CNS Disorders Pathophysiology of CNS Emergencies u Structural

CNS Disorders

Pathophysiology of CNS Emergencies u Structural Changes l l Often due to Trauma but not always Circulatory Changes u l Alterations of ICP u u Response to insult Toxic Metabolic states l u Inadequate Perfusion Alteration to blood chemistry or introduction of toxins Psychiatric ‘mimicking’

ICP Review u CBF is a factor of CPP & CVR l l u CPP = MAP - ICP l l u If CPP , then CBF If CVR , then CBF most likely MAP = Diastolic + 1/3 PP PP = SBP - DBP PCO 2 has greatest effect on CVR l Sympathomimetics may CVR

ICP Review u As PCO 2 , CVR l l u u u Therefore, if PCO 2 , CVR Then, as CVR , CBF Normal ICP < 15 mm Hg As ICP , CPP then CBF Compensation for ICP via MAP l l Cushing’s Reflex (Triad) Cushing’s triad with coma indicates possible herniation

Altered Mental Status

Coma u u A decreased state of consciousness from which a patient cannot be aroused Mechanisms Structural lesions l Toxic Metabolic states l Psychiatric ‘mimicking’ l

Brain injury u Recall that Brain injury is often shown by: Altered Mental Status l Seizures l Localizing signs l

Is unconsciousness itself an immediate life threat? YES, IT IS! Loss of airway u Vomiting, aspiration u

Altered Mental State Manage ABC’s Before Investigating Cause!

Initial Assessment/Management u Airway l l u Breathing l l l u Open, clear, maintain If trauma or + history, control C-spine Presence? Adequacy (rate, tidal volume)? High concentration O 2 on ALL patients with altered mental status Assist ventilations prn Circulation l Pulses? Adequate Perfusion?

Investigate Cause u DERM D = Depth of Coma l E = Eyes l R = Respiratory Pattern l M = Motor Function l

D = Depth of Coma What does patient respond to? u How does he respond? u Avoid use of non-specific terms like “stuporous”, “semi-conscious”, “lethargic”, “obtunded”

D = Depth of Coma AVPU u Glasgow Scale (later) u Describe level of consciousness in terms of reproducible findings

E = Eyes u Pupils l Size - mid, dilated or constricted u measurement - e. g. 4 mm Shape - round, oval, pontine l Equality - equal in size l Symmetry - equal in reaction/response l Response to light l u Yes or No u How?

R = Respiratory Pattern u Depth l u Unusually deep or shallow? Pattern l Regular or Unusual pattern u. Can you identify the pattern?

M = Motor Function u Paralysis? l u Muscle tone? l u Where? What is it like? Posturing? l u Rigid or Flaccid Movement? l u Where? How? Symmetrical Motor Function?

Physical Exam u Vital Signs Shock? l Increased ICP? l Hypoxia/Hypercarbia l u Diagnostics Dysrhythmias? l Blood glucose l Oxygen saturation l

Physical Exam u Detailed (Head-to-Toe) Exam Injuries causing coma? l Injuries caused by coma? l Clues to the cause l

Probable Causes of AMS u u Not enough Oxygen Not enough Sugar Not enough blood flow to deliver oxygen, sugar Direct brain injury l Structural l Metabolic

Differentiating AMS Causes u Structural l l Asymmetrical deficits Unequal pupils Afebrile History of trauma, structural abnormality Often a rapid onset u Metabolic l l l Symmetrical deficits Equal pupils (? altered function) ? Fever History of metabolic disorder or illness Rapid onset less likely

Management Maintain ABCs u Attempt to identify cause u Mainstays of therapy u Oxygenation/Ventilation l IV fluids appropriate for the patient l D 50 (if hypoglycemic) l Narcan if possibility of opiate OD l Flumazenil in known benzo only OD l

AEIOU TIPS Alcohol u Epilepsy u Insulin u Overdose u Uremia (Metabolic causes) u Trauma u Infection u Psychogenic u Stroke/Syncope u

Cerebrovascular Accident AEIOU TIPS

Cerebrovascular Accident Any disease process that disrupts blood flow to a distinct region of the brain u Transient Ischemic Attack (TIA) u l S/S less than 24 hours without permanent neuro deficits

Cerebrovascular Accident 500, 000/yr in US u 25% die u Survivors often socially, financially devastated u $20 billion in medical costs, lost wages u

Cerebrovascular Accident (CVA) u Pathophysiology Thrombosis (brain itself) l Embolus (head, neck or heart) l Hemorrhage (within brain) l Ischemia (systemic blood flow) l

Predisposing Factors: Modifiable Hypertension u Chronic atrial fibrillation u Cigarette smoking u Diabetes Mellitus u Sickle cell disease u Polycythemia u Heart disease u Hypercoagulability u Hyperlipidemia u Birth control pill use u Cardiovascular disease u Cocaine use u

Predisposing Factors: Unmodifiable Age u Gender u Race u Prior stroke u Heredity u

CVA Mechanisms Ischemic stroke--80 to 85% u Hemorrhagic stroke--15 to 20% u

CVA Origin Thrombus u Embolus u Aneurysm u Arrhythmia u Hypovolemia u

Ischemic Stroke u Blood vessel occlusion l l Thrombosis Embolism u Plaque fragments from carotids u Chronic atrial fibrillation u Fat particles u IV substance abuse particulates u Systemic hypoperfusion l l Pump failure Hypovolemia

Ischemic Stroke Syndromes u Transient Ischemic Attack (TIA) l l l Neurological deficits that resolve in 24 hours or less (most in 30 minutes) Commonly result from carotid artery disease Same symptoms as CVA Often warning sign of impeding CVA 5% risk of stroke per year

Ischemic Stroke Syndromes u Dominant Hemisphere Infarction l l Contralateral weakness, numbness Contralateral blurring of vision of half the visual field in both eyes Difficulty pronouncing words (dysarthria) Difficulty speaking or understanding speech (dysphasia or aphasia)

Ischemic Stroke Syndromes u Nondominant Hemisphere Infarction l l l Contralateral weakness, numbness Contralateral visual field cut Neglect of contralateral extremities Constructional apraxia (difficulty drawing figures like a clock face) Dysarthria Usually NOT dysphasic or aphasic

Ischemic Stroke Syndromes u Vertebrobasilar Syndrome l l l Involves blood flow to brainstem, cerebellum, and visual cortex Dizziness, vertigo Diplopia Dysphagia Ataxia, bilateral limb weakness

Hemorrhagic Stroke 30 to 50% 30 -day mortality u Younger patient population u Two subtypes: u l l Intracerebral, usually 2 o to hypertension Subarachnoid, usually from berry aneurysms

Hemorrhagic Stroke Syndromes u Intracerebral Hemorrhage l l Headache, nausea, vomiting precede deficits Patients commonly have decreased LOC with extreme hypertension Contralateral hemiplegia, hemianesthesia Possible aphasia, extremity neglect depending on hemisphere involved

Hemorrhagic Stroke Syndromes u Subarachnoid Hemorrhage

CVA Assessment u Presentation of CVA varies with area(s) of brain involved and type of CVA

CVA Presentation u Brain can show injury in only three ways: l l l Decreased LOC Seizures Localizing signs u Hemiparesis or hemiplegia u Dysphasia (Receptive or expressive) u Visual disturbances u Gait disturbances u Inappropriate affect u Bizarre behavior u Incontinence

Cincinnati Prehospital Stroke Scale u Have patient smile (“Facial Droop”) l l u Have patient close eyes and hold arms out (“Arm Drift”) l l u Normal: Both sides of face move equally well Abnormal: One side does not move as well as other Normal: Both arms drift same amount or do not drift Abnormal: One arm does not drift or one drifts down compared to other or can’t move arms Have patient say, “You can’t teach an old dog new tricks. ” (“Speech”) l l Normal: Correct words, no slurring Abnormal: Slurs words, uses inappropriate words, or unable to speak

Assessment u Signs & Symptoms l Ischemic S&S usually of slower onset u Hemiparesis or hemiplegia u Numbness or decreased sensation of face or unilateral u Altered LOC or coma u Convulsions u Visual disturbances u Slurred or inappropriate speech u Headache or dizziness

Assessment u Signs & Symptoms l Cerebral Embolus with rapid onset u Emboli from valvular HD or Afib u rapid onset u Often with an identifiable cause (e. g. Afib, Valvular heart disease, recent long bone fracture)

Assessment u Signs & Symptoms l Cerebral hemorrhage associated with rapid onset u high mortality rate u Often with severe HA (“Worst headache ever”) u N/V u Rapid decrease in LOC or seizure u Coma, Cushing’s and Herniation

u History l l l Associated Altered LOC or Seizure? Onset/Precipitating factors? Initial symptoms and progression? u l l l Assessment Dizziness, Severe HA, N/V Previous CVA or TIA? Previous neuro deficits? Concomitant illnesses? Sickle Cell Disease u Atrial fibrillation u l Risk factors for stroke & thrombus formation? BCP, Smoking u HTN, CVD u

Assessment u Physical Exam l l Mental Status & Behavior Extremity Motor & Sensory u l l Gait Pupils & Vision Cincinnati Prehospital Stroke Scale Evidence of Cushing’s or Herniation Blood glucose level

CVA Management Basic Objective Improve cerebral blood flow and oxygenation

CVA Management u Airway l l l u If no gag reflex, intubate Otherwise, position to ensure drainage of secretions Suction prn Breathing l l l Oxygen via NRB Ventilate with BVM and O 2 if rate or tidal volume inadequate Intubate if herniating

CVA Management Controlled hyperventilation if intracranial hemorrhage suspected with increased ICP and neurologic deterioration u Indicators u l l l Sudden onset Headache Rapid loss of consciousness Seizures Unequal pupils

CVA Management u Circulation l Check blood glucose level u Hypoglycemia may mimic CVA u Treat hypoglycemia with D 50 l Establish IV Access u Draw blood samples u TKO u avoid l solutions with glucose Monitor ECG u 10% of CVAs are associated with cardiac event u 12 Lead ECG if suspected ischemia

CVA Management Do not assume patient cannot understand because they cannot talk u Position appropriately: u l l l If hypertensive, semireclined (head slightly elevated) If normotensive, on affected side If hypotensive, supine

CVA Management u Increased Blood pressure treated ONLY if strongly suggestive of ischemic stroke l If systolic >220 or diastolic >120 consider gradual blood pressure reduction u Labetalol u Nitropaste u Nitroprusside l l Controlled reduction Return to pre-CVA levels, NOT to “normal”

CVA Management u Thrombolytic agents l l l Consider for all patients with ischemic CVA presenting within 3 hours of onset Early recognition of ischemic stroke and administration of thrombolytics can prevent/limit loss of neurologic function Requires CT scan!!!

CVA Management u Think like AMI of the Brain l u Time is tissue Therapy Mainstays l l l Oxygenation/Ventilation IV Access Rapid assessment & differential u Treat associated conditions (hypoglycemia, hypoxia, hypotension) l Rapid Transport to appropriate facility u CT Scan & Thrombolytics vs. CT Scan & Neurosurgery

Syncope AEIOU TIPS

Syncope aka Fainting u Pathophysiology u Brief loss of consciousness caused by transient cerebral hypoxia l May be caused by lack of glucose or seizure activity in the brain l

Syncope u Types l Postural u Inadequate l blood flow to brain due to position Vasovagal u Excessive vagal stimulation u Carotid Sinus stimulation/pressure l Cardiogenic u Dysrhythmia, usually bradycardia u Stokes-Adams Syndrome

Syncope u Types l Tussive spell” resulting in intrathoracic pressure causing venous return to the heart u most often in overweight male smokers with chronic bronchitis u “coughing l Micturation u associated with urination, usually in patients who have consumed Et. OH and compounded by increased vagal stimulation

Syncope u Assessment l History of the event u Often preceded by sensation of light-headedness u Rapid return of consciousness is most common l Past History u History of vertigo u Similar past episodes l Many possible causes

Syncope u Management l Manage ABCs u Clear airway and Assist ventilations as needed u Oxygen NRB (initially) u Calm & Reassure u Assess for underlying cause ECG v Blood glucose v History (present and past) v Physical Exam v u Treatment based on underlying cause

Seizures AEIOU TIPS

Seizures u Alteration in behavior/consciousness 2° unstable, uncoordinated electrical activity in the brain l l Often a result of altered membrane permeability Manifested by sudden, brief episodes of: u altered consciousness u altered motor activity u altered sensory phenomena u unusual behavior

Seizure Categories u Generalized l Tonic-Clonic (grand mal) u AKA l u Absence (petit mal) Partial l l u Convulsions Simple partial Complex partial Hysterical

Seizure Etiology CVA u Hypoxia u Infection/Fever u Drug/alcohol withdrawal u Poisoning/OD u Thyrotoxicosis u Head trauma u Hypoglycemia u Brain neoplasms u Psychiatric disorders u Eclampsia u Hypocalcemia u

Seizures Etiology Most epileptic seizures are idiopathic in origin

Generalized Seizures u Petit Mal Absence Sz l Children l No LOC l u Grand mal aka Convulsions l Common l Often w/Aura l Sudden LOC l Tonic / Clonic l Postictal phase l Status epilepticus l

Generalized Seizures Symmetrical u No local onset u Irritable focus difficult to identify u l l Near simultaneous activation of entire cortex Focus may begin deep in brain and spread outward

Generalized Seizures u Tonic-Clonic Seizures (Grand Mal) l l l l Aura (preictal phase) Loss of consciousness/postural tone Tonic phase Hypertonic (tetanic) phase Clonic phase Post-ictal phase May experience transient neurologic deficits (Todd’s paralysis)

Generalized Seizures u Absence Seizure (Petit Mal) l l l Brief loss of awareness (10 - 30 seconds) Usually no loss of postural tone May occur 100+ times a day Primarily pediatric problem Often described as “daydreaming”, not paying attention Usually disappear as child matures

Partial Seizures Seizure begins locally u May remain localized or spread to entire cortex u Result from focal structural lesion in brain u

Partial Seizures u Simple u Localized clonic activity l Abnormal sensory symptoms l Usually no LOC l May progress l u Jacksonian (Seizure) March Complex Change in behavior l Preceded by aura l Repetitive motor behavior l No recall l May progress l

Partial Seizures u Simple partial seizures (No loss of consciousness) l Focal motor seizures u Local clonic activity u May display Jacksonian march Sensory seizures l Autonomic seizures l

Partial Seizures u Complex partial seizure (psychomotor or temporal lobe seizures) l Distinctive aura l Loss of consciousness l Automatisms l May be mistaken for drunks or psychotics l May experience episodes of rage

Hysterical “Seizures” Usually in front of audience u Usually follow interpersonal stress u Movements asymmetrical or purposeful u Does not fall, hit head, bite tongue u Incontinence rare u Recalls things said, done during “seizure” u

Assessment u Seizure Assessment l Duration u Seizure u Postictal phase u Typical for the patient? l Onset u Events before u HA u Aura u Trauma u Vision Disturbances

Assessment u Recent History l l l l Trauma to the head/brain HA / Neck Pain Pregnancy Brain tumor Recent Infection/Illness CVA Symptoms Introduction of Poisons into body

Assessment u Past History l l l l Diabetes Mellitus Seizure Disorder Tumor CVA Medications Recreational Drug Use Alcohol abuse

Assessment u Physical Exam l l l Evidence of trauma Evidence of alcohol, drug abuse Rash, stiff neck Pregnant CVA Signs Incontinence

Status Epilepticus Two or more seizures without intervening conscious period u Usually due to medication noncompliance u Management same as for other Seizures just more aggressive u

Seizure Management u Patient actively seizing l l l Do NOT restrain Do NOT put anything in mouth Oxygen NRB if possible ECG Monitor when possible IV Access u Lg Bore, NS u Assess blood glucose

Seizure Management u Patient actively seizing l If hypoglycemic: Assess IV patency FIRST!! u Dextrose 50% 12. 5 - 25 grams IV push u Consider Thiamine 100 mg slow IV push l Diazepam, slow IV administration until seizure stops or until ~ 10 mg u Usually l aimed at 2. 5 mg doses, one after another Phenobarbital, 100 mg/min IV push to a total ~390 mg or seizure stops Barbiturate coma u NMB & Intubation u

Seizure Management u Current Mainstays of Therapy for Actively Seizing Patient l l l u “New” Therapy l u Diazepam Lorazepam Phenobarbital Phosphenytoin Other Considerations l l Glucose Mg. SO 4 Paraldehyde Dilantin (phenytoin) 18 mg/kg at 25 mg/min

Seizure Management u After seizure stops: l l l l u Open -Clear- Maintain airway O 2 via NRB Assist ventilations if needed Roll patient onto side protecting head Reassess ABCDs Assess blood glucose Physical Exam and History Most seizure deaths are due to anoxia

Seizure Management If the patient is epileptic, do these seizures match what is “normal” for him? Just because the patient is epileptic, he does NOT have to be having an epileptic seizure!

Mandatory Transports u u u u First time seizures Seizure patient off medications Change in seizure pattern Associated with trauma Pregnant patient Status epilepticus Associated with increased body temperature l l Not always; Seldom in young children Has infection been diagnosed and treatment initiated?

Insulin: Hypo/Hyperglycemia AEIOU TIPS

Insulin Hypoglycemia u Hyperglycemia u l l DKA HHNC

Insulin u Assessment l l l Medical Alert Tag/Bracelet Evidence of DM Medications Fruity breath odor Signs of repeated SQ injections Blood glucose level (See Endocrine for further assessment)

Insulin u Management l Hypoglycemia u Management ABCs: Oxygen/IV/ECG u Dextrose 50% (adult), 12. 5 - 25 grams IV push via patent line u Consider Thiamine 100 mg slow IV push u Dextrose 25% (children), 0. 5 - 1 grams IV push (24 cc/kg) via patent line u Carbohydrate meal u Assess for underlying cause u Consider transport

Insulin u Management l DKA/HHNC u Management ABCs: Oxygen/IV/ECG u Ventilate/Intubate prn u Fluid administration titrated to signs of shock v 250 cc boluses and reassess u Consider administration of Regular Insulin (consult medical control) u Assess for underlying cause u Transport

Alcohol AEIOU TIPS

Alcohol Et. OH present in up to 40% of AMS patients “Dead drunk” u Mixed overdose u May be associated with u l l Head trauma Hypoglycemia

Alcohol Is it alcohol or is it something else? A patient is never “Just Drunk”

u Management l Alcohol Manage ABCs u Clear airway and ventilate as needed u Oxygen u IV access prn l Assess for other causes of AMS u ECG Monitor u Blood glucose level u History of mixed poisoning or Et. OH poisoning u Physical exam l Treat other causes

Overdose/Poisoning AEIOU TIPS

Overdose/Poisoning u Possible Overdose/Poisonings resulting in AMS l l l Alcohol: Ethanol/Methanol Narcotics Sedative-hypnotics Solvent inhalation Stimulants

Overdose u Assessment l l l Needle marks? Pupil responses? Slow respirations? u Associated l l hypotension Odd behavior? Breath odors? Color of oral mucosa, vomitus? History of Recent Drug/Poison use?

Uremia/Metabolic Causes AEIOU TIPS

Uremia (Metabolic Causes) Uremia/Renal Failure u Hyperthyroidism u Hypothyroidism u Addisonian Crisis u Hepatic Coma/Encephalopathy u

Uremia (Metabolic Causes) u Assessment Med Alert? l Patient medications? l Physical findings? l l The Physical Exam and History (recent and past) are most useful

Trauma AEIOU TIPS

Trauma Concussion u Cerebral contusion u Intracranial hematoma u Hypovolemia u Hypoxia u

Trauma u Assessment l Physical findings? u Evidence l of brain injury History of recent or remote trauma?

Trauma Altered Mental Status = Head Injury Until Proven Otherwise

Trauma Head injury severity cannot be evaluated accurately in presence of shock

Trauma u Management l l l Manage ABCs Spinal motion restriction if indicated Clear airway and secure prn Ventilate prn Oxygen Establish IV access, NS u l l Fluid to titrate BP to ~ 90 mm Hg systolic Assess for other causes: ECG, Blood glucose Transport to trauma center

Infection/Fever AEIOU TIPS

Infection Meningitis u Encephalitis u Brain abscess u Sepsis u Fever u

Infection u Assessment Headache? l Fever? l Sore throat? l Stiff neck (nuchal rigidity)? l Rash? l Associated symptoms of systemic infection l

Infection u Management l l Infection Control Measures Manage ABCs u clear airway and ventilate prn u oxygen u IV access prn l Consider acetaminophen for fever u fluid / rehydration u

Psychogenic AEIOU TIPS

Psychogenic Hysterical faking u Catatonia u l l “psychomotor disturbances characterized by physical rigidity, negativism, or stupor” may occur in schizophrenia, mood disorders or organic mental disorders

Psychogenic u Assessment l Circumstances? u. Events l Prior behavior? u. Similar l leading up to this point past episodes Medications & PMHx

Assessment & Management of AMS

Primary Assessment u Onset l l u Level of Consciousness l l u Mechanism (Kinematics) Preceding S/S AVPU GCS (later) Airway obstruction or compromise l l Fluid Unprotected airway (e. g. coma)

Primary Assessment u Ventilatory ability l l u Adequate Ventilatory rate and depth? Respiratory Insufficiency 2° to ICP? (e. g. irregular patterns) Cardiovascular compromise l l Shock /hypotension /hypovolemia Hypertension

Primary Assessment u Neuro Exam (motor & sensory) Posturing? Muscle Tone? l Pupillary Reflexes? l Extraocular Movements? l Symmetry l u History Present and Recent l Past l

Management of AMS u Goals: l Airway control/ maintenance u Avoid l Cardiovascular stabilization u Avoid l hypotension/shock Interruption of cerebral injury u Fix l hypoxia the root cause problem Protection from further harm u Avoid secondary brain injury

Other Neurologic Conditions

Headache u Common complaint l l l u Characteristics l l l u Many persons experience regularly ~ 1/3 due to migraine HA May be associated with significant pathology Sudden vs Constant vs Recurring Generalized vs Localized Mild to Moderate to Severe Intensity of Pain Cause is often unknown

Headache u Vascular l Migraines u Last minutes to hours to days u Usually very intense, throbbing pain u Photosensitivity u N/V u Often unilateral u May be preceded by aura (not common) u Occur commonly in women

Headache u Vascular l Cluster u Series of headaches u Usually last for a few minutes or a few hours u Sudden, intense pain u Usually unilateral u May be accompanied by nasal congestion, irritated or watery eye (same side) u Occur commonly in men

Headache u Tension l l l Most common headache Occur regularly Often awake in a. m. and worsens throughout the day Dull, ache Feels like pressure on neck and/or head

Headache u Organic l l Not very common Due to some specific cause (illness/injury) in the body u Tumor u Infection u Meningitis u Hypoglycemia u etc.

Headache u Potentially Serious Pathologies l Complaint u “Worst headache ever” u “It hurts right here” u May localize at posterior neck at base of skull v l Possible subarachnoid hemorrhage Concern for possible intracranial hemorrhage

Neoplasms Less common neoplasm u Risk factors u l l l genetic exposure to radiation tobacco use occupational exposure to toxins medications/drugs/poisons diet

Neoplasms u Pathophysiology l u Most often a result of metastasis from another cancer (malignant) Assessment l l focused on the detailed neuro exam not a diagnosis BUT should be included in the differential dx

Muscular Dystrophy Genetic disorder u Results in degeneration of muscle fibers u Types u l l Duchenne Fascioscapulohumeral Limb Girdle Myotonic

Muscular Dystrophy u Duchenne dystrophy l l l most common childhood muscular dystrophy onset usually by age 6 symmetrical weakness and wasting of first the pelvic and leg muscles u then pectoral and proximal upper extremities u l progresses and results in early death u usually in adolescence

Multiple Sclerosis u u Common demyelinating disorder of the CNS Results in patches of sclerosis (patches) in brain and SC Occurs primarily in young adults Typical S/S l l visual loss, diplopia nystagmus weakness, paresthesias symptoms may have periods of exacerbation and remission

Parkinson’s Disease u u u Degenerative changes in the basal ganglia result in deficiency of dopamine Characterized by rhythmical muscular tremors, rigidity of movement, and droopy posture Usually occurs after 40 years of age Leading cause of neuro disability > 60 years Estimated 500, 000 in US

Central Pain Syndrome u u Known as Trigeminal Neuralgia paroxysmal bursts of pain in one or more branches of the trigeminal nerve Often induced by touching trigger points in or about the mouth Causes l l tumor some medications (phenothiazines)

Bell’s Palsy u Paresis or paralysis of the facial muscles l u u usually unilateral Occurs in 23 of 100, 000 persons Caused by dysfunction of the 7 th cranial nerve l l cause is usually a viral infection other causes post trauma u herpes simplex u lyme disease u idiopathic u

Amyotrophic Lateral Sclerosis u u u Progressive motor neuron disease aka ALS or Lou Gehrig disease of the motor tracts of the lateral columns and anterior horns of the SC l results in progressive muscular atrophy, increased reflexes, and spastic irritability of muscles

Spina Bifida u An embryolgic failure of fusion of one or more vertebral arches l l l u results in spinal cord exposure spinal cord may protrude outward various types based upon type of deformity Child requires frequent surgeries l increased risk of latex allergies

Poliomyelitis u u An inflammatory process of the Spinal Cord’s gray matter May be caused by the poliomyelitis virus l l u Enters bloodstream and nervous system results in paralysis of the limbs Uncommon today in the US due to polio vaccine