1. tremor
2. bradykinesia
3. rigidity
4. pregressive posutral instability

1. tremor : worse @ rest, emotional stress (lessened w/ voluntary activity/intentional movement & sleep).  usually confined to one side or limb for years before becoming generalized. 
2. Bradykinesia: slowness of voluntary movement & decrease of automatic movements: lack of swinging of arms while walking/shuffle gait
3. rigidity: increased resistance to passive movement (flexed posture).  Festination - increased speed while walking. 
4. face involvement: relative immobile face, widened palpebral fissures, seborrhea of skin common. decreased blinking.
5. instability: postural instability usually a late finding ("pull test" - stand behind pt pull shoulders - pt falls or takes steps backwards)

1. Levodopa/Carbidopa
2. Dopamine agonists
3. anticholinergics
4. amantadine
5. selective MAO-B inhibitors
6. COMT inhibitors

• treats Parkinson's disease
• levodopa converted to dopamine 
• carbidopa reduces amount of levodopa needed reducing SE of the levodopa
• SE: N/V, hypotension, somnolence, dyskinesia & "wearing off" assoc w/ long term us
• Most effective tx 

• treats Parkinson's disease
• bromocriptine, pramiprexole, ropinirole
• less s/e than levodopa
• somtimes used in young pts to delay use of levodopa
• if pt is not sensitive to levodopa, DA useless
• SE: orthostatic hypotension, N, HA, dizziness, unpredictable sleepiness

• used for Parkinson's disease
• blocks excitatory cholinergic effects
• Ind: pts < 70 w. tremor as predominant sx 
• doesnt improve bradykinesia
• benztropine (cogentin), trihexyphenidyl
• help w/ tremor & rigidity, NOT BRADYKINESIA
• SE: constipation, dry mouth, thirst, blurred vision, tachycardia, urinary retention
• CI: BPH & acute glaucoma

• Parkinson's disease
• may hlep early on with mild sx
• MOA: increases presynaptic dopamine release & improves long term levodopa-induced dyskinesias

• Parkinson's disease
• Selegiline, rasagiline
• MOA: increases dopamine in striatum (MOA_B normally breaks down dopamine)

• Parkinson's disease
• MOA : prevents dopamine breakdown
• entacapone, tolcapone
• SE: GI (diarrhea), brown urine discoloration
• Rulminant hepatic failure w. Tolcapone (so Entacapone preferred

1. initial behavioral changes (personality, cognitive intellectual, psych
2. chorea - rapid, involuntary, or arrhythmic movement of the face, neck, trunk, & limbs initially. May have facial grimacing, ataxia
3. dementia

restlessnesss

fragility

quick involuntary hand movements

• no cure
• chorea dominant: antidopaminergic agents (phenothiazines, haloperidol) & benzo's
• tetrabenzine for dyskinesia
• amantadine may help w/ chorea

worse @ night

ETOH

stress 

ingestion of specific foods

• IPSILATERAL Horner's syndrome (ptosis, miosis, anhydrosis)
• nasal congestion/rhinorrhea
• conjunctivitis
• lacrimation

• 100% O2 1st line (6-10L)
• anti-migraine meds helps during attack (SQ sumatriptan or dihydroergotamin) : vasoconstriction

verapamil (1st line)

steroids, ergotamine, valproic acid, lithium

treated as migraines

NSAIDS

anti-migraine meds

TCA's (ex ampitriptyline)

BB

1. common migraine (w/o aura)
2. classic migrane (w/ aura) --> rarer

physical activity

stress

lack/excessive sleep

ETOH

specific foods (ex chocolate)

OCPs/menstruation

• visual changes MC light flashes (photopsia), zig zag lines of light, scotomas (blind spots that may scintilate)
• aphasia (impairement of language)
• weakness, numbness lasting for 5-20 min 
• Aura lasts <60 minutes --> HA

Anti-HTN meds

BB

CCB

TCA's

anticonvulsants (valproate, topiramate)

• triptans, IV dihydroergotamine (triptans & ergots are serotonin 5HT-agonists - vasoconstriction), SE: chest tightness from constriction.  CI: CAD, peripheral vascular dz, HTN, hepatic or renal dz
• Dopamin blockers: for N/V. IV phenothiazines: metoclopramide, promethazine, prochlorperazine.  MOA: blocks dopamine receptors (given w/ benadryl to prevent EPS & dystonic reactions, parkinsonism sx d/t decreased dopamine)
• IV fluids, NSAIDs/acetaminophen
• Codeine, barbiturates for mild symptoms
• dark, quiet room helps

1. confusion: confused or blank expression, blunted affected
2. amnesia: pretraumatic (retrograde) or posttraumatic (antegrade) amnesia.  The duration of retrograde amnesia is usually breif
3. Ha, Dizziness, visual disturbances: blurred or double vision
4. Signs of increased ICP: persistent vomiting, worsening HA, increasing dsorientation, changing levels of consciousness

1. CT : test of choice.  PET scan may be done to look at glucose uptake (not done often)
2. MRI: study of choice if prolonged symptoms > 7-14 days or w/ worsening of symptoms not explained by concussion syndrome

• cognitive & physical rest is the main management of pts w/ concussion
• pt's may resume strenuous activity after resolution of sxs & recovery of memory & cognitive fcns

idiopathic by definition

strong assoc w/ HSV reactivation (MC)

VZV

lyme disease

MC right side

DM

pregnancy (esp 3rd trimester)

post URI

inappropiratley placed dental n. block

• sudden onset (24-48h) of ipsilateral hyperacusis (ear pain) 
• unilateral facial paralysis
• unable to lift affected eyebrow
• wrinkle forehead
• smile on affected side
• loss of nasolabial fold
• drooping of corner of mouth
• taste disturbance (anterior 2/3)
• biting inner cheek
• eye irritation (d/t decreased lacrimation & inability to fully close eyelid)
• weakness/paralysis ONLY affects face (not extremities)

eye on affected side moves laerally & superiorly when eye closure is attempted 

bell's palsy

1. prednisone (esp if started w/n 1st 72h of sx onset).  decreases n. inflammation. 60mg/d x 1 week
2. artifical tears (replaces lacrimation & reduces vision probs) may need eye patch to sleep if severe
3. +- acyclovir in severe cases
4. function often begins to return w/n 2 weeks w/ significant improvements w/n 4 months 
5. restoration of taste usually precedes motor recovery

• immune-mediated demyelination & axonal degeneration slows impulses 
• symmetric weakness & paresthesias 
• thought 2ry to post-infection immune response which cross-reacts w/ peripheral n. components (molecular mimicry)

• CSF: high protein w/ normal WBC-albuminocytological dissociation
• high protein in absence of increased cell count may be d/t altered n. capillary-CSF barrier defect
• high protein (>400mg/L) usually seen after 1-3 weeks of sx

1. plasmapheresis (done early) removes harmful circulating autoantibodies that causes demyelination. equally effective as IVIG
2. IVIG: suppresses harmful inflammation/auto-Ab & induces remyelination. Most recover w/n mos (10-20% left w/ persisting disability)
3. Prednisone CI
4. Mechanical ventilation if respiratory failure
5. IVIG used in children as well