Neuro Test 1 Set 1

Front 1

Levodopa/carbidopa brand name

Back 1

Sinement

Front 2

Divalproex brand name

Back 2

Depakote/Valproic Acid

Front 3

Phenytoin brand name

Back 3

Dilantin

Front 4

Dorsal column =....

Back 4

touch

Front 5

Spinothalamic tract=...

Back 5

pain/temperature

Front 6

Trigeminal nerve=...

Back 6

face (sensory, pain, temperature)

Front 7

Hyperkinetic tremors (3)

Back 7

1)postural/terminal tremor
2)essential tremor
3)rest tremor

Front 8

Hypokinetic tremor (2)

Back 8

1)masked face
2)shuffling gaits (pedastel turning seen w/ this)

Front 9

Postural/Terminal tremor?

Back 9

finger shakes as reaching target

Front 10

Essential tremor (7)

Back 10

1)head wobble
2)no resting tremor
3)finger shakes whole time during finger to target test
4)involves hands, head, face
5)familial tremor (seen b4 25yo)
6)Senile tremor (seen in 7th decade)
7)other tremors include cerebellar tremor, neuropathic tremor, alcohol withdrawal tremor

Front 11

Resting tremor (3)

Back 11

1)continues during sustension of posture
2)but resolves w/ movement
3)gone while sleeping

Front 12

Chorea (4 and last has 4 causes)

Back 12

1)completely random/jerky movments
2)Huntington's Chorea
3)Senile Chorea

4)acute chorea commonly caused by drugs
a)anticonvulsants
b)neuroleptics
c)levodopa
d)dopamine agonists

Front 13

Dystonia (2)

Back 13

1)intense, irregular, sustained torsion spasms of musculature
2)marked abnormalities of body posture

Front 14

Akathisia (2)

Back 14

1)RESTLESSNESS/irresistible urge to move
2)often caused by neuroleptic use

Front 15

Tardive Dyskinesia (2)

Back 15

1)persistent, repetitive abnormal movements
2)associated w/ chronic neuroleptic meds that block and bind dopamine receptor

Front 16

Hemiballisms (2)

Back 16

1)violent, involuntary movement
2)happens ONLY ONE 1 SIDE

Front 17

Parkinson's Disease (PD) 4 cardinal features

Back 17

TRAP

Tremor at rest (resting tremor---see NC for def)

Rigidity- tone @ all/some joints increased ("cog wheeling")

Akinesia/bradykinesia- slow movements, delay in blinking, blink/swallow less frequently (see the 2 hypokinesia's)

Postural abnormalities- flexion giving the appearance of exaggerated old age, balance is affect so incr risk of falling

Front 18

Other characteristics of PD (6)

Back 18

1)Gait disturbance- slow walking movement, slow small shuffling to start then rapid shuffling to catch up (then hard to slow down)
2)Micrographia (bad handwriting)
3)urinary urgency
4)hypophonia
5)stuttering
6)depression/dementia

Front 19

Classifying symptoms (HOEHN-YAHR CLASSIFICATION) (6)

Back 19

Stage 0) no clinical signs

Stage 1) unilateral involvement

Stage 2) bilateral involvement, no postural changes

Stage 3) bilateral involvement w/ mild postural imbalance, pt leads independent life

Stage 4) bilateral involvement w/ postural instability, pt requires substantial help

Stage 5) severe, fully developed disease, pt is restricted to bed/chair

Front 20

Essential Tremor (5)

Back 20

1)peak incidence in 15-20 and 50-70yo (most common movement disorder in world)
2)bilateral posture or action tremor varies in intensity
3)often more intense as hands near face
4)voice tremor common
5)SMALL QUANTITY OF ALCOHOL MAY IMPROVE TREMOR

Front 21

Differentiating ESSENTIAL TREMOR from Parkinson's
a)tremor type
b)onset
c)symmetry
d)family history
e)affected parts
f)bradykinesia
g)rigidity
h)postural instability
i)responds to what drugs?
j)worsened by emotional stress?

Back 21

a)postural, KINETIC, RARELY RESTING
b)bimodal (15-20yo and 50-70yo)
c)BILATERAL
d)50%
e)Hands>head>voice (LEGS UNCOMMON)
f)absent
g)absent
h)absent
i)propanolol, primidone, alcohol (think peach schnapps--3P's)
j)yes

Front 22

Differentiating PARKINSON'S from Essential tremor
a)tremor type
b)onset
c)symmetry
d)family history
e)affected parts
f)bradykinesia
g)rigidity
h)postural instability
i)responds to what drugs?
j)worsened by emotional stress?

Back 22

a)RESTING, postural, RARELY KINETIC
b)55-66yo
c)unilateral OR bilateral
d)less than 10%
e)Hands>legs (HEAD/VOICE UNCOMMON)
f)present
g)present
h)present
i)anticholinergic drugs, LEVODOPA, small amt to propanolol
j)yes

Front 23

Primary PD causes (6)

Back 23

1)neurodegeneration (loss of basal ganglia leading to motor abnormalities)
2)genetic
3)environment
4)excitotoxicity
5)mitochondria/energy metabolism
6)oxidative stress/generation of free radicals from dopamine metabolism

Front 24

In ____ pts PD can also be seen b/c....

Back 24

Alzeheimer's; loss of cerebral cortex and hippocampus

Front 25

Genetic (2) and Environment (3) causes of PD

Back 25

G1)Parkin gene
G2)alpha-synnuclein

E1)rural living, well water
E2)heavy metal/hydrocarbon exposure
E3)cigs and caffeine shown to be mildly protective

Front 26

Excitotoxicity cause of PD (2)

Back 26

1)neural injury caused by excess glutamate
2)NMDA receptor mediated damage

Front 27

Mitochondria/Energy metabolism cause of PD (2)

Back 27

1)compromised energy sustaining capacity in neurons
2)caused by aging, exposure to toxins/drugs

Front 28

Neuropathology of PD (3 and clinical significance(2))

Back 28

1)loss of dopamine containing neurons in substantia nigra compact
2)disruption b/w substantia nigra and striatum
3)decr in dopamine fxn w/ reflexive/relative INCR of striatal cholinergic interneuron activity

1)positive correlation b/w degree of nigrostriatal dopamine loss and severity of sx
2)threshold of PD appears to be loss of 80% or more of these neurons

Front 29

Secondary PD
a)causes (5)
b)tx (2)

Back 29

1)DRUG INDUCED
a)antipsychotics (haloperidol, chlorpromazine)
b)antiemetics (prochlorperazine, droperidol)
c)gastric motility agents (metoclopramide)

1)amantadine
2)anticholinergics

Front 30

Tardive dyskinesia (2desc and 4 causes)

Back 30

1)persistent (over 4wks) DRUG INDUCED movement disorder
2)due to greater than 3months exposure to dopmaine-receptor blocker

a)antiemetics (metoclopramide, prochlorperazine)
b)antiepileptics (phenytoin)
c)psychotropics (haloperidol)

Front 31

Tardive dyskinesia
a)incidence
b)onset
c)tx

Back 31

a)incr w/ tx duration w/ offending drug (5% after 1yr, 7% after 2yr, 15% after 4yr)

b)insidious, initially mild and unnoticeable

c)DC OF OFFENDING AGENT

Front 32

Type of involuntary motions in tardive dyskinesia (3 and each has desc)

Back 32

1)choreiform (rapid/jerky and nonrepititive)
2)athetoid (slow, sinuous, writhing)
3)stereotypic (rhythmic and repetitive)

Front 33

stimulation of D1=
stimulation of D2=
(by frontal cortex)

Back 33

D1)incr cAMP
D2)decr cAMP

Front 34

Loss of substantia nigra compacta in PD= (3)

Back 34

1)loss of signal from GPe to STN
2)this causes MASSIVE incr in signal to GPi/SNr
3)resulting in large inhibition of VA/VL of thalamus (= DECR MOTOR)

Front 35

Progressive Supranuclear Palsy? (3)

Back 35

1)akinetic syndrome
2)abnormal eye movements where pts are unable to look up and down voluntarily
3)can't turn head either

Front 36

Nonpharmacological tx of PD (4)

Back 36

1)education
2)exercise
3)nutrition
4)group support

Front 37

PD pharmacologic tx is individualized based on...(3)

Back 37

1)age of onset
2)coexisting conditions
3)troublesome symptoms

Front 38

Pharmacology of PD is all based upon....(2)

Back 38

1)REQUIRES LIVE DOPAMINE NEURONS
2)balance of dopamine and ACh

Front 39

Balance of dopamine/ACh (4)

Back 39

1)incr dopamine = motor fluxuations (hemiball/chorea), dyskineaseas, incr oxidative stress
2)decr dopamine = rigidity and bradykineasea

3)incr ACh = tremor
4)decr ACh = anti-SLUD, confusion/hallucinate

Front 40

Dopamine synthesis steps (4)

Back 40

1)phenylalanine
2)tyrosine
3)dopa
4)dopamine via dopa decarboxylase

Front 41

Dopamine catabolism steps (2pathways w/ 7 total steps)

Back 41

1)dopamine via MAO to...
2)DHPA
3)DOPAC
4)HVA via COMT

1)dopamine to 3-O-MD via COMT
2)MHPA via MAO
3)HVA

Front 42

L-dopa/carbidopa
a)brand name
b)MOA
c)ADR's (4)

Back 42

a)Sinemet
b)DA precursor/decarboxylation inhibitor

c1)postural hypotension
c2)GI
c3)hallucinations/confusion
c4)chorea/dyskinesias

Front 43

Pramipexole
a)brand name
b)MOA
c)ADR's (6)

Back 43

a)Mirapex
b)DA agonist (D2/3)

c1)postural hypotension
c2)n/v
c3)hallucinations/psychosis
c4)dyskinesias
c5)sedation
c6)PERIPHERAL EDEMA

Front 44

Ropinorol
a)brand name
b)MOA
c)ADR's (5)

Back 44

a)Requip
b)DA Agonist (D2/3)

c1)postural hypotension
c2)n/v
c3)hallucinations/psychosis
c4)dyskinesias
c5)sedation

Front 45

Rotigotine
a)brand name
b)MOA
c)ADR's (4)

Back 45

a)Neupro
b)DA agonist

c1)n/v
c2)local rxn
c3)sedation/dizzy
c4)insomnia

Front 46

Amantidine
a)brand name
b)MOA
c)ADR's (4)

Back 46

a)Symmetrel
b)DA releaser

c1)depression
c2)postural hypotension
c3)psychosis
c4)urinary retention

Front 47

Benzotropine
a)brand name
b)MOA
c)ADR's (2)

Back 47

a)Cogentin
b)DA reuptake & anticholinergic

c1)dry mouth
c2)confusion

Front 48

Entacapone
a)brand name
b)MOA
c)ADR's (2)

Back 48

a)Comtan
b)COMT inhibitor (PERIPHERAL ONLY)

c1)brown/orange urine
c2)dopaminergic effects may require Sinement dose reductions

Front 49

Tolcapone
a)brand name
b)MOA
c)ADR's (2)

Back 49

a)Tasmar
b)COMT inhibitor (peripheral and central)

c1)HEPATOTOXICITY
c2)delayed onset diarrhea

Front 50

Selegiline
a)brand name
b)MOA
c)ADR's (3)

Back 50

a)Eldepryl
b)MOA-B inhibitor & antioxidant

c1)nausea
c2)dizzy
c3)confusion/hallucination

Front 51

Rasagiline
a)brand name
b)MOA
c)ADR's (4)

Back 51

a)Azilect
b)SELECTIVE MAO-B inhibitor & neuroprotective

c1)dyskineasia
c2)orthostasis
c3)HA
c4)GI

Front 52

Trihexylphenidyl
a)brand name
b)MOA
c)ADR's (3)

Back 52

a)Artane
b)anticholinergic

c1)dry mouth
c2)blurred vision
c3)confusion

Front 53

Drugs that incr dopamine synthesis (2)

Back 53

1)L-dopa
2)sinemet (carbidopa inhibits peripheral decarboxylation of L-dopa making more precursor available to brain

Front 54

Drugs that enhance dopamine synthesis

Back 54

amantadine

Front 55

Drugs blocking dopamine reuptake (2)

Back 55

1)TCA
2)benztropine

Front 56

Drugs that inhibit dopamine catabolism/degredation (4)

Back 56

a)COMT inhibitors (tolcapone, entacapone)
b)MAO-B inhibitors (selegiline, rasagiline)

Front 57

Drugs that act as DA agonists (3)

Back 57

1)pramipexole
2)ropinirol
3)rotigotine

Front 58

Role of anticholinergics in tx of PD and 2 of em

Back 58

1)trihexyphenidyl
2)benztropine

maintain balance b/w dopamine and ACh activity

Front 59

Drugs that halt progression of neurotoxicity (3)

Back 59

a)antioxidants (vitE, selegiline)
b)memantine as neuroprotective (but currently only indicated for Alzeheimer's)

Front 60

Reversing neuropathology and nonpharmachologic tx (3)

Back 60

1)brain implants
2)ablative surgery
3)deep brain stimulation

Front 61

Drugs commonly used for tx of Essential tremor and these are due to....

Back 61

1)PROPANOLOL
2)metoprolol

adrenergic overload

Front 62

BB and Essential Tremor
a)impact of lipophilicity
b)impact of selectivity
c)impact of ISA

Back 62

a)does NOT influence efficacy
b)must have B1 and B2 blockade
c)agents w/ ISA are no good (pindolol)

Front 63

Anticonvulsants used to tx Essential Tremor and these are...(4)

Back 63

1)gabapentin
2)primidone
3)topamax
4)Zonisamide

2ND LINE

Front 64

Role of BZD's and which ones w/ Essential Tremor and one other thing used

Back 64

1)Clonazepam
2)valium
3)lorazepam (SA so best w/ old ppl)
Adjunctive agents for symptoms not controlled w/ other agents

Botox- dosage varies by muscle injected

Front 65

Dx criteria for PD

Back 65

Bradykinesia w/ ATLEAST 2 OF THE OTHER 3 IN TRAP
1)ridigity
2)resting tremor
3)postural instability

Front 66

Secondary features of PD
a)behavioral/psychiatric (3)
b)sensory disturbances (3)
c)autonomic dysfxn (4)

Back 66

a1)depression
a2)dementia/hallucinations
a3)sleep disturbances

b1)pain/tingling/burning
b2)loss of smell
b3)numbness

c1)orthostatic hypotension
c2)genitourinary (sex dysfxn, dysurination)
c3)dermatitis
c4)GI (hard to swallow, delayed gastric empty, constipation, salivation)

Front 67

MAO-B inhibitors
a)drugs (2)
b)MOA
c)efficacy (2)

Back 67

a)Selegiline, Rasagiline
b)irreversible inhibition of MAO-B (which is involved in oxidative deamination of dopamine in the brain)

c1)delays need to add levodopa
c2)supplement to levopdopa allowing 20-50% decr in L-dopa dose

Front 68

MAO-B inhibitors
a)dosage (SELEGILINE ONLY) (3)
b)Interactions

Back 68

a1)LIMIT TO 10MG/DAY (5mg bid) AND GIVE W/ FOOD!!!
a2)avoid late afternoon/evening doses b/c metabolites are amphetamines
a3)when used w/ L-dopa reduce doses of L-dopa after 2-3 days by 20-50%

b1)foods w/ tyramine (cheese/beer/wine)

Front 69

Rasagiline
a)diff from Selegiline (3)

Back 69

a1)not metabolized to amphetamines
a2)10-15x more potent than selegiline
a3)taken qd NOT bid

Front 70

Anticholinergic Agents
a)drugs (2)
b)MOA
c)efficacy

Back 70

a)benztropine, trihexyphenidyl
b)decr axn of ACh in CNS to balance ACh/dopamine in corpus striatum
c)SPECIFIC FOR TREMOR AND RIGIDITY

Front 71

Anticholinergics
a)ADR's (major and minor)
b)role in therapy
c)special thing****

Back 71

major)confusion, hallucination, memory impairment
minor)anti-SLUD (hold everything in)

b)LESS than 70yo w/ TREMOR
c)avoid dc due to rebound deterioration

Front 72

Amantadine
a)MOA
b)efficacy (2)
c)dosage (2)

Back 72

a)dopamine releaser (acts at NMDA)

b1)MORE effective than anticholinergics for akinesia and rigidity, but less effective for tremor
b2)Refractoriness occurs: beneficial effects last only 2months-1yr

c1)100mg bid-tid
c2)limit dose to 200mg/d in old due to incr risk of cognitive impairment

Front 73

Amantadine
a)ADR's (5)
b)role (3)

Back 73

a1)n/v
a2)hallucinations/confusion
a3)PERIPHERAL EDEMA
a4)WORSENING CHF
a5)livido reticularis (benign rose colored rash)

b1)Early monotherapy (if effect wanes, add another agent and dc amantadine slowly)
b2)For tremors in pts over 70yo
b3)L-dopa induced dyskinesia

Front 74

L-dopa
a)MOA
b)ADR's (6)

Back 74

a)dopamine precursor to restore balance b/w dopamine and ACh in corpus striatum

b1)emetic (stim vomiting center in medulla)
b2)orthostatic hypotension
b3)cardiac arrhythmias
b4)confusion/hallucination
b5)insomnia
b6)DYSKINETIC MVMNTS*****

Front 75

L-dopa/Sinemet
a)adv of Sinement over L-dopa (2)
b)dosing of IR Sinemet (3)
c)dosing of CR Sinemet (3)

Back 75

a1)need 50-75% less L-dopa (minimizes L-dopa ADR's)
a2)induction phase is decr to weeks instead of months

b1)start sinemet @ 25/100 TID
b2)incr by 100mg l-dopa every other day until 600-750mg l-dopa
b3)switch to sinemet 25/250 TID as approaching lower end of usual therapeutic dose (750-1000mg/day)

c1)start w/ 25/100 or 50/200 BID in am and early afternoon
c2)adding a dopamine agonist if doses greater than 500-800mg l-dopa are necessary
c3)slow titration decreases ADR's

Front 76

Guidelines for switch from IR to CD (4)

Back 76

1)start w/ 50% reduction in frequency (like qid to bid)
2)begin w/ 100% of total daily dose of LD/CD IR
3)if wearing off persists but is LESS than 60min, incr DOSE
4)if wearing off persists but is MORE than 60min, incr FREQ

Front 77

Special considerations relating to the slower onset of Sinemet CR (3)

Back 77

1)halve tablets to incr erodible surface
2)supplement first AM dose of CR w/ IR
3)diphasic dyskinesia may be more common w/ CR (so avoid CR in later stages of disease)

Front 78

When to start L-dopa (1) and why do they delay starting it (3)

Back 78

1)when disease interferes w/ pt's occupation or ADL

1)efficacy decr over time
2)associated w/ motor complications and dyskinesias
3)freezing, constipation, dermatitits, postural instability, psychosis RESISTANT to L-dopa

Front 79

What if pt fails L-dopa? (2)

Back 79

1)only 15% of PD pts fail to improve w/ L-dopa
2)so if pt fails it is probably a misdiagnosis of PD

Front 80

Direct DA agonists
a)drugs (4)
b)advantages over Sinemet (4)

Back 80

a1)ropinirole
a2)pramipexole
a3)Apomorphine SQ injexn
a4)Rotigotine (transdermal)

b1)acts directly on striatal dopamine receptors w/o requiring metabolic conversion
b2)no free radicals or induced oxidative stress (neuroprotective)
b3)no competition w/ circulating AAs for absorption and transport into brain
b4)LONGER DURATION OF RESPONSE*****

Front 81

Direct DA agonists
a)disadvantages (4)
b)ADR's (6)

Back 81

a1)neuropsychiatric effects (hallucinations/psychosis)
a2)sedative/sleep attacks
a3)does NOT tx all features of PD (freezing, posture, dementia, autonomic dysfxn)
a4)does NOT stop disease progression

b1)n/v
b2)HIGHER INCIDENCE OF NEURO PROBLEMS VS. Sinemet
b3)erythromelagia
b4)pulmonary/retroperitoneal fibrosis
b5)hypotension/dizzy
b6)START AT LOW DOSES AND TITRATE UP TO DECR N/V

Front 82

Apomorphine SQ Injexn
a)indication
b)requirment w/ it (3)
c)ADR's (4)

Back 82

a)ACUTE tx of "off"/freezing episodes

b1)big n/v rxn so requires apomorphine challenge by specialist
b2)trimethobenzamide 300mg TID for 3d
b3)(+) if 20% improvement in UPDRS

c1)orthostatic hypotension
c2)dyskinesias
c3)sleep attacks
c4)needle-site rxns

Front 83

Adv of Rotigotine (2)

Back 83

1)transdermal
2)continuous delivery and relative stable blood []s

Front 84

Role of DA agonist
a)as monotherapy (3)
b)as adjunct (2)

Back 84

a1)comparable benefit to Sinemet in HY stages 1-2
a2)low incidence of dystonia, motor fluctuations
a3)NOT for posture, autonomic dysfxn, dementia

b1)sig reduction in L-dopa dosage
b2)lower incidence of L-dopa complications (dyskinesia, oxidative stress)

Front 85

COMT inhibitors
a)MOA (2)
b)benefit (3)
c)ADR's (5)

Back 85

a1)COMT is major pathway for degredation in presence of carbidopa
a2)Entacapone inhibits O-methylation mainly in periphery; tolcapone also inhibits centrally

b1)reduces off time
b2)incr on-time by 1-3h
b3)reduces maintenance L-dopa dose in pt w/ wearing off

c1)diarrhea (explosive)
c2)nausea
c3)HA
c4)discoloration of urine to dark yellow/orange
c5)severe hepatotoxicity w/ Tolcapone

Front 86

Entacapone dosing (3)

Back 86

1)200mg tablet w/ each Sinemet dose
2)max of 8 doses per day
3)adjust L-dopa down 20-30%

Front 87

Mechanism/Management of DELAYED "ON" RESPONSE AND DOSE FAILURES (w/ L-dopa)

Back 87

1)delay in absorption/crossing of BBB of L-dopa b/c it is a large neutral AA competing w/ other LNAA for GI/CNS absorption

1)take med on empty stomach to reduce protein load @ time of med

Front 88

Mechanism(2)/Management(3) of WEARING OFF (w/ L-dopa)

Back 88

1)pt develops loss of response to dose of a med b4 taking next dose
2)degeneration of presynaptic dopaminergic neurons resulting in lack of storage for dopamine

1)incr freq and/or dose of L-dopa
2)combine therapy w/ DA agonist
3)add COMT inhibitor (= 20-30% decr in L-dopa dose)

Front 89

On-Off Phenomena
a)what is it
b)prevalence
c)management (2)

Back 89

a)rapid fluctuation from symptom free to extreme symptoms
b)in 40% of pts after 5yrs of therapy; due to progression of disease and fluctuating of CNS drug levels

c1)direct DA agonist
c2)extra L-dopa IR

Front 90

Freezing
a)what is it
b)management

Back 90

a)unable to initiate or complete a movement (unknown cause)
b)attempt to find relationship to meds so that can recommend incr/decr

Front 91

Peak dose dyskinesia (w/ L-dopa)
a)aka.../what is it
b)Control (5)

Back 91

a)improvement-dyskinesia-improvement IDI, over 1 dose (dyskinesia due to peak dopamine level)

b1)switch from XR to IR
b2)reduce/eliminate selegiline or COMT inhibitor
b3)reduce dose of Sinement or DA agonist
b4)add amantadine
b5)pallidotomy or deep brain stimulatino surgery

Front 92

Diphasic dyskinesia
a)aka.../what is it
b)control (4)

Back 92

a)dyskinesia-improvement-dyskinesia DID, due to more advance disease and in pts who HAD IDI

b1)prolong "on" state: higher dose/more frequent Sinemet
b2)can overlap 4-5 doses of Sinemet IR to prevent dyskinetic phase @ end of dosing cycle
b3)add DA agonist
b4)pallidotomy or globus pallidus stimulation

Front 93

"Off" dystonia
a)what is it
b)control

Back 93

a)foot posturing on waking (MOST COMMON SIGN)
b)add dopaminergic agents

Front 94

Cognitive Impairment management (4)

Back 94

1)tx underlying problems (dehydration, electrolyte imbalance, infexn, metabolic abnormality)
2)eliminate unecessary meds (especially sedatives, anxiolytics)
3)gradually decr L-dopa dose
4)Decr/dc Antiparkinson agents in this order: anticholinergic, amantadine, selegiline, DA agonist*******

Front 95

Hallucinations/delirium management (3)

Back 95

1)dc drugs in this order: anticholinergics, amantadine, selegiline, DA agonists
2)THEN consider reduction of L-dopa
3)Drug tx of psychosis is QUETIAPINE, CLOZAPINE (BUT CLOZ HAS ANTICHOLINERGIC EFFECTS)****

Front 96

If over 70yo what to consider in drug tx (5)

Back 96

1)anticholinergics make for greater propensity for ADR's AND ARE AVOIDED
2)amantadine- incr chance of cognitive impairment
3)Sinemet- fewer motor fluxuation in over 70yo
4)Sinemet reqd earlier in this age group
5)BUT Sinemet has greater incidence of hallucination, cofusion, psychosis

Front 97

What drugs to use if...
a)Tremor Predominant (2)
b)Tremor NOT predominant (mainly have bradykinesia) (2)

Back 97

a1)in over 70yo use amantadine
a2)in under 70yo use anticholinergics

b1)in under 65yo OR cognitively normal use DA agonist
b2)in over 65yo OR cognitively impaired use Sinemet

Front 98

Drugs that require dose reduction of L-dopa (3)

Back 98

1)Selegiline (10-50% reduction)
2)Entacapone (20-30% reduction)
3)DA agonists