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.
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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.
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
General/Global onset seizures
Generalized motor seizure (Grand mal)
Absence seizure (Petite mal)
Focal onset seizures
Simple partial seizure
Motor cortex (Jacksonian)
Complex partial seizure (libmbic)
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)
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
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
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.
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
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
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
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
Association with streptococcal infection
Association with other neuropsychiatric symptoms (including any of the PANS �accompanying� symptoms)
Blood tests for strep
Anti-DNase B Titer
Test for other infectious agents
MRI preferred but PET can be used if necessary
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
Injury Medical Clinic: Chiropractor (Recommended)
�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.
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.
�Introduction to Autism.� Interactive Autism Network, iancommunity.org/introduction-autism.
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.
�What Is PANDAS?� PANDAS Network, www.pandasnetwork.org/understanding-pandaspans/what-is-pandas/.
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.
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.
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
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
Nerve Conduction Velocity (NCV) Studies
Evoked Potential Studies
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
Diagnostic Needle EMG
Recorded depolarizations may be:
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
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
Increased amplitude and duration can be the result of reinnervation after chronic denervation
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
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
Positive Sharp Waves
DO NOT occur in normally functioning fibers
Spontaneous depolarization due to increased resting membrane potential
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
Tables of normal, adjusted for age, height and other factors are available for practitioners to make comparison
Time between stimulus and the appearance of a response
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.
Blurred eyesight or other vision problems, such as dilated or uneven pupils
Ringing in the ears
Nausea or vomiting
Delayed response to questions
Continued or persistent memory loss
Irritability and other personality changes
Sensitivity to light and noise
Mood swings, stress, anxiety or depression
Disorders of taste and smell
Rigidity and inflexibility
Lack of empathy
Lack of motivation or initiative
Depression or anxiety
Symptoms In Children
Concussions can present differently in children
Loss of appetite
Loss of interest in favorite toys or activities
Unsteadiness while standing
Memory loss and failure to form new memories
Inability to remember things that happened before the injury
Due to failure in recall
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
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.
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
Loss of concentration and memory
Ringing in the ears
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
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
Improve stress coping skills
MSK treatment of the cervical and thoracic regions
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
Other light blocking glasses
Cotton in ears
Treatment Of PCS
Manage each symptom individually as you otherwise would
Manage CNS inflammation
Fish oil/Omega-3s � (***after r/o bleed)
Cognitive behavioral therapy
Mindfulness & relaxation training
Brain balancing physical therapy exercises
Refer for psychological evaluation/treatment
Refer to mTBI specialist
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
�A Head for the Future.� DVBIC, 4 Apr. 2017, dvbic.dcoe.mil/aheadforthefuture.
Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
�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/.
�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: 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.
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