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80 Cards in this Set
- Front
- Back
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neurological system hx
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History
A. OPQRST B. impact on patient’s life 1. ADL C. patient’s perceptions vs. those around him/her D. headache, fainting, blackouts, dizziness, clumsiness, seizures, convulsions, paralysis, local weakness, difficulty speaking, difficulty walking with coordination, tremors, numbness, tingling, difficulty with bladder or bowel control, trouble thinking, memory lapses, nervousness, irritability, depression, worrying, sleep, dreams, uncontrollable feelings E. frightened patient with a lot of subjective complaints F. localization of the lesion 1. muscle, nerve, spinal cord, brain G. ROS 1. neuro deficits common in systemic disorders H. family hx 1. metabolic & degenerative disorders often inherited I. social & travel 1. infectious causes |
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cranial nerves: olfactory, optic, oculomotor
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E. cranial nerves
1. 1st - olfactory a. identify odors (coffee, soap, mint) to each nostril with eyes closed 2. 2nd - optic a. visual acuity, fields b. fundus 3. 3rd - oculomotor; 4th - trochlear; 6th - abducens a. PERRLA b. EOM |
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cranial nerves: 5th, trigeminal
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4. 5th - trigeminal
a. 3 divisions - ophthalmic (corneal reflux, touch white), maxillary, mandibular b. motor only in mandibular (masseter + temporalis) i. palpate clenched masseter c. sensory in all i. pinprick d. corneal reflex i. touch limbus with a wisp of cotton |
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cranial nerves: 7th, facial
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7th - facial
a. watch face during conversation for asymmetries b. depressed nasolabial fold c. raise eyebrows, frown, close eyes tightly so cannot be opened, show teeth, smile, puff out cheeks d. taste to anterior 2/3 of tongue i. stroke side of tongue with sweet, sour, salty, or bitter |
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cranial nerves: 8th - vestibulocochlear, acoustic,
9th - glossopharyngeal; 10th - vagus |
6. 8th - vestibulocochlear, acoustic (acoustic neuroma)
a. hearing (unilateral hearing loss w/dizzy///or menieres) b. specialized tests for vestibular function (eyes back + forth rapidly cause dizzy/nausea) 7. 9th - glossopharyngeal; 10th - vagus a. hoarseness b. gag reflex c. symmetric upward movement of soft palate and uvula on saying “ah” |
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cranial nerves: 11th - spinal accessory, 12th - hypoglossal
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8. 11th - spinal accessory
a. palpate SCM while turning head against resistance (+trapezius innerv) 9. 12th - hypoglossal a. inspect tongue for atrophy, fasciculations, deviation i. deviates toward side of lesion when tongue is stuck out |
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neuro: motor system
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1. observe gait - watch patient walk down hall
2. inspect limbs and girdles for atrophy, asymmetry, fasciculations 3. walk heel to toe 4. walk on toes and then on heels 5. shallow knee bends unilaterally 6. Romberg sign 7. passive flexion and extension of limbs 8. muscle strength 9. coordination a. rapid rhythmic alternating movements i. pat leg fast with hand ii. rapidly turn hand over and back iii. touch each of fingers with thumb rapidly b. point to point testing c. heel on opposite knee and run it down shin |
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neuro: sensory system screening
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1. screening testing
a. face, torso, 4 limbs b. pain, vibration in hands and feet c. light touch in arms and legs d. stereognosis 2. ability to perceive stimulus 3. symmetry - always do bilaterally 4. vibration and position sense distally a. if normal, omit proximal 5. pain, temperature, touch both distally and proximally 6. cover most dermatomes and major peripheral nerves 7. meticulously map out boundaries of areas of hypo or hyperesthesia a. begin centrally at point of reduced sensation and move outward progressively until normal |
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neuro: sensory system screening / specific testing
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8. specific testing - done with closed eyes
a. pain i. safety pin ii. sharp or dull - use point and dull end b. temperature i. tubes filled with hot and cold water ii. omit if pain normal c. light touch i. cotton d. vibration (1st effected w/diabetes) i. low pitched tuning fork ii. dip joints of finger, ip joint of great toe iii. if impaired, test more proximal bony prominences e. position i. terminal phalanges of toes and fingers up and down ii. usually just great toe and index finger f. discriminative sensation i. stereognosis - identify object in hand ii. number id - draw number on palm iii. 2 point discrimination (on back pts feel closer sooner, dont need fine discrim) |
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reflexes general
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H. reflexes
1. DTR’s a. relaxed b. mild stretch on muscle then strike tendon briskly 2. lateral differences (check good side b4 affected side) 3. strength a. graded 0 - +4 b. hypo - lower motor neuron disease c. LMN - anterior horn cell, spinal root, peripheral nerve d. hyper - upper motor neuron disease e. UMN - motor cortex, brain stem, corticospinal tract down to LMN |
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reflexes specific
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4. biceps C5,6
5. triceps C7,8 6. brachioradialis C5,6 7. abdominal a. above umbilicus T8-10 b. below umbilicus T10-12 8. cremasteric (males) L1,2 9. patellar (knee, quadriceps) L2-4 10. ankle S1,2 a. if hyper, check for clonus b. rapid, rhythmic oscillations between dorsi and plantar flexion 11. plantar L4-S2 a. plantar flexion of toes b. Babinski’s sign - dorsiflexion of great toe with fanning of other toes i. upper motor neuron disease |
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nerve reflex arcs
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peripheral nerve, cord level at that nerve + peripheral nerve going back out = reflex arc
*hypo reflexia: lower motor neuron disease (something blocking stimulus, dont get reflux) *hyper reflexia: upper motor neuron disease: corticospinal tract, brain, stem, cord down to where u r looking at, nothing to regulate the response) |
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meningeal signs
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1. if suspecting meningeal inflammation
2. Brudzinski’s sign a. patient supine, flex neck, watch for flexion of hips and knees 3. Kernig’s sign a. patient supine, flex one of hips and same knee, pain indicates meningeal inflammation or disc disease |
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neuro lab + imaging
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III. Lab
A. none specific IV. Imaging A. x-ray B. CT scan 1. bony structures 2. contrast cerebral angiography C. MRI 1. neural structures 2. demyelination, edema |
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special studies
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A. lumbar puncture
1. spinal tap 2. information about intracranial pressure and CSF 3. CSF usually clear, colorless (w/MS find immunoglobulins) a. blood, cells, glucose, protein, stain, culture B. cerebral angiography (dye into vessels, take pics) C. myelography: looking for abn in spinal columns (h.a. for weeks/days) 1. x-ray of spinal cord after dye injected into subarachnoid space 2. mostly replaced by MRI D. PET scan 1. uptake of radioisotopes 2. blood flow, glucose, oxygen metabolism E. functional MRI (FMRI + PET vying for attention: all relatively new) F. SPECT scan G. electroencephalography (EEG) 1. recording of electrical currents in the brain H. electromyography EMG 1. recording of electrical properties of muscle I. nerve conduction velocities NCV 1. time for an impulse to travel a length of nerve |
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h.a. emergencies
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A. headache
1. may or may not be emergency 2. questions to ask yourself a. head trauma b. seizures c. acute onset d. rapidly changing pattern e. meningitis f. pg and hypertensive 3. if yes to any of the above questions, refer to ER 4. persistent hypertension with HA, refer to cardiologist 5. increasingly severe HA not responding to tx, refer to PCP |
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veritigo/meningitis: emergencies
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B. vertigo
1. with HA or CNS signs like diplopia (dbl vision), slurred speech, extremity discoordination, unilateral weakness all indicate central lesion a. refer for evaluation ASAP C. meningitis 1. acute bacterial meningitis 2. can be lethal in hours 3. uri 4. fever, HA, stiff neck, vomiting 5. purpural rash with above sxs indicates meningococcal meningitis (often trunk, blotchy, anywhere: amputations: destroys tissue) 6. refer to ER immediately |
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stroke/epilepsy: emergencies
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D. stroke
1. abrupt or gradual onset of neurological deficits 2. hypertension, DM, AS, embolism 3. refer to ER, may need to call 911 E. status epilepticus 1. seizures with no intervening periods of consciousness 2. call 911 |
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Dementia def + classification
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VII. Dementia
A. chronic, global (whole brain), usually irreversible deterioration of cognition 1. progressive decline in intellectual function that interferes substantially with the person’s social or occupational activity B. classification 1. Alzheimer’s Disease 2. mild cognitive impairment MCI 3. vascular (atherosclerosis, hypertns) 4. mixed 5. Lewy body (abn. protein bodies in brain) |
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dementia risk factors
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C. risk factors
1. age a. after age 60 b. doubles every 5 years thereafter c. at age 85, 50% have dementia i. 2/3 is Alzheimer’s 2. family hx a. environmental b. genetic (apolipoproteins) i. risk genes - APOE-e4 ii. deterministic genes - ADAD 3. head injury 4. cardiovascular disease (esp. vascular dementia) |
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dementia sxs + sns
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D. sxs & sns
1. short term memory loss 2. aphasia a. word finding difficulty 3. apraxia a. inability to perform motor tasks 4. agnosia a. inability to recognize objects 5. visuospatial dysfunction 6. executive dysfunction (cant think of things easily) 7. apathy 8. clock drawing with 3 item word recall a. full mental status exam |
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dementia: alzheimer's
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1. Alzheimer’s Disease
a. most common age related neurodegenerative disease b. beta-amyloid senile plaques c. neurofibrillary tangles of tau protein i. both cause decrease in Ach d. 10 sxs that warn of AD development *memory loss, problem solving (planning out/following plan), familiar tasks problematic, time or place confusion, visuospacial relationships, speech/writing difficulties, misplacing things, poor judgement, withdrawl, mood + personality changes |
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dementia: mild cognitive impairment
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2. mild cognitive impairment
a. mental dysfunction sxs noticeable by others but not enough to interfere with dailylife |
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dementia: vascular
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3. vascular dementia
a. 2nd most common type b. post stroke dementia i. sxs appear after stroke c. multi-infarct dementia i. vascular cognitive impairment ii. small infarcts iii. over time, sxs develop d. sxs i. memory loss ii. confusion iii. difficulty concentrating, planning, following instructions, communicating iv. difficulties with ADLs |
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dementia: mixed
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4. mixed dementia
a. vascular disease and AD i. 45% autopsies of people with AD have both |
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dementia: lewy body type
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5. Lewy body
a. abnormal deposits of alpha-synuclein protein inside neurons b. sxs i. AD sxs - memory loss, poor judgment, confusion ii. daytime drowsiness iii. visual hallucinations iv. fluctuation of cognitive sxs and alertness v. movement sxs - stiffness, shaking, mask-like facies, falling vi. REM sleep disorders - normal suppression of body movement while dreaming does not occur -vivid, violent movement while asleep |
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dementia labs/other studies
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F. lab
1. serum B12 2. thyroid function 3. CBC 4. CMP 5. lipid panel 6. heavy metal testing 7. HIV G. other studies 1. MRI 2. CT scan a. often N cortical atrophy with age 3. PET |
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dementia tx
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H. treatment
1. prevention a. exercise b. mental stimulation c. learning new tasks d. prevention of AS e. prevention of head injuries f. regular ingestion of curcumin 2. tx underlying cause if one found 3. aerobic exercise 4. mental stimulation 5. community activity 6. cholinesterase inhibitors 7. Ginkgo biloba – 40 mg TID 8. acetyl-L-carnitine – 500-1,000 mg TID 9. vit. E – 2,000 IU/day 10. Melissa (lemon balm) |
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H.A. definition + etiology
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A. cephalalgia - head pain
B. etiology 1. common sx of systemic or intracranial infection, head injury, intracranial tumor, severe hypertension, cerebral hypoxia, EENT 2. most patients however suffer from muscle tension or migraine 3. try to determine what hurts a. nerves, arteries, other tissues b. intracranial vs extracranial |
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H.A. history
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C. history
1. OPQRST a. rapidity of onset b. times of day c. location d. recent head trauma e. hypertension 2. relationship to meals, foods 3. stress 4. eyestrain, visual defects 5. fevers, sinusitis 6. occupation 7. toxic exposure 8. allergies 9. improper yoga, exercise 10. family history |
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H.A. sxs + sns
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D. sxs & sns
1. must determine frequency, duration, character, location, severity 2. palpate head, mastoid processes, occiput 3. neck - stiffness, tightness 4. ophthalmoscopic, press on eyeballs 5. jaundice, herpes lesions on face 6. malocclusion of teeth 7. full physical exam of EENT |
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primary H.A. definition
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F. primary
1. muscle tension a. from muscle spasm, postural strain, anxiety b. gradual onset c. worse at end of day d. cyclical periods of tension and relaxation e. intermittent, moderate tightness f. viselike pain g. general or fronto-occipital h. tender neck and skull muscles i. tx i. massage ii. relaxation and stress reduction |
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migraine H.A. def. + etiology
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2. migraine
a. most common cause of recurrent moderate to severe HA b. neurovascular pain syndrome with altered central neuronal processing and trigeminovascular involvement i. cortical hyperexcitability followed by depression ii. inflammation in cranial vasculature and dura mater c. 18% women, 6% men i. often gone after age 50 d. etiology i. positive family hx ii. fluctuating estrogen levels iii. red wine iv. glucose fluctuations v. stimuli (flashing lights, strong odors) vi. weather changes vii. insomnia viii. stress |
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migraine sxs + sns
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e. sxs & sns
i. prodrome may be due to vasoconstriction of cerebral blood vessels ii. HA from vasodilation iii. short period of depression, irritability, restlessness, anorexia iv. prodrome - scintillating scotomas, visual field defects, paresthesias, dizziness, mood swings v. unilateral or bilateral vi. pulsating or throbbing vii. sx usually follow a pattern in each pt viii. behind one eye spreading out ix. nausea, vomiting x. photophobia, sonophobia xi. lasts hours to days |
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migraine tx
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f. tx
i. triptans - SSRAs that block vasoactive neuropeptide release ii. vasoconstrictors (caffeine, ergotamine) iii. food sensitivities iv. Mg 600 mg/daytanacetum parthenium(feverfew) v.. vitamin B2 (riboflavin) 400 mg/day (25 mg/day) vi. Tanacetum parthenium (feverfew) 20-500 mg/day vii. Petasites hybridus (butterbur) 75 mg BID viii. CoQ10 150 mg/day |
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cluster H.A.
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3. cluster
a. mostly in males i. aged 20 – 40 b. appear in clusters of days to weeks and then not for months or years c. paroxysmal d. abrupt onset of severe pain usually at same time of day e. last 1/4-3 hours f. agitated, restless g. unilateral - eye, neck, temple, face h. histaminic sx ipsilaterally i. vasodilation ii. periorbital edema, flushed cheek, rhinorrhea, lacrimation |
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secondary H.A d/t: first half
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1. intracerebral hemorrhage
a. rupture of atherosclerotic vessel from hypertension or thrombus b. abrupt onset, severe c. steadily increasing neurological deficits 2. subarachnoid hemorrhage a. rupture of intracranial aneurysm, usually congenital b. abrupt onset, severe c. syncope, vomiting, dizziness, stiff neck, positive Kernig’s and Babinski’s signs 3. hypertension a. throbbing, paroxysmal b. vertex, occiput 4. EENT lesions a. eyestrain, otitis, sinusitis, TMJ syndrome b. variable depending on cause |
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secondary H.A d/t: second half
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5. brain tumor
a. mild to severe, localized initially then becomes generalized as tumor grows, intermittently persistent b. slowly progressive weakness, convulsions, visual changes, aphasia, vomiting, mental changes c. better or worse with postural changes 6. brain abscess a. hx of EENT infection, lung abscess, RF 7. meningitis a. constant, severe, generalized b. fever, vomiting c. preceding uri 8. subdural hematoma a. trauma, changes in consciousness |
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Vertigo definition + etiology
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IX. Vertigo
A. the false sensation of the movement of self or the environment B. often accompanied by nausea, vomiting, and/or loss of equilibrium C. etiology 1. benign positional vertigo (BPV) (otoliths) 2. dysfunction of equilibratory apparatus a. vestibule, semi-circular canals, 8th cranial nerve, brainstem, cortex, eyes 3. otogenic (Meniere’s, otitis, labyrinthitis), 4.toxic, 5.environmental (motion sickness) 6. psychogenic 7. ocular (diplopia), 8. circulatory, 9. neurologic (MS, seizures), 10. neoplastic (tumors) |
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vertigo sxs + sns
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Vertigo: peripheral vs. central
1. peripheral - labyrinth, 8th nerve 2. central - brainstem, cortex E. sxs & sns 1. HA, hearing loss, tinnitus 2. diplopia, slurred speech, discoordination of an extremity 3. orthostatic hypotension |
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vertigo diagnosis + tx
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F. diagnosis
1. pulse oximetry 2. serum glucose 3. vestibular function tests 4. MRI G. treatment 1. find cause |
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Epilepsy def + etiology
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X. Epilepsy (Seizures)
A. an abnormal, unregulated discharge that transiently disrupts normal brain function 1. characterized by altered awareness, abnormal sensations, focal involuntary movements, or convulsions (widespread violent involuntary contraction of voluntary muscles) D. etiology 1. before age 2 – developmental defects, birth injury, metabolic disorders 2. ages 2-14 – idiopathic 3. adults – tumors, strokes, alcohol, hypoglycemia, idiopathic |
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Epilepsy classification
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E. classification
1. partial a. specific sensory, motor, psychic change that reflects the affected part of the brain 2. generalized a. aura often first b. motor + consciousness affected |
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partial seizure sxs + sns
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F. sxs & sns
1. partial a. simple partial (focal) i. specific sensory, motor, psychomotor phenomena without loss of consciousness ii. jacksonian - focal sxs begin in hand or foot and march up extremity b. complex partial (psychomotor) i. 1-2 minute loss of contact with surroundings ii. purposeless movements, unintelligible sounds, staggering iii. confusion, disorientation, amnesia |
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generalized seizures: sxs + sns
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2. generalized
a. loss of consciousness and motor function b. absence (petit mal) i. generalized ii. 10-30 second loss of consciousness with eye or muscle fluttering iii. stops activity and then resumes it after attack is over iv. often when sitting quietly v. genetic vi. predominantly in children c. grand mal (tonic-clonic) i. generalized ii. occasional aura iii. loss of consciousness iv. tonic-clonic contractions of muscles of extremities, trunk, head v. 1-2 minutes vi. postictal state - sleep, HA, muscle soreness d. atonic i. brief, generalized ii. in children iii. complete loss of muscle tone and consciousness e. myoclonic i. brief, quick jerks ii. may be repetitive iii. no loss of consciousness f. febrile i. 3 months to 5 years old ii. fever iii. in 4% of all children - 2% of those develop epilepsy |
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seizure: diagnosis + tx
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G. diagnosis
1. hx - family, trauma, infection, toxic exposure 2. lab - serum glucose, CBC, CMP 3. imaging - CT scan, MRI, EEG H. treatment 1. prevent injury during convulsion 2. identify cause if possible and then tx 3. anticonvulsant agents i. use until 2 years without seizures |
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Cerebrovascular Disease def + etiology + risk factors
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A. stroke, CVA
1. sudden, focal interruption of cerebral blood flow resulting in neurologic deficits B. most common cause of neurologic disability in the West 1. 3rd most common cause of death C. risk factors 1. older age 2. family hx 3. alcohol abuse 4. male 5. hypertension 6. cigarette smoking 7. hypercholesterolemia 8. diabetes |
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Cerebrovascular Disease: ischemic def. + etiology
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E. ischemic
1. 80% 2. insufficient cerebral circulation 3. etiology a. AS plaques i. thrombosis, emboli b. interruption of blood supply c. brain ischemia d. infarction if ischemia longer than a few minutes |
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Cerebrovascular Disease: ischemic stroke: TIA's
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4. TIA’s (transient ischemic attack)
a. focal neurologic abnormality b. sudden onset, brief duration c. AS - cerebral emboli d. sudden onset, last 2-30 minutes, no permanent sx e. sxs, with variable frequency depend on area of brain involved i. confusion, vertigo, blindness, paresthesia, weakness, dysarthria f. may indicate upcoming stroke g. treatment i. address underlying cause ii. hypertension, DM, hyperlipidemia, smoking |
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Cerebrovascular Disease: ischemic: stroke in evolution
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5. stroke in evolution
a. enlarging infarction b. neuro deficits increase over 24-48 hours c. unilateral sxs d. continuous stepwise progression over days |
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Cerebrovascular Disease: ischemic completed stroke
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6. completed stroke (ischemic
a. infarction manifested by neuro deficits of varying degree i. reflect area of brain involved b. abrupt onset c. AS thrombosis, embolism, stenosis d. very common e. rapid sxs, maximum within a few minutes i. numbness ii. weakness iii. paralysis iv. aphasia v. confusion vi. visual disturbance vii. dizziness viii. loss of balance ix. headache |
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Cerebrovascular Disease: ischemic stroke: diagnosis/prognosis
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f. diagnosis
i. clinical suspicion ii. AS thrombosis, embolism, stenosis iii. carotid vascular bruits iv. possible HA v. CT, MRI g. prognosis i. 20% die ii. age, health, site, size all important iii. the sooner improvement begins, the better the outcome iv. deficits after 12 months usually permanent |
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Cerebrovascular Disease: hemorrhagic def + etiology, sxs + sns
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1. 20%
2. bleeding into brain or meningeal spaces 3. intracerebral a. rupture of AS vessel from hypertension or made ischemic from thrombus - some from aneurysm b. sxs & sns i. abrupt severe HA ii. steadily inc neuro deficits iii. N,V, delirium, seizures, loss of consciousness iv. large hemorrhages fatal in >50% v. neuro deficits dec as blood resorbed vi. some degree of deficits remain c. diagnosis i. CT, MRI d. tx i. anti-coagulants contra-indicated ii. anti-platelet drugs |
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Cerebrovascular Disease: hemorrhagic: subarachnoid
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4. subarachnoid
a. bleeding into subarachnoid space b. ruptured congenital intracranial aneurysm c. head trauma d. sxs & sns i. asx until rupture ii. sudden, severe HA iii. syncope (quickly) iv. V, dizziness v. stiff neck vi. focal sns in 25% e. diagnosis i. CT, MRI ii. LP f. mortality 35%, 15% more die of another in a few weeks g. after 6 months, second rupture 3%per year h. overall bad prognosis i. tx i. anti-coagulants contra-indicated ii. surgery |
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MS definition + etiology
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XII. Multiple Sclerosis
A. demyelination in brain and spinal cord B. etiology 1. autoimmune 3. viral 4. genetic predisposition 5. 2-3x more in women 6. temperate climates 7. linked to geographic area where 1st 15 yrs spent 8. onset at age 20-40 yrs |
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MS "courses"...
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C. 4 courses
1. relapsing-remitting a. clearly defined attacks followed by remissions b. 85% 2. primary-progressive a. slowly worsening neurologic function b. 10% (often don't live for more than 10 yrs) 3. secondary-progressive a. initial relapsing-remitting course but then disease worsens steadily b. before DMARDs, (disease modifying anti rheumatic) 50% with relapsing-remitting developed this 4. progressive-relapsing a. disease steadily worsens with attacks of even worse neurologic function b. 5% (very severe pattern) |
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MS sxs + sns
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D. sxs & sns (* heat makes sx worse)
1. paresthesias 2. weakness, clumsiness of hand or leg 3. visual disturbances a. optic neuritis (comes and goes) b. partial blindness and pain in one eye c. fleeting ocular palsy (extraocular eye muscles don't work/tracking) 4. fatigue 5. gait disturbances 6. bladder dysfunction 7. bowel dysfunction 8. vertigo 9. MCI (mild cog impairment) a. emotional lability b. apathy c. depression 10. scanning speech 12. sexual dysfunction 13. sx worse with heat 14. fundus + optic nerve/, visual field changes 15. hyperreflexia (upper motor n prob - can't control reflex below) 16. tremors, muscular weakness, spasticity |
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MS diagnosis + prognosis
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E. diagnosis
1. clinical 2. MRI (with demyelination/brain + spinal cord) 3. CSF (lumbar puncture, cerebrospinal fluid) immunoglob G, lipoproteins a. increased IgG, lymphocytes, protein 4. visual evoked potentials (firing of neurons testing) F. prognosis 1. variable, remitting course 2. months, years of remittance 3. sx free intervals grow shorter often 4. permanent, disabling changes |
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MS tx
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G. treatment
1. corticosteroids 2. immunosuppresants 3. interferons 4. avoid overwork, fatigue, and stress 5. food sensitivities (elim diet) 6. low fat diet a. saturated fat less than 20 gm/day 7. EFA a. EPO 3-6 gm/d evening primrose b. sunflower oil 2 tbsp/d c. cod liver oil 1 tsp/d 8. avoid lipid peroxidation a. anti-oxidants to avoid this (myelin phospholipid layer) 9. vitamin B12 - 1-3 mg/day IM 10. vitamin D |
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Parkinson's definition + etiology
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A. slowly progressive degenerative CNS disorder
B. idiopathic C. slowness and decreased (poverty of) movement, muscular rigidity, resting tremor, postural instability D. onset usually after age 40 E. etiology 1. synuclein filled Lewy bodies in nigrostriatal system a. idiopathic b. loss of substantia nigra cells from basal ganglia c. *dopamine depletion 2. genetics a. 20% have positive family hx |
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Parkinson's sxs + sns
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1. insidious onset
a. loss of smell b. small handwriting c. soft or low voice d. dizziness 2. resting “pill-rolling” tremor a. maximum at rest, decreased during movement, absent during sleep 3. progressive rigidity 4. bradykinesia - slowness and poverty of movement 5. akinesia - difficulty initiating movement 6. masklike facies, open mouth, decreased blinking 7. stooped posture 8. shuffling gait 9. arms do not swing with stride 10. festination (gait small, fall over can't keep up w/ it) 11. lead-pipe rigidity interspersed with cogwheel rigidity 12. depression common 13. dementia in 50% a. AD 14. seborrheic dermatitis |
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Parkinson's diagnosis + tx
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H. treatment
1. levodopa usually with carbidopa 2. amantadine 3. remain active 4. PT 5. stool softeners |
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Peripheral Neuropathies def + classification
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A. syndrome of sensory loss, muscle weakness and atrophy, hyporeflexia, vasomotor sx
B. classification 1. mononeuropathy a. single and multiple 2. polyneuropathy a. many nerves simultaneously |
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Peripheral Neuropathies etiology
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1. mono
a. single (like carpal tunnel / common peronial=tibial nerve when head of fibula kicked etc // drop foot i. trauma ii. pressure b. multiple i. collagen-vascular diseases ii. metabolic (DM) iii. infectious (Lyme, HIV) 2. poly a. autoimmune b. toxic /I.e. Mercury c. nutritional def (B vitamins) d. metabolic (hypothyroidism, DM) e. malignancy |
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Peripheral Neuropathies mono, single + multiple sxs + sns
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D. sxs & sns
1. mono, single and multiple a. pain, weakness, paresthesia b. positive Tinel’s sign i. percussion over nerve producing distal paresthesias c. compression and entrapment syndromes i. ulnar nerve palsy -claw hand deformity ii. carpal tunnel syndrome - compression of median nerve - sensory deficits and paresthesias in radio-palmar hand - differentiate from C6 nerve root compression - vitamin. B6 100 mg TID iii. radial nerve palsy - wrist drop(sat. Night palsy) iv. peroneal nerve palsy - foot drop (tibialis ant. / common peronial (part of sciatic nerve) |
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Peripheral Neuropathies poly sxs + sns
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2. poly
a. symmetric b. sensory, motor, vasomotor sxs c. insidious d. sensory abnormalities in lower extremities e. tingling, numbness, burning f. worse at night g. position and vibration senses decreased h. objective sensory loss in stocking-glove distribution i. decreased or absent DTR’s j. distal muscle weakness and atrophy k. nocturnal diarrhea l. bladder and bowel incontinence m. impotence n. orthostatic hypotension o. pitted, ridged nails p. smooth, shiny skin that is dry, pale or dusky, sweaty |
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Peripheral Neuropathies diagnosis
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1. CBC - pernicious anemia,(macrocytosis/ B12 xu: very common cause) lead poisoning (bssophilic stippling) - dots
2. CMP - liver, kidney failure, DM (glucose, bilirubin...) 3. HbA1c (amt. of glucose erythrocyte been exposed to in 120 days) 4. thyroid function tests (hypo or hyper) 5. EMG, nerve conduction velocities 6. muscle biopsy (muscular or peripheral nerve etc.) |
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Peripheral Neuropathies / thoracic outlet
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1. thoracic outlet syndrome
a. compression of brachial plexus or subclavian vessels b. sx as in peripheral neuropathies c. positive Adson’s test |
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Peripheral Neuropathies / Guillain-Barre Syndrome
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Guillain-Barre Syndrome
a. acute rapidly progressive inflammatory polyneuropathy b. muscle weakness and distal sensory loss c. onset 5 days to 3 weeks after mild infectious disorder, surgery, immunization d. probably autoimmune e. most common acquired demyelinating neuropathy f. sxs & sns i. symmetric weakness with paresthesias beginning in legs and moving to arms ii. absent DTR’s iii. facial and oropharyngeal muscle weakness iv. 5-10% respiratory failure v. BP fluctuations, arrhythmias vi. 5% die v. 90% reach maximal weakness in 2-3 weeks h. treatment i. severe is medical emergency ii. maintain airway iii. plasmaphoresis i. prognosis i. 2% fatality ii. considerable improvement over a period of months is usual iii. 30% have residual weakness at 3 yrs iv. 10% relapse after initial improvement and develop chronic relapsing polyneuropathy |
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Peripheral Neuropathies / Bell's palsy
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Bell’s palsy
a. unilateral 7th cranial nerve palsy b. sudden onset c. swelling of facial nerve possibly autoimmune or viral d. extent of recovery varies on extent of nerve damage |
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Peripheral Neuropathies / Trigeminal neuralgia
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trigeminal neuralgia (opthalmic, maxillary/ sensory + mandibular)
a. sharp, lancinating pain usually over mandibular or maxillary divisions of trigeminal nerve b. last from seconds to minutes c. no signs only hx i. if sns, look for another cause d. often arterial compression of trigeminal nerve |
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Peripheral Neuropathies / amyotrophic lateral sclerosis (ALS)
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amyotrophic lateral sclerosis (ALS) MOTOR (no sensory abnormalities)
a. progressive degeneration of anterior horn cells, corticospinal tracts, bulbar motor nuclei b. combined motor neuron disease - UMN & LMN c. muscular weakness and atrophy initially in hands d. progression asymmetric e. initial hyporeflexia (LMN) f. then muscle fasciculations, spasticity g. hyperreflexia, extensor plantar reflexes (moves up UMN) h. dysarthria, dysphagia (speek, chew, swallow, breathe) i. dx by onset during middle to late life, progressive and generalized motor involvement with no sensory abnormalities j. 50% die within 3 years of onset |
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Meningitis def + etiology
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Meningitis
A. inflammation of meninges of brain or spinal cord B. acute bacterial meningitis 1. etiology a. Neisseria meningitidis - meningococcus i. most in 1st year of life ii. epidemics in closed populations b. Streptococcus pneumoniae - pneumococcus i. most common in adults ii. alcohol abuse, chronic otitis, sinusitis, mastoiditis, pneumococcal pneumonia, sickle cell disease, asplenism, closed head injury c. hematogenous spread d. direct communication with exterior |
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Meningitis sxs + sns
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2. sxs & sns
a. uri b. fever, HA, stiff neck, vomiting c. desperately ill within hours d. irritability, confusion, drowsiness, stupor, coma e. seizures, cranial neuropathies f. infants up to 2 years of age - fever, vomiting, irritability, convulsions, high-pitched cry, bulging fontanelles g. purpural rash with meningeal sns - meningococcemia |
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Meningitis diag/prog/tx
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3. diagnosis
a. accurate dx essential because it can be lethal in hours b. positive Brudzinski’s and Kernig’s signs c. blood culture 4. lab a. LP b. CSF - stain, culture 5. prognosis a. early antibiotics – less than 10% fatality b. late dx, neonates, elderly - often fatal 6. treatment a. dexamethasone b. antibiotics |
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aseptic meningitis
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C. aseptic meningitis
1. inflammation of meninges without apparent cause 2. etiology a. viruses b. tumors 3. sxs & sns a. uri b. fever c. HA d. meningeal sns i. milder than in bacterial meningitis 4. dx a. LP i. CSF examination to R/O bacteria 5. tx a. resolves on its own |
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subacute + chronic meningitis
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D. subacute and chronic meningitis
1. subacute a. meningeal inflammation that lasts more than 2 weeks 2. chronic a. meningeal inflammation that lasts more than 1 month 3. etiology a. fungi, TB, Lyme disease, AIDS, syphilis, neoplasm 4. sxs & sns a. as in acute meningitis but evolves slowly over weeks b. minimal fever c. progressive course to fatality within a few weeks to months 5. diagnosis a. must R/O structural lesions (tumors, abscess) because of slow development of sxs b. CSF examination 6. treatment a. depends on cause |
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CNS neoplasms def + etiology
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CNS Neoplasms
A. intracranial tumors 1. brain parenchyma or extraneural structures 2. metastases 10x more common than primary tumors B. CNS changes from invasion and destruction by tumor and from secondary effects like increased ICP C. found in 2% of routine autopsies D. most common in early adulthood or middle life E. severity depends on size, location, rate of growth, grade of malignancy F. benign grow more slowly with no necrosis or vascular proliferation 1. may reach considerable size before causing sxs 2. if cannot be excised entirely, lethal due to size G. malignant have rapid growth, necrosis, vascular proliferation, and endothelial hyperplasia 1. rarely metastasize out of CNS 2. death by large local growth |
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CNS neoplasms sxs + sns
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H. sxs & sns
1. HA most common sx a. increased ICP b. vomiting c. papilledema 2. mental status deterioration a. seizures i. more common with primary than metastatic tumors b. drowsiness c. lethargy d. personality changes e. disordered conduct f. impaired cognition g. impaired consciousness 3. focal brain dysfunction a. suggest location of tumor b. focal sxs & sns c. altered endocrine function |
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CNS neoplasms diagnosis + tx
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I. diagnosis
1. suspect in patients with the following a. progressive sns of focal or global cerebral dysfunction b. seizures of new onset c. persistent, unexplained HA of recent onset i. often worse with sleep d. sxs of increased ICP i. vomiting, papilledema e. pituitary of hypothalamic endocrinopathy 2. complete neuro exam 3. chest x-rays 4. CT scan 5. MRI J. treatment 1. depends on type and location of tumor 2. corticosteroids 3. surgical excision 4. radiation 5. chemotherapy only in a few selected types |
