HOSA Neurologic Diseases and Conditions

Nervous System

Complex, sophisticated, elaborate network of many interlaced neuron making up brain, spinal cord, nerves; E impulses throughout body by neurons, regulating activity, responds to stimuli, helps body adjust to env changes int/ext; CNS, PNS; CNS brain, spinal cord, processes and stores sensory/motor info and governs consciousness

Cerebellum

Coordination, equilibrium, posture controls

Hypothalamus

Regulates hormone secretions from pituitary; many visceral activities controls

Brain Anatomy

5 pairs of 12 cranial nerves in medulla oblongata, extension of spinal cord; medulla has vital centers regulating heart rate, BP, respiration; all sensory and motor nerve fibers pass thru medulla oblongata, connecting brain to spinal cord

Spinal Cord

Continuation of medulla oblongata, extends to first lumbar vertebra, divided into 31 segments, each w/ pair of spinal nerves acting as telephone switchboard or reflex center, carrying impulses to/from brain

Peripheral Nervous System (PNS)

all nerves not brain/spinal cord; connects nerves from spinal cord to body, w/ info impulses carried to brain; contains 12 pairs of cranial nerves, 31 pairs spinal nerves, and sympathetic and parasympathetic nerves; controls all conscious activities which affect unconscious processes (heart rate, bowel functions)

Afferent Nerves

Sensory nerves transmitting impulses from parts of body (skin, ear, eye, nose) to spinal cord and brain

Efferent Nerves

Transmit impulses away from CNS and prod responses in muscles and glands

Autonomic Nervous System (ANS)

(Para)sympathetic nerves, regulating involuntary movements and glandular actions

Carotid Arteries

Two int/ext each; originates from two common carotid arteries and located in anterior of neck; two vertebral arteries within vertebral column join two anterior and posterior cerebral arteries and two anterior and posterior communicating arteries to form brain’s vascular system; in shape of circle, the circle of Willis; branches from circle supply blood to all portions of brain; areas of brain which depends on one branch are esp vulnerable to any disruptions of blood flow

Stroke / Cerebrovascular Accident (CVA)

occurs when brain damaged by sudden disruption in flow of blood to part of brain (embolic) or bleeding in head (hemorrhagic); #1 cause of adult disability; signs of stroke depend on brain affected; common stroke symptoms are sudden severe headache, aphasia, dysphasia, difficulty understanding language, sudden weakness, numbness, paralysis of face w/ one-sided drooping of mouth/eyelid (hemiparesis); sudden confusion or impaired consciousness, sudden loss of vision, blurred vision, unequal pupils, diplopia, sudden onset dizziness, loss of balance, loss of coordination; if left brain damage, right side paralysis, speech/memory deficits, slow cautious behavior; if right brain damage, left side paralysis, perceptual/memory deficits, quick/impulsive behavior; severe can cause coma or death; early recognition req to avoid; sudden symptoms req immediate assessment as emergency; often result of (1) cerebral thrombosis (clot) (2) cerebral bleed (3) cerebral embolism (moving clot); three induced by atherosclerosis, hypertension; blood disorders, arrhythmias, systemic diseases (diabetes mellitus, syphilis), hyperlipidemia, rheumatic heart disease, head trauma; high-fat diet, no exercise, smoking, obesity, family history atherosclerosis contributes; embolus/hemorrhages can have sudden onset, thrombus cause if one cerebral arteries narrows due to plaque can enlarge until part/complete blockage, starving tissue of O2; cerebral embolism is blockage, but from foreign object, e.g. piece of arterial wall, small blood clot from diseased heart, bacteria; often a platelet fibrin from ulcerated arterial wall of heart or valve carried by bloodstream until obstructing blood flow to brain; in hemorrhage, artery ruptures flooding brain w/ blood; more serious initial symptoms and long-term effects; phys exam of patient suspects and gauges impairments; MRI, CT, cerebral angiography, electroencephalography (EEG), blood tests if bleeding/clotting disorders Rx; immediate intervention limits brain damage; anticoagulants (warfarin sodium, thrombolytic agents, antiplatelet meds) given PO or thrombolytic agent heparin by IV; new protocol has patients chew aspirin if possible; surgery to improve circulation or remove clots Rx; surgery to repair broken vessels, drugs to reverse brain swelling; long-term treatment varies w/ size, location, w/ goal to restore lost function; rehabilitation w/ family member, med speech, phys, occupational therapists; recovery varies w/ rate of improvement w/ rehabilitation; some permanent disability may remain, as destroyed brain cells do not recover; patients learn new ways of functioning using undamaged brain cells; prevention of positive lifestyle changes can control risk factors, no smoking, limiting alcohol, lowering BP

Arteriovenous Malformations (AVMs)

formed during fetal development, abnormal structures of blood vessels; etiology rarely discovered before 20, often unknown; mainly in brain, can be anywhere; abnor connection noted in which capillaries are lacking, causing arterial blood moving directly into veins, giving vessels appearance of tangled mass of arteries/veins, a fragile vascular structure w/ tendency to bleed and often hemorrhage; when in brain, can yield stroke symptoms; general, region-specific headache; vomiting, stiff neck, confusion, lethargy, generalized weakness, visual problems, irritability; w/ progression, speech impaired, muscle weakness, paralysis in face, ringing in ears, dizziness and syncope may follow, potential loss of consciousness; imaging, CT scans, brain MRIs diagnosis; prompt treatment req w/ surgery, radiation, embolization of involved vessel; cerebral AVMs mortality 10%; possible for residual conditions from insult of O2, nutrition deprivation of brain tissue; seizure activity, other neurologic problems may follow; no prevention known

Transient Ischemic Attack (TIA)

temporary episodes w/ duration <24 hours of impaired neurologic functioning from inadequate flow of blood to part of brain; “little strokes” “ministrokes” resembling stroke from embolism; sudden weakness, numbness of ½ body, dizziness, dysphagia, confusion’ often no unconsciousness; manifested as recurring episodes, lasting seconds to hours, w/ symptoms gradually subsiding; can signal impending stroke, varies w/ location; req immediate intervention to reduce residual effect; commonly piece of plaque from atherosclerosis breaks from artery or heart valve and travels to brain, an embolus; platelet fibrin embolic from arterial ulcer often; arterial vascular spasms, minute blood clots can cause; phys exam, history first, then cranial MRI, CT, EEG grounds diagnosis; however, all can appear normal; treatment varies w/ location and cause; anticoagulants commonly lessen freq and recurrence; chewing of aspirin ASAP; surgery to inc blood flow to area Rx; prognosis varies w/ extent and duration, w/ most resolving w/ min residual effects; can warn of future CVAs; stress reduction, lifestyle changes to avoid risk factors done; positive lifestyle to avoid smoking, excesses in diet/alc, untreated BP, uncontrolled diabetes; oral contraceptives can cause in women

Epidural/Subdural Hematomas

Epidural collection of mass forming btwn skulls and dura mater, the outermost of three meningeal layers covering brain; subdural hematoma is blood pooling btwn dura mater and arachnoid membrane the second meningeal membrane; pressure on brains from either hematomas can impair brain function or death; epidural typically within few hours of head trauma, w/ sudden headache, dilated pupils, nausea, vomiting, inc drowsiness, sometimes hemiparesis; if untreated, unconsciousness, coma, death occurs; neurologic emergences; subdural similar symptoms but onset delayed w/ slower accumulation of blood, mimicking TIA, stroke, dementia; diplopia common; emergency; if head injury not obvious, onset insidious; both from blood from ruptured vessels seeping into and around meningeal layers, often from head trauma; blow to head can cause epidural, head striking an immovable objects (sudden accel/deceleration injurY) can cause subdural, where brain strikes skull or tears vessels; subdural can occur in elderly or alc from falls; often follows skull fractures; clinical findings on exam, history of recent trauma suggests; cranial radiographs, CT scans, cerebral arteriograms locates and rules out other causes; mechanism of injury and time of initial insult can aid diagnosis; craniotomy, cranial trephination (bur hole made into skull w/ drill to relieve P by draining accumulated blood) Rx; procedures remove blood to cauterize bleeding vessels, allowing complete recovery; if no loss of consciousness but symptoms, immediate/delayed physician should be seen; unchecked bleeding enlarges hematomas and inc P on blood vessels; sooner treatment better prognosis; safety measure deterring head trauma best prevents

Cerebral Concussion

possible bruising of cerebral tissue from back/forth movement of head, a accel/decel insult; blunt force trauma can result; loss of consciousness from few seconds to several minutes, followed by varying periods of amnesia 12-24 hours, shallow respirations, pulse depressed, muscle tone flaccid; once consciousness back, headache, nausea, vomiting, diplopia, blurred vision, photophobia, irritability, dec concentration; any head injury w/ loss of consciousness req immediate assessment, oftentimes emergency; disrupts normal E activity of brain, but brain itself usually not permanently injured; complete neurologic exam w/ history of injury req; CT shows no evidence of brain tissue damage; history from from others of what happened vital; quiet bed rest w/ observation for behavioral changes general treatment; prognosis unpredictable, based on extent of insult; often recovery w/ no residual damage; difficult to prevent, but seat belts, helmets can reduce severity

Cerebral Contusion

More serious than concussion, where brain tissues bruises along/beneath surface of brain; a contra-coup insult; symptoms vary w/ site/extent, can persist for 24 hours; ranges from temporary loss of consciousness to coma; if conscious, headache, hemiparesis; symptoms progressive, a person can appear drowsy or hostile; permanent damage can occur if dural hematomas, impairing intellect, dysphasia, paralysis, epilepsy, impaired gait, continuing stupor; head injury w/ severe headache or hemiparesis req immediate assessment, often an emergency; caused by blow to head or impacting against hard surface, e.g. car accident; twisting/shearing force against two hemisphere of brain occurs when colliding w/ cranial bones, damaging deep structures of brain, often associated w/ skull fractures; thorough neurologic exam req, w/ history of mechanism of injury; CT shows location, extent of damage; cranial radiographs rule out skull fracture; hospitalization to monitor vital signs, rapid med intervention available Rx; specific treatment based on site and severity; prognosis unpredictable, based on health of ind; underlying pathology may compromise a favorable outcome; inc intracranial P, possible herniations complicate; difficult to prevent, but seatbelts, helmets can help

Depressed Skull Fracture

break/fracture of 1+ bones of cranium; if skull bones depressed or torn loose, they are pushed below normal surface of skull; when part of skull breaks and pushes onto brain; symptoms vary w/ sitel if affecting motor area, hemiplegia; not progressive, static symptoms until depressed bone elevated and pressure relieves; epilepsy common; emergency, should be considered life-threatening until said otherwise; direct impact on skull w/ blunt object most common cause; industrial, car accidents; fractured bone may cut artery/vein, hemorrhage; phys exam of patient reveals defect in skull; cranial radiographic films show whether and where brain is crushed; CT shows life-threatening cerebral edema; craniotomy done, depressed bone elevated into place; head protection worn until fracture partially healed; prognosis unpredictable, depending on extent of insult, timely intervention, possible complications, additional trauma, underlying med conditions; successful surgery often positive outcome; prevention difficult; seatbelts, helmets help

Basilar Skull Fracture

Fracture of bones of floor of cranial vault, resulting from massive insult to cranial, car accident, other violent trauma where head struck anteriorly/laterally in midportion; injuries, symptoms, signs, treatments depends on area; raccoon eyes, Battle signs are manifestations, alerting physician to order imaging of cranial vault to assess; Cerebrospinal fluid flowing from ears/nares associated; level of consciousness assessed, as are other neurologic signs; treatment akin to other head injuries, w/ surgery to relieve intracranial P; sometimes severity causes severing of pituitary stalk, causing panhypopituitarism

Para/Quadplegia

Injuries to spinal cord affected innervation of any spinal nerves distal to point of insult; extent of injury and consequential edema results in failure of spinal nerve functioning w/ resulting loss of motor/sensory function; para is loss of nerve function below waist paralyzing lower trunk and legs; quadri is loss of nerve function at cervical region, resulting in paralysis of arms, hands, trunks, legs; damage to cord can be temporary, but can lead to degree of impairment as nerve pathways control many different bodily functions; loss of bowel, bladder, sex function common; hypotension,  hypothermia, bradycardia, respiratory problems all sometimes, req mechanical ventilation; if accel/decl emergency, req emergency care; spinal cord injuries cause, w/ site of injury, type of trauma, severity of trauma can determine if para/quadri; trauma to thoracic, lumbar regions T1 or below paraplegia; vertical compression, hyperflexion of spine prod this injury; trauma to cervical vertebrae C5 or above quadriplegia, w/ injuries btwn C5 and C7 prod differing degrees of paresis to shoulders/arms; damage above C3 often fatal, w/ cause hyperextension, flexion of portion of spine; complete neurologic functioning, spinal radiograph films, MRI, CT determine type/extent of injury; restoration to normal alignment, decompression of spine, nerves, vertebrae, early rehab, surgery Rx; prgnosis guarded, but early treatment yields better prognosis; partial/total severing of spinal cord results in permanent, irreversible damage and paralysis below insult; absolute prevention impossible, but preventing injury after insult by immediate stabilization can help; types of insults include compression from fall, hyperflexion of neck from car accident, hyperextension of spine from falling head-first

Degenerative Disk Disease

Degeneration of intervertebral disk may result in pain in areas served by spinal nerves of involved disk space; natural part of aging, occurring in almost all; w/ pain it radiates down nerve path, burns, is constant, can become intractable; constant back pain and severe radiation pain down to 1+ legs can accompany some loss of function, numbness, tingling, weakness; severe back pain req prompt assessment; w/ age water in disk dec, causing; can be mechanical or result of constant wear on disk; misalignment of vertebrae causes continual rubbing on disk, causing infla and gradual destruction of it; infla eventually involves spinal nerve roots causing scarring; sequela is spinal stenosis, where nerve roots become trapped in foramen as they leave spinal canal; clinical findings, history leads to investigation; radiograph, MRI, myelogram w/ contrast to show disk status, rarely CT; narrowing of intervertebral space consistent w/ condition; electromyogram (EMG) and neurologic exams show involvement of dependent nerves and measures nerve conduction; observation of neurologic deficits, e.g. footdrop, dragging of leg when walking, adds to suspicion; advising activity, analgesics, NSAIDs for pain; oral steroids Rx; epidurals or selective nerve root blocks for pain or spinal stenosis recommended; phys therapy helps; TENs units Rx w/ positive results; sometimes injections before surgery; surgery of spinal fusion and freeing of spinal nerve roots from entrapment; pumps are last resort, w/ continuous infusion of morphine into epidural space for intractable pain; prognosis varies w/ extent of degenerative process and response to treatment; prevention difficult w/ main cause aging

Herniated / Bulging Disk

Ruptured/Slipped disk is rupture of nucleus pulposus thru annular wall of disk and into spinal cavity; intervertebral disks are soft pads of cartilage and gelatinous material located btwn each vertebrae; each disk is shock-absorbing cushion allowing flexibility of movement; in each disk is gelatinous center the nucleus pulposus, surrounded by circular wall-like annulus; nucleus pulposus contained by wall, is bulging, thus protrusion into spinal canal not severe; rupture induces severe back pain, disability if it presses against or pinches nerves; sudden sharp pain worsens w/ movement, can radiate to butt, thigh, eg causing paresthesia and muscle weakness; if pain from pinching nerve roots of sciatic nerve, called sciatica; most in lower back btwn 4th-5th lumbar vertebrae and 5th lumbar and 1st sacral vertebrae, lumbosacral area; if cervical region, pain, weakness in arm/neck; pain uni/bilateral; req immediate med attention; more often men; often from accumulated trauma (improper mechanics when lifting) or sudden impact; poor posture, age can cause; rupture may occur at time or shortly thereafter trauma; thorough history of back pain req, phys exam on back to rule out other causes; diagnosis considered if sciatic pain on straight leg raising test; MRI< CT, myelogram can help confirm; when severe, nucleus pulposus penetrates both inner/outer annulus; hot/cold packs, muscle relaxants, analgesics (aspirin), oral prednisone, epidural injections, phys therapy; if conservative not successful, surgical excision of disk Rx, where percutaneous discectomy introduces needle into intravertebral space and encroaching area of nucleus pulposus aspirated; microdisketomy w/ small incision to aspirate offending material; discectomy uses laser ablation and evaporation of disk; laminectomy w/ fusion of vertebrae can remove; often pain goes away w/ drug therapy; prognosis varies w/ extent and duration of herniation, most resolve w/ conservative care; surgery often favorable; good proper body mechanics can prevent

Spinal Stenosis

Sciatic Nerve Injury; rupture of nucleus pulposus within intervertebral disks L4 to S3; narrowing of spinal canal or nerve root foramen, often sciatica due to compression of spinal cord and spinal nerve roots; pressure on sciatic nerve sends impulses down it, prod severe sharp pain radiating down leg to food; pain cont/intermittent, areas of skin may feel numb; if rupture toward neural canal, P on nerve root can cause lower back and leg pain; anterior/lateral ruptures may or may not prod symptoms; symptoms vary w/ extent of rupture, proximity of nerves to site, strength of muscles and ligaments surrounding spine; nerve injury can prod severe disability, temp/permanent; reflexes of lower extremities asymmetric, sensation dec; req appointment or emergency visit; a fall, poor body mechanics, gunshot/stab wounds, aging; infla autoimmune response can induce more rapid degeneration w/ arthritic changes, narrowing vertebrae; osteophytes on foramen where spinal nerves exit can induce pain; congenital narrowing possible; med history, phys exam, then MRI, spinal radiographs, CT, myelogram, blood serum tests Rx; radiographs often show changes; EMG can show neurologic changes; conservative oral prednisone, phys therapy, ultrasound diathermy w/ massage; after acute pain and infla gone, exercise program to strengthen back/ab muscles Rx; analgesics (aspirin, Tylenol), muscle relaxants (Valium, Robaxin), antiinfla meds (Fledene, Motrin, Advil), antiseizure meds use slows nerve transmission to relieve pain; if severe pain not resolved, narcotics (demerol, morphine) Rx; phys therapy w/ applications of heat/cold and gental massage (myofascial release) can help acute pain; corticosteroid epidural injections can relieve pain and reduce infla of spinal nerve, does not cure but relieves pain; disabling pain or inc weakness may req surgery; if disk causing pain, (micro)diskectomy, spinal fusing, or chem dissolving by chemonucleolysis (enzyme of nucleus pulposus) can help; decompression of spinal nerve foramen can be used to free trapped nerves; prognosis varies w/ extent of degeneration and traumatic insult; preventing injury can only help

Cephalalgia

Headache, pain in head not confined to any one specific nerve dist area; acute/chronic, frontal/temporal/occipital regions; can be confined to 1_ side; pain dull/unbearable, intense/intermittent, throbbing pain, pressure pain, penetrating pain; brain tissues themselves never ache as they have no sensory nerves; meninges do have pain receptors, so sensitivity in this area exists only in meninges, skin, muscle covering skull, and nerves traveling from brain to head/face; common, self-limiting; secondary headache sometimes symptom of underlying disorder (hypertension, stroke), often caused by nothing more than fatigue/tension; cluster version w/ severe pain around one eye w/ abrupt onset/cessation, where affected eye can tear, often night for weeks-months then disappearing for years, common in men associated w/ congestion and partial Horner’s; stress too little/much sleep, overeating, overdrinking, stuffy/noisy env, heavy phys labor; physiologically there are actually only two causes (1) strain on facial/neck/scalp muscles from tension, causing a tension headache (2) edema in blood vessels, changing arterial size, a vascular headache; med history vital to identifying pattern of headaches; phys exam, neurologic testing if recurring pattern revealed; cranial, spinal radiographs, EEG, cranial CT Rx to rule out other causes; cause determines treatment; if no underlying cause, analgesics (Aspirin, NSAIDs), muscle relaxants, minor tranquilizers, muscle massages, relaxation w/ warm bath yields temporary relief; prognosis typically good; if intractable head pain prognosis variable; drug therapy can relieve, stress reduction and relaxation yield positive outcomes; avoiding known triggers prevents

Migraine

Periodic severe headaches that are completely incapacitating w/ nausea, vomiting, anorexia, intense hemicranial/bilateral throbbing pain, visual signs/symptoms are this type of headache; before onset, visual auras (flashing lights, zigzagging lines, ares of total darkness), photophobia; nature of each attack varies w/ person, but a warning period w/ abnor fatigue and irritability universally experienced; less common numbness, tingling in 1+ arm or 1+ side of body, dizziness, temporary confusion; can begin in adolescence, less freq and intense w/ age, more often women; if known to patient common migraines, req prompt treatment; it is unknown why some are more subject than others; susceptibility tends to appear familially, potential genetic aspect; certain foods (aged cheese, chocolate, red wine) can provoke attack; biologic cause is changes in cerebral blood flow, presumably attributable to vasoconstriction followed by vasodilation of cerebral/cranial arteries; medical history suggests; EEG, CT, MRI Rx to rule out organic conditions; bed rest in quiet, dark room and analgesics at first sign can completely treat; other times, vascoconstrictors, antiemetics for vomiting Rx; use of ergot prep effective for some to stall impending attacks and lessen symptoms; Beta-blockers and tricyclic antidepressants Rx to prevent; Imitrex for pain relief; relaxation therapy, biofeedback successful for some; prognosis favorable w/ good response to therapy; avoiding known triggers can prevent, w/ drug therapy vastly helping

Epilepsy

Chronic brain disorder w/ sudden episodes of abnor intense E activity in brain; many forms and manifestations, 30+ types known, possible for one person to have 1+ type; recurring seizures entail involuntary contractions of muscles (convulsions) w/ disturbances of consciousness and sensory phenomena; seizures partial/generalized; status epilepticus complicated prolonged seizure activity; partial do not involve entire brain, arising from localized area; rhythmic twitching of group of muscles, compulsive lip smacking or picking at clothing; behavioral, psychic, sensory manifestations (auras) can occur; amnesia of attack, but no loss of consciousness; generalized seizures have diffuse E abnor in brain w/ absence (petit mal) and tonic-clonic (grand mal) attacks; absence version, or petit mal epilepsy are brief change of level of consciousness, starting w/ staring, blinking, loss of awareness of surroundings, few seconds or sometimes many in one day if not treated, often children or young adults; tonic-clonic or grand mal epilepsy begins w/ loud cry, falling to ground,  then loss of consciousness, where body stiffens, tongue bites, prolonged contraction of respiratory muscles induces cyanotic look; generalized rhythmic muscle spasms followed by relaxation (clonic phase), patient incontinent to urine/feces, subsiding in 1-2 minutes, but consciousness regained slowly; drowsiness, confusion, weakness, no memory of attack; status epilepticus occurs when one seizure followed another w/ no recovery of consciousness btwn attacks, a medical emergency req immediate anticonvulsant therapy to prevent cerebral anoxia, hyperpyrexia, vascular collapse, death; req immediate intervention; idiopathic has no apprent cause for abnor E discharge, but greater freq familially; symptomatic epilepsy, abnor in brain from pathologic process, genetic/acquired, triggering seizures, e.g. scar tissue on cerebral cortex from infection/trauma, cortical neoplasms, cerebral edema, CVAs, cerebral palsy, drug toxicity, diabetes, hypoglycemia, whatever deprives brain w/ O2; not all seizures implies epilepsy, so med history req; EEG shows semispecific brain activity, suggesting diagnosis; MRI Rx; classification based on location; CT shows structural changes, tumors, scars, malformations; cerebral angiography can identify vascular changes; skull radiograph film may reveal fracture, separation of cranial structures, movement of pineal gland; blood serum chem shows metabolic disease, drug toxicity, hypoglycemia; anticonvulsant meds treat, often Dilantin, Tegretol, Mysoline, valproic acid; close monitoring to adjust dosage Rx best; rarely, surgery to excise lesion in brain; based on state regulations, license to drive may not be allowed until seizure free; prognosis varies, drug therapy can control somewhat; initial onset impossible to prevent

Parkinson’s Disease

Common, slowly progressive neurologic disorder charact by onset of recognizable disturbances, a pill-rolling tremor of thumb forefinger, muscular rigidity, slowness of movement, postural instability; often insidious, symptoms vary person to person, associated w/ aging until recognizable paradigm emerges; posture stooped, peculiar shuffling gait, head bowed, body flexed forward, knees slightly bent, patient tendency to fall; face takes masklike expressionless appearance, speech muffled, swallowing difficult; gradual behavioral/mental activity changes; mean onset 60, often younger, more men, life span after diagnosis about 10 years; vague symptoms warrant appointment; what causes nerve degeneration of nerves in motor system/ brain stem unknown; deficiency in dopamine, a neurotransmitter in midbrain, demonstrated in patients; Parkinsonism as a syndrome can occur after ingestion of poison, after encephalitis, after certain tranquilizers, after certain antihypertensive drugs; diagnosis based on characteristic history and careful neurologic exam, dec dopamine in urine noted; cannot be cured, so med management uses supportive measures to control symptoms; drugs (levodopa, carbidopa, antidepressants, anticholinergics) for tremor, rigidity; improvement w/ deprenyl sometimes; phys therapy helps max mobility; treatment encourages independence and self-care; no prevention known

Huntington’s Chorea

Hereditary degenerative disease of cerebral cortex and basal ganglia; progressive atrophy of brain; chronic, progressive chorea (ceaseless, uncontrolled movements) w/ insidious onset, loss of musculoskeletal control by subtle, semipurposeful movements; arms/face first involved typically, w/ movements ranging from mild fidgets to tongue smacking;  speech difficulties, emotional state deteriorates, dementia, disruption of personality, careless appearance, apathetic moody behavior, loss of memory, paranoia; often in early middle age; often family history makes patient aware beforehand; exact etiology uncertain, but transmitted by autosomal-dominant trait in either sex; no definitive diagnosis known; careful neurologic appraisal, detection of defective gene by DNA analysis, progressive chorea, dementia, familial trait, cerebral CT shows brain atrophy; no cure known; Haldol, Prolixin can control choreic movements and reduce agitation; phys therapy, occupational therapy, speech therapy, psychosocial support can help; eventually, institutionalization may be req for deteriorating condition; prevention unknown

Amyotrophic Lateral Sclerosis (ALS) / Lou Gehrig Disease

progressive, destructive motor neuron disease causing muscular atrophy; fasciculations (small local involuntary muscle contractions) w/ atrophy and weakness in forearms/hands noted; difficulty in speech, chewing, swallowing, breathing, eventually ventilator req; no sensory neuron involvement noted, functioning of mind not affected; more men, onset 50-60; complaints of symptoms should be assessed; etiology uncertain, but sometimes caused by autosomal inherited traits; upper/lower motor neuron involvement w/o sensory neuron involvement suggests; EMG, muscle biopsy confirms diagnosis; no cure known; death often within 6-10 years onset; prevention unknown

Transient Global Amnesia

Usually benign but frightening at first; temporary 1-12 hours, global in nature encompassing entire memory of current events; manifests as total loss of recent memory, learning process completely blocked; sudden memory loss of current/recent events; constant questioning typical, confusion, but ability to recall personal identity and orientation to place as long as place is normal env; memory loss often precedes 3-5 years of specific events; usual tasks involving mechanical abilities often done w/o difficulty; neurologic signs normal, no numbness, tingling, weakness noted; PERLE and vocalization normal; communication skills concerning current events and status suffer from amnesic event, beginning and ending abruptly; memory often returns 6-12 hours, but period of amnesia will remain unavailable to recall; sometimes headache; to reduce anxiety of family, should be seen in office for evaluation; etiology unknown; precursors of stress, emotional events, swimming in cold water, driving a car, or having sex; migraine, headaches, w/(o) nausea, vomiting, photosensitivity; diagnosis by observing symptoms and signs and finding negative neurologic exam; TIA, cerebral accident, seizure must be ruled out; treatment supportive, given reassurance during/after episode; prognosis good, recurrence unlikely; patient will never learn of what happened during episode; prevention unknown, but suggested to lower stress

Neuropathy

Degeneration of peripheral nerves; affects distal muscles of extremities; unless precipitating factors are severe infection or chronic alc intoxication, onset insidious; clumsiness, loss of sensation in hands/feet, flaccid paralysis and wasting of muscles in areas; deep tendon reflexes diminished, tenderness in atrophied muscles; skin may appear glossy, red, and sweating dec; footdrop, sometimes pain in affected regions; loss of sensations in hands/feet req prompt assessment; alcohol intoxication, toxicity from Ar/Pb?CS2/benzene/P, infectious diseases (Mumps, pneumonia, diphtheria), metabolic, infla disorders (diabetes, rheumatoid arthritis, gout, lupus), certain nutritional deficiencies can cause; history w/ clinical findings of motor/sensory involvement suggests; motor/sensory nerve impairment detected by EMG/NCS nerve conduction study, two different tests; must ascertain cause and eliminate it; toxic substances removed, vitamin/nutrition restored if possible; avoiding alcohol; anticonvulsants, tricyclic antidepressants, rest, phys therapy for pain; control of underlying cause and good nutrition has good prognosis; prevention difficult, but avoiding alcohol can prevent recurrence

Trigeminal Neuralgia / Tic Douloureux

pain of area innervated by 5th cranial nerve, the trigeminal nerve; transient, excruciating pain radiates along nerve, distributing to any of three fifth cranial nerve branches, mainly affecting 2nd/3rd; if ophthalmic branch affected, pain in eye/forehead; maxillary branch involves nose, upper lip, cheek; mandibular branch involves lower lip, outer portion of tongue, area of cheek close to ear; 1+ branch can be involved; pain always unilateral, not crossing midline as one side of face is involved; abrupt onset of pain triggered by mechanical/thermal stimulation; poor sleep, undernourished, dehydrated, chewing, swallowing, touching of area may set off pain; pain so severe req immediate pain relief, immediate appointment; cause uncertain, some related to compression of nerve root by tumor/lesion; sometimes sequela of multiple sclerosis or herpes, but often no cause identified; symptom and abrupt onset suggests; observation during both normal times and times of attack demonstrates; face protected from even gentle breezes as it may set off attack; no impairment of sensory or motor function noted; episodes lasts months to years then subsides, infection of sinus or tooth and tumor must rule out; analgesics, sometimes carbamazepine; if no relief, surgery to dissect nerve roots performed; no more smoking; prognosis depends on underlying cause ; sometimes resolving spontaneously or to drugs; surgery as last resort will relieve pain, but nerve function will be compromised; no prevention known

Bell’s Palsy

Disorder of facial nerve (7th cranial) causing sudden onset of weakness, paralysis of facial muscles; severity of paralysis varies widely; patient may be aware of pain or drawing sensation behind ear followed by inability to open/close eye and drooping of mouth w/ drool; often first noticed in morning, developing overnight; initially unable to smile, whistle, grimace, distorted face; taste diminished, loss of appetite; often unilateral, may be transient or permanent, often 20-60, M/F equally; symptoms req prompt assessment; cause not always certain; symptoms result from blockage of impulses from facial nerve, caused by compression of nerve in bony canal; bilateral facial paralysis in small # of Lyme disease patients; diagnosed by symptoms, characteristic history; early treatment critical; warm moist heat, gentle massage, facial exercises to stimulate muscle tone; prednisone for infla of nerve, analgesics, artificial tears or eye patch for protection needed unless case is mild; electrotherapy stimulates nerve and prevents atrophy; complete recovery possible if treated early, but residual effects remain for undetermined period; prevention unknown

Meningitis

Infla of meninges, membranous coverings of brain/spinal cord; vomiting, headache inc intensity w/ movement or shaking of head; nuchal rigidity when moving head, stiffness in neck resisting sideways/flexion-extension motion is a classic sign; positive Kernig’s sign (resistance to leg extension after flexing thigh on body) and Brudzinski’s sign (neck flexion causing flexion on hips from supine position) indicates meningeal irritation; deep tendon reflexes inc, irritability, photophobia, hypersensitivity to skin; seizures by cortical irritation can be late manifestations; drowsiness, stupor, then coma w/ progression; early symptoms easily overlooked, prompt assessment w/ worsening symptoms; bacterial/viral cause, can originate from brain, spinal cord, or sinuses; open head injuries allow entry; Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae responsible for most; clinical findings suggests; diagnostic lumbar puncture shows cerebrospinal fluid (CSF) pressure and WBCs, protein, glucose in CSF; cultures of CSF show microbes, confirming diagnosis; treated aggressively w/ IV antibiotics; anticonvulsive drugs to control seizures, aspirin/acetaminophen for headache, low stimuli, room kept dark/quiet; prognosis unpredictable, depends on source of infection and response to drug therapy; bacterial good response from antibiotics, most viral forms run their course; degree of residual damage based on drug response; prevention difficult; prophylactic antibiotics for those w/ known cases; good hand washing can help

Encephalitis

Infla of brain tissue; insidious/sudden onset; headache, elevated temperature, stiffness in neck/back, muscular weakness, restlessness, visual disturbances, lethargy, mental confusion progresses to coma; symptoms warrant emergency appointment; infla leads to cerebral edema and subsequent cell destruction, caused by viruses/toxins (chickenpox, measles, mumps), most from infected mosquito bites; Eastern equine, western equine, Venezuelan equine encephalomyelitis and St. Louis encephalitis are forms found in US; recently, West Nile viral encephalitis is a form not endemic to US but has evolved and spread to US; clinical findings suggest, e.g. lumbar puncture; Blood/CSF studies reveal virus; EEG abnor, MRI to look for HSV encephalitis and rule out other pathology; antiviral agents effective only against Herpes Simplex encephalitis; otherwise, treatment symptomatic, w/ mild analgesics, antipyretics for elevated temp, anticonvulsants for seizure activity, antibiotics for any intercurrent infection; prognosis unpredictable, based on type of infection and response to drug therapy; most viral forms run their course; residual damage to brain tissue possible prevention difficult; avoiding mosquitoes w/ spray, long sleeves, etc. helps

Guillain-Barre Syndrome

Acute, rapidly progressive disease of spinal nerves; numbness/tingling of feet/hands on onset, w/ inc muscle pain and tenderness; progressive muscle weakness, paralysis in lower extremities moving up body in 24-72 hours; most find ascending paralysis, sometimes descending weakness/paralysis; respiratory insufficiency, difficulty swallowing sometimes; symptoms req immediate assessment; knowledge of etiology limited, syndrome autoimmune basis w/ current knowledge; known to follow respiratory infection of gastroenteritis in 10-21 days; demyelination of nerves occurs; confirmation w/ elevated protein in CSF, peaking in 4-6 weeks after onset; hospitalization req for observation; plasmapheresis washes plasma to remove antibodies, shortening time req for recovery; IV human immunoglobulin may help; prognosis varies, but recovery often complete; prevention unknown

Brain Abscess

Collection of pus anywhere in brain tissue; primary symptom headache; other signs depend on location and extent; inc intracranial P, nausea/vomiting, visual disturbances, unequal pupil size, seizures; many times eyes look toward insult, moving to side of head where abscess is located; nuchal rigidity maybe; symptoms warrants emergency services; CNS abscesses from local infection, can be 2ndary to infection elsewhere in body; staphylococci, streptococci, pneumococci organisms can cause; any occurrence breaches integrity of CNS, including head trauma, craniotomy wound can be portal of entry for microorganisms; abscess can be secondary to infection from sinusitis, otitis, dental abscess, subdural empyema, bacterial endocarditis; history of infection, esp of sinuses/ear, or insult to CNS w/ charact clinical features of inc intracranial P suggests; EEG, CT verifies diagnosis; lumbar puncture is contraindicated as resulting inc intracranial P may cause brain stem to herniate, inducing death; blood cultures Rx; IV antibiotics resolves; mannitol, steroids reduce cerebral edema; surgical drainage Rx to relieve intracranial P and culture offending organism; prognosis varies w/ location, size, causative agent of abscess; underlying pathology and health status of patient affects; when intracranial P cannot be controlled, death; prevention difficult; prompt treatment of secondary sources of infection helps

Poliomyelitis / PostPolio

Poliomyelitis is viral infection of anterior horn cells of gray matter of spinal cord, causing selective destruction of motor neurons; highly contagious, no longer threat since 1960s since Salk/Sabin vaccines have eliminated it in West; low-grade fever, profuse discharge from nose, malaise; symptoms followed by progressive muscle weakness, stiff neck, nausea/vomiting, flaccid paralysis of affected muscles; atrophy of muscle follows, w/ dec tendon reflexes, muscle/joint deterioration following; involves muscles supplied by spinal nerves termed spinal, whereas involvement of muscles supplied by cranial nerves (gray matter of medulla) termed bulbar; symptoms req prompt assessment; if previously had polio (often 30 years beforehand) req prompt appointment w/ symptoms; poliovirus enters body thru nose/throat crossing into GI tract by bloodstream, soon reaching CNS, incubation 7-21 days, transmitted btwn ppl by oropharyngeal secretions or feces w/ virus; clinical symptoms w/ exposure to infected person primary diagnosis; isolation of poliovirus from throat washings or feces confirms; if CNS involved, culture of CSF positive for virus; analgesics, moist head applied, bed rest until acute stage resolves, phys therapy w/ braces Rx; if difficulty respirating, mechanical ventilation Rx; Sabin/Salk vaccines has rendered poliomyelitis nonexistent; three serotypes exist (1,2,3), all found worldwide, w/ immunization from Sabin trivalent oral vaccine giving immunity to all three; Salk vaccine, or monovalent vaccines grant immunity to only one kind; immunosuppressive patients should not be given trivalent vaccine;  two more vaccines being developed, IPV and OPV; postpolio syndrome occurs later in life w/ those previously experienced disease, w/ functional deterioration of muscles w/ loss of strength, often 30 years after initial attack, involving affected muscles; fasciculations, muscular atrophy may accompany, treatment supportive; prognosis fair, depending on muscles involved; vaccines prevents

Brain Tumors

can be primary, neoplasms in brain itself, or secondary metastasized from other areas (lungs, liver, kidney, skin); primary can arise from any cell in cranium, named according to tissue originated; symptoms from displacement/compression of normal brain tissue by tumor, inducing progressive neurologic deficits, expansion of brain (cerebral edema), inc intracranial P (ICP), possible herniation; headache (dull, constant, worse at night/morning), focal/generalized seizures (common in gliomas or secondary tumors), nausea/vomiting, loss of consciousness, cognitive dysfunction (memory problems, personality changes), muscle weakness, sensory loss, aphasia, gait disturbance, visual dysfunction; cerebellar tumors (medulloblastoma) have classic symptoms of gait disturbance, nystagmus, lethargy, dysarthric speech pattern, clumsiness, balance difficulty; elevated ICP from cranial nerve defects; edema of optic nerve (papilledema) seen w/ ophthalmoscope; if P too high, herniation of brain tissue is life-threatening condition; symptoms req prompt assessment, w/ seizures, loss of consciousness, reduced cognitive functioning being more emergency; classified by predominant cell type; gliomas glial cells, meningiomas from arachnoid membrane, embryonal tumors in children; incidence of gliomas inc after 45, w/ embryonal rarely after 20; for most under 15, brain tumors most common solid malignancy; incidence greater in developed, industrialized countries (west, Australia), whites more affected; only therapeutic ionizing radiation and genetic predisposition (neurofibromatosis, von Hippel-Lindau syndrome) are established risk factors, only fraction of cases however; evaluation of patient w/ suspected brain tumor includes detailed history, neurologic exam, diagnostic neuroimaging studies; neurologic exams find associated regions affected by destruction of neural tissue; cranial MRI is most common, measuring blood flow thru regions during various activities, helpful for pre-op planning; CSF cytology abstained by lumbar puncture to check for neoplastic cells or metastasis done; tissue obtained during surgery or from stereotactic biopsy req for diagnosis; staged by modified TNM, w/ N not informative as CNS has no lymphatic structures; can be benign/malignant, but even benign brain tumors have same symptoms as malignant tumors; a benign tumors w/o metastasis can be fatal; primary tumors symptomatic treatments, anticonvulsants for seizures, corticosteroids to dec ICP, anticoagulants to prevent venous thromboembolic disease; surgery initially most time, providing tissue samples for definitive diagnosis and reliving symptoms by reducing tumor bulk; extent or surgery limited by goal of not inflicting incapacitating neurologic damage on patient; surgery w/ radiotherapy and/or chemo, based on tumor type/stage; while experimental, immunotherapy shows promise as another method; secondary tumors based on location, size, # metastases, age, neurologic status, extent of systemic cancer; solitary brain lesions and no other metastasis use surgery and whole brain radiation therapy (WBRT), improving quality of life and lowering chance of death; multiple metastases req WBRT w/o surgery, w/ recurrent brain metastases treated w/ surgery, radiation w/ palliative intent; could be long-term treatment, esp children, complications of neurocognitive defects, growth hormone deficiency, learning disability, loss of vision, second malignancies possible; 5-year survival 32%, one of the poorest of all cancers; poorer prognosis for older age, higher tumor grade, mental changes at time of diagnosis, larger tumors, CSF cytology positive for neoplastic cells, and inability to fully resect tumor w/ surgery; no prevention known