Neurology and Movement disorders – Flashcards

Nearly 800,000 strokes/year in u.s. 90% ischemic, 10% hemorrhagic. 1 in 5 in children and young adults. Important to include cva in your differential diagnosis if someone comes in with focal deficits even if they are younger than you would expect.

-facial drooping, one sided arm or leg weakness, verbal deficits( slurring,dysarthria, aphasia, verbal agnosia, altered LOC) may also have ataxia, gait disturbances, visual field deficits (particularly homonomous hemianopsia (sp), imbalance, vertigo, etc. symptoms depend on location of lesion in cerebral circulation.

non-contrast head CT, allows you to differentiate between hemorrhagic and ischemic stroke. Diffusion weighted MRI is technically most accurate but is rarely performed (because it takes much more time to do than CT). After this routine labs include: CMP, CBC, glucose, INR's, EKG(looking for a.fib which is a risk factor for CVA).

-supplemental o2 -airway management (if ;94%) - blood pressure control (labetalol) immediately if systolic bp more than 220 mmHg (blood pressure will need to be less than 220 if going to give clot-busting drugs) - treat hypoglycemia if 100.4.

Due to stenosis of a critical vessel (most common type of ischemic stroke).

Due to embolism from distal site. Major risk factors include atrial fibrillation and DVT. also risk in pt. with PFO.

Blockage of smaller penetrating vessels of brain parenchyma. much more subtle, usually presenting with only a few neurological deficits (pure motor stroke, pure sensory stroke, ataxic hemiparesis-etc) -much smaller area of brain affected because smaller vessel is blocked.

-10% of strokes -Most caused by SAH: "the worst headache of my life", "Thunderclap headache", Particularly consider in acute focal neuro sx acc. w/ headache. usually d/t ruptured aneurysm. -Be aware of the Saccular "berry aneurysm"whichhave a tendency to show up in the anterior /posterior communicating arteries, as well as the MCA.

SHAME mneumonic: Smoking Hypertension adult polyposis kidney disease marfan syndrome Ehler-danlos syndrome

Surgery is generally indicated for coiling or clipping. management focuses on reducing BP to below 160 systolic (nicardipine most commonly employed) and if the pt. is on warfarin administration of FFP. -be vigilant for seizures (true of any patient with increased intracranial pressure). -keep pt inclined to 30 degrees to keep ICP in control.

-question becomes whether the pt is eligible for thrombolytic therapy w/ rtPA (alteplase). No benefit to heparin, Coumadin, or antiplatelet administration for an ongoing stroke.

-Stroke/significant head trauma in last 3 months -arterial puncture in non-compressible site in past 7 days -bp;185/110 mmHg (can use nicardipine or nitroprusside to make pt eligible for TPA) -INR ;1.7 -platelets should be above 100 K -Elevated PTT -Glucose ;50 mg/dl -any PMHx of intracranial bleed -Multilobar infarct (multiple areas of infarction rather than just 1).

-All stroke pts. should be transferred to neuro ICU, SICU or MICU -hemorrhagic: management will be based on surgical method.

-All stroke patients should be given aspirin as prophylaxis for secondary stroke (if pt is allergic to aspirin clopidogrel or dipyridamole may be substituted. if pt. has another stroke it should be given in addition to aspirin. -seizure prophylaxis is not necessary, but it is important to be prepared for the event. (5 mg of lorazepam or diazepam IV). Approximately 1 in every 5 patients have seizures after stroke. -If EKG showed atrial fibrillation that should be managed with warfarin(to INR of 2-3), and a calcium channel blocker (diltiazem). -echocardiography(checking to see if they have a P.F.O.) -carotid angiography (surgery if blockage more than 70%) -Lifestyle modifications -anticoagulation: heparin/LMWH, warfarin, factor X blockers (Used in all ischemic stroke patients). -rehabilitation.

-of utmost importance in any patient with a.fib to assess their risk of stroke! CHF(1) Hypertension OR treated for HTN (1) Age ;75 years (1) Diabetes mellitus (1) Stroke (2) -Score 0-1: aspirin QD, 1+ Warfarin to an INR of 2-3. CCB is the anti- arrhythmic of choice for A.Fib. -Another more complex scoring system called CHAD-S2 vasc.

0= 1.9% 1= 2.8% 2= 4.0% 3= 5.9% 4= 8.5% 5= 12.5% 6= 18.2%

Hx: hypertension, hypercoagulability(inherited, acquired, OCP's or estrogen use), hyperlipidemia, diabetes, obesity, amyloid angiopathy.

Spinning often accompanied with nystagmus

Single prolonged episode: -vestibular neuronitis -labyrinthine damage -lateral medullary (Wallenberg's) or cerebellar infarctin Recurrent episodes -Meniere's disease -vertebrobasilar insufficiency -migraine aura -perilymphatic fistula Postitional -benign positional paroxysmal vertigo Other -otosclerosis, acoustic neuroma, CP angle tumor, multiple sclerosis, Ramsay-Hunt syndrome, disequilibrium syndrome, anxiety, drugs. VERTIGO NEEDS TO BE DIFFERENTIATED FROM PRE-SYNCOPE

Common complaint with myriad causes. Helpful approach is to ask: How often (episodic or constant), Hearing loss associated with it( hearing loss almost always points toward a peripheral cause of vertigo), other symptoms. -Most pressing diagnosis to rule out particularly in older patients is stroke(Wallenberg's syndrome, cerebellar infarct) and space occupying lesion. -Base index of suspicion on risk factors and other symptoms (i.e. cranial nerves, particularly hemisthesias, dysphagia, papilledema) -Err on the side of caution if not sure: non-contrast CT.

Central: diplopia, dysarthria, dysphagia(esp. brainstem lesions), ataxia; vertical nystagmus which is more notable with gaze fixation; absence of hearing loss and tinnitus, central vertigo tends to last longer (with major exception of infarcts) Peripheral: tinnitus, hearing loss, severe nausea/vomiting, horizontal nystagmus which lessens w/ gaze fixation; peripheral vertigo tends to be episodic. -Is it acute or recurrent -Physical findings: Romberg test( universally abnormal if pt has vertigo), caloric stimulation test, Dix-Hallpike maneuver -Provoking factors: particularly consider: head position, head injury, recent URTI, "pop"sensation or changes in ear pressure, headache.

Cold Other Warm Same

Pt side lying pour cold water into ear. normal response is to get fast beat nystagmus toward opposite ear. indicates healthy vestibular nerve. If you pour hot water into ear the normal response is for the nystagmus to go toward ear that is being tested. If this is not your result you have vestibular nerve problems.

Peripheral is all things peripheral TO THE BRAIN. Central vertigo is within the brain.

-Acute peripheral vertigo commonly associated with an upper respiratory tract infection. Idiopathic (may be some association with HSV) -Hx: usually relatively healthy patient, young or old (age doesn't matter). -Sx; few other symptoms besides the vertigo (and associated nausea and vomiting, imbalance), vertigo is severe. -Px: +Romberg's test, abnormal caloric vestibular stimulation test (abnormal caloric test is not diagnostic but if the hx of URI is present this is the most likely Dx). -Dx: clinical -Tx: rehydration (as for any significant N/V; IV if necessary, supportive care, antiemetics(diphenhydramine, Phenergan, metoclopramide), anticholinergics/vestibulosuppressants: meclizine, scopolamine.

-Acute, peripheral vertigo associated w/ head injury or trauma to the ear. remember that any pt who presents with a head injury and CNS sx or nausea/vomiting should first get a head CT to r/o intracranial bleed. -Hx; trauma to head or ear -Sx: few other besides vertigo (and associated nausea and vomiting, imbalance) -Px; +Romberg, signs of head or ear injury on general or otoscopic exam, carefully examine head and neck for injury. -Dx: trauma w/ CNS warrant Immediate head CT. May be unremarkable in pts solely with labyrinthine concussion -Tx; supportive, vestibulosuppressants, consult ENT if medical treatment fails (should resolve in a week, if longer then consult).

stroke to posterior inferior cerebellar artery. Not a lot of things cause vertigo and sensory heminanesthesia problems.

-Acute central vertigo secondary to infarct of the lateral medulla, associated with other CNS sx. MEDICAL EMERGENCY! -Hx: risk factors for stroke(age, hypertension, smoking, hyperlipidemia, hypercoagulability, atrial fibrillation -Sx: severe vertigo, N/V, facial hemianesthesia (ipsilateral), contralateral body hemianesthesia;dysphagia, dysarthria, horner's syndrome (ptosis, miosis, anhidrosis) -Dx; make presumptive diagnosis on clinical presentation. The best initial test is a non-contrast head CT -Tx; stroke protocol, TPA if within 3 hours of symptom onset.

-Recurrent, peripheral vertigo strongly associated with constant tinnitus and progressive hearing loss. Caused by unilateral intermittent increases in perilymphatic volume, resulting in unequal and abnormal vestibular function -Hx/Sx: More common in older adults, women more than men; salient features apart from vertigo are "feeling of fullness" in one ear, progressive hearing loss and constant ringing (tinnitus). symptoms may wax and wane (the higher the blood pressure, the more fluid goes into the semicircular canal). -Dx: primarily clinical. Unilateral and chronic nature may incline the clinician to get imaging to exclude acoustic neuroma (especially if pt has neurofibromatosis). progressive hearing loss, dizziness and tinnitus are common triad of diagnosis in Meniere's. -Px: ensure there is abnormality in hearing, unilateral supports dx. -Tx: supportive, Lasix or any other kind of diuretic with low sodium diet will help to decrease the fluid in the inner ear (keep them low normal hydration). ENT surgical therapy is available for protracted cases.

-very uncommon diagnosis -Recurrent, peripheral vertigo caused by rupture of bony capsule in inner ear, resulting in leakage of perilymph into the middle ear. -Hx is often useful in diagnosing this condition as the patient can often note the onset of the vertigo with a "pop", associated with an increase in middle ear pressure (valsalva maneuver, straining, coughing, sneezing etc.) consider in pilots and scuba divers (d/t drastic changes in pressure). -Sx: like Meniere's disease can also cause sensation of fullness and progressive decline in hearing. -Dx: differential from Meniere's disease is elusive and often based on hx of onset. if perilymhpatic fistula is suspected ENT consult should be obtained immediately. Tx: supportive, ENT surgery, much more easily treated with surgery than Meniere's.

-Recurrent central vertigo caused by intermittent hypoxia due to insufficiency of the posterior/ vertebral circulation which primarily feeds the cerebellum, brainstem, occipital cortex (causes vertigo because cerebellum and brainstem manage balance). Important because of the risk it implies, approximately 25% of the strokes/TIA's in the U.S. are of posterior circulation. anyone with spells of central vertigo should be worked up for VBI. -Hx: Pts w/ vertebrobasilar insufficiency will generally have multiple risk factors for stroke, they are often older adults. -Sx: apart from vertigo patients may report visual changes, diplopia, numbness and tingling, weakness,dysarthria, dysphagia. Notably these are often sudden attacks. -Dx; always keep a high index of suspicion for vascular disease in pts w/ risk factors for stroke. If VBI is most likely dx then get a head CT, follow by angiography(either traditional or MR) to identify stenotic vessels. -Tx: therapy is similar for pts w/ carotid artery disease: reduction of modifiable risk factors (smoking, htn, cholesterol), anti-platelet therapy, various surgical repair therapies if deemed necessary by a vascular surgeon (specifics are outside scope of USMLE).

-recurrent peripheral vertigo caused by dislocation of otoliths in the semicircular canals. notably exacerbated with changes in head position. -Otoliths are normal and are responsible for telling your hairs/nerves where your head is in space. In BPPV they are dislocated from where they need to be. -Most common cause of vertigo in U.S. -Sx: vertigo exacerbated with changes in head position. vertigo comes on severely and dissipates within a minute. few other symptoms not related to vertigo. -Dx; the best initial test is the Dix Hallpike maneuver. This maneuver should elicit nystagmus with a fast-phase toward the affected ear (positive maneuver). -tx: the Epley maneuver (otolith repositioning ) is the best treatment BPPV. supportive care should be prescribed for any residual sx.

Pt sitting up with you supporting their head and move them quite quickly to a lying down position and head rotated 45 degrees to left or right.

-The therapy for BPPV -effective more than half the time, may not always take all the symptoms away but may partly help.

`-Multiple sclerosis: focal neurologic signs, particularly numbness/tingling, weakness, diplopia, eye pain, focally enhancing white matter lesions on CT -Panic attack: classic panic attack symptoms, short lived, look for symptoms of anxiety, depression. -Ramsay hunt syndrome Type 2: complication of shingles, Hx of shingles, facial muscle palsy(one side of face will be much weaker than the other), vesicles on tympanic membrane seen on otoscopy and hard palate. Loss of taste sensation over anterior 2/3 of tongue. -Cholesteatoma: waxy white-yellow tumor seen on otoscopy; looks like cerumen but you will not be able to get it out. Hx of chronic ear infection, drainage, conductive hearing loss (especially Peds). Weber test helps to diagnose. -Otosclerosis: autosomal dominant, conductive hearing loss. -migraine aura, seizure aura -Drugs: aminoglycosides, diuretics (especially furosemide); antihypertensives; antidepressants, alcohol

eye pain and diplopia associated with Multiple Sclerosis.

Immune mediated disease of the CNS. Disease of myelin and axons. The immune system destroys the normal protective myelin coating necessary for normal conduction of electrical impulses. conduction is slowed and axons are exposed. exposed axons may then be severed leading to permanent loss of the axon and permanent loss of function.

-usually diagnosed between 20 and 50 (occasionally diagnosed in young children and older adults). -more common in women than men (;2-3:1) -most common in those of northern European ancestry(more common in Caucasians than Hispanics or African Americans. rare in Asians). -most common in temperate areas of the world. (environmental factors, genetics, lower vitamin D exposure???)

-20% of those with MS have a blood relative with MS. -Risk is 1/750 for general population, 1/40 for those with 1st degree relative, 1/4 for identical twins. -Risk is higher in any family where there are several family members with the disease(multiplex families).

-clinical diagnosis based on signs and symptoms and medical history. -paraclinical tests provide support (MRI, spinal fluid, evoked potentials). -Diagnostic criteria: dissemination in time and space: evidence that damage has occurred in at least 2 separate areas of the CNS at different points in time (evidence of plaques). There must be no other explanation. (see Revised McDonald criteria).

-a first neurological event suggestive of demyelination -Individuals with CIS are at high risk for developing clinically definite MS if the neurologic event is accompanied by multiple clinically silent (asymptomatic) lesions on MRI typical of MS.

-relapsing-remitting (55%) -secondary progressive (30%) -primary progressive (10%) -progressive relapsing. (5%)

neurologist, urology, nurse, PCP, physiatrists, physical therapy, OT, SLP, psychiatry, psychotherapist, neuropsychologist, social worker, pharmacist.

Cannot predict who will do well but can predict who will not do well. -frequent multifocal attacks. -heavy MRI burden on initial scans -pyramidal involvement -ataxia -cognitive difficulties -5 year accumulation of disability -spinal progression (primary progressive MS).

-Relapse = new symptom or sudden worsening of old symptom lasting at least 24 hours and usually accompanied by an objective change in neurologic findings. -treatment with corticosteroids recommended if relapse significantly interferes with every day functioning. (3-5 day course of high dose intravenous methylprednisolone with or without oral taper. -high dose oral steroids may also be used. -rehabilitation can help restore function following a relapse.

Most are not outwardly visible: fatigue(most common), loss of sensation, decreased visual acuity, diplopia, bladder/bowel dysfunction. pain, sexual dysfunction, paresthesias(tingling, numbness, burning), emotional disturbances (depression, mood swings), cognitive difficulties(memory, attention, processing), heat sensitivity. Visible symptoms: spasticity. Gait, balance and coordination problems. speech/swallowing problems, tremor, weakness.

MS lassitude can be treated with amantadine, SSRI's, modafinil, armodafinil etc.

-only needs to be treated if it is causing decrease in function. -first important to reduce sources of pain in the body. -Exercises and therapy stretching, ROM, weight bearing, cryotherapy, inhibitory casting, pool therapy, aerobic exercise, EMG biofeedback, electrical stimulation. -multiple medications and procedures as well.

While exercise is important, it is important to remember the muscles are not the source of the weakness, the nerves are.

-reaction to disease as well as part of the disease process. -underdiagnosed and undertreated in MS. -best treatment is exerices+Medication+psychotherapy. -Suicide 7.5 x more common in MS than in general population -Depression+ETOH+isolation =85% accuracy for SI.

cognitive function correlates with lesion load/brain atrophy and cognitive difficulties can occur anywhere along the course of the disease. depression worsens cognition. anticholinergic medications can also worsen cognition.

-Memory: acquisition and retrieval -attention and concentration: working memory -speed of information processing -executive functioning -visual/spatial organization -verbal fluency, word finding.

-to establish baseline -there are reported changes in ability -there is a potentially treatable condition -person is being started on new treatment -when considering application for SSDI or vocational rehabilitation -when there is a need to know. -standard mental status exam used neuro exam will miss 50% of cognitively impaired patients.

-most common cause of unilateral facial palsy worldwide -paralysis generally clears in 6-8 weeks. -Signs and symptoms include: acute onset of unilateral upper and lower facial paralysis (over a 48 hour period), posterior auricular pain, decreased tearing, hyperacusis, taste disturbances, otalgia, weakness of the facial muscles, poor eyelid closure, aching of ear or mastoid, tingling or numbness of cheek/mouth, epiphora, ocular pain, blurred vision, flattening of forehead and nasolabial fold on the side affected by the palsy. inability to raise eyebrows on affected side. distorted smile.

overflow of tears onto face indicating that tear ducts are not draining properly.

-patch/protect affected eye if not producing enough tears and use artificial tears/ointment as needed. -start corticosteroids in 72 hours. -possible antivirals if virus suspected.

-RPR -HIV elisa/western blot -CBC, ESR, thyroid, glucose, CSF analysis, HgbA1C, antineutrophil cytoplasmic antibody levels, salivary flow, schemer blotting test, nerve excitability test, computed tomography, MRI.

in central motor neuron disorder the paralysis will only by the bottom half of face.