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Clinical Neurology

El Paso, TX. Chiropractor, Dr. Alexander Jimenez discusses clinical neurology. Dr. Jimenez provides an advanced understanding of the systematic investigation of common and complex neurological complaints including headache, dizziness, weakness, numbness, and ataxia. The focus will be on the pathophysiology, symptomatology, and management of pain in relation to headache and other neurologic conditions, with the capacity to distinguish serious from benign pain syndromes.

Our clinical focus and personal goals are to help your body heal itself naturally in a quick and effective manner.  At times, it may seem like a long path; nevertheless, with our commitment to you, it’s a sure to be an exciting journey. The commitment to you in health is to, never loose our deep connection to each one of our patients in this journey.

When your body is truly healthy, you will arrive at your optimal fitness level proper physiological fitness state.  We want to help you live a new and improved lifestyle. Over the last 2 decades while researching and testing methods with thousands of patients we have learned what works effectively at decreasing pain while increasing human vitality. For Answers to any questions you may have please call Dr. Jimenez at 915-850-0900.


Seizures, Epilepsy And Chiropractic

Seizures, Epilepsy And Chiropractic

El Paso, TX. Chiropractor, Dr. Alexander Jimenez takes a look at seizures, epilepsy and treatment options.
Seizures are defined as, abnormal movements or behavior from unusual electrical activity in the brain. Seizures are a symptom of epilepsy but not all who have seizures have epilepsy. As there is a group of related disorders characterized by recurrent seizures. Epilepsy is a group of disorders that are related and characterized by recurrent seizures. There are different types of epilepsy and seizures. There are medications for epilepsy that are prescribed to control seizures, and surgery is rarely needed if medication is ineffective.

Seizures & Epilepsy

  • Seizures occur when there is spontaneous depolarization and synchronized firing of groups of neurons, often in response to a trigger such as metabolic compromise
  • Any brain can have a seizure if the conditions are right
  • Epilepsy or seizure disorder, is the pathologically increased likelihood of seizure activity occurring in a persons brain

Seizure Categories

  • General/Global onset seizures

  • Generalized motor seizure (Grand mal)
  • Absence seizure (Petite mal)
  • Focal onset seizures

  • Simple partial seizure
  • Motor cortex (Jacksonian)
  • Sensory cortex
  • Somatosensory
  • Auditory-vestibular
  • Visual
  • Olfactory-gustatory (uncinate)
  • Complex partial seizure (libmbic)
  • Continuous/Ongoing seizures

  • Generalized (status epilepticus)
  • Focal (epilepticus partialis continua)

Generalized Motor Seizure

  • Electrical depolarization of neurons in the entire cerebral cortex simultaneously
  • Trigger assumed to be outside of the cerebral cortex, such as in thalamus or brainstem
  • Episodes begin with loss of consciousness followed by tonic contraction (extension)
  • Respiration is halted, and hair is expelled past the closed glottis (“cry”)
  • Elevated blood pressure, dilated pupils
  • Intermittent contraction and relaxation (clonic activity)
  • Usually lasts a few minutes, but for some patients can last hours or even days (status epilepticus)
  • Generally begin in childhood

Tonic Clonic Seizure

seizures epilepsy chiropractic el paso tx.http://nanfoundation.org/neurologic-disorders/epilepsy/what-is-epilepsy

My Tonic Clonic/Grand Mal Seizure

Seizure Triggers

  • Ionic abnormalities (Na, K, Ca, Mg, BUN, pH)
  • Sedative withdrawal in addicts (alcohol, barbiturates, benzodiazepines)
  • Hypoglycemia
  • Hypoxia
  • Hyperthermia (especially patients under 4 years old)
  • Toxin exposure
  • Genetic abnormal sensitivity of neurons (rarely)

EEG Of Grand Mal Seizure

  • Tonic phase
  • Clonic phase
  • Postictal phase

seizures epilepsy chiropractic el paso tx.

Swenson, R. Epilepsy. 2010

Absence (Petit Mal) Seizures

  • Most often occur in children
  • Originate in the upper brainstem
  • Often look like losing train of thought or staring off into space
  • These children may go on to develop focal seizures later in life
  • Spontaneous remission possible as neurons mature

Absence Seizure Caught On Camera

EEG Of Petit Mal Seizure

  • 3 spike-waves/second
  • Can be elicited by hyperventilation
  • Spike = excitation
  • Wave = inhibition

seizures epilepsy chiropractic el paso tx.

Swenson, R. Epilepsy. 2010

Simple Focal/Partial Seizures

  • May be with or without secondary generalization
  • Patient generally retains consciousness
  • Begin in a localized primary functional area of the cortex
  • Different symptoms and classifications depending on where in the brain the epileptiform activity originates
  • Sensory areas usually produce positive phenomenon (seeing lights, smelling something, etc, as opposed to lack of sensation)
  • Motor areas may produce positive or negative symptomology
  • Function of area of involvement may be reduced during the postictal phase
  • If the primary motor cortex is involved = “Todd paralysis

Partial (Focal Seizure) 12 Yr Old Boy

Partial Seizure In The Motor Cortex

  • May begin as a jerking of one body area, on the side contralateral to the epileptiform activity, but may spread through the body in a homuncular pattern (Jacksonian seizure/march)

seizures epilepsy chiropractic el paso tx.

https://www.maxplanckflorida.org/fitzpatricklab/homunculus/science/

Partial Seizure In The Somatosensory Cortex

Produces paresthesia on the contralateral side to the epileptiform activity and can also spread in a homuncular pattern (march) similar to the motor type

seizures epilepsy chiropractic el paso tx.https://en.wikipedia.org/wiki/Cortical_homunculus

Partial Seizure In The Auditory – Vestibular Area

  • Posterior temporal region involvement
  • May produce tinnitus and/or vertigo
  • Audiometry will be normal

Partial Seizure In The Visual Cortex

  • May produce hallucinations in the contralateral visual field
  • Visual cortex (calcarine cortex) produced flashes, spots, and/or zig-zags of light
  • Visual association cortex produces more complete hallucinations such as floating balloons, stars, and polygons

Partial Seizure In The Olfactory – Gustatory Cortex

  • May produce olfactory hallucinations
  • Likely area to spread to more generalized seizure

Complex Partial Seizures

  • Involves the association cortices of the frontal, temporal or parietal lobes
  • Similar to simple partial seizures but there may be more confusion/reduced consciousness
  • Limbic Cortex (hippocampus, parahippocampal temporal cortex, retro-splenial-cingulate-subcallosal cortex, orbito- frontal cortex, and insula) is the most susceptible to metabolic injury
  • Therefore this is the most common type of epilepsy

  • May produce visceral and affective symptoms (most likely), peculiar and unpleasant smells and tastes, bizarre abdominal sensations, fear, anxiety, rarely rage, and excessive sexual appetite, visceral and behavioral phenomena such as sniffing, chewing, lip smacking, salivation, excessive bowel sounds, belching, penile erection, feeding, or running

Clips Of Different Seizures In Same Child

Continuous/Ongoing Seizures

  • 2 Types

  • Generalized (status epilepticus)

  • Focal (epilepticus partialis continua)

  • Continuous or recurrent seizures over a 30-minute period without return to normal over the period
  • Prolonged seizure activity or multiple seizures occurring close together without full recovery in between
  • Most often seen as the result of acute sensation of anticonvulsive medications due to rebound hyperexcitability
  • Emotional excess, fever, or other hypermetabolic states, hypoglycemia, hypocalcemia, hypomagnesemia, hypoxemia, toxic states (e.g., tetanus, uremia, exogenous, excitatory agents such as amphetamine, aminophyline, lidocaine, penicillin) and sedative withdrawal may also predispose to ongoing seizure

Status Epilepticus

  • Ongoing grand mal seizure is a medical emergency because it may result in brain damage or death if prolonged seizure is not stopped
  • Elevated temperature due to sustained muscle activity, hypoxia due to inadequate ventilation and severe lactic acidosis can damage neurons
  • Death can result from shock and overtaxation of cardiopulmonary

Epilepsia Partialis Continua

  • Less life threatening than status epilepticus, but seizure activity must be terminated as it may progress to generalized seizure form if allowed to go on for prolonged periods
  • May be a result of neoplasm, ischemia-infarction, stimulant toxicity or hyperglycemia

Treatment Of Seizures

  • If the seizures are the result of an underlying condition, such as infection, disorders of fluid and electrolyte balance, exogenous and endogenous toxicities, or renal failure, treatment of the underlying condition should ameliorate seizure activity
  • Most antiepileptic medications treat multiple seizure types – not perfect though
  • Some are slightly more effective (phenytoin, carbamazepine, valproic acid and phenobarbital)
  • There are those that have fewer side effects (gabapentin, lamotrigine and topiramate)
  • Certain medications only treat one seizure type (such as ethosuximide for absence seizures)

Sources

Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
Swenson, R. Epilepsy. 2010.

Childhood Neurodevelopmental Disorders

Childhood Neurodevelopmental Disorders

El Paso, TX. Chiropractor, Dr. Alexander Jimenez looks at childhood developmental disorders, along with their symptoms, causes and treatment.

Cerebral Palsy

  • 4 Types
  • Spastic Cerebral Palsy
  • ~80% of CP cases
  • Dyskinetic Cerebral Palsy (also includes athetoid, choreoathetoid, and dystonic cerebral palsies)
  • Ataxic Cerebral Palsy
  • Mixed Cerebral Palsy

Autism Spectrum Disorder

  • Autistic Disorder
  • Asperger’s Disorder
  • Pervasive Developmental Disorder–Not Otherwise Specified (PDD-NOS)
  • Childhood Disintegrative Disorder (CDD)

Autism Spectrum Disorder Red Flags

  • Social Communication
  • Limited use of gestures
  • Delayed speech or lack of babble
  • Odd sounds or unusual tone of voice
  • Difficulty making eye contact, gestures and words at the same time
  • Little imitation of others
  • No longer uses words they used to use
  • Uses another person’s hand as a tool
  • Social Interaction
  • Difficulty making eye contact
  • Lack of joyful expression
  • Lack of responsiveness to name
  • Does not try to show you things they’re interested in
  • Repetitive Behaviors & Restricted Interests
  • Unusual way of moving their hands, fingers or body
  • Develops rituals, such as lining up objects or repeating things
  • Focuses on unusual objects
  • Excessive interest in a particular object or activity which interferes with social interaction
  • Unusual sensory interests
  • Under or over reaction to sensory input

ASD Diagnostic Criteria (DSM-5)

  • Persistent deficits in social communication and social interaction across multiple contexts, as manifested by the following, currently or by history (examples are illustrative, not exhaustive; see text):
  • Deficits in social-emotional reciprocity, ranging, for example, from abnormal social approach and failure of normal back-and-forth conversation; to reduced sharing of interests, emotions, or affect; to failure to initiate or respond to social interactions.
  • Deficits in nonverbal communicative behaviors used for social interaction, ranging, for example, from poorly integrated verbal and nonverbal communication; to abnormalities in eye contact and body language or deficits in understanding and use of gestures; to a total lack of facial expressions and nonverbal communication.
  • Deficits in developing, maintaining, and understand relationships, ranging, for example, from difficulties adjusting behavior to suit various social contexts; to difficulties in sharing imaginative play or in making friends; to absence of interest in peers.

ASD Diagnostic Criteria

  • Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least two of the following, currently or by history (examples are illustrative, not exhaustive; see text):
  • Stereotyped or repetitive motor movements, use of objects, or speech (e.g., simple motor stereotypes, lining up toys or flipping objects, echolalia, idiosyncratic phrases).
  • Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behavior (e.g., extreme distress at small changes, difficulties with transitions, rigid thinking patterns, greeting rituals, need to take same route or eat same food every day).
  • Highly restricted, fixated interests that are abnormal in intensity or focus (e.g., strong attachment to or preoccupation with unusual objects, excessively circumscribed or perseverative interests).
  • Hyper – or Hyporeactivity to sensory input or unusual interest in sensory aspects of the environment (e.g. apparent indifference to pain/temperature, adverse response to specific sounds or textures, excessive smelling or touching of objects, visual fascination with lights or movement).

ASD Diagnostic Criteria

  • Symptoms must be present in the early developmental period (but may not become fully manifest until social demands exceed limited capacities, or may be masked by learned strategies in later life).
  • Symptoms cause clinically significant impairment in social, occupational, or other important areas of current functioning.
  • These disturbances are not better explained by intellectual disability (intellectual developmental disorder) or global developmental delay. Intellectual disability and autism spectrum disorder frequently co-occur; to make comorbid diagnoses of autism spectrum disorder and intellectual disability, social communication should be below that expected for general developmental level.

ASD Diagnostic Criteria (ICD- 10)

A. Abnormal or impaired development is evident before the age of 3 years in at least one of the following areas:
  • Receptive or expressive language as used in social communication;
  • The development of selective social attachments or of reciprocal social interaction;
  • Functional or symbolic play.
B. A total of at least six symptoms from (1), (2) and (3) must be present, with at least two from (1) and at least one from each of (2) and (3)
1. Qualitative impairment in social interaction are manifest in at least two of the following areas:

a. failure adequately to use eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction;

b. failure to develop (in a manner appropriate to mental age, and despite ample opportunities) peer relationships that involve a mutual sharing of interests, activities and emotions;

c. lack of socio-emotional reciprocity as shown by an impaired or deviant response to other people’s emotions; or lack of modulation of behavior according to
social context; or a weak integration of social, emotional, and communicative behaviors;

d. lack of spontaneous seeking to share enjoyment, interests, or achievements with other people (e.g. a lack of showing, bringing, or pointing out to other people objects of interest to the individual).

2. Qualitative abnormalities in communication as manifest in at least one of the following areas:

a. delay in or total lack of, development of spoken language that is not accompanied by an attempt to compensate through the use of gestures or mime as an alternative mode of communication (often preceded by a lack of communicative babbling);

b. relative failure to initiate or sustain conversational interchange (at whatever level of language skill is present), in which there is reciprocal responsiveness to the communications of the other person;

c. stereotyped and repetitive use of language or idiosyncratic use of words or phrases;

d. lack of varied spontaneous make-believe play or (when young) social imitative play

3. Restricted, repetitive, and stereotyped patterns of behavior, interests, and activities are manifested in at least one of the following:

a. An encompassing preoccupation with one or more stereotyped and restricted patterns of interest that are abnormal in content or focus; or one or more interests that are abnormal in their intensity and circumscribed nature though not in their content or focus;

b. Apparently compulsive adherence to specific, nonfunctional routines or rituals;

c. Stereotyped and repetitive motor mannerisms that involve either hand or finger flapping or twisting or complex whole body movements;

d. Preoccupations with part-objects of non-functional elements of play materials (such as their oder, the feel of their surface, or the noise or vibration they
generate).

C. The clinical picture is not attributable to the other varieties of pervasive developmental disorders; specific development disorder of receptive language (F80.2) with secondary socio-emotional problems, reactive attachment disorder (F94.1) or disinhibited attachment disorder (F94.2); mental retardation (F70-F72) with some associated emotional or behavioral disorders; schizophrenia (F20.-) of unusually early onset; and Rett’s Syndrome (F84.12).

Asperger’s Syndrome Diagnostic Criteria (ICD-10)

  • A. Qualitative impairment in social interaction, as manifested by at least two of the following:
  • marked impairments in the use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction.
  • failure to develop peer relationships appropriate to developmental level.
  • a lack of spontaneous seeking to share enjoyment, interests, or achievements with other people (e.g. by a lack of showing, bringing, or pointing out objects of interest to other people).
  • lack of social or emotional reciprocity.
  • B. Restricted repetitive and stereotyped patterns of behavior, interests, and activities, as manifested by at least one of the following:
  • encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus.
  • apparently inflexible adherence to specific, nonfunctional routines or rituals.
  • stereotyped and repetitive motor mannerisms (e.g., hand or finger flapping or twisting, or complex whole-body movements).
  • persistent preoccupation with parts of objects.
    C. The disturbance causes clinically significant impairment in social, occupational, or other important areas of functioning
    D. There is no clinically significant general delay in language (e.g., single words used by age 2 years, communicative phrases used by age 3 years).
    E. There is no clinically significant delay in cognitive development or in the development of age-appropriate self- help skills, adaptive behavior (other than social interaction), and curiosity about the environment in childhood.
    F. Criteria are not met for another specific Pervasive Developmental Disorder or Schizophrenia.

Attention-Deficit/Hyperactivity Disorder (ADHD)

  • Inattention – gets off task easily
  • Hyperactivity – seems to move about constantly
  • Impulsivity – makes hasty actions that occur in the moment without first thinking about them

ADHD Risk Factors

  • Genetics
  • Cigarette smoking, alcohol use, or drug use during pregnancy
  • Exposure to environmental toxins during pregnancy
  • Exposure to environmental toxins, such as high levels of lead, at a young age
  • Low birth weight
  • Brain injuries

Developmental Screening

childhood neurodevelopmental disorders el paso tx.

https://www.cdc.gov/ncbddd/autism/hcp- screening.html

Primitive Reflexes

  • Moro
  • Spinal Galant
  • Asymmetrical Tonic Neck Reflex
  • Symetrical Tonic Neck Reflex
  • Tonic Labrynthine Reflex
  • Palmomental Reflex
  • Snout Reflex

Treatment Of Developmental Delays

  • Remediate any retained reflexes
  • Educate parents on providing a structured environment
  • Promote brain balancing activities
  • Address food sensitivities and remove likely problematic foods
  • Treat the patient’s gut – probiotics, glutamine, etc.

Pediatric Acute-Onset Neuropsychiatric Syndrome

(PANS)

  • Abrupt dramatic onset of OCD or severely restricted food intake
  • Symptoms are not better explained by a known neurologic or medical disorder
  • Also at least two of the following:
  • Anxiety
  • Emotional lability and/or depression
  • Irritability, aggression and/or severely oppositional behaviors
  • Behavioral/Developmental regression
  • Deterioration in school performance
  • Sensory or motor abnormalities
  • Somatic signs including sleep disturbances, enuresis or urinary frequency
  • *The onset of PANS may start with infectious agents other than strep. It also includes onset from environmental triggers or immune dysfunction

Pediatric Autoimmune Disorders Associated With Streptococcus

(PANDAS)

  • Presence of significant obsessions, compulsions and/or tics
  • Abrupt onset of symptoms or a relapsing-remitting course of symptom severity
  • Pre-pubertal onset
  • Association with streptococcal infection
  • Association with other neuropsychiatric symptoms (including any of the PANS “accompanying” symptoms)

PANS/PANDAS Tests

  • Swab/Strep culture
  • Blood tests for strep
  • Strep ASO
  • Anti-DNase B Titer
  • Streptozyme
  • Test for other infectious agents
  • MRI preferred but PET can be used if necessary
  • EEG

False Negatives

  • Not all children who have strep have elevated labs
  • Only 54% of children with strep showed a significant increase in ASO.
  • Only 45% showed an increase in anti–DNase B.
  • Only 63% showed an increase in either ASO and/or anti–DNase B.

Treatment Of PANS/PANDAS

  • Antibiotics
  • IVIG
  • Plasmaphoresis
  • Anti-Inflammatory protocols
  • Steroid medications
  • Omega-3’s
  • NSAIDS
  • Probiotics

Injury Medical Clinic: Chiropractor (Recommended)

Sources

  1. “Attention Deficit Hyperactivity Disorder.” National Institute of Mental Health, U.S. Department of Health and Human Services, www.nimh.nih.gov/health/topics/attention-deficit-hyperactivity-disorder-adhd/index.shtml.
  2. Autism Navigator, www.autismnavigator.com/.
    “Autism Spectrum Disorder (ASD).” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 29 May 2018, www.cdc.gov/ncbddd/autism/index.html.
  3. “Introduction to Autism.” Interactive Autism Network, iancommunity.org/introduction-autism.
  4. Shet, Anita, et al. “Immune Response to Group A Streptococcal C5a Peptidase in Children: Implications for Vaccine Development.” The Journal of Infectious Diseases, vol. 188, no. 6, 2003, pp. 809–817., doi:10.1086/377700.
  5. “What Is PANDAS?” PANDAS Network, www.pandasnetwork.org/understanding-pandaspans/what-is-pandas/.
Degenerative And Demyelinating Diseases Of The Nervous System

Degenerative And Demyelinating Diseases Of The Nervous System

El Paso, TX. Chiropractor, Dr. Alexander Jimenez focuses on degenerative and demyelinating diseases of the nervous system, their symptoms, causes and treatment.

Degenerative & Demyelinating Diseases

Motor Neuron Diseases

  • Motor weakness without sensory changes
  • Amyotrophic lateral sclerosis (ALS)
  • ALS Variants
  • Primary lateral sclerosis
  • Progressive bulbar palsy
  • Inherited conditions that cause anterior horn cell degeneration
  • Werdnig-Hoffmann disease in infants
  • Kugelberg-Welander disease in children and young adults

Amyotrophic Lateral Sclerosis (ALS)

  • Affects patients 40-60 years of age
  • Damage to:
  • Anterior horn cells
  • Cranial nerve motor nuclei
  • Corticobulbar and corticospinal tracts
  • Lower motor neuron findings (atrophy, fasciculations) AND upper motor neuron findings (spasticity, hyperreflexia)
  • Survival ~three years
  • Death results from weakness of the bulbar and respiratory musculature and resultant superimposed infection

ALS Variants

  • Usually eventually evolve into typical ALS pattern
  • Primary Lateral Sclerosis
  • Upper motor neuron signs begin first, but patients do eventually have lower motor neuron signs as well
  • Survival can be ten years or longer
  • Progressive Bulbar Palsy
  • Selectively involves the head and neck musculature

Inherited Motor Neuron Conditions

degenerative diseases el paso tx.Church, Archibald. Nervous and Mental Diseases. W.B. Saunders Co., 1923.

Alzheimer Disease

  • Characterized by neurofibrillary tangles (aggregates of hyperphosphorylated tau protein) & beta-amyloid plaques
  • Generally occurring after age 65
  • Hereditary risk factors
  • Mutations in the beta amyloid gene
  • Epsilon 4 version of apolipoprotein

Diagnosis

  • Pathologic diagnosis is the only way to definitively diagnose the condition
  • Imaging may be able to rule out other causes of dementia
  • Functional imaging studies may be further developed to become diagnostically useful in the future
  • CSF studies examining for tau proteins and beta amyloid may become useful as diagnostic tests in the future

Amyloid Plaques & Neurofibrillary Tangles

degenerative diseases el paso tx.http://sage.buckinstitute.org/wp-content/uploads/2015/01/plaque-tanglesRNO.jpg

Brain Areas Affected by Alzheimer Disease

  • Hippocampus
  • Loss of recent memory
  • Posterior temporo-parietal association area
  • Mild anomia & constructional apraxia
  • Nucleus basalis of Meynert (cholinergic neurons)
  • Changes in visual perception

Progression

  • As more and more cortical areas become involved, the patient will develop more severe cognitive deficits, however paresis, sensory loss, or visual field defects are features.

Treatment Options

  • Medications that inhibit central nervous system acetylcholinesterase
  • Donepezil
  • Galantamine
  • Rivastigmine
  • Aerobic Exercise, 30 minutes daily
  • PT/OT care to maintain activities of daily living
  • Antioxidant and anti-inflammatory therapies
  • In advanced stages, may require full time, in home care

Vascular Dementia

  • Cerebral arteriosclerosis leading to stroke
  • Patient will have documented stroke history or signs of prior stroke (spasticity, paresis, pseudobulbar palsies, aphasia)
  • May be associated with Alzheimer Disease if due to amyloid angiopathy

Frontotemporal Dementia (Pick’s Disease)

  • Familial
  • Affects the frontal and temporal lobes
  • May be seen on imaging if advanced degeneration in these areas
  • Symptoms
  • Apathy
  • Disordered behavior
  • Agitation
  • Socially inappropriate behavior
  • Impulsivity
  • Language difficulties
  • Generally no memory or spatial difficulties
  • Pathology reveals Pick bodies within the neurons
  • Results in death in 2-10 years

Pick Bodies/Cytoplasmic Inclusions

degenerative diseases el paso tx.http://slideplayer.com/9467158/29/images/57/Pick+bodies+Silver+stain+Immunohistochemistry+for+Tau+protein.jpg

Treatment

  • Antidepressants
  • Sertraline
  • Citalopram
  • Discontinue medications that can cause memory impairment or confusion
  • Sedatives
  • Benzodiazepines
  • Exercise
  • Lifestyle modification
  • Behavioral modification therapy

Parkinson Disease

  • May occur at any age, but rare before age 30, and increases prevalence increases in older populations
  • Familial tendency but can also without family history
  • Can be induced by certain environmental factors
  • Exposure 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)
  • Compounds which produce excessive free radicals
  • Affects substantia nigra pars compacta
  • Dopaminergic neurons
  • On pathology, the presence of Lewy Bodies
  • Accumulation of alpha-synuclein

Lewy Bodies

degenerative diseases el paso tx.https://scienceofpd.files.wordpress.com/2017/05/9-lb2.jpg

Symptoms of Parkinsonism

  • Rigidity (all planes)
  • Passive ROM
  • Active movement
  • May be of cogwheel nature due to tremor symptoms
  • Bradykinesia
  • Slowness of movement
  • Inability to initiate movement
  • Freezing
  • Resting tremor (“pill-rolling”)
  • Created by oscillation of opposing muscle groups
  • Postural defects
  • Anteriorly flexed (stooped) posture
  • Inability to compensate for perturbations, resulting in retropulsion
  • Mask-like facies
  • Mild to moderate dementia
  • Later in progression, due to lewy body accumulation

Pathology

  • Deficiency of dopamine in the striatum (caudate and putamen) of the basal ganglia
  • Dopamine normally has the effect of stimulating the direct circuit through the basal ganglia, while inhibiting the indirect pathway

Carbidopa/Levodopa

  • Most common treatment is a combination drug

  • Levodopa
  • A dopamine precursor that crosses the blood-brain barrier
  • Carbidopa
  • Dopamine decarboxylase inhibitor that does not cross the BBB
  • Amino acids will reduce effectiveness (competition) and so medication should be taken away from protein

Prolonged Treatment With Carbidopa/Levodopa

  • The patient’s capacity to store dopamine declines with medication use and therefore the improvements from the medications will last for shorter and shorter periods the longer the medication is used
  • Over time can result in proliferation of dopamine receptors
  • Peak-dose dyskinesia
  • Long term use puts stress on the liver
  • Other side effects can include nausea, hypotension and hallucinations

Other Treatment Options

  • Medications
  • Anticholinergics
  • Dopamine agonists
  • Dopanime breakdown inhibitors (Monoamine oxidase or catechol-O-methyl transferase inhibitors)
  • High dose glutathione
  • Brain balancing functional neuro-rehab exercises
  • Vibration
  • Retropulsive stimulation
  • Repeated reflex stimulation
  • Targeted CMT/OMT

Multiple System Atrophy

  • Symptoms of Parkinson Disease paired with one or more of the following:
  • Pyramidal signs (Striatonigral degeneration)
  • Autonomic dysfunction (ShyDrager syndrome)
  • Cerebellar finding (Olivopontocerebellar atrophy)
  • Generally not responsive to standard Parkinson Disease treatments

Progressive Supranuclear Palsy

  • Fast progressing degeneration involving tau proteins in many areas including the rostral midbrain
  • Symptoms usually start around ages 50-60
  • Gait difficulty
  • Significant dysarthria
  • Voluntary vertical gaze difficulty
  • Retrocollis (dystonic extension of the neck)
  • Severe dysphagia
  • Emotional lability
  • Personality changes
  • Cognitive difficulty
  • Does not respond well to standard PD treatment

Diffuse Lewy Body Disease

  • Progressive dementia
  • Severe hallucinations and possible paranoid delusions
  • Confusion
  • Parkinsonian symptoms

Multiple Sclerosis

  • Multiple white matter lesions (plaques of demyelination) in the CNS
  • Variable in size
  • Well-circumscribed
  • Visible on MRI
  • Optic nerve lesions are common
  • Peripheral nerves are not involved
  • Uncommon in children under 10, but usually presents before age 55
  • Viral infection may trigger an inappropriate immune response with antibodies to a common virus-myelin antigen
  • Infectious and immune mechanisms contribute

Types Of MS

  • Primary progressive MS (PPMS)
  • Secondary progressive MS (SPMS)
  • Relapsingremitting multiple sclerasis (RRMS)
  • Most common type
  • Can develop acutely, spontaneous appear to resolve and return
  • Eventually becomes like SPMS

Optic Nerve Involvement

  • In 40% of MS cases
  • Pain with eye movements
  • Visual field defect (central or paracentral scotoma)
  • Funduscopic examination
  • May reveal papilledema if the plaque involves the optic disk
  • May not appear unusual if plaques are behind the optic disk (retrobulbar neuritis)

Medial Longitudinal Fasciculus Involvement

  • Demyelination of the MLF results in internuclear ophthalmoplegia
  • During lateral gaze there is paresis of the medial rectus and nystagmus of the contralateral eye
  • Convergence remains normal

Other Possible MS Symptoms

  • Myelopathy
  • Spastic hemiparesis
  • Impaired sensory tracts (DC-ML)
  • Paresthesias
  • Cerebellar involvement
  • Ataxia
  • Dysarthria
  • Vestibular system involvement
  • Imbalance
  • Mild vertigo
  • Nystagmus
  • Tic douloureux (trigeminal neuralgia)
  • Lhermitte’s symptom
  • Shooting or tingling sensation referred to the trunk and limbs during neck flexion
  • Fatigue
  • Hot bath often exacerbates symptoms

Differentials To Consider

  • Multiple emboli and vasculitis
  • May appear as white matter damage on MRI
  • Central nervous system sarcoidosis
  • Can produce reversible optic neuritis and other CNS signs
  • Whipple disease
  • Inflammatory lesions
  • Usual eye movements
  • Vitamin B12 deficiency
  • Dementia
  • Spasticity
  • Dorsal column
  • Meningovascular syphilis
  • Multifocal CNS damage
  • CNS Lyme disease
  • Multifocal disease

Differential Diagnosis: Diagnostic Studies

  • Blood tests can help to distinguish
  • Complete blood count
  • Antinuclear antibodies (ANA)
  • Serum test for syphilis (RPR, VDRL, etc.)
  • Fluorescent treponemal antibody test
  • Lyme titer
  • ESR
  • Angiotensin converting enzyme level (to r/o sarcoidosis)

Diagnostic Studies Of MS

  • MRI with and without contrast
  • 90% of MS cases have detectable MRI findings
  • CSF findings
  • Elevation of mononuclear white blood cells
  • Oligoclonal IgG bands
  • Increased globulin to albumin ratio
  • This is also seen in 90% of MS cases
  • Increased myelin basic protein levels

Prognosis

  • Average survival after diagnosis is ~ 15 to 20 year
  • Death is usually from superimposed infection and not due to the effects of the disease itself

Sources

Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
Swenson, R. Degenerative Diseases of the Nervous System. 2010.

Cerebrovascular Disorders

Cerebrovascular Disorders

Cerebrovascular disease is a designated group of conditions that can lead to cerebrovascular event/s, i.e. stroke. These events affect the blood supply and vessels to the brain. With a blockage, malformation, or hemorrhage happens, this prevents brain cells from getting enough oxygen, which can cause brain damage. Cerebrovascular diseases can develop in different ways. These include deep vein thrombosis (DVT) and atherosclerosis.

Types of cerebrovascular disease: Stroke, transient ischemic attack, aneurysms, and vascular malformations

In the U.S. cerebrovascular disease is the fifth most common cause of death.

Cerebrovascular Disorders

The Brain

  • Makes up ~2% of the body weight
  • Accounts for ~10% of the body’s oxygen use
  • Accounts for ~20% of the body’s glucose use
  • Receives ~20% of the cardiac output
  • Per minute, requires ~50-80cc of blood per 100g of grey matter brain tissue and ~17-40cc of blood per 100g of white matter
  • If blood supply to the brain is <15cc per 100g of tissue, per minute, neurologic dysfunction occurs
  • As with all tissues, the longer there is ischemia, the more likely there is to be cell death and necrosis
  • The brain depends on a constant, uninterrupted supply of oxygen and glucose
  • 3-8 minutes of cardiac arrest can result in irreversible brain damage!

cerebrovascular el paso tx.

Autoregulation In The Brain

  • Systemic hypotension causes reactive cerebral vasodilation to allow more blood flow to the brain
  • The brain can extract enough oxygen from the brain if systolic pressure is 50 mmHg
  • Atherosclerotic narrowing can produce reactive vasodilation to attempt to reduce excess pressure
  • Increased blood pressure can result in vasoconstriction, reducing likelihood of hemorrhage
  • If systolic pressure averages >150 mmHg for prolonged periods, this compensation may fail
  • Labelled hypertensive encephalopathy

Blood Supply To The Head

cerebrovascular el paso tx.http://madeinkibera.com/lingual-arterie-anatomie

Collateral Circulation

  • In slowly developing occlusion such as atherosclerotic thrombosis, collateral circulation has time to develop
  • Circle of Willis connects the carotid and basilar systems
  • Anterior and posterior communicating arteries provide collateral supply
  • Anastomoses between main cerebral and cerebellar arteries in some people
  • Internal and external carotid artery connection via the ophthalmic & maxillary arteries

Circle Of Willis

  • Connects the vertebrobasilar system with the internal carotid system
  • While providing helpful collateral circulation, is also the most susceptible area to Berry Aneurysms which can lead to hemorrhagic stroke

cerebrovascular el paso tx.https://en.wikipedia.org/wiki/Circle_of_Willis

Blood Supply To The Brain

cerebrovascular el paso tx.http://teachmeanatomy.info/neuro/vessels/arterial-supply/

Maxillary & Ophthalmic aa.

cerebrovascular el paso tx.

cerebrovascular el paso tx.

Cerebrovascular Disorders

  • ~700,000 adults in the US have a stroke each year
  • Third most common cause of death in the US
  • ~2 million people are disabled due to stroke
  • By far more common in persons of advanced age
  • Occlusive/Ischemic Disease
  • 80% of all strokes
  • Most common site of occlusion is at the internal carotid artery just above the bifurcation of the common carotid a.
  • Atherothrombotic
  • Embolic
  • Small vessel
  • Hemorrhagic Disease

Occlusive/Ischemic Stroke

  • Can be due to artery OR vein occlusion
  • Artery occlusion is much more common
  • Due to lack of blood & oxygen supply reaching a particular area of the brain
  • Sudden onset of neurologic deficits, correlating to the distribution of a specific artery
  • Deficits will differ depend on which artery’s distribution has been disrupted

Venous Occlusion

  • Hyperviscocity
  • Dehydration
  • Thombocytosis
  • Elevated red or white blood cells counts
  • Polycythemia
  • Hypercoagulability
  • Elevated homocysteine
  • Prolonged immobility or airplane travel
  • Genetic clotting factor disorders
  • Pregnancy
  • Cancer
  • Hormone replacement & OCP use

Atherothrombotic

  • Neurologic deficits may be transient or develop slowly over time
  • Possible causes/types:
  • Dissection of the tunica intima and tunica adventitia
  • Can occur in younger patients with connective tissue disorders
  • Inflammatory materials deposit & build up in the vessel walls
  • Oxidized LDLs deposit in vessel walls

Embolic

  • Neurologic deficits likely to have sudden onset
  • Dislodged tissue from dissection of the tunica intima and tunica adventitia
  • Any dislodged thrombus can become an embolus blocking/closing the lumen of smaller vessels

Small Vessel

  • Lipohyalinosis
  • Vessel wall micro-trauma & ballooning
  • Amyloid Angiopathy
  • Accumulation of amyloid proteins in vessel walls
  • More common in patients >65 years old
  • Causes narrowing (leading to ischemia) but can also cause vessel fragility (leading to hemorrhage)
  • Associated with Alzheimer’s disease
  • Inflammatory
  • Spasmotic

Risk Factors For Occlusive Stroke

  • Hypertension
  • Diabetes Mellitus
  • Cardiac abnormalities
  • Right-left shunts (Patent foramen ovale, VSD, tetralogy of fallot, etc)
  • Atrial fibrillation
  • Valve disease/artificial heart valves
  • Advanced age
  • Obesity
  • Hyperlipidemia
  • Especially high LDL and low HDL
  • Sedentary lifestyle
  • Cigarette/Tobacco smoking
  • High oxidation status
  • Elevated homocysteine
  • Contributed to by low folic acid, B6 & B12 statuses
  • Interacts with LDL cholesterol
  • Hyperviscocity and hypercoagulability states as shown on previous slide

Transient Ischemic Attack (TIA)

  • Fully reversible episodes of neurologic deficit due to vascular insufficiency generally lasting no more than 30 minutes at a time
  • Occasionally can last 24 hours or more
  • Half of patients who suffer from a complete occlusive stroke previously had transient ischemic attack(s)
  • 20-40% of patients with TIA go on to have complete stroke
  • In is important to identify patients with TIAs to that they can be appropriately managed and modifiable risk factors reduced

History of Transient Neurologic Deficit In Patient > 45 y/o

  • DDx
  • TIA most likely dx
  • Migraine
  • Focal seizures
  • BPPV
  • Meniere’s
  • Demyelinating diseases
  • Temporal arteritis
  • Hypoglycemia
  • Tumor
  • Arteriovenous malformations

Carotid Artery Disease

  • High pitched systolic bruit heard over the carotid artery may indicate carotid stenosis
  • Requires duplex ultrasound evaluation
  • Lesions narrowing the lumen >70% can possibly cause ischemia
  • Many carotid occlusions do not cause ischemia due to slow development allowing for collateral circulation to be developed as well
  • Fast forming occlusions or emboli can produce problems with <70% stenosis
  • Surgical intervention should be considered for patients with >70% stenosis and symptoms of TIA

Occlusive Stroke

  • If there is an onset of definitive substantial neurologic deficit, the patient should have a CT to rule out hemorrhage
  • If hemorrhage is ruled out, tissue plasminogen activator should be given within the first 4.5 hours
  • It should not be given later than this because it can increase risk of bleeding during reperfusion of brain tissue
  • After this initial period, focused thrombolysis or mechanical extraction of the embolus

Intracranial Hemorrhage

  • Approximately 20% of stroke cases
  • Severe HA or vomiting suggest hemorrhage over occlusion
  • Two types
  • Spontaneous intracranial hemorrhage
  • Hypertension
  • Arterial aneurysms
  • Arteriovenous malformations
  • Bleeding disorders
  • Vessel weakening due to amyloid angiopathy
  • Traumatic

Aneurysm Sites

  • Intraparenchymal hemorrhage
  • 50% – Lenticulostriate branches of the middle cerebral artery
  • Affects the putamen and external capsule
  • 10% – Penetrating branches of the posterior cerebral artery
  • Affects the thalamus
  • 10% – Penetrating branches of the superior cerebellar artery
  • Affects the cerebellum
  • 10% – Paramedian branches of the basilar artery
  • Affects the basilar pons
  • 20% – Various vessels affecting areas of white matter
  • Subarachnoid hemorrhage
  • Berry aneurysms at communicating artery junctions

Bleeding Disorders

  • Thrombocytopenia
  • Leukemia
  • Excess anticoagulant therapies

Risk Factors For Hemorrhagic Stroke

  • Hypertension
  • Arterial aneurysms
  • Arteriovenous malformations
  • Bleeding disorders
  • Vessel weakening due to amyloid angiopathy
  • Head trauma

Signs Of Stroke: Teach Patients F.A.S.T

cerebrovascular el paso tx.http://chrcsf.org/expert-tips-to-help-with-detecting-the-early-signs-of-stroke/

Common Transient Symptoms

  • Vertigo
  • Bilateral blurring or loss of vision
  • Ataxia
  • Diplopia
  • Bilateral or unilateral sensory and motor deficits
  • Syncope
  • Weakness in the distribution of a motor cranial nerve one side of the head with a contralateral hemiparesis (medial brainstem damage)
  • Damage to a sensory cranial nerve & Horner’s syndrome on one side of the head and loss of contralateral pain and temperature sensation in the body (lateral brainstem damage)

Long-Term Symptoms Depend On Area Affected

  • Monocular visual obscuration (amaurosis fugax) that is due to retinal ischemia
  • Contralateral hemiparesis
  • Hemisensory deficit
  • Visual field deficits
  • Dysphasia
  • Receptive aphasia (Wernicke’s area lesion)
  • Expressive aphasia (Broca’s areas lesion)
  • Contralateral neglect (on-dominant parietal lobe lesion)
  • Problemswithinitiationofmovement(Supplementarymotorcortex lesion)
  • Difficulty with voluntary gaze to the contralateral side (Frontal eye field lesions)
  • Short-term memory deficits(medial temporal lobes lesioned)

Brain-Stem Syndromes

cerebrovascular el paso tx.http://roho.4senses.co/stroke- syndromes/common-stroke- syndromes-chapter-9-textbook-of- stroke-medicine.html

Stroke Recovery

  • Rehab needs depend upon the area of brain tissue that was affected by the stroke
  • Speech therapy
  • Restriction of functioning limbs
  • Balance and gait exercises
  • Encourages neuroplastic restructuring
  • Symptoms may improve within the first 5 days due to reduction in edema
  • Edema may cause herniation through the foramen magnum which can cause brainstem compression and death – patients with this problem may require craniectomy (last resort)

Sources

Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
Swenson, R. Cerebrovascular Disorders. 2010

Neurological Advanced Studies

Neurological Advanced Studies

After a neurological exam, physical exam, patient history, x-rays and any previous screening tests, a doctor may order one or more of the following diagnostic tests to determine the root of a possible/suspected neurological disorder or injury. These diagnostics generally involve neuroradiology, which uses small amounts of radioactive material to study organ function and structure and ordiagnostic imaging, which use magnets and electrical charges to study organ function.

Neurological Studies

Neuroradiology

  • MRI
  • MRA
  • MRS
  • fMRI
  • CT scans
  • Myelograms
  • PET scans
  • Many others

Magnetic Resonance Imaging (MRI)

Shows organs or soft tissue well
  • No ionizing radiation
Variations on MRI
  • Magnetic resonance angiography (MRA)
  • Evaluate blood flow through arteries
  • Detect intracranial aneurysms and vascular malformations
Magnetic resonance spectroscopy (MRS)
  • Assess chemical abnormalities in HIV, stroke, head injury, coma, Alzheimer’s disease, tumors, and multiple sclerosis
Functional magnetic resonance imaging (fMRI)
  • Determine the specific location of the brain where activity occurs

Computed Tomography (CT or CAT Scan)

  • Uses a combination of X-rays and computer technology to produce horizontal, or axial, images
  • Shows bones especially well
  • Used when assessment of the brain needed quickly such as in suspected bleeds and fractures

Myelogram

Contrast dye combined with CT or Xray
Most useful in assessing spinal cord
  • Stenosis
  • Tumors
  • Nerve root injury

Positron Emission Tomography (PET Scan)

Radiotracer is used to evaluate the metabolism of tissue to detect biochemical changes earlier than other study types
Used to assess
  • Alzheimer’s disease
  • Parkinson’s disease
  • Huntington’s disease
  • Epilepsy
  • Cerebrovascular accident

Electrodiagnostic Studies

  • Electromyography (EMG)
  • Nerve Conduction Velocity (NCV) Studies
  • Evoked Potential Studies

Electromyography (EMG)

Detection of signals arising from the depolarization of skeletal muscle
May be measured via:
  • Skin surface electrodes
  • Not used for diagnostic purposes, more for rehab and biofeedback
Needles placed directly within the muscle
  • Common for clinical/diagnostic EMG

neurological studies el paso tx.Diagnostic Needle EMG

Recorded depolarizations may be:
  • Spontaneous
  • Insertional activity
  • Result of voluntary muscle contraction
Muscles should be electrically silent at rest, except at the motor end-plate
  • Practitioner must avoid insertion in motor end-plate
At least 10 different points in the muscle are measured for proper interpretation

Procedure

Needle is inserted into the muscle
  • Insertional activity recorded
  • Electrical silence recorded
  • Voluntary muscle contraction recorded
  • Electrical silence recorded
  • Maximal contraction effort recorded

Samples Collected

Muscles
  • Innervated by the same nerve but different nerve roots
  • Innervated by the same nerve root but different nerves
  • Different locations along the course of the nerves
Helps to distinguish the level of the lesion

Motor Unit Potential (MUP)

Amplitude
  • Density of the muscle fibers attached to that one motor neuron
  • Proximity of the MUP
Recruitment pattern can also be assessed
  • Delayed recruitment can indicated loss of motor units within the muscle
  • Early recruitment is seen in myopathy, where the MUPs tend to be of low amplitude short duration

neurological studies el paso tx.Polyphasic MUPS

  • Increased amplitude and duration can be the result of reinnervation after chronic denervation

neurological studies el paso tx.Complete Potential Blocks

  • Demyelination of multiple segments in a row can result in a complete block of nerve conduction and therefore no resulting MUP reading, however generally changes in MUPs are only seen with damage to the axons, not the myelin
  • Damage to the central nervous system above the level of the motor neuron (such as by cervical spinal cord trauma or stroke) can result in complete paralysis little abnormality on needle EMG

Denervated Muscle Fibers

Detected as abnormal electrical signals
  • Increased insertional activity will be read in the first couple of weeks, as it becomes more mechanically irritable
As muscle fibers become more chemically sensitive they will begin to produce spontaneous depolarization activity
  • Fibrillation potentials

Fibrillation Potentials

  • DO NOT occur in normal muscle fibers
  • Fibrillations cannot be seen with the naked eye but are detectable on EMG
  • Often caused by nerve disease, but can be produced by severe muscle diseases if there is damage to the motor axons

neurological studies el paso tx.Positive Sharp Waves

  • DO NOT occur in normally functioning fibers
  • Spontaneous depolarization due to increased resting membrane potential

neurological studies el paso tx.Abnormal Findings

  • Findings of fibrillations and positive sharp waves are the most reliable indicator of damage to motor axons to the muscle after one week up to 12 months after the damage
  • Often termed “acute” in reports, despite possibly being visible months after onset
  • Will disappear if there is complete degeneration or denervation of nerve fibers

Nerve Conduction Velocity (NCV) Studies

Motor
  • Measures compound muscle action potentials (CMAP)
Sensory
  • Measures sensory nerve action potentials (SNAP)

Nerve Conduction Studies

  • Velocity (Speed)
  • Terminal latency
  • Amplitude
  • Tables of normal, adjusted for age, height and other factors are available for practitioners to make comparison

Terminal Latency

  • Time between stimulus and the appearance of a response
  • Distal entrapment neuropathies
  • Increased terminal latency along a specific nerve pathway

Velocity

Calculated based on latency and variables such as distance
Dependent on diameter of axon
Also dependent on thickness of myelin sheath
  • Focal neuropathies thin myelin sheaths, slowing conduction velocity
  • Conditions such as Charcot Marie Tooth Disease or Guillian Barre Syndrome damage myelin in large diameter, fast conducting fibers

Amplitude

  • Axonal health
  • Toxic neuropathies
  • CMAP and SNAP amplitude affected

Diabetic Neuropathy

Most common neuropathy
  • Distal, symmetric
  • Demyelination and axonal damage therefore speed and amplitude of conduction are both affected

Evoked Potential Studies

Somatosensory evoked potentials (SSEPs)
  • Used to test sensory nerves in the limbs
Visual evoked potentials (VEPs)
  • Used to test sensory nerves of the visual system
Brainstem auditory evoked potentials (AEPs)
  • Used to test sensory nerves of the auditory system
Potentials recorded via low-impedance surface electrodes
Recordings averaged after repeated exposure to sensory stimulus
  • Eliminates background “noise”
  • Refines results since potentials are small and difficult to detect apart from normal activity
  • According to Dr. Swenson, in the case of SSEPs, at least 256 stimuli are usually needed in order to obtain reliable, reproducible responses

Somatosensory Evoked Potentials (SSEPs)

Sensation from muscles
  • Touch and pressure receptors in the skin and deeper tissues
Little if any pain contribution
  • Limits ability to use testing for pain disorders
Velocity and/or amplitude changes can indicate pathology
  • Only large changes are significant since SSEPs are normally highly variable
Useful for intraoperative monitoring and to assess the prognosis of patients suffering severe anoxic brain injury
  • Not useful in assessing radiculopathy as individual nerve roots cannot be easily identified

Late Potentials

Occur more than 10-20 milliseconds after stimulation of motor nerves
Two types
  • H-Reflex
  • F-Response

H-Reflex

Named for Dr. Hoffman
  • First described this reflex in 1918
Electrodiagnostic manifestation of myotatic stretch reflex
  • Motor response recorded after electrical or physical stretch stimulation of the associated muscle
Only clinically useful in assessing S1 radiculopathy, as the reflex from the tibial nerve to triceps surae can be assessed for velocity and amplitude
  • More quantifiable that Achilles reflex testing
  • Fails to return with after damage and therefore not as clinically useful in recurrent radiculopathy cases

F-Response

So named because it was first recorded in the foot
Occurs 25 -55 milliseconds after initial stimulus
Due to antidromic depolarization of the motor nerve, resulting in a orthodromic electrical signal
  • Not a true reflex
  • Results in a small muscle contraction
  • Amplitude can be highly variable, so not as important as velocity
  • Reduced velocity indicates slowed conduction
Useful in assessing proximal nerve pathology
  • Radiculopathy
  • Guillian Barre Syndrome
  • Chronic Inflammatory Demyelinating Polyradiculopathy (CIDP)
Useful in assessing demyelinative peripheral neuropathies

Sources

  1. Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
  2. Day, Jo Ann. “Neuroradiology | Johns Hopkins Radiology.” Johns Hopkins Medicine Health Library, 13 Oct. 2016, www.hopkinsmedicine.org/radiology/specialties/ne uroradiology/index.html.
  3. Swenson, Rand. Electrodiagnosis.

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Concussions & Post-Concussion Syndrome

Concussions & Post-Concussion Syndrome

Concussions are traumatic brain injuries that affect brain function. Effects from these injuries are often temporary but can include headaches, problems with concentration, memory, balance and coordination. Concussions are usually caused by a blow to the head or violent shaking of the head and upper body. Some concussions cause loss of consciousness, but most do not. And it is possible to have a concussion and not realize it. Concussions are common in contact sports, such as football. However, most people gain a full recovery after a concussion.

Concussions

Traumatic Brain Injuries (TBI)

  • Most often the result of head trauma
  • Can also happen due to excessive shaking of the head or acceleration/deceleration
  • Mild injuries (mTBI/concussions) are the most common type of brain injury

Glasgow Coma Scale

concussions el paso tx.

Common Causes Of Concussion

  • Motor vehicle collisions
  • Falls
  • Sports injuries
  • Assault
  • Accidental or intentional discharge of weapons
  • Impact with objects

Blog Image Concussion Demonstration e

Prevention

Prevention of concussive injuries can be paramount

Encourage Patients To Wear Helmets
  • Competitive sports, especially boxing, hokey, football and baseball
  • Horseback riding
  • Riding bicycles, motorcycles, ATVs, etc.
  • High elevation activates such as rock climbing, zip lining
  • Skiing, snowboarding
Encourage Patients To Wear Seatbelts
  • Discuss the importance of wearing seatbelts at all times in vehicles with all of your patients
  • Also encourage use of appropriate booster or car seats for children to ensure adequate fit and function of seat belts.
Driving Safely
  • Patients should never drive while under the influence of drugs, including certain medications or alcohol
  • Never text and drive
concussions el paso tx.
Make Spaces Safer For Children
  • Install baby gates and window latches in the home
  • May in areas with shock-absorbing material, such as hardwood mulch or sand
  • Supervise children carefully, especially when they’re near water
Prevent Falls
  • Clearing tripping hazards such as loose rugs, uneven flooring or walkway clutter
  • Using nonslip mats in the bathtub and on shower floors, and installing grab bars next to the toilet, tub and shower
  • Ensure appropriate footwear
  • Installing handrails on both sides of stairways
  • Improving lighting throughout the home
  • Balance training exercises

Balance Training

  • Single leg balance
  • Bosu ball training
  • Core strengthening
  • Brain balancing exercises

Concussion Verbiage

Concussion vs. mTBI (mild traumatic brain injury)

  • mTBI is the term being used more commonly in medical settings, but concussion is a more largely recognized term in the community by sports coaches, etc.
  • The two terms describe the same basic thing, mTBI is a better term to use in your charting

Evaluating Concussion

  • Remember that there does not always have to be loss of consciousness for there to be a concussion
  • Post-Concussion Syndrome can occur without LOC as well
  • Symptoms of concussion may not be immediate and could take days to develop
  • Monitor for 48 post head injury watching for red flags
  • Use Acute concussion evaluation (ACE) form to gather information
  • Order imaging (CT/MRI) as needed if concussion red flags are present

Red Flags

Requires imaging (CT/MRI)

  • Headaches worsening
  • Patient appears drowsy or can’t be awakened
  • Has difficulty recognizing people or places
  • Neck pain
  • Seizure activity
  • Repeated vomiting
  • Increasing confusion or irritability
  • Unusual behavioral change
  • Focal neurologic signs
  • Slurred speech
  • Weakness or numbness in extremities
  • Change in state of consciousness

Common Symptoms Of Concussion

  • Headache or a sensation of pressure in the head
  • Loss of or alteration of consciousness
  • Blurred eyesight or other vision problems, such as dilated or uneven pupils
  • Confusion
  • Dizziness
  • Ringing in the ears
  • Nausea or vomiting
  • Slurred speech
  • Delayed response to questions
  • Memory loss
  • Fatigue
  • Trouble concentrating
  • Continued or persistent memory loss
  • Irritability and other personality changes
  • Sensitivity to light and noise
  • Sleep problems
  • Mood swings, stress, anxiety or depression
  • Disorders of taste and smell
Concussions el paso tx.

Mental/Behavioral Changes

  • Verbal outbursts
  • Physical outbursts
  • Poor judgment
  • Impulsive behavior
  • Negativity
  • Intolerance
  • Apathy
  • Egocentricity
  • Rigidity and inflexibility
  • Risky behavior
  • Lack of empathy
  • Lack of motivation or initiative
  • Depression or anxiety

Symptoms In Children

  • Concussions can present differently in children
  • Excessive crying
  • Loss of appetite
  • Loss of interest in favorite toys or activities
  • Sleep issues
  • Vomiting
  • Irritability
  • Unsteadiness while standing

Amnesia

Memory loss and failure to form new memories

Retrograde Amnesia
  • Inability to remember things that happened before the injury
  • Due to failure in recall
Anterograde Amnesia
  • Inability to remember things that happened after the injury
  • Due to failure to formulate new memories
Even short memory losses can be predictive of outcome
  • Amnesia may be up to 4-10 times more predictive of symptoms and cognitive deficits following concussion than is LOC (less than 1 minute)

Return To Play Progression

WhyMeniscalTearsOccur ElPasoChiropractor
Baseline: No Symptoms
  • As the baseline step of the Return to Play Progression, the athlete needs to have completed physical and cognitive rest and not be experiencing concussion symptoms for a minimum of 48 hours. Keep in mind, the younger the athlete, the more conservative the treatment.
Step 1: Light Aerobic Activity
  • The Goal: Only to increase an athlete’s heart rate.
  • The Time: 5 to 10 minutes.
  • The Activities: Exercise bike, walking, or light jogging.
  • Absolutely no weight lifting, jumping or hard running.
Step 2: Moderate activity
  • The Goal: Limited body and head movement.
  • The Time: Reduced from typical routine.
  • The Activities: Moderate jogging, brief running, moderate-intensity stationary biking, and moderate-intensity weightlifting
Step 3: Heavy, non-contact activity
  • The Goal: More intense but non-contact
  • The Time: Close to typical routine
  • The Activities: Running, high-intensity stationary biking, the player’s regular weightlifting routine, and non- contact sport-specific drills. This stage may add some cognitive component to practice in addition to the aerobic and movement components introduced in Steps 1 and 2.
Step 4: Practice & full contact
  • The Goal: Reintegrate in full contact practice.
Step 5: Competition
  • The Goal: Return to competition.

Microglial Priming

After head trauma microglial cells are primed and can become over active

  • To combat this, you must mediate the inflammation cascade
Prevent repeated head trauma
  • Due to priming of the foam cells, response to follow-up trauma may be far more severe and damaging

What Is Post-Concussion Syndrome (PCS)?

  • Symptoms following head trauma or mild traumatic brain injury, that can last weeks, months or years after injury
  • Symptoms persist longer than expected after initial concussion
  • More common in women and persons of advanced age who suffer head trauma
  • Severity of PCS often does not correlate to severity of head injury

PCS Symptoms

  • Headaches
  • Dizziness
  • Fatigue
  • Irritability
  • Anxiety
  • Insomnia
  • Loss of concentration and memory
  • Ringing in the ears
  • Blurry vision
  • Noise and light sensitivity
  • Rarely, decreases in taste and smell

Concussion Associated Risk Factors

  • Early symptoms of headache after injury
  • Mental changes such as amnesia or fogginess
  • Fatigue
  • Prior history of headaches

Evaluation Of PCS

PCS is a diagnosis of exclusion

  • If patient presents with symptoms after head injury, and other possible causes have been ruled out => PCS
  • Use appropriate testing and imaging studies to rule out other causes of symptoms

Headaches In PCS

Often “tension” type headache

Treat as you would for tension headache
  • Reduce stress
  • Improve stress coping skills
  • MSK treatment of the cervical and thoracic regions
  • Constitutional hydrotherapy
  • Adrenal supportive/adaptogenic herbs
Can be migraine, especially in people who had pre-existing migraine conditions prior to injury
  • Reduce inflammatory load
  • Consider management with supplements and or medications
  • Reduce light and sound exposure if there is sensitivity

Dizziness In PCS

  • After head trauma, always assess for BPPV, as this is the most common type of vertigo after trauma
  • Dix-Hallpike maneuver to diagnose
  • Epley’s maneuver for treatment

Light & Sound Sensitivity

Hypersensitivity to light and sound is common in PCS and typically exacerbates other symptoms such as headache and anxiety
Management of excess mesencephalon stimulation is crucial in such cases
  • Sunglasses
  • Other light blocking glasses
  • Earplugs
  • Cotton in ears

Treatment Of PCS

Manage each symptom individually as you otherwise would

Manage CNS inflammation
  • Curcumin
  • Boswelia
  • Fish oil/Omega-3s – (***after r/o bleed)
Cognitive behavioral therapy
  • Mindfulness & relaxation training
  • Acupuncture
  • Brain balancing physical therapy exercises
  • Refer for psychological evaluation/treatment
  • Refer to mTBI specialist

mTBI Specialists

  • mTBI is difficult to treat and is an entire specialty both in the allopathic and complementary medicine
  • Primary objective is to recognize and refer for appropriate care
  • Pursue training in mTBI or plan to refer to TBI specialists

Sources

  1. “A Head for the Future.” DVBIC, 4 Apr. 2017, dvbic.dcoe.mil/aheadforthefuture.
  2. Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
  3. “Heads Up to Health Care Providers.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 16 Feb. 2015, www.cdc.gov/headsup/providers/.
  4. “Post-Concussion Syndrome.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 28 July 2017, www.mayoclinic.org/diseases-conditions/post- concussion-syndrome/symptoms-causes/syc-20353352.
Origin Of Head Pain | El Paso, TX.

Origin Of Head Pain | El Paso, TX.

Origin: The most common cause of migraines/headaches can relate to neck complications. From spending excessive time looking down at a laptop, desktop, iPad, and even from constant texting, an incorrect posture for extended periods of time can begin to place pressure on the neck and upper back leading to problems that can cause headaches. The majority of these type of headaches occurs as a result of tightness between the shoulder blades, which in turn causes the muscles on the top of the shoulders to also tighten and radiate pain into the head.

Origin Of Head Pain

  • Arises from pain sensitive structures in the head
  • Small diameter fibers (pain/temp) innervate
  • Meninges
  • Blood vessels
  • Extracranial structures
  • TMJ
  • Eyes
  • Sinuses
  • Neck muscles and ligaments
  • Dental structures
  • The brain has no pain receptors

Spinal Trigeminal Nucleus

  • Trigeminal nerve
  • Facial nerve
  • Glossopharyngeal nerve
  • Vagus nerve
  • C2 nerve (Greater occipital nerve)

Occipital Nerves

origin headache el paso tx.http://dailymedfact.com/neck-anatomy-the-suboccipital-triangle/

Sensitization Of Nociceptors

  • Results in allodynia and hyperalgesia

origin headache el paso tx.http://slideplayer.com/9003592/27/images/4/Mechanisms+associated+with+peripheral+sensitization+ to+pain.jpg

Headache Types

Sinister:
  • Meningeal irritation
  • Intracranial mass lesions
  • Vascular headaches
  • Cervical fracture or malformation
  • Metabolic
  • Glaucoma
Benign:
  • Migraine
  • Cluster headaches
  • Neuralgias
  • Tension headache
  • Secondary headaches
  • Post-traumatic/post-concussion
  • “Analgesic rebound” headache 
  • Psychiatric

HA Due To Extracranial Lesions

  • Sinuses (infection, tumor)
  • Cervical spine disease
  • Dental problems
  • Temporomandibular joint
  • Ear infections, etc.
  • Eye (glaucoma, uveitis)
  • Extracranial arteries
  • Nerve lesions

HA Red Flags

Screen for red flags and consider dangerous HA types if present

Systemic symptoms:
  • Weight loss
  • Pain wakes them from sleep
  • Fever
Neurologic symptoms or abnormal signs:
  • Sudden or explosive onset
  • New or Worsening HA type especially in older patients
  • HA pain that is always in the same location
Previous headache history
  • Is this the first HA you’ve ever had?
    Is this the worst HA you’ve ever had?
Secondary risk factors:
  • History of cancer, immunocompromised, etc.

Dangerous/Sinister Headaches

Meningeal irritation
  • Subarachnoid hemorrhage
  • Meningitis and meningoencephalitis
Intracranial mass lesions
  • Neoplasms
  • Intracerebral hemorrhage
  • Subdural or epidural hemorrhage
  • Abscess
  • Acute hydrocephalus
Vascular headaches
  • Temporal arteritis
  • Hypertensive encephalopathy (e.g., malignant hypertension, pheochromocytoma)
  • Arteriovenous malformations and expanding aneurysms
  • Lupus cerebritis
  • Venous sinus thrombosis
Cervical fracture or malformation
  • Fracture or dislocation
  • Occipital neuralgia
  • Vertebral artery dissection
  • Chiari malformation
Metabolic
  • Hypoglycemia
  • Hypercapnea
  • Carbon monoxide
  • Anoxia
  • Anemia
  • Vitamin A toxicity
Glaucoma

Subarachnoid Hemorrhage

  • Usually due to ruptured aneurysm
  • Sudden onset of severe pain
  • Often vomiting
  • Patient appears ill
  • Often nuchal rigidity
  • Refer for CT and possibly lumbar puncture

Meningitis

  • Patient appears ill
  • Fever
  • Nuchal rigidity (except in elderly and young children)
  • Refer for lumbar puncture – diagnostic

Neoplasms

  • Unlikely cause of HA in average patient population
  • Mild and nonspecific head pain
  • Worse in the morning
  • May be elicited by vigorous head shaking
  • If focal symptoms, seizures, focal neurologic signs, or evidence of increased intracranial pressure are present rule our neoplasm

Subdural Or Epidural Hemorrhage

  • Due to hypertension, trauma or defects in coagulation
  • Most often occurs in the context of acute head trauma
  • Onset of symptoms may be weeks or months after an injury
  • Differentiate from the common post-concussion headache
  • Post-Concussive HA may persist for weeks or months after an injury and be accompanied by dizziness or vertigo and mild mental changes, which will all subside

Increase Intracranial Pressure

  • Papilledema
  • May cause visual changes

origin headache el paso tx.

https://openi.nlm.nih.gov/detailedresult.php?img=2859586_AIAN-13-37- g001&query=papilledema&it=xg&req=4&npos=2

origin headache el paso tx.

Temporal (Giant-Cell) Arteritis

  • >50 years old
  • Polymyalgia rheumatic
  • Malaise
  • Proximal joint pains
  • Myalgia
  • Nonspecific headaches
  • Exquisite tenderness and/or swelling over the temporal or occipital arteries
  • Evidence of arterial insufficiency in the distribution of branches of the cranial vessels
  • High ESR

Cervical Region HA

  • Neck trauma or with symptoms or signs of cervical root or cord compression
  • Order MR or CT cord compression due to fracture or dislocation
  • Cervical instability
  • Order cervical spine x-rays lateral flexion and extension views

Ruling Out Dangerous HA

  • Rule our history of serious head or neck injury, seizures or focal neurologic symptoms, and infections that may predispose to meningitis or brain abscess
  • Check for fever
  • Measure blood pressure (concern if diastolic >120)
  • Ophthalmoscopic exam
  • Check neck for rigidity
  • Auscultate for cranial bruits.
  • Complete neurologic examination
  • If needed order complete blood cell count, ESR, cranial or cervical imaging

Episodic Or Chronic?

<15 days per month = Episodic

>15 days per month = Chronic

Migraine HA

Generally due to dilation or distension of cerebral vasculature

Serotonin In Migraine

  • AKA 5-hydroxytryptamine (5-HT)
  • Serotonin becomes depleted in migraine episodes
  • IV 5-HT can stop or reduce severity

Migraine With Aura

History of at least 2 attacks fulfilling the following criteria

One of the following fully reversible aura symptoms:
  • Visual
  • Somatic sensory
  • Speech or language difficulty
  • Motor
  • Brain stem
2 of the following 4 characteristics:
  • 1 aura symptom spreads gradually over ≥5 min, and/or 2 symptoms occur in succession
  • Each individual aura symptom lasts 5-60 min
  • 1 aura symptom is unilateral
  • Aura accompanied or followed in <60 min by headache
  • Not better accounted for by another ICHD-3 diagnosis, and TIA excluded

Migraine Without Aura

History of at least 5 attacks fulfilling the following criteria:
  • Headache attacks lasting 4-72 h (untreated or unsuccessfully treated)
  • Unilateral pain
  • Pulsing/pounding quality
  • Moderate to severe pain intensity
  • Aggravation by or causing avoidance of routine physical activity
  • During headache nausea and/or sensitivity to light and sound
  • Not better accounted for by another ICHD-3 diagnosis

Cluster Headache

  • Severe unilateral orbital, supraorbital and/or temporal pain
  • “Like an ice pick stabbing me the eye”
  • Pain lasts 15-180 minutes
At least one of the following on the side of headache:
  • Conjunctival injection
  • Facial sweating
  • Lacrimation
  • Miosis
  • Nasal congestion
  • Ptosis
  • Rhinorrhea
  • Eyelid edema
  • History of similar headaches in the past

Tension Headache

Headache pain accompanied by two of the following:
  • Pressing/tightening (non-pulsing) quality
  • “Feels like a band around my head”
  • Bilateral location
  • Not aggravated by routine physical activity
Headache should be lacking:
  • Nausea or vomiting
  • Photophobia and phonophobia (one or the other may be present)
  • History of similar headaches in the past

Rebound Headache

  • Headache occurring on ≥15 days a month in a patient with a pre-existing headache disorder
  • Regular overuse for >3 months of one or more drugs that can be taken for acute and/or symptomatic treatment of headache
  • Due to medication overuse/withdrawal
  • Not better accounted for by another ICHD-3 diagnosis

Sources

Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.

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Benign and Sinister Types of Headaches

Benign and Sinister Types of Headaches

Headaches are very common health issues, and lots of people treat themselves by using basic painkillers, drinking additional water, with rest, or by simply waiting for the headache to go away on its own. As a matter of fact, a headache is among the most common reasons for doctor office visits.

 

Just about everyone will experience a headache sometime during their life. Most headaches are not caused by serious or sinister conditions. However, people understandably worry if headaches feel different, whether they’re especially severe, particularly frequent or unusual in any other manner. But, the most common concern is whether the headache may be a symptom of an underlying health issue, such as a brain tumor.

 

The following article discusses headaches generally. It explains the various types of headaches you may experience and describes those very rare situations where a headache may be a symptom of a serious disease.

 

Types of Headaches

 

Headaches can be categorized as primary, or they can be classified as secondary, meaning they are a side-effect of another injury or condition.

 

A healthcare professional can usually determine the possible cause of your headaches from speaking to you and examining you. When they have found the cause then you’ll have the ability to decide the best treatment approach for your head pain symptoms. This may involve taking drugs only when you get the headaches, taking daily medication to stop them altogether, and/or even stopping medication you’re already taking. Very occasionally, headaches may need further diagnosis to rule out more serious underlying causes. Chiropractic care and physical therapy are also commonly utilized to help treat headaches. Below, we will discuss the different types of headaches.

 

Primary Headaches

 

The most common types of headaches, by far, are tension headaches and migraines.

 

Tension Headaches

 

Tension headaches are generally felt as a band around the forehead. They may last for many days. They may be tiring and uncomfortable, but they don’t normally disturb sleep. Most people can carry on working with a tension headache. These often have a tendency to worsen as the day progresses, however, they aren’t usually made worse with physical activities, though it’s not strange to be somewhat sensitive to bright light or noise.

 

Migraines

 

Migraines are also very common types of headaches. A typical migraine is described as a throbbing sensation. Headaches which are one-sided, headaches which throb and headaches that make you feel sick are more inclined to be migraines compared to anything else. Migraines are often severe enough to be disabling. Some individuals will need to go to bed to sleep off their aggravation.

 

Cluster Headaches

 

Cluster headaches are extremely severe headaches, sometimes called “suicide headaches”. They occur in clusters, often every day for a number of days or maybe weeks. Then they vanish for weeks on end. These types of headaches are rare and often occur particularly in adult male smokers. They’re intense, one-sided headaches, which are very disabling, meaning they stop routine activity. People often describe them as the worst pain they have ever felt. Cluster headaches are typically one-sided. Patients frequently have a red watery eye on the other hand, a stuffy runny nose and a droopy eyelid.

 

Chronic Tension Headaches

 

Chronic tension headaches (or chronic daily headache) is generally caused by muscle tension in the back of the neck and affects women more frequently than men. Chronic means that the problem is persistent and ongoing. These headaches can develop due to neck injuries or tiredness and may worsen with drug/medication overuse. A headache that occurs virtually every day for 3 weeks or more is known as a chronic daily headache or a chronic tension headaches.

 

Medication-Overuse Headaches

 

Medication-overuse headaches or medication-induced aggravation, is an unpleasant and long-term headache. It’s brought on by taking painkillers usually meant for headaches. Unfortunately, when painkillers are taken regularly for headaches, the body reacts by creating additional pain sensors in the brain. Finally, the pain sensors are so many that the head becomes super-sensitive and the headache won’t go away. Individuals who have these headaches often take an increasing number of painkillers to attempt and feel much better. But, the painkillers may have regularly long ceased to work. Medication-overuse headaches are the most common cause of secondary headache.

 

Exertional Headaches/Sexual Headaches

 

Exertional headaches are headaches associated with physical activity. They may get severe very quickly following a strenuous activity like coughing, running, with intercourse, and straining with bowel movements. They’re more commonly experienced by patients that also have migraines, or who have relatives with migraine.

 

Headaches associated with sex particularly worry patients. They can occur as sex starts, at orgasm, or following sex. Headaches at orgasm would be the most common type. They are generally acute, at the back of the head, behind the eyes or all around. They last about twenty minutes and aren’t usually an indication of any other underlying health issues or problems.

 

Exertional and sexual intercourse-related headaches aren’t typically an indication of serious underlying problems. Very occasionally, they can be a sign that there is a leaky blood vessel on the surface of the brain. As a result, if they are marked and repeated, it’s sensible to talk about them with your healthcare professional.

 

Primary Stabbing Headaches

 

Primary traumatic headaches are sometimes called “ice-pick headaches” or “idiopathic stabbing headache”. The term “idiopathic” is used by doctors for something that comes without a clear cause. These are brief, stabbing headaches that are extremely sudden and severe. They generally last between 5 and 30 seconds and they occur at any time of the day or night. They feel as though a sharp object, like an ice pick, is being stuck into your head. They frequently occur in or just behind the ear and they are sometimes quite frightening. Even though they aren’t migraines they’re more prevalent in those who suffer from migraines, nearly half of individuals who experience migraines have principal stabbing headaches.

 

They are often felt at the place on the head where the migraines have a tendency to happen. Primary stabbing headaches are too brief to take care of, even though migraine prevention medications may reduce their number.

 

Hemicrania Continua

 

Hemicrania continua is a major chronic daily headache. It typically induces a continuous but shifting pain on one side of the brain. The pain is generally continuous with episodes of severe pain, which can last between 20 minutes and several days. During those episodes of severe pain there may be other symptoms, such as watering or redness of the eye, runny or blocked nose, and drooping of the eyelid, around precisely the same side as the aggravation. Similar to a migraine, there may also be sensitivity to light, feeling sick, such as nausea, and being sick, such as vomiting. The headaches do not go away but there may be periods when you don’t have any headaches. Hemicrania continua headaches respond to medicine called indometacin.

 

Trigeminal Neuralgia

 

Trigeminal neuralgia causes facial pain. The pain consists of very short bursts of electric shock-like sensations in the face, particularly at the area of the eyes, nose, scalp, brow, lips or limbs. It’s usually one-sided and is more common in people over age 50. It may be triggered by touch or a light breeze on the surface area.

 

Headache Causes

 

Occasionally, headaches have underlying causes, and treatment of the headache involves treating the cause. Individuals often fear that headaches are caused by serious illness, or by high blood pressure. Both of these are extremely uncommon causes of headache, really increased blood pressure usually causes no symptoms in any way.

 

Chemicals, Drugs and Substance Withdrawal

 

Headaches can be because of a substance, or its withdrawal, for example:

 

  • Carbon monoxide, that is made by gas heaters which aren’t properly ventilated
  • Drinking alcohol, with headache often experienced the morning afterwards
  • Deficiency of body fluid or dehydration

 

Headaches Due to Referred Pain

 

Some headaches may be caused by pain in some other portion of the head, such as ear or tooth pain, pain in the jaw joint and pain in the neck.

 

Sinusitis is also a frequent cause of headaches. The sinuses are “holes” in the skull which are there to stop it from becoming too heavy for the neck to transport around. They are lined with mucous membranes, such as the lining of the nose, and this creates mucus in response to colds or allergy. The liner membranes also swell and can block the drainage of the mucus out of the space. It subsequently becomes cracked and infected, resulting in headache. The headache of sinusitis is often felt at the front of the head and also in the face or teeth.

 

Frequently the face feels tender to tension, particularly just below the eyes beside the nose. You might have a stuffy nose and the pain is often worse when you bend forwards. Acute sinusitis is the kind that comes on fast in conjunction with a cold or abrupt allergy. You may have a temperature and be generating a lot of mucus. Chronic sinusitis may be caused by allergy, by overusing decongestants or with the acute sinusitis that doesn’t settle. The sinuses become chronically infected and the nasal linings chronically swollen. The contents of this uterus may be thick but frequently not infected.

 

Acute glaucoma can cause severe headaches. In this condition, the pressure inside the eyes goes up suddenly and this causes a surprisingly, very severe headache behind the eye. Even the eyeball can feel really hard to touch, the eye is red, the front part of the eye, or cornea, can seem cloudy and the eyesight is generally blurred.

 

What Types of Headaches are Dangerous or Serious?

 

All headaches are unpleasant and some, such as headache from medication abuse, are serious in the sense that if not treated correctly they might never go away. But a few headaches are indications of serious underlying issues. These are uncommon, in many cases very rare. Dangerous headaches often occur suddenly, and also eventually become increasingly worse over time. They are more common in elderly people. They comprise of the following:

 

Bleeding Around the Brain (Subarachnoid Haemorrhage)

 

Subarachnoid haemorrhage is a really serious condition which occurs when a tiny blood vessel pops on the surface of the brain. Patients develop a serious headache and stiff neck and may become unconscious. This is a rare cause of acute headache.

 

Meningitis and Brain Infections

 

Meningitis is infection of the tissues around and on the surface of the brain and encephalitis is infection of the brain itself. Brain infections can be caused by germs called bacteria, viruses or parasites and they are thankfully rare. They cause a severe, disabling headache. Normally, patients may feel sick or vomit and can’t bear bright lights, something known as photophobia. Often they have a rigid neck, too stiff for your physician to have the ability to bend the head down so that the chin touches the chest, even in the event that you attempt to relax. Patients are generally also unwell, experiencing hot, sweaty and overall sick sensations.

 

Giant Cell Arteritis (Temporal Arteritis)

 

Giant cell arteritis (temporal arteritis) is, generally, just seen in people over the age of 50. It is due to swelling, or inflammation, of the arteries at the temples and behind the eye. It causes a headache behind the forehead, also referred to as a sinus headache. Typically the blood vessels at the forehead are tender and individuals detect pain from the scalp when they comb their own hair. Frequently the pain gets worse with chewing. Temporal arteritis is severe because if it’s not treated it can cause sudden loss of eyesight. Treatment is with a course of steroids. The need to keep these steroids is generally monitored by the GP through blood tests, and they are typically needed for several months.

 

Brain Tumors

 

Brain tumors are a very uncommon cause of headache, although most patients with long-term, severe or persistent headaches start to worry that this might be the reason. Brain tumors can lead to headaches. Usually the aggravation of brain tumors exists on waking in the morning, is worse on sitting up, and becoming steadily worse in the day to day, never easing and never disappearing. It can sometimes be worse on coughing and sneezing, as may sinus headaches and migraines.

 

When Should I Worry About a Headache?

 

Most headaches do not have a serious underlying cause. However, healthcare professionals are trained to ask you about the signs and symptoms that might suggest your headache needs further diagnosis, just to make certain it’s nothing serious.

 

The things which would suggest to your physician and nurse that your headache may need additional evaluation include the following. They don’t mean that your headache is severe or sinister, but they imply that the healthcare professional may wish to do some additional evaluations to make sure if:

 

  • You have had a substantial head injury in the previous three months.
  • Your headaches are worsening and accompanied with high temperature or fever.
  • Your headaches begin extremely unexpectedly.
  • You’ve developed problems with speech and balance as well as headache.
  • You’ve developed problems with your memory or changes in your behavior or personality in addition to headache.
  • You’re confused or muddled along with your headache.
  • Your headache started when you coughed, sneezed or strained.
  • Your headache is much worse when you sit or stand.
  • Your headache is associated with red or painful eyes.
  • Your headaches are not like anything you’ve ever experienced before.
  • You have unexplained nausea together with the aggravation.
  • You have low immunity, for instance, when you have HIV, or are about oral steroid medicine or immune suppressing drugs.
  • You have or have had a type of cancer that can spread throughout the body.

 

Dr-Jimenez_White-Coat_01.png

Dr. Alex Jimenez’s Insight

Headaches are extremely common health issues which affect a wide range of the population around the world. Although frequent, a headache which is described to be like no other ever experienced before, may often become a concern. There are several types of headaches which can be caused by a variety of injuries and/or underlying conditions. As a healthcare professional, it’s essential to be able to determine between sinister or dangerous types of headaches and benign types of headaches, in order to decide the best treatment approach. By properly diagnosing the source of a patient’s headaches, both benign and sinister types of headaches can be treated accordingly.

 

Overview

 

Many headaches, whilst unpleasant, are harmless and react to a variety of treatments, including chiropractic care. Migraine, tension headaches and medication-overuse headaches are very common. The majority of the populace will experience one or more of these. Working out exactly the underlying cause of any headaches through discussion with your doctor is often the best method to resolve them. It is possible to develop a persistent or chronic and constant headache through taking drugs and/or medications that you took to get rid of your headache. Your physician can support you through the practice of quitting painkillers when that is the case.

 

Headaches are, quite infrequently, an indication of a serious or sinister underlying illness, and many headaches go away on their own.

 

If you have a headache which is uncommon for you then you need to discuss it with your doctor. You should also speak to your doctor about headaches which are particularly severe or that affect your regular activities, those that are associated with other symptoms, such as tingling or weakness, and those which make your own scalp tender, especially if you’re over 50 years old. Finally, always speak to a healthcare professional when you have an unremitting morning headache which is present for at least three days or is becoming gradually worse.

 

Remember that headaches are not as likely to occur in people who:

 

  • Handle their anxiety levels well.
  • Eat a balanced, regular diet.
  • Take balanced routine exercise.
  • Focus on posture and core muscles.
  • Sleep on two pillows or fewer.
  • Drink loads of water.
  • Have plenty of sleep.

 

Anything that you can do to enhance one or more of these aspects of your life will improve your health and well-being and cut back the number of headaches you experience. Make sure to seek the appropriate medical attention from a qualified and experienced healthcare professional in the event of a severe headache unlike anything you’ve ever experienced before. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

Curated by Dr. Alex Jimenez

 

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Additional Topics: Back Pain

 

Back pain is one of the most prevalent causes for disability and missed days at work worldwide. As a matter of fact, back pain has been attributed as the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience some type of back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.

 

 

 

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EXTRA IMPORTANT TOPIC: Low Back Pain Management

 

MORE TOPICS: EXTRA EXTRA: Chronic Pain & Treatments

 

Cerebral Palsy And Chiropractic Treatment | El Paso, TX. | Video

Cerebral Palsy And Chiropractic Treatment | El Paso, TX. | Video

Robert “Bobby” Gomez was born with cerebral palsy. Bobby describes how he felt like an outcast, growing up with the disorder, but he explains how much he is able to accomplish when he’s not being underestimated. While Robert Gomez describes experiencing no set-backs due to his cerebral palsy, he suffered from pain and limited mobility. That’s when he decided to seek chiropractic care with Dr. Alex Jimenez and he found much more help than he expected. Through spinal adjustments, manual manipulations and rehabilitation exercises, Robert “Bobby” Gomez has started to regain some of his mobility and has experienced decreased pain symptoms. Bobby recommends Dr. Jimenez as the non-surgical choice for back pain and he encourages other to educate themselves on cerebral palsy.

Chiropractic Treatment For Cerebral Palsy

 

Cerebral palsy is a set of permanent movement disorders that appear in early youth. Signs and symptoms vary among people. Many times, symptoms include poor coordination, stiff muscles, weak muscles and tremors.There may be problems with feeling, vision, hearing, swallowing and talking. Often, infants with cerebral palsy don’t roll over, sit, walk or crawl as early as other kids of their age. Other symptoms may include seizures and problems with reasoning or thinking, both which happens in about one third of individuals with cerebral palsy. While the symptoms may get more noticeable over the first few years of life, the underlying problems don’t worsen over time. Cerebral palsy is caused by abnormal development or damage to the areas of the brain that control movement, balance and posture. Most often, the problems occur during pregnancy; however, they may also happen during childbirth or soon after birth.

cerebral palsy el paso tx.

We are blessed to present to you El Paso’s Premier Wellness & Injury Care Clinic.

Our services are specialized and focused on injuries and the complete recovery process. Our areas of practice include: Wellness & Nutrition, Chronic Pain, Personal InjuryAuto Accident Care, Work Injuries, Back Injury, Low Back Pain, Neck Pain, Migraine Headaches, Sport Injuries, Severe Sciatica, Scoliosis, Complex Herniated Discs, Fibromyalgia, Chronic Pain, Stress Management, and Complex Injuries.

As El Paso’s Chiropractic Rehabilitation Clinic & Integrated Medicine Center, we passionately are focused treating patients after frustrating injuries and chronic pain syndromes. We focus on improving your ability through flexibility, mobility and agility programs tailored for all age groups and disabilities.

If you have enjoyed this video and/or we have helped you in any way please feel free to subscribe and share us.

Thank You & God Bless.

Dr. Alex Jimenez DC, C.C.S.T

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Injury Medical Clinic: Herniated Disc Treatment & Recovery

Brainstem And The Rule Of 4 | El Paso, TX.

Brainstem And The Rule Of 4 | El Paso, TX.

The rule of 4 of the brainstem: a simplified method for understanding brainstem anatomy and brainstem vascular
syndromes for the non-neurologist.

The Rule Of 4 & The Brainstem

The rule of 4 is a simple method developed to help ‘students of neurology’ to remember the anatomy of the brainstem and thus the features of the various brainstem vascular syndromes. As medical students, we are taught detailed anatomy of the brainstem containing a bewildering number of structures with curious names such as superior colliculi, inferior olives, various cranial nerve nuclei and the median longitudinal fasciculus. In reality when we do a neurological examination we test for only a few of these structures. The rule of 4 recognizes this and only describes the parts of the brainstem that we actually examine when doing a neurological examination. The blood supply of the brainstem is such that there are paramedian branches and long circumferential branches (the anterior inferior cerebellar artery (AICA), the posterior inferior cerebellar artery (PICA) and the superior cerebellar artery (SCA). Occlusion of the paramedian branches results in medial (or paramedian) brainstem syndromes and occlusion of the circumferential branches results in lateral brainstem syndromes. Occasionally lateral brainstem syndromes are seen in unilateral vertebral occlusion. This paper describes a simple technique to aid in the understanding of brainstem vascular syndromes.

Any attempt to over simplify things runs the risk of upsetting those who like detail and I apologize in advance to the anatomists among us, but for more than 15 years this simple concept has helped numerous students and residents understand, often for the first time, brainstem anatomy and the associated clinical syndromes that result.

In The Rule Of 4 There Are 4 Rules:
  1. There are 4 structures in the ‘midline’ beginning with M.
  2. There are 4 structures to the side beginning with S.
  3. There are 4 cranial nerves in the medulla, 4 in the pons and 4 above the pons (2 in the midbrain).
  4. The 4 motor nuclei that are in the midline are those that divide equally into 12 except for 1 and 2, that is 3, 4, 6 and 12 (5, 7, 9 and 11 are in the lateral brainstem).

If you can remember these rules and know how to examine the nervous system, in particular the cranial nerves, then you will be able to diagnose brainstem vascular syndromes with ease.

brainstem el paso tx.

Figure 1 shows a cross-section of the brainstem, in this case at the level of the medulla, but the concept of 4 lateral and 4 medial structures also applies to the pons, only the 4 medial structures relate to midbrain vascular syndromes.

brainstem el paso tx.

The 4 Medial Structures & The Associated Deficit Are:
  1. The Motor pathway (or corticospinal tract): contra lateral weakness of the arm and leg.
  2. The Medial Lemniscus: contra lateral loss of vibration and proprioception in the arm and leg.
  3. The Medial longitudinal fasciculus: ipsilateral inter- nuclear ophthalmoplegia (failure of adduction of the ipsilateral eye towards the nose and nystagmus in the opposite eye as it looks laterally).
  4. The Motor nucleus and nerve: ipsilateral loss of the cranial nerve that is affected (3, 4, 6 or 12).
The 4 Lateral Structures & The Associated Deficit Are:
  1. The Spinocerebellar pathways: ipsilateral ataxia of the arm and leg.
  2. The Spinothalamic pathway: contra lateral alteration of pain and temperature affecting the arm, leg and rarely the trunk.
  3. The Sensory nucleus of the 5th: ipsilateral alteration of pain and temperature on the face in the distribution of the 5th cranial nerve (this nucleus is a long vertical structure that extends in the lateral aspect of the pons down into the medulla).
  4. The Sympathetic pathway: ipsilateral Horner’s syndrome, that is partial ptosis and a small pupil (miosis)

These pathways pass through the entire length of the brainstem and can be likened to ‘meridians of longitude’ whereas the various cranial nerves can be regarded as ‘parallels of latitude’. If you establish where the meridians of longitude and parallels of latitude intersect then you have established the site of the lesion.

Figure 2 shows the ventral aspect of the brainstem.

brainstem el paso tx.

The 4 Cranial Nerves In The Medulla Are:

9 Glossopharyngeal: ipsilateral loss of pharyngeal sensation.
10 Vagus: ipsilateral palatal weakness.
11 Spinal accessory: ipsilateral weakness of the trapezius and sternocleidomastoid muscles.
12 Hypoglossal: ipsilateral weakness of the tongue.

The 12th cranial nerve is the motor nerve in the midline of the medulla. Although the 9th, 10th and 11th cranial nerves have motor components, they do not divide evenly into 12 (using our rule) and are thus not the medial motor nerves.

The 4 Cranial Nerves In The Pons Are:

5 Trigeminal: ipsilateral alteration of pain, temperature and light touch on the face back as far as the anterior two-thirds of the scalp and sparing the angle of the jaw.
6 Abducent: ipsilateral weakness of abduction (lateral movement) of the eye.
7 Facial: ipsilateral facial weakness.
8 Auditory: ipsilateral deafness.

The 6th cranial nerve is the motor nerve in the pons.

The 7th is a motor nerve but it also carries pathways of taste, and using the rule of 4 it does not divide equally in to 12 and thus it is not a motor nerve that is in the midline. The vestibular portion of the 8th nerve is not included in order to keep the concept simple and to avoid confusion. Nausea and vomiting and vertigo are often more common with involvement of the vestibular connections in the lateral medulla.

The 4 Cranial Nerves Above The Pons Are:

4 Olfactory: not in midbrain.
5 Optic: not in midbrain.
6 Oculomotor: impaired adduction, supraduction and infraduction of the ipsilateral eye with or without a dilated pupil. The eye is turned out and slightly down.
7 Trochlear: eye unable to look down when the eye is looking in towards the nose.

The 3rd and 4th cranial nerves are the motor nerves in the midbrain.

Thus a medial brainstem syndrome will consist of the 4 M’s and the relevant motor cranial nerve, and a lateral brainstem syndrome will consist of the 4 S’s and either the 9–11th cranial nerve if in the medulla, or the 5th, 7th and 8th cranial nerve if in the pons.

MEDIAL (PARAMEDIAN) BRAINSTEM SYNDROMES

Let us assume that the patient you are examining has a brainstem stroke. If you find upper motor neurone signs in the arm and the leg on one side then you know the patient has a medial brainstem syndrome because the motor pathways is paramedian and crosses at the level of the foramen magnum (decussation of the pyramids). The involvement of the motor pathway is the ‘meridian of longitude’. So far the lesion could be anywhere in the medial aspect of the brainstem, although if the face is also affected it has to be above the mid pons, the level where the 7th nerve nucleus is.

The motor cranial nerve ‘the parallels of latitude’ indicates whether the lesion is in the medulla (12th), pons (6th) or midbrain (3rd). Remember the cranial nerve palsy will be ipsilateral to the side of the lesion and the hemiparesis will be contralateral. If the medial lemniscus is also affected then you will find a contra lateral loss of vibration and proprioception in the arm and leg (the same side affected by the hemiparesis) as the posterior columns also cross at or just above the level of the foramen magnum. The median longitudinal fasciculus (MLF) is usually not affected when there is a hemiparesis as the MLF is further back in the brainstem.

The MLF can be affected in isolation ‘a lacunar infarct’ and this results in an ipsilateral internuclear ophthalmoplegia, with failure of adduction (movement towards the nose) of the ipsilateral eye and leading eye nystagmus on looking laterally to the opposite side of the lesion in the contra lateral eye. If the patient had involvement of the left MLF then, on being asked to look to the left, the eye movements would be normal, but on looking to the right the left eye would not go past the midline, while there would be nystagmus in the right eye as it looked to the right.

Figure 3 shows the clinical features of the medial brainstem syndromes.

brainstem el paso tx.LATERAL BRAINSTEM SYNDROMES

Once again we are assuming that the patient you are seeing has a brainstem problem, most likely a vascular lesion. The 4 S’s or ‘meridians of longitude’ will indicate that you are dealing with a lateral brainstem problem and the cranial nerves or ‘parallels of latitude’ will indicate whether the problem is in the lateral medulla or lateral pons.

A lateral brainstem infarct will result in ipsilateral ataxia of the arm and leg as a result of involvement of the Spinocerebellar pathways, contralateral alteration of pain and temperature sensation as a result of involvement of the Spinothalamic pathway, ipsilateral loss of pain and temperature sensation affecting the face within the distribution of the Sensory nucleus of the trigeminal nerve (light touch may also be affected with involvement of the spinothalamic pathway and/or sensory nucleus of the trigeminal nerve). An ipsilateral Horner’s syndrome with partial ptosis and a small pupil (miosis) is because of involvement of the Sympathetic pathway. The power tone and the reflexes should all be normal. So far all we have done is localize the problem to the lateral aspect of the brainstem; by adding the relevant 3 cranial nerves in the medulla or the pons we can localize the lesion to this region of the brain.

brainstem el paso tx.The lower 4 cranial nerves are in the medulla and the 12th nerve is in the midline so that 9th, 10th and 11th nerves will be in the lateral aspect of the medulla. When these are affected, the result is dysarthria and dysphagia with an ipsilateral impairment of the gag reflex and the palate will pull up to the opposite side; occasionally there may be weakness of the ipsilateral trapezius and/or sternocleidomastoid muscle. This is the lateral medullary syndrome usually resulting from occlusion of the ipsilateral vertebral or posterior inferior cerebellar arteries.

The 4 cranial nerves in the pons are: 5th, 6th, 7th and 8th. The 6th nerve is the motor nerve in the midline, the 5th, 7th and 8th are in the lateral aspect of the pons, and when these are affected there will be ipsilateral facial weakness, weakness of the ipsilateral masseter and pterygoid muscles (muscles that open and close the mouth) and occasionally ipsilateral deafness. A tumour such as an acoustic neuroma in the cerebello-pontine angle will result in ipsilateral deafness, facial weakness and impairment of facial sensation; there may also be ipsilateral limb ataxia if it compresses the ipsilateral cerebellum or brainstem. The sympathetic pathway is usually too deep to be affected.

If there are signs of both a lateral and a medial (paramedian) brainstem syndrome, then one needs to consider a basilar artery problem, possibly an occlusion.

In summary, if one can remember that there are 4 pathways in the midline commencing with the letter M, 4 pathways in the lateral aspect of the brainstem commencing with the letter S, the lower 4 cranial nerves are in the medulla, the middle 4 cranial nerves in the pons and the first 4 cranial nerves above the pons with the 3rd and 4th in the midbrain, and that the 4 motor nerves that are in the midline are the 4 that divide evenly into 12 except for 1 and 2, that is 3, 4, 6 and 12, then it will be possible to diagnose brainstem vascular syndromes with pinpoint accuracy.

P. GATES

The Geelong Hospital, Barwon Health, Geelong, Victoria, Australia

REFERENCES

1 Chapter 7. Neurology. In: Williams PL, Warwick R, Dyson M, Bannister LH, eds. Gray’s Anatomy, 37th edn. Edinburgh: Churchill Livingstone; 1989; 860–1243.

Testing the Function of the Cranial Nerves in El Paso, TX

Testing the Function of the Cranial Nerves in El Paso, TX

Physicians, neurologists, and other healthcare professionals may often run a cranial nerve examination as part of a neurological evaluation to analyze the operation of the cranial nerves. This involves a highly formalized series of tests that evaluate the status of each cranial nerve. A cranial nerve test begins with observation of the patient partly due to the fact that cranial nerve lesions may ultimately affect the symmetry of the face or eyes, among other signs and symptoms.

 

The visual fields for neural lesions or nystagmus are tested via an evaluation of particular eye movements. The sensation of the face is tested by asking patients to execute different facial movements, like puffing out their cheeks. Hearing is tested through voice and tuning forks. The position of the individual’s uvula is also examined because asymmetry in its placement could indicate a lesion of the glossopharyngeal nerve. After the capability of the individual to use their shoulder to test the accessory nerve (XI), the patient’s tongue operation is generally assessed by detecting various tongue movements.

 

Damage or Injury of the Cranial Nerves

 

Compression

 

Cranial nerves may be compressed due to increased intracranial pressure, a profound effect of an intracerebral haemorrhage, or tumour which presses against the cranial nerves and interferes with the communication of impulses along the length of a nerve. In some instances, a loss of functionality of one cranial nerve may on occasion be the first symptom of an intracranial or skull base cancer.

 

An increase in intracranial pressure can lead to dysfunction of the optic nerves (II) because of the compression of the surrounding veins and capillaries, resulting in swelling of the eyeball, known as papilloedema. A cancer, such as an optic glioma, can also affect the optic nerve (II). A pituitary tumour can compress the optic tracts or the optic chiasm of the optic nerve (II), causing visual field loss. A pituitary tumour may also extend into the cavernous sinus, compressing the oculuomotor nerve (III), the trochlear nerve (IV) and the abducens nerve (VI), often leading to double-vision and strabismus. These cranial nerves may also be impacted by herniation of the temporal lobes of the brain via the falx cerebri.

 

The cause of trigeminal neuralgia, where one side of the face experiences painful signs and symptoms, is believed to be due to the compression of a cranial nerve by an artery as the nerve exits from the brain stem. An acoustic neuroma, especially at the junction between the pons and medulla, may compress the facial nerve (VII) and the vestibulocochlear nerve (VIII), resulting in hearing and sensory loss on the affected side.

 

Stroke

 

Occlusion of blood vessels which supply the cranial nerves or their nuclei, or an ischemic stroke, might cause specific signs and symptoms which could localize where the occlusion happened. A clot in a blood vessel draining the cavernous sinus, also known as the cavernous sinus thrombosis, may affect the oculomotor (III), the trochlear (IV), and the opthalamic branch of the trigeminal nerve (V1) and the abducens nerve (VI).

 

Inflammation

 

Inflammation caused by an infection may impair the operation of any of the cranial nerves. Infection of the facial nerve (VII), for instance, can result in Bell’s palsy. Multiple sclerosis, an inflammatory process which can produce a loss of the myelin sheathes that encircle the cranial nerves, may cause a variety of shifting signs and symptoms which can ultimately affect multiple cranial nerves.

 

Other

 

Trauma to the skull, bone disease like Paget’s disease, and damage or injury to the cranial nerves through neurosurgery, by way of instance, through tumor removal, are other potential causes of cranial nerve health issues.

 

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Dr. Alex Jimenez’s Insight

There are 12 pairs of cranial nerves which exit the brain, one in each side. These cranial nerves are named and numbered (I-XII) according to their location in the brain as well as their specific function in the body. Common conditions, such as multiple sclerosis, may affect one or more of the cranial nerves, resulting in dysfunction of the specific regions innervated by them. Signs and symptoms associated with health issues affecting specific cranial nerves can help healthcare professionals determine the source of the problem. Testing the cranial nerves involves a number of steps in order to be certain which function of the human body has been ultimately affected.

 

Clinical Significance of the Cranial Nerves

 

Most commonly, humans are believed to have twelve pairs of cranial nerves which have been assigned Roman numerals I-XII for identification. The numbering of the cranial nerves is based on the order in which they emerge from the brain, or from the front to the back of the brainstem. These include: the olfactory nerve (I), the optic nerve (II), the oculomotor nerve (III), the trochlear nerve (IV), the trigeminal nerve (V), the abducens nerve (VI), the facial nerve (VII), the vestibulocochlear nerve (VIII), the glossopharyngeal nerve (IX), the vagus nerve (X), the accessory nerve (XI), and the hypoglossal nerve (XII). Below we will narrow down the clinical significance of the cranial nerves.

 

Olfactory Nerve (I)

 

The olfactory nerve (I) communicates the sensation of smell to the brain. Lesions resulting in anosmia, or loss of the sense of smell, have been previously described to occur through trauma, damage or injury to the head, especially in the instance that a patient hits the back of their head. In addition, frontal lobe masses, tumors, and SOL have also been associated with the loss of the sense of smell. Healthcare professionals have previously identified that the loss of the sense of smell is one of the first symptoms seen in Alzheimer’s and early dementia patients.

 

Healthcare professionals may test the function of the olfactory nerve (I) by having the patient close their eyes and cover one nostril at a time in order to have them breathe out through their nose while placing a scent under the nostril and having them breathe in. The doctor will ask the patient, “do you smell anything?”, and record the findings. This tests whether the nerve is operating appropriately. If the patient says yes, the doctor will then ask the patient to identify the scent. This tests whether the processing pathway, known as the temporal lobe, is functioning accordingly.

 

Optic Nerve (II)

 

The optic nerve (I) communicates visual information to the retina. Lesions to this cranial nerve can be the result of CNS disease, such as MS, or CNS tumors and SOL. Most health issues associated with the visual system emerge from direct trauma, metabolic or vascular diseases. FOV lost in the periphery can also indicate that SOL may be affecting the optic chiasm, including a pituitary tumor.

 

A healthcare professional will often test the function of the optic nerve (II) by asking whether the patient can see. If the patient describes having vision in each eye, the optic nerve is functional. Doctors may also perform visual acuity testing using the Snellen chart, first one eye at a time, then the two eyes together, or they may perform distance vision testing. Near vision testing will often involve the Rosenbaum chart, first one eye at a time, then the two eyes together. Additional associated testing for the visual system can include, the ophthalmoscopic or funduscopic exam, which assess the A/V ratio and vein/artery health as well as assess cup to disc ratio of the visual system. Other testing methods include field of vision testing, intraoccular pressure testing and the iris shadow test.

 

Oculomotor Nerve (III), Trochlear Nerve (IV), and Abducens Nerve (VI)

 

The oculomotor nerve (III), the trochlear nerve (IV), the abducens nerve (VI) and the ophthalmic division of the trigeminal nerve (V1) travel through the cavernous sinus to the superior orbital fissure, passing out of the skull into the orbit. These cranial nerves control the tiny muscles that move the eye and also offer sensory innervation to the eye and orbit.

 

The clinical significance of the oculomotor nerve (III) includes diplopia, lateral strabismus (unopposed lateral rectus m.), head rotation away from the side of the lesion, a dilated pupil (unopposed dilator pupillae m.), and ptosis of the eyelid (loss of function of the levator palpebrae superioris m.). Lesions to the oculomotor nerve (III) can occur due to inflammatory diseases, such as syphilitic and tuberculous meningitis, aneurysms of the posterior cerebral or superior cebellar aa., and SOL in the cavernous sinus or displacing the cerebral peduncle to the opposite side. Testing this cranial nerve is performed by moving a light in front of the patient’s pupil from the lateral side and hold for 6 seconds. The doctor should watch for direct (ispilateral eye) and consensual (contralateral eye) pupillary constriction in order to distinguish dysfunction of the oculomotor nerve (III).

Testing Cranial Nerve III | El Paso, TX Chiropractor

 

The clinical significance of the trochlear nerve (IV) is characterized where the patient presents diplopia and difficulty while maintaining a downward gaze, often complaining of having difficulties when walking down stairs, resulting in more frequent tripping and/or falling, followed by extortion of the affected eye (unopposed inferior oblique m.) and a head tilt to the unaffected side. Lesions to the trochlear nerve (IV) can commonly be the result of inflammatory diseases, aneurysms of the posterior cerebral or superior cerebellar aa., SOL in the cavernous sinus or superior orbital fissure and surgical damage during mesencephalon procedures. Head tilts in superior oblique palsy (CN IV failure) may also be identified.

 

The clinical significance of the abducens nerve (VI) includes diplopia, medial strabismus (unopposed medial rectus m.), and head rotation towards the side of the lesion. Lesions to this cranial nerve can be the result of aneurysms of the posterior inferior cerebellar or basilar aa., SOL in the cavernous sinus or 4th ventricle, such as a cerebellar tumor, fractures of the posterior cranial fossa, and increased intracranial pressure. Testing this cranial nerve is performed through the H-Pattern testing, where the healthcare professional will have the patient follow an object no bigger than 2 inches. It’s essential for the doctor to follow these specific guidelines as patient’s can have difficulties focusing on items that are too large, and it’s also important for the doctor not to hold the object too close to the patient. Convergence and accommodation testing is performed by bringing the object close to the bridge of the patient’s nose and back out at least 2 times. The physician must look for pupillary constriction response as well as convergence of the eyes.

 

Trigeminal Nerve (V)

 

The trigeminal nerve (V) is made up of three different parts: The . When put together, these nerves provide sensation to the skin of the face and also controls the muscles of mastication, or chewing. Cranial nerve dysfunction along any of the separate sections of the trigeminal nerve (V) can manifest as decreased bite strength on the ipsilateral side of the lesion, loss of sensation along the distribution of V1, V2, and V3, and loss of corneal reflex. Lesions to the trigeminal nerve (V) can be the result of aneurysms or SOL affecting the pons, particularly tumors at the cerebellopontine angle, skull fractures on the facial bones or damage to the foramen ovale, and Tic doloureux, most frequently referred to as trigeminal neuralgia, characterized by sharp pain along the distributions of the different parts of the trigeminal nerve (V). Physicians may utilize analgesic, anti-inflammatory or contralateral stimulation to control the signs and symptoms.

 

Testing the trigeminal nerve (V) includes pain & light touch testing along the ophthalmic (V1), the maxillary (V2), as well as the Mandibular (V3) nerves of the cranial nerve. Testing is best done toward the more medial or proximal areas of
the face, where the V1, the V2 and the V3 are better delineated. A healthcare professional may also assess dysfunction along this cranial nerve using the blink/corneal reflex testing, performed by puffing air or doing a small tissue tap from the lateral side of the eye on the cornea. If normal, the patient blinks. The CN V provides the sensory (afferent) arc of this reflex. Bite strength may also be tested by having the patient bite down on a tongue depressor while the doctor tries to remove it. The jaw jerk/Masseter reflex may also be performed with the patient’s mouth slightly open, by placing the thumb on a patient’s chin and tapping the own thumb with a reflex hammer. Strong closure of the mouth indicates UMN lesion. CN V provides both the motor and sensory of this reflex.

 

Facial Nerve (VII) and Vestibulocochlear Nerve (VIII)

 

The facial nerve (VII) and the vestibulocochlear nerve (VIII) both input the inner auditory canal in the temporal bone. The facial nerve subsequently extends to the side of the face then distributes to control and reach all of the muscles in charge of facial expressions. The vestibulocochlear nerve reaches the organs which control equilibrium and hearing in the temporal bone.

 

As with all cranial nerves, signs and symptoms along the facial nerve (VII) describe the location of the lesion. Lesion in the lingual nerve will manifest as loss of taste, general sensation in the tongue and salivary secretion. Lesion proximal to the branching of the chorda tympani, such as in the facial canal, will result in the same signs and symptoms, without the loss of general sensation of the tongue, partly due because the V3 has not yet joined the facial nerve (VII). Corticobulbar innervation is asymmetric to the upper and lower parts of the facial motor nucleus. In the instance of an UMN lesion, or a lesion to the corticobulbar fibers, the patient will experience paralysis of the muscles in charge of facial expression in the contralateral lower quadrant. If there is an LMN lesion, or a lesion to the facial nerve itself, the patient will experience paralysis of the muscles of facial expression in the ipsilateral half of the face, otherwise known as Bell’s palsy.

 

A healthcare professional will test the facial nerve (VII) initially by asking the patient to mimic or follow specific instructions to make certain facial expressions. The doctor should make sure to evaluate all four quadrants of the face by asking the patient to raise their eyebrows, puff their cheeks, smile and then close their eyes tightly. Subsequently, the doctor will test the facial nerve (VII) by checking the strength of the buccinator muscle against resistance. The healthcare professional will achieve this by asking the patient to hold air in their cheeks as they press gently from the outside. The patient should be able to hold air in against the resistance.

 

Signs and symptoms of dysfunction in the vestibulocochlear nerve (VIII) often involve changes in hearing alone, most commonly as a result of infections in the otitis media and/or as a result of skull fractures. The most common lesion to this nerve is caused by an acoustic neuroma which affects the CN VII and the CN VIII, particularly the cochlear and vestibular divisions, as a result of proximity in the internal auditory meatus. Signs and symptoms of the health issue include nausea, vomiting, dizziness, hearing loss, tinnitus, and Bell’s palsy, etc.

 

Testing the vestibulocochlear nerve (VIII) for dysfunction commonly involves an otoscopic exam, the scratch test, which determines whether a patient can hear equally on both sides, the Weber test, tests for lateralization, a 256 Hz tuning fork placed on top of the patient’s head in the center, which can help point out whether a patient hears it louder on one side than the other, and finally the Rinne test, which compares air conduction to bone conduction. Normally, air conduction should last twice as long as bone conduction.

 

Testing Cranial Nerve VIII | El Paso, TX Chiropractor

 

Glossopharyngeal Nerve (IX), Vagus Nerve (X) and Accessory Nerve (XI)

 

The glossopharyngeal (IX), the vagus nerve (X) and the accessory nerve (XI) all emerge from the skull to enter the neck. The glossopharyngeal nerve (IX) provides innervation to the upper throat and the back of the tongue, the vagus nerve (X) offers innervation to the muscles at the voicebox, and proceeds down to provide parasympathetic innervation to the chest and abdomen. The accessory nerve (XI) controls the trapezius and sternocleidomastoid muscles at the neck and shoulder.

 

The glossopharyngeal nerve (IX) is rarely damaged alone, due to it’s proximity to the CN X and XI. A healthcare professional should perform a test to look for signs of CN X & XI damage as well if CN IX involvement is suspected.

 

Patients with clinical signs and symptoms caused by vagus nerve (X) dysfunction may experience dysarthria, or difficulty speaking clearly, as well as dysphagia, or difficulty swallowing. These may present as food or liquid coming out of their nose or frequent chocking or coughing when eating and/or drinking. Further clinical presentations include hyperactivity of a visceral motor component, leading to the hypersecretion of gastric acid and resulting in ulcers. Hyper-stimulation of the general sensory component can cause coughing, fainting, vomiting and reflex visceral motor activity. The visceral sensory component of this nerve only provides general feelings of un-wellness but visceral pain may transfer on to the sympathetic nerves.

 

Testing for the glossopharyngeal nerve (IX) and the vagus nerve (X) can include the gag reflex, where the CN IX provides the afferent (sensory) arc and the CN X provides the efferent (motor) arc. Approximately 20 percent of patients have a minimal or absent gag reflex. Other tests may include wwallowing, gargling, etc., as it requires CN X function. Healthcare professionals may also test palatal elevation because it requires CN X function. Furthermore, the doctor will see whether the palate elevates and uvula deviates
contralateral to damaged side. Finally, the healthcare professional will test the auscultation of the heart, since the R CN X innervates SA node (more rate regulation) and the L CN X the AV node (more rhythm regulation).

 

Testing Cranial Nerve IX and X | El Paso, TX Chiropractor

 

Lesions in the accessory nerve (XI) may occur due to radical surgeries in the neck area, such as the removal of the laryngeal carcinomas. Testing for the accessory nerve (XI) may include the strength test SCM m. Patients with clinical signs and symptoms due to lesions in the accessory nerve (XI) will experience difficulties turning their head against the resistance of a healthcare professional, particularly toward the side opposite of the lesion. Testing for the accessory nerve (XI) may also include the strength test trapezius m. Patients with clinical signs and symptoms due to lesions in the accessory nerve (XI) will experience difficulties with shoulder elevation on the side of the lesion.

 

Hypoglossal Nerve (XII)

 

The hypoglossal nerve (XII) originates from the skull to reach the tongue in order to control essentially all of the muscles involved in the movements of the tongue. The clinical significance of health issues associated to the hypoglossal nerve (XII) can manifest as a deviating tongue towards the side of an inactive genioglossus m. upon tongue protrusion. This may often be contralateral to a corticobulbar, or UMN, lesion or from an ipsilateral to a hypoglossal n., or LMN, lesion.

 

Testing Cranial Nerve XII | El Paso, TX Chiropractor

 

Testing for the hypoglossal nerve (XII) involves the healthcare professional asking a patient to stick out their tongue. The doctor will look for any deviation which may signal a health issue along the length of the hypoglossal nerve (XII). Another test the doctor may perform as a part of the evaluation may include the physician asking the patient to place their tongue inside their cheek and apply light resistance, one side at a time. The patient should be able to resist moving their tongue with pressure.

 

Clinical Examination of Cranial nerves I-VI

 

 

Clinical Examination of Cranial nerves VII-XII

 

 

The clinical significance of the signs and symptoms which manifest as a result of cranial nerve dysfunction are essential in order for the healthcare professional to properly diagnose the patient’s specific health issue. The clinical findings described above are often unique to the affected cranial nerve and the tests and evaluations for each can help confirm a diagnosis. Proper diagnosis is fundamental in order for the doctor to continue with the patient’s appropriate treatment. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

Curated by Dr. Alex Jimenez

 

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Additional Topics: Sciatica

Sciatica is medically referred to as a collection of symptoms, rather than a single injury and/or condition. Symptoms of sciatic nerve pain, or sciatica, can vary in frequency and intensity, however, it is most commonly described as a sudden, sharp (knife-like) or electrical pain that radiates from the low back down the buttocks, hips, thighs and legs into the foot. Other symptoms of sciatica may include, tingling or burning sensations, numbness and weakness along the length of the sciatic nerve. Sciatica most frequently affects individuals between the ages of 30 and 50 years. It may often develop as a result of the degeneration of the spine due to age, however, the compression and irritation of the sciatic nerve caused by a bulging or herniated disc, among other spinal health issues, may also cause sciatic nerve pain.

 

 

 

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EXTRA IMPORTANT TOPIC: Chiropractor Sciatica Symptoms

 

 

MORE TOPICS: EXTRA EXTRA: El Paso Back Clinic | Back Pain Care & Treatments

Ataxia And Dizziness | El Paso, TX.

Ataxia And Dizziness | El Paso, TX.

Ataxia is a degenerative disease of the nervous system. Symptoms can mimic those of being inebriated/intoxicated, with  slurred speech, stumbling, falling, and unable to maintain coordination. This comes from degeneration of the cerebellum, which is the part of the brain responsible for coordinating movement. It is a disease that affects people of all ages. However, age of symptom onset can vary, from childhood to late adulthood. Complications from the disease can be serious, even debilitating and life shortening.

Symptoms can vary from person to person, as well as, the type of Ataxia. Symptom onset and progression can vary as well. Symptoms can worsen slowly, over decades or quickly, over a few months. The common symptoms are lack of coordination, slurred speech, trouble eating, swallowing, eye movement abnormalities, motor skill deterioration, difficulty walking, gait abnormalities, tremors, and heart problems. People with Ataxia usually require wheelchairs, walkers, and/or scooters to aid in mobility.

Ataxia

The Loss Of Full Control Of Bodily Movements, Especially Gait

History Of Ataxia

  • How long has it been present?
  • Slow onset ➔ Degenerative disease?
  • Acute onset ➔ Stroke?
  • When does it occur?
  • If worsened by walking on uneven surfaces, or with limited vision ➔ Sensory ataxia?
  • Are there any coexisting symptoms?
  • Vertigo, weakness, stiffness, cognitive changes, etc.
  • Have others noticed this gait disturbance?
  • If no, consider psychogenic cause
  • Is the gait change explainable by physical problems such as pain or weakness?
  • Antalgic gait, limp, etc.
  • Weakness
  • Proximal muscle weakness ➔ Myopathy?
  • Distal muscle weakness ➔ Neuropathy?
  • UMN signs?
  • LMN signs?
  • Has the patient fallen? Or at risk for fall?
  • Is ataxia limiting ADLs?

Balance

  • Utilizes
  • Vestibular system
  • Cerebellar system
  • Conscious proprioceptive information (joint position sense)
  • Visual information
  • Motor strength and coordination

Vestibular System

  • Generally, if the problem lies in the vestibular system the patient will experience dizziness, possibly having vertigo or nystagmus
  • Unable to walk a straight line
  • When walking, will tend to veer to one side

Testing The Vestibular System

  • Fukuda Stepping Test
  • Patient marches in place with eyes closed and arms raised to 90 degrees in front of them
  • If they rotate more than 30 degrees = positive
  • Patient will rotate toward the side of vestibular dysfunction
  • Rhomberg Test
  • If patient sways a different direction every time their eyes are closed, this may indicate vestibular dysfunction

Cerebellar System

  • Cerebellar gaits present with a wide-base and generally involve staggering and titubation
  • Patient will have difficulty doing Rhomberg’s test with eyes open or closed, because they cannot stand with their feet together
  • Afferent information helps make assessments about where the body is in space
  • Ventral spinocerebellar tract
  • Dorsal spinocerebellar tract
  • Cuneocerebellar tract
  • Olivocerebellar tract
  • Efferent tracts carry responsive information to make adjustments to muscle tone and position to maintain balance

Testing The Cerebellar System

  • Piano-playing test & hand-patting test
  • Both assess for dysdiadochokinesia
  • Both tests, patient will have more difficulty moving the limb on the side of cerebellar dysfunction
  • Finger-to-nose test
  • Patient may be hyper/hypo metric in movement
  • Intention tremor may be reveled

Joint Position Sense

  • Conscious proprioception may be diminished, especially in elderly patients and patients with neuropathy

Visual Information

  • Patients with joint position sense losses often rely on visual information to help compensate.
  • When visual input is removed or diminished these patient’s have exaggerated ataxia.

Motor Strength & Coordination

  • If patient has reduced frontal lobe control they may end up with an apraxia of gait, where they have difficult with the volitional control of movement
  • Extrapyramidal disorders such as Parkinson disease result in inability to control motor coordination
  • Pelvic girdle muscle weakness due to a myopathy will produce an abnormal gait pattern

Commonly Seen Abnormal Gait Patterns

  • Circumduction gait
  • Hemiplegia
  • Often due to stroke
  • Bilaterally (Diplegic gait), causes toe walking
  • Typical gait of cerebral palsy patients
  • Festinating gait
  • Small steps due to spasticity
  • Often seen in Parkinson Disease
  • Myopathicgait(waddling)
  • Seen in disorders of proximal muscle weakness
  • Steppage gait/Neuropathic gait
  • Leg is lifted from the hip, without dorsiflexion at the ankle
  • Often seen in patients with foot-drop due to a LMN lesion
  • Wide-BasedCerebellargait

Gait Deviations

 

Dizziness

The Sensation Of Loss Of Balance

  • 4 Main Types
  • Vertigo
  • Peripheral
  • Central
  • Pre-Syncope/Light-headedness
  • Disequilibrium
  • Other/Floating type

Peripheral Vertigo

  • More common than central vertigo
  • Due to damage to the inner ear or CN VIII
  • Usually produces abnormal eye movements
  • Nystagmus – May be horizontal or rotary
  • Usually jerky in nature, with a fast and slow phase
  • Named for the direction of the fast phase
  • Vertigo usually worsens when patient looks to the side of the fast phase of nystagmus
  • Severity of nystagmus usually correlates with severity of vertigo
  • No other symptoms/signs of CNS dysfunction
  • Patient may have nausea or difficulty walking, but only because of vestibular dysfunction
  • Patient may also have hearing loss or tinnitus due if CN VIII or auditory mechanism function is damaged
  • Typically the causes are benign, including
  • Benign paroxysmal positional vertigo (BPPV)
  • Cervicogenic vertigo
  • Acute labyrinthitis/Vestibular neuronitis
  • Meniere’s Disease
  • Perilymph fistula
  • Acoustic Neuroma

Narrowing It Down

  • If movement, particularly of the head/neck exacerbate vertigo, consider:
  • BPPV
  • Vertebrobasilar artery insufficiency
  • Cervicogenic vertigo
  • If noise brings on episodes, consider:
  • Meniere’s disease
  • Perilymph fistula

Vertigo Hx Questions

  • Does your dizziness feel like you’re on an amusement park ride?
  • Do you get nauseous when you’re dizzy?
  • Are you spinning?
  • Or is the world spinning?

Benign Paroxysmal Positional Vertigo (BPPV/BPV)

  • benign paroxysmal positional vertigo el paso tx.May develop spontaneously, especially in the elderly
  • May arise due to head trauma
  • Vertiginous episodes associated with specific movements:
  • Looking at a high shelf (“top-shelf vertigo”)
  • Bending over
  • Rolling over in bed
  • Onset of vertigo begins a few seconds after the movement, and resolves within about a minute
  • Diagnostic test
  • Dix-Hallpike Maneuver
  • Treatment procedure
  • Epley Maneuver
  • Brandt-Daroff Exercises
  • Can self resolve as crystals dissolve, but it may take months and new otoliths can become displaced

Cervicogenic Vertigo

  • Occurs after head/neck injuries, but is not very common
  • Usually accompanied by pain and/or joint restriction
  • Usually vertigo and nystagmus will be less severe than in BPPV
  • Vertigo begins with change in head position but does not subside as quickly as it does in BPPV

Vertebrobasilar Artery Insufficiency

  • Occurs if the vertebral artery is compressed during head rotation/extension
  • Onset of vertigo is delayed more than in BPPV or cervigogenic vertigo, because ischemia will take up to 15 seconds to occur
  • Orthopedic test may help in evaluation
  • Barré-Liéou Sign
  • DeKlyn Test/Hallpike Maneuver
  • Hautant test
  • Underberg Test
  • Vertebrobasilar After Functional Maneuver

Acute Labyrinthitis/ Vestibular Neuronitis

  • Not well understood, but believed to be inflammatory in origin
  • Follows viral infection or arise seemingly without cause
  • Single, monophasic attack of vertigo
  • Resolves in days to a few weeks and generally does not reoccur

Meniere’s Disease

  • Increased pressure in the endolymph causes membrane ruptures and sudden mixture of endolymph and perilymph
  • Episodes last 30 minutes to several hours, until equilibrium between the fluids is reached
  • Over time, episodes damage vestibular and cochlear hair cells
  • Low-pitch buzzing tinnitus
  • Loss of hearing of low tones

Meniere’s Disease vs. Syndrome

  • Meniere’s syndrome is when then symptoms of Meniere’s disease are found to be secondary to another condition, such as:
  • Hypothyroidism
  • Acoustic neuroma
  • Superior semicircular canal dehiscence (SCDS)
  • Perilymph fistula
  • True Meniere’s disease is idiopathic

Perilymph Fistula

  • Small leak due to trauma, especially barotrauma
  • Can look very similar symptomatically to Meniere’s disease/syndrome
  • Exacerbated by changes in pressure
  • Airplane rides
  • Driving uphill
  • Hennebert’s sign
  • Vertigo or nystagmus episode brought on by sealing pressure of the ear (such as by inserting an otoscope)

Central Vertigo

  • Less common than peripheral vertigo
  • Caused by damage to the processing centers of vestibular information in the brain stem and the cerebral cortex
  • Typically “dizziness” is less severe than with peripheral vertigo
  • Nystagmus
  • Usually more severe than the description/patient’s complaint
  • May go in multiple directions, including vertical
  • May or may not have other CNS findings on examination
  • No change in hearing expected

Causes Include:

  • Cerebrovascular disease (such as transient ischemic attacks)
  • Multiple Sclerosis
  • Arnold-Chiari Malformation
  • Damage to caudal brainstem or vestibulocerebellum
  • Migraine condition

Pre-Syncope Hx Qustions

  • Does it feel like you’re going to pass out?
  • Does the dizziness feel similar to when you stand up too fast?

Pre-Syncope

  • “Light-headedness”
  • CardiacOrigin
  • Output disorders
  • Arrhythmias
  • Holter monitor testing
  • Postural/Orthostatic hypotension
  • May be secondary to other problems (diabetic neuropathy, adrenal hypofunction, Parkinsons, certain medications, etc.)
  • Vasovagal episodes
  • Slow heart rate with low blood pressure
  • Often brought on by stress, anxiety or hyperventilation
  • Migraine
  • Due to cerebrovascular instability
  • Blood sugar dysregulation

Disequilibrium Hx Questions

  • Does the dizziness only occur when you’re on your feet?
  • Does it get better if you touch/hold onto something?

Disequilibrium

  • Common in the elderly
  • Due to sensory deficits
  • Gradual onset
  • Worsened by reduced vision
  • Dark
  • Eyes closed
  • Visual acuity losses
  • Improved by touching a stationary object
  • Subjective of dizziness often improves with a gait assistive device (cane, walker, etc.)

Other Causes

  • Psychological stress
  • Often patient will describe dizziness as “floating”
  • Rule out hyperventilation and other types of dizziness

Sources

Blumenfeld, Hal. Neuroanatomy through Clinical Cases. Sinauer, 2002.
Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.

Benign Paroxysmal Positional Vertigo | El Paso, TX.

Benign Paroxysmal Positional Vertigo | El Paso, TX.

You have been diagnosed with Benign Paroxysmal Positional Vertigo. This brochure is designed to help increase your understanding of this disorder and its potential treatments.

Benign Paroxysmal Positional Vertigo

What Is BPPV?

Benign paroxysmal positional vertigo (BPPV) is a disorder of the inner ear. People with BPPV typically experi­ence brief episodes of vertigo (dizziness) when they change the position of their head with respect to gravity. Approximately 20 percent of all vertigo is due to BPPV.

What Causes BPPV?

benign paroxysmal positional vertigo el paso tx.

Benign Paroxysmal Positional Vertigo is thought to be due to tiny crystals, called otoconia, that have collected within a sensitive part of the inner ear. Otoconia are crystals of calcium carbonate that are normally located in a structure of the ear called the utricle.

Dizziness occurs when the crystals are displaced from the utricle into the semicircular canals of the inner ear.
Otoconia may become displaced when the utricle is injured, if there is an infection or other disorder of the inner ear, or simply due to advanced age. When you change the position of your head, the otoconia move within the semicircular canals and this causes the dizziness. The dizziness subsides when the otoconia stop moving.

The most common cause of BPPV in people under age 50 is head injury. In older people, the most common cause is degeneration of the vestibular system of the inner ear. BPPV becomes much more common with advancing age. Other causes include minor strokes, Meniere’s disease, and viruses such as those causing vestibular neuritis. In approximately half of all BPPV cases, no cause can be determined.

What Are The Symptoms?

The symptoms of BPPV include dizziness or vertigo, lightheadedness, imbalance, and nausea. Activities that
bring on symptoms vary among individuals, but symptoms are usually associated with a change in the position of the head with respect to gravity. Getting out of bed, rolling over in bed, and tipping the head back to look up are common “problem” motions. The use of shampoo bowls in hair salons may bring on symptoms. An intermittent pattern is common. BPPV may be present for a few weeks, then stop, and then come back again.

How Is Benign Paroxysmal Positional Vertigo (BPPV) Diagnosed?

BPPV is diagnosed with the Dix-Hallpike test. This test involves observing the eyes with the head and body positioned in specific ways. It can be performed either by the clinician, or as part of a laboratory test called an electronystagmography, or ENG. If the Dix-Hallpike test is abnormal and the findings are “dassic” for BPPV, then additional testing is not necessary. If the results are normal or not “classic” then the diagnosis of BPPV is less certain and other tests may be suggested.

What Are The Treatments For BPPV?

There are four approaches to treating BPPV.

1. Do Nothing And Wait For It To Go Away By Itself

BPPV symptoms sometimes go away within six months of onset, therefore you might want to wait and see if your symptoms subside on their own. During this waiting period, medications to prevent motion sickness or nausea are sometimes helpful in controlling the nausea associated with BPPV.

2. Physical Maneuvers Performed In The Clinic

benign paroxysmal positional vertigo el paso tx.(The Epley and Semont Maneuvers)
The Epley and Semont maneuvers, named for their inventors, are treat­ments that are performed in the clinic. These treatments are specifi­cally intended to move the otoconia from the semicircular canals to a less sensitive location within the inner ear. Your clinician will select the treatment that is most appropriate for you.

Each of these treatments takes about 15 minutes and alleviates symptoms in about 80 percent of patients. In the remaining 20 percent, a second treatment may be necessary, or you may be instructed to perform the Brandt-Daroff exercises (see “Home Treatment”).

The Epley maneuver, also called the canalith reposi­tioning procedure (CRP) and particle repositioning, is a procedure in which the clinician moves your head into five positions, maintaining each position for ap­proximately 30 seconds. The Semont maneuver (also called the liberatory maneuver) is a procedure in which the clinician rapidly moves you from lying on one side to lying on the other side. These maneuvers may not be appropriate for patients with neck or back problems. Pa­tients who experience nausea or anxiety may wish to take medication prior to the treatment.

INSTRUCTIONS FOR PATIENTS AFTER CLINIC TREATMENTS

Follow these instructions after the Epley or Semont maneuver. B.Y doing so you will minimize the opportunity for otoconia to return to the semicircular canals of the inner ear and reduce the potential that your dizziness will recur.

Wait at least 10 minutes after the maneuver before going home.

This is to avoid “quick spins” or brief bursts of vertigo as the otoconia reposition themselves immedi­ately after the maneuver. If possible, arrange to have someone drive you home.

The following two days:
  • benign paroxysmal positional vertigo el paso tx.Sleep semi-recumbent for the next two nights. This means sleeping with your head halfway between flat and upright, at a 45-degree angle. This is most easily done by sleeping in a recliner chair or by sleeping with pillows appropriately arranged on a couch.
  • During the day, try to keep your head vertical. A soft neck brace may be helpful.
  • Do not go to the barber, hairdresser or dentist.
  • When shaving, keep your head vertical by bending forward at your hips with your neck extended.
  • If you need to administer eye drops, try to keep your head as vertical as possible.
  • Sham­poo only under the shower.
During the following week, avoid provoking head positions that might bring on BPPV.
  • Use two pillows when you sleep.
  • Avoid sleeping on the affected side.
  • Don’t turn your head far up or far down.
  • Avoid tilting your head back especially when lying on your back with your head turned toward the affected side.
  • If possible, postpone elective surgery and going to the beauty parlor or the dentist’s office.
  • Avoid far head-forward positions and exercises where the head is not kept upright, for example toe touches.
The effectiveness of the clinic treatment cannot be determined for one week.

Wait one week after treatment to test the effectiveness of treatment. Place yourself in the position that usually makes you dizzy. Be sure to position yourself cautiously and under conditions in which you can’t fall or hurt yourself.

3. Home Treatment Of Benign Paroxysmal Positional Vertigo (Brandt-Daroff Exercises)

When the clinic treatment (Epley or Semont) fails, when the involved side is not determined, or when a case is mild, the Brandt-Daroff exercises may be recommended. These exercises succeed in 95 percent of cases but take longer to work than the clinic treatments. You should perform these exercises only if instructed to do so by your clinician. If your clini­cian performed the Epley or Semont maneuver, you must wait one week after that treatment before you begin the Brandt-Daroff exercises.

These exercises should be performed on a flat surface, without a pillow.

benign paroxysmal positional vertigo el paso tx.

Start sitting upright on the edge of the bed or on the floor.

(Position 1) Turn your head 45 degrees to the left and lie down on your right side.

(Position 2) When in the right side-lying position, your head should be at a 45-degree angle turned halfway between the flat surface and the ceiling. Stay in the side-lying position for at least 30 seconds. If you are still dizzy, stay until the dizziness subsides or one minute, whichever is less.

Then sit up (Position 3} and stay in the sitting posi­tion for 30 seconds. Turn your head 45 degrees to the right and lie down on your left side.

(Position 4) Again keeping your head turned halfway toward the ceiling for 30 seconds or until the dizziness subsides. Return to Position 1 (sit upright) for 30 seconds. This is one repetition.

One set (five repetitions) takes about 10 minutes to complete and should be performed each morning, mid-day and evening.

The Brandt-Daroff exercises should be performed for two weeks, three sets each day, or for three weeks, two sets each day (52 sets total). In most individuals, complete relief from symptoms is obtained after 30 sets, or about 10 days. In approximately 30 percent of patients, BPPV will recur within one year. If BPPV recurs you may wish to add one 10-minute exercise (one set) to your daily routine.

4. Surgical Treatment Of Benign Paroxysmal Positional Vertigo

If the maneuvers or exercises do not control symptoms that have persisted for a year or longer and the diagnosis is very clear, surgery may be recommended. The most common surgical procedure, called posterior canal plugging, blocks most of the posterior canal’s function without affecting the functions of the other canals or parts of the ear. There is, however, a small risk of hearing loss. This surgery is effective in about 90 percent of individuals who have not responded to other treatments and when symptoms are severe and long-standing.

©️2000 Northwestern University.
Authors: Timothy C. Hain, MD, Janet Odiry Helminski, PhD, PT.

This information is for educational purposes and is not intended as a substitute for examination, diagnosis, or medical care provided by a licensed and qualified health professional. This work was supported by the Center for Sensory and Communicotion Disorders at Northwestern University, a national research and training center funded by the National Institute on Deafness and Other Communication Disorders.

Structure and Function of the Cranial Nerves in El Paso, TX

Structure and Function of the Cranial Nerves in El Paso, TX

The cranial nerves are the nerves which come out straight from the brain, including the brainstem, in comparison to the spinal nerves, which come out from sections of the spinal cord. Of those, 10 out of 12 of these cranial nerves originate in the brainstem. Cranial nerves transfer information between the brain and parts of the human body, particularly to and from areas of the head and neck.

 

Spinal nerves exit from the spinal cord with the spinal nerve closest to the head (C1) exiting in the space above the first cervical vertebra. The cranial nerves, however, exit from the central nervous system above this region. Each cranial nerve is paired and is present on either side of the brain. Based on the definition in humans, there are twelve, sometimes thirteen, cranial nerve pairs, which have been assigned Roman numerals I-XII for identification, sometimes including cranial nerve zero as well. The numbering of the cranial nerves is based on the order in which they emerge from the brain, or from the front to the back of the brainstem.

 

The terminal nerves, olfactory nerves (I) and optic nerves (II) come out from the cerebrum, or forebrain, where the rest of the ten pairs of cranial nerves arise in the brainstem, which is the lower portion of the brain. The cranial nerves are considered components of the peripheral nervous system (PNS), though on a structural level, the olfactory, the optic and the trigeminal nerves are more accurately considered a portion of the central nervous system (CNS).

 

Most commonly, humans are believed to have twelve pairs of cranial nerves (I-XII). These include: the olfactory nerve (I), the optic nerve (II), the oculomotor nerve (III), the trochlear nerve (IV), the trigeminal nerve (V), the abducens nerve (VI), the facial nerve (VII), the vestibulocochlear nerve (VIII), the glossopharyngeal nerve (IX), the vagus nerve (X), the accessory nerve (XI), and the hypoglossal nerve (XII). There may be a thirteenth cranial nerve, known as the terminal nerve, or nerve N or O, which Is quite small and may or may not be functional in humans.

 

Cranial Nerves Diagram 1 | El Paso, TX Chiropractor

 

Cranial Nerves Diagram 2 | El Paso, TX Chiropractor

 

Anatomy of the Cranial Nerves

 

The cranial nerves are usually named according to their structure or function. For instance, the olfactory nerve (I) supplies smell, and the facial nerve (VII) supplies motor innervation to the face. Since Latin was the common language of the study of anatomy once the nerves were documented, recorded, and mentioned, many nerves maintain Greek or Latin names, including the trochlear nerve (IV), named based on its arrangement, as it supplies a muscle which attaches to a pulley (Greek: trochlea). The trigeminal nerve (V) is named based on its three components (Latin: trigeminus meaning triplets), and the vagus nerve (X) is known because of its wandering course (Latin: vagus).

 

In addition, cranial nerves are numbered according to their rostral-caudal, or front-back, position, when looking at the brain. If the brain is carefully removed from the skull, the nerves are typically visible in their numeric order, with the exception of the final nerve, the CN XII, which seems to come out from above, into the CN XI.

 

Cranial nerves have pathways within and away from the skull. The pathways inside the skull are known as “intracranial paths” and the pathways outside the skull are known as “extracranial pathways”. There are a number of holes in the skull known as “foramina”, by which the nerves may exit from the skull. All cranial nerves are paired, meaning that they can be found on both the left and right sides of the human body. The skin, muscles, or other structural function provided by a nerve on the same side of the human body as the side it originates from, is referred to as an ipsilateral function. In case the function is on the other hand from the origin of the nerve, then this is referred to as a contralateral function.

 

Location of the Cranial Nerves

 

After coming out from the brain, the cranial nerves from inside the skull must leave this bony structure in order to arrive to their destinations. Several of the cranial nerves pass through the foramina, holes in the skull, as they journey to their destinations. Other nerves pass through bony canals, longer pathways enclosed by bone. The foramina and canals might contain more than just one cranial nerve, and may also include blood vessels. Below is a list of the twelve cranial nerves and a brief summary of their function.

 

  • The olfactory nerve (I), composed of many small separate nerve fibers, which passes through perforations from the cribiform plate component of the ethmoid bone. These fibers end in the upper part of the nasal cavity and also operate to communicate impulses containing information about scents or odors into the brain.
  • The optic nerve (II) passes through the optic foramen from the sphenoid bone in order to reach the eye. It communicates visual information to the brain.
  • The oculomotor nerve (III), the trochlear nerve (IV), the abducens nerve (VI) and the ophthalmic division of the trigeminal nerve (V1) journey through the cavernous sinus to the superior orbital fissure, passing out of the skull into the orbit. These cranial nerves control the tiny muscles that move the eye and also offer sensory innervation to the eye and orbit.
  • The maxillary division of the trigeminal nerve (V2) moves through the foramen rotundum from the sphenoid bone to supply the skin of the middle of the face.
  • The mandibular branch of the trigeminal nerve (V3) moves through the foramen ovale of the sphenoid bone to supply the lower face with sensory innervation. This nerve also extends to nearly all the muscles that control chewing.
  • The facial nerve (VII) and the vestibulocochlear nerve (VIII) both input the inner auditory canal in the temporal bone. The facial nerve subsequently extends to the side of the face using the stylomastoid foramen, also from the temporal bone. Its fibers then distribute to control and reach all of the muscles in charge of facial expressions. The vestibulocochlear nerve reaches the organs which control equilibrium and hearing in the temporal bone, and therefore doesn’t reach the outside surface of the skull.
  • The glossopharyngeal (IX), the vagus nerve (X) and the accessory nerve (XI) all emerge from the skull via the jugular foramen to enter the neck. The glossopharyngeal nerve provides innervation to the upper throat and the back of the tongue, the vagus nerve offers innervation to the muscles at the voicebox, and proceeds down to provide parasympathetic innervation to the chest and abdomen. The accessory nerve controls the trapezius and sternocleidomastoid muscles at the neck and shoulder.
  • The hypoglossal nerve (XII) exits the skull using the hypoglossal canal at the occipital bone and also reaches the tongue to control virtually all the muscles involved in movements of this organ.

 

Cranial Nerves Diagram 3 | El Paso, TX Chiropractor

 

Function of the Cranial Nerves

 

The cranial nerves give motor and sensory innervation particularly to the structures found inside the neck and head. The sensory innervation contains both “overall” feelings, such as temperature and touch, and “particular” innervation, such as flavor, vision, smell, balance and hearing. For instance, the vagus nerve (X) gives sensory and autonomic, or parasympathetic, motor innervation to structures in the neck and to many of the organs in the chest and abdomen. Below, we will discuss the function of each cranial nerves in further detail.

 

Smell (I)

 

The olfactory nerve (I) communicates the sense of smell. Damage to the olfactory nerve (I) may cause an inability to smell, referred to as anosmia, a distortion in the sense of odor, referred to as parosmia, or even a distortion or absence of flavor. When there’s suspicion of a change in the sense of smell, every nostril is tested with compounds of known odors, such as coffee or soap. Intensely smelling chemicals, such as ammonia, can lead to the activation of pain receptors, known as nociceptors, of the trigeminal nerve which are situated in the nasal cavity, which may ultimately confound olfactory testing.

 

Vision (II)

 

The optic nerve (II) communicates visual information. Damage to the optic nerve (II) affects specific aspects of vision which are based on the area of the lesion. An individual may not be able to observe objects in their left or right sides, known as homonymous hemianopsia, or might have difficulty seeing objects on their outer visual areas, known as bitemporal hemianopsia, if the optic chiasm is included. Vision may be analyzed by examining the visual field, or simply by analyzing the retina with an ophthalmoscope, with a procedure called funduscopy. Visual field testing can be employed to pin-point structural lesions in the optic nerve, or further along the visual pathways.

 

Eye Movement (III, IV, VI)

 

The oculomotor nerve (III), the trochlear nerve (IV) and the abducens nerve (VI) coordinate eye motion. Damage to nerves III, IV, or VI can impact the movement of the eyeball globe. One or both eyes may be influenced; in either case, double vision, referred to as diplopia, will likely occur since the movements of the eyes are no longer synchronized. Nerves III, IV and VI are tested by observing the way the eye follows an object in different directions. This object may be a finger or even a pin, and may be moved at several directions to test for pursuit velocity. If the eyes don’t work together, the most likely cause is harm to a specific cranial nerve or its nuclei.

 

Damage to the oculomotor nerve (III) can lead to double vision, or diplopia, and inability to coordinate the movements of both eyes, known as strabismus, as well as eyelid drooping, referred to as ptosis, and pupil dilation, or mydriasis. Lesions may also lead to theinability to open the eye due to paralysis of the levator palpebrae muscle. People suffering from a lesion in the oculomotor nerve may compensate by leaning their heads to relieve symptoms because of paralysis of one or more of the eye muscles it regulates.

 

Damage to the trochlear nerve (IV) may also cause diplopia with all the eye adducted and raised. The result will be an eye which can’t move downwards properly, especially downwards when within an inward position. This is a result of impairment from the superior oblique muscle, which is innervated by the trochlear nerve.

 

Damage to the abducens nerve (VI) can also result in diplopia This is a result of impairment in the lateral rectus muscle, which is innervated by the abducens nerve.

 

Trigeminal nerve (V)

 

The trigeminal nerve (V) is made up of three different parts: The ophthalmic (V1), the maxillary (V2), as well as the Mandibular (V3) nerves. When put together, these nerves provide sensation to the skin of the face and also controls the muscles of mastication, or chewing. Conditions affecting the trigeminal nerve (V) include, trigeminal neuralgia, cluster headaches, and trigeminal zoster. Trigeminal neuralgia may occur later in life, from middle age onwards, most often after the age of 60, and it is a condition commonly associated with a very strong pain that spreads over the region innervated by the maxillary or mandibular nerve divisions of the trigeminal nerve (V2 and V3).

 

Facial expression (VII)

 

Lesions of the facial nerve (VII) may manifest as facial palsy. This is where a individual is unable to move the muscles on one or both sides of the face. An extremely frequent and generally temporary facial palsy is called Bell’s palsy. Bell’s Palsy is the end result of an idiopathic (unknown cause), unilateral lower motor neuron lesion of the facial nerve and is characterized by an inability to move the ipsilateral muscles of facial expression, including altitude of the eyebrow and furrowing of their forehead. Patients with Bell’s palsy frequently have a drooping mouth over the affected side and often have difficulty chewing since the buccinator muscle is affected. Bell’s palsy occurs very rarely, affecting around 40,000 Americans annually. Facial paralysis may be caused by other conditions including, stroke. Related conditions to Bell’s Palsy are sometimes misdiagnosed as Bell’s Palsy. Bell’s Palsy is a temporary condition usually lasting 2-6 months, but can have life-changing results and may reoccur often. Strokes typically also impact the cranial nerve by cutting off blood flow to nerves within the brain which is a clear indication that the nerve is present with similar symptoms.

 

Hearing and Equilibrium (VIII)

 

The vestibulocochlear nerve (VIII) divides into the vestibular and cochlear nerve. The vestibular region is in charge of innervating the vestibules and semicircular canal of the inner ear; this structure communicates information regarding equilibrium, and is a significant element of the vestibuloocular reflex, which keeps the brain stable and allows the eyes to track moving objects. The cochlear nerve communicates data from the cochlea, allowing sound to be heard. If damaged, the vestibular nerve can manifest the sensation of spinning and dizziness. Function of the vestibular nerve may be analyzed by placing warm and cold water in the ears and watching eye motions caloric stimulation. Damage to the vestibulocochlear nerve may also pose as repetitive and involuntary eye movements, previously described as nystagmus, particularly when looking in a horizontal plane. Damage to the cochlear nerve may cause partial or complete deafness in the affected ear.

 

Oral Sensation, Taste, and Salivation (IX)

 

The glossopharyngeal nerve (IX) innervates the stylopharyngeus muscle and supplies sensory innervation to the oropharynx and back of the tongue. The glossopharyngeal nerve additionally supplies parasympathetic innervation to the parotid gland. Unilateral absence of a gag reflex suggests a lesion of the glossopharyngeal nerve (IX), and perhaps the vagus nerve (X).

 

Vagus Nerve (X)

 

Reduction of function of the vagus nerve (X) can lead to a reduction of parasympathetic innervation to quite a high number of structures. Important consequences of damage to the vagus nerve could include an increase in blood pressure and heart rate. Isolated dysfunction of just the vagus nerve is rare, but can be diagnosed with a hoarse voice, because of dysfunction of one of its branches, the recurrent laryngeal nerve. Damage to this nerve may result in difficulties swallowing.

 

Shoulder Elevation and Head-Turning (XI)

 

Damage to the accessory nerve (XI) can lead to ipsilateral weakness in the trapezius muscle. This can be tested by asking the patient to elevate their shoulders or shrug, where the shoulder blade, or scapula, will protrude to a winged position. Additionally, if the nerve is damaged, weakness or an inability to elevate the scapula may be present because the levator scapulae muscle is only able to provide this function. Based on the location of the lesion, there may also be weakness within the sternocleidomastoid muscle, which then acts to reverse the head so that the face points to the other side.

 

Tongue Movement (XII)

 

The hypoglossal nerve (XII) is unique in that it is innervated in the motor cortices of both hemispheres of the brain. Damage to the nerve at lower motor neuron level may cause fasciculations or atrophy of the muscles of the tongue. The fasciculations of the tongue are sometimes said to look like a”bag of worms”. Upper motor neuron damage won’t cause atrophy or fasciculations, but only weakness of the innervated muscles. Once the nerve is damaged, it will lead to weakness of tongue movement on one side. When damaged and extended, the tongue will move towards the weaker or damaged side, as shown in the image.

 

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Dr. Alex Jimenez’s Insights

The cranial nerves are a set of 12 nerves which emerge directly from the brain. The first two nerves, known as the olfactory nerve and the optic nerve, come out from the cerebellum, where the remaining ten cranial nerves emerge from the brain stem. The names of the cranial nerves relate directly to their function and they are also numerically identified in roman numerals I-XII by their specific location of the brain and by the order in which they exit the cranium. Damage to any of the above mentioned cranial nerves can cause health issues associated to the specific structure and function of each nerve. Common signs and symptoms in these regions can help healthcare professionals identify the affected cranial nerves.

 

The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

Curated by Dr. Alex Jimenez

 

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Additional Topics: Sciatica

Sciatica is medically referred to as a collection of symptoms, rather than a single injury and/or condition. Symptoms of sciatic nerve pain, or sciatica, can vary in frequency and intensity, however, it is most commonly described as a sudden, sharp (knife-like) or electrical pain that radiates from the low back down the buttocks, hips, thighs and legs into the foot. Other symptoms of sciatica may include, tingling or burning sensations, numbness and weakness along the length of the sciatic nerve. Sciatica most frequently affects individuals between the ages of 30 and 50 years. It may often develop as a result of the degeneration of the spine due to age, however, the compression and irritation of the sciatic nerve caused by a bulging or herniated disc, among other spinal health issues, may also cause sciatic nerve pain.

 

 

 

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EXTRA IMPORTANT TOPIC: Chiropractor Sciatica Symptoms

 

 

MORE TOPICS: EXTRA EXTRA: El Paso Back Clinic | Back Pain Care & Treatments

Cranial Nerves: Introduction | El Paso, TX.

Cranial Nerves: Introduction | El Paso, TX.

Human Cranial nerves are a set of 12 paired nerves that come directly from the brain. The first two (olfactory and optic) come from the cerebrum, with the remaining ten come from the brain stem. The names of the these nerves relate to what function they perform and are also numerically identified in roman numerals (I-XII). The nerves serve in functions of smell, sight, eye movement, and feeling in the face. These nerves also control balance, hearing, and swallowing.

Cranial Nerves: Review

  • CN I – Olfactory
  • CN II – Optic
  • CN III – Oculomotor
  • CN IV – Trochlear
  • CN V – Trigeminal
  • CN VI – Abducens
  • CN VII – Facial
  • CN VIII – Vestibulocochlear
  • CN IX – Glossopharyngeal
  • CN X – Vagus
  • CN XI – Accessory
  • CN XII – Hypoglossal

Location Of Nerves

cranial el paso tx.

http://www.strokeeducation.info/images/cranial%20nerves%20chart.jpg

 

cranial el paso tx.

https://upload.wikimedia.org/wikipedia/commons/thumb/8/84/Brain_human_normal_inferior_view_ with_labels_en.svg/424px-Brain_human_normal_inferior_view_with_labels_en.svg.png

cranial el paso tx.

https://diagramchartspedia.com/cranial-nerve-face-diagram/cranial-nerve-face-diagram-a- synopsis-of-cranial-nerves-of-the-brainstem-clinical-gate/

CN I – Olfactory

cranial el paso tx.CN I Clinically

  • Lesions resulting in anosmia (loss of the sense of smell) can be caused by:
  • Trauma to the head, especially patient’s hitting the back of their head
  • Frontal lobe masses/tumors/SOL
  • Remember that loss of the sense of smell is one of the first symptoms seen in Alzheimer’s and early dementia patients

Testing CN I

  • Have the patient close their eyes and cover one nostril at a time
  • Have them breathe out through their nose, THEN place the scent under the nostril while they breathe in.
  • Ask them “do you smell anything?”
  • This tests if the nerve is functioning
  • If they say yes, ask them to identify it
  • This tests if the processing pathway (temporal lobe) is functional

Cranial Nerve II – Optic

cranial el paso tx.Cranial Nerve II Clinically

Lesions to this nerve can be the result of:

  • CNS disease (such as MS)
  • CNS tumors and SOL
  • Most problems with the visual system arise from direct trauma, metabolic or vascular diseases
  • FOV lost in the periphery can mean SOL affecting the optic chiasm such as a pituitary tumor

Testing Cranial Nerve CN II

  • cranial el paso tx.

    https://upload.wikimedia.org/wikipedia/commons/9/9f/Snellen_chart.svg

    Can the patient see?

  • If patient has vision in each eye, nerve is functional
  • Visual acuity testing
  • Snellen chart (one eye at a time, then two eyes together)
  • Distance vision
  • Rosenbaum chart (one eye at a time, then two eyes together)
  • Near vision

 

 

 

 

 

Associated Testing For Visual System

  • Ophthalmoscopic/Funduscopic exam
  • Assessment of A/V ratio and vein/artery health
  • Assessment of cup to disc ratio
  • Field of vision testing
  • Intraoccular pressure testing
  • Iris shadow test

Cranial Nerve III – Oculomotor

cranial el paso tx.Cranial Nerve III Clinically

  • Diplopia
  • Lateral strabismus (unopposed lateral rectus m.)
  • Head rotation (yaw) away from the side of the lesion
  • Dilated Pupil (unopposed dilator pupillae m.)
  • Ptosis of the eyelid (loss of function of levator palpebrae superioris m.)
  • Lesions to this nerve can be the result of:
  • Inflammatory diseases
  • Syphilitic and tuberculous meningitis
  • Aneurysms of the posterior cerebral or superior cerebellar aa.
  • SOL in the cavernous sinus or displacing the cerebral peduncle to the opposite side

Testing Cranial Nerve CN II & III

  • Pupillary reflex testing
  • Move the light in front of the pupil from the lateral side and hold 6 seconds
  • Watch for direct (ispilateral eye) and consensual (contralateral eye) pupillary constriction

cranial el paso tx.Testing Cranial Nerve CN II & III

cranial el paso tx.

https://commons.wikimedia.org/wiki/File:1509_Pupillary_Reflex_Pathways.jpg

Cranial Nerve IV – Trochlear

cranial el paso tx.Cranial Nerve IV Clinically

  • Patient has diplopia & difficulty in downward gaze
  • Often complain of difficulty walking down stairs, tripping,falling
  • Extortion of the affected eye (unopposed inferior oblique m.)
  • Head tilt (roll) to the unaffected side
  • Lesions to this nerve can be the result of:
  • Inflammatory diseases
  • Aneurysms of the posterior cerebral or superior cerebellar aa.
  • SOL in the cavernous sinus or superior orbital fissure
  • Surgical damage during mesencephalon procedures

Head Tilt In Superior Oblique Palsy (CN IV Failure)

cranial el paso tx.

Pauwels, Linda Wilson, et al. Cranial Nerves: Anatomy and Clinical Comments. Decker, 1988.

Cranial Nerve VI – Abducens

cranial el paso tx.Cranial Nerve VI Clinically

cranial el paso tx.

  • Diplopia
  • Medial strabismus (unopposed medial rectus m.)
  • Head rotation (yaw) toward the side of the lesion
  • Lesions to this nerve can be the result of:
  • Aneurysms of the posterior inferior cerebellar or basilar aa.
  • SOL in the cavernous sinus or 4th ventricle (such as a cerebellar tumor)
  • Fractures of the posterior cranial fossa
  • Increased intracranial pressure

Testing Cranial Nerve CN III, IV & VI

  • H-Pattern testing
  • Have the patient follow an object no larger than 2 inches
  • Patient’s can have focus difficulty if the item is too large
  • It’s also important not to hold the object too close to the patient.
  • Convergence and accommodation
  • Bring object close to the bridge of the patient’s nose and back out. Perform at least 2 times.
  • Look for pupillary constriction response as well as convergence of the eyes

Cranial Nerve V – Trigeminal

cranial el paso tx.Cranial Nerve V Clinically

  • Decreased bite strength on the ipsilateral side of lesion
  • Loss of sensation in V1, V2 and/or V3 distribution
  • Loss of corneal reflex
  • Lesions to this nerve can be the result of:
  • Aneurysms or SOL affecting the pons
  • Specifically tumors at the cerebellopontine angle
  • Skull fractures
  • Facial bones
  • Damage to foramen ovale
  • Tic doloureux (Trigeminal neuralgia)
  • Sharp pain in V1-V3 distributions
  • Tx with analgesic, anti-inflammatory, contralateral stimulation

Testing Cranial Nerve CN V

  • V1 – V3 pain & light touch testing
  • Testing is best done toward the more medial or proximal areas of the face, where V1, V2 &V3 are better delineated
  • Blink/Corneal reflex testing
  • Puff of air or small tissue tap from the lateral side of the eye on the cornea, if normal, the patient blinks
  • CN V provides the sensory (afferent) arc of this reflex
  • Bite strength
  • Have patient bite down on tongue depressor & try to remove
  • Jaw jerk/Masseter Reflex
  • With patient’s mouth slightly open place thumb on patient’s chin and tap your own thumb with a reflex hammer
  • Strong closure of the mouth indicates UMN lesion
  • CN V provides both the motor and sensory of this reflex
cranial el paso tx.

https://upload.wikimedia.org/wikipedia/commons/a/ab/Trigeminal_Nerve.png

Cranial Nerve VII – Facial

cranial el paso tx.Cranial Nerve VII Clinically

  • As with all nerves, symptoms describe the location of the lesion
  • Lesion in the lingual nerve will result in loss of taste, general sensation in tongue & salivary secretion
  • Lesion proximal to the branching of the chorda tympani such as in the facial canal will result in the same symptoms without the loss of general sensation of the tongue (because V3 has not yet joined the CN VII)
  • Corticobulbar innervation is asymmetric to the upper and lower parts of the Facial Motor Nucleus
  • If there is an UMN lesion (lesion to the corticobulbar fibers) the patient will have paralysis of the muscles of facial expression in the contralateral lower quadrant
  • If there is a LMN lesion (lesion to the facial nerve itself) the patient will have paralysis of the muscles of facial expression in the ipsilateral half of the face
  • Bell’s Palsy

Testing Cranial Nerve CN VII

  • Ask the patient to mimic you or follow instructions to make certain facial expressions
  • Be sure to assess all four quadrants of the face
  • Raise eyebrows
  • Puff cheeks
  • Smile
  • Close eyes tightly
  • Check for strength of the buccinator muscle against resistance
  • Ask patient to hold air in their cheeks as you press gently from the outside
  • Patient should be able to hold air in against resistance

Cranial Nerve VIII – Vestibulocochlear

cranial el paso tx.Cranial Nerve VIII Clinically

  • Changes in hearing alone are most often due to
  • Infections (otitis media)
  • Skull fracture
  • The most common lesion to this nerve is caused by an acoustic neuroma
  • This affects CN VII and CNVIII (cochlear AND vestibular divisions) due to proximity in the internal auditory meatus
  • Symptoms include nausea, vomiting, dizziness, hearing loss, tinnitus, and bell’s palsy etc.

Testing Cranial Nerve CN VIII

  • Otoscopic Exam
  • Scratch Test
  • Can the patient hear equally on both sides?
  • Weber Test
  • Tests for lateralization
  • 256 Hz tuning fork placed on top of the patient’s head in the center, is it louder on one side than the other?
  • Rinne Test
  • Compares air conduction to bone conduction
  • Normally, air conduction should last 1.5-2 as long as bone conduction

Testing Cranial Nerve CN VIII

https://informatics.med.nyu.edu/modules/pub/neurosurgery/cranials.html

Cranial Nerve IX – Glossopharyngeal

cranial el paso tx.Cranial Nerve IX Clinically

  • This nerve is rarely damaged alone, due to it’s proximity to CN X & XI
  • Look for signs of CN X & XI damage as well if CN IX involvement is suspected

Cranial Nerve X – Vagus

cranial el paso tx.Cranial Nerve X Clinically

  • Patient may have dysarthria (difficulty speaking clearly) and dysphagia (difficulty swallowing)
  • May present as food/liquid coming out their nose or frequent choking or coughing
  • Hyperactivity of the visceral motor component can cause hypersecretion of gastric acid leading to ulcers
  • Hyper-stimulation of the general sensory component can cause coughing, fainting, vomiting and reflex visceral motor activity
  • The visceral sensory component of this nerve only provides general feelings of un-wellness, but visceral pain is carried on the sympathetic nerves

Testing Cranial Nerve IX & X

cranial el paso tx.

https://d1yboe6750e2cu.cloudfront.net/i/172ce0f0215312cee9dec6211a2441606df26c97

  • Gag reflex
  • CN IX provides the afferent (sensory) arc
  • CN X provides the efferent (motor) arc
  • ~20% of patients have a minimal or absent gag reflex
  • Swallowing, gargling, etc.
  • Requires CN X function
  • Palatal elevation
  • Requires CN X function
  • Is it symmetrical?
  • Palate elevates and uvula deviates contralateral to damaged side
  • Auscultation of the heart
  • R CN X innervates SA node (more rate regulation) and L CN X the AV node (more rhythm regulation)

 

Cranial Nerve XI – Accessory

cranial el paso tx.Cranial Nerve XI Clinically

  • Lesions may result from radical surgeries in the neck region, such as removal of laryngeal carcinomas

Testing Cranial Nerve XI

  • Strength test SCM m.
  • Patient will have difficulty turning head against resistance toward the side opposite of the lesion
  • Strength test trapezius m.
  • Patient will have difficulty with shoulder elevation on the side of the lesion

Cranial Nerve XII – Hypoglossal

cranial el paso tx.Cranial Nerve XII Clinically

cranial el paso tx.

https://openi.nlm.nih.gov/imgs/512/71/4221398/PMC4221398_arm-38-689-g001.png

  • On tongue protrusion, the tongue deviates toward the side of the inactive genioglossus m.
  • This could be contralateral to a corticobulbar (UMN) lesion OR ipsilateral to a hypoglossal n. (LMN) lesion

 

 

 

 

 

 

Testing Cranial Nerve XII

  • Ask patient to stick out their tongue Look for deviation as in above slide
  • Have patient place tongue inside cheek and apply light resistance, one side at a time
  • Patient should be able to resist moving the tongue with pressure

Clinical Examination – CN’s I – VI (Lower CN’s)

Clinical Examination – CN’s VII – XII

Sources

Blumenfeld, Hal. Neuroanatomy through Clinical Cases. Sinauer, 2002.
Pauwels, Linda Wilson, et al. Cranial Nerves: Anatomy and Clinical Comments. Decker, 1988.