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Clinical Neurology

Back Clinic Clinical Neurology Support. 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 sure to be an exciting journey. The commitment to you in health is to, never lose 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

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.

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

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)


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

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. 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


  • 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


  • 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)


  • 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
  • Probiotics

Injury Medical Clinic: Chiropractor (Recommended)


  1. �Attention Deficit Hyperactivity Disorder.� National Institute of Mental Health, U.S. Department of Health and Human Services,
  2. Autism Navigator,
    �Autism Spectrum Disorder (ASD).� Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 29 May 2018,
  3. �Introduction to Autism.� Interactive Autism Network,
  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,
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


  • 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

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


  • 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


  • 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

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


  • 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


  • 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


  • 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


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

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

Blood Supply To The Brain

cerebrovascular el paso

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


  • 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


  • 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

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 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)


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


  • 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


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


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

  • 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)

  • 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

  • Measures compound muscle action potentials (CMAP)
  • 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


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


  • 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


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


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


  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, 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.


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 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


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


  1. �A Head for the Future.� DVBIC, 4 Apr. 2017,
  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,
  4. �Post-Concussion Syndrome.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 28 July 2017, 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

Sensitization Of Nociceptors

  • Results in allodynia and hyperalgesia

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Headache Types

  • Meningeal irritation
  • Intracranial mass lesions
  • Vascular headaches
  • Cervical fracture or malformation
  • Metabolic
  • Glaucoma
  • 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
  • Hypoglycemia
  • Hypercapnea
  • Carbon monoxide
  • Anoxia
  • Anemia
  • Vitamin A toxicity

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


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


  • 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

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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


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

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