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Clin Med-Neuro > Disorders of Extrapyramidal System > Flashcards

Disorders of Extrapyramidal System Flashcards

1
Q

function of extrapyramidal system

A

involuntary movement (dampens reflex arc)

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2
Q

hypo-kinetic disorder

A

dopamine

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3
Q

Hyperkinetic disorder

A

dopamine> Ach

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4
Q

epidemiology of PD

A

progressive neurodegenerative disorder

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5
Q

cause of primary PD

A

primary or idopathic

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6
Q

cause of secondary PD

A

damage to the basal ganglia

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7
Q

what is parkinsons PD

A

loss of dopaminergic cells in substantia nigra causes an imbalance between dopamine and Ach

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8
Q

cardinal symptoms of PD

A

bradkinesia
rigidity
postural instability (head tends to fall forward)
tremor (resting)

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9
Q

pathological hallmark of PD

A

lewey bodies

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10
Q

onset of PD

A

insidious and asymmetric

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11
Q

freezing

A

sudden interruption of movement

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12
Q

festination

A

tendency of gait to alternate between speeding up and slowing down

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13
Q

dysautonomia (PD)

A

associated with lewey bodes

  • sweating
  • ortho HTN
  • trouble with temperature ocontrol
  • drooling
  • insomnia
  • digestive problems (compounded by inactivity and use of anticholinergics)
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14
Q

when is a non-ergonline dopamine agonist used?

A

younger than 50

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15
Q

when is carbidopa/levodopa used?

A

older than 70

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16
Q

COMT inhibitors

A
  • Entacapone

- inhibits enzyme so that dopamine isn’t broken down = increase dopamine

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17
Q

Glutamate (NMDA) antagonists

A
  • Amantadine

- decreases ach levels by blocking glutamate receptors (good for treating tremor)

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18
Q

Levodopa

A
  • loses effectiveness after 5 years
  • pro drug
    combine with carbidopa ( a peripheral DOPA decarboxylase inhibitor) that does not cross BBB (reduces side effects)
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19
Q

treatment of on-off phenomenon

A

amantadine
addition of COMT or MAO-B inhibitor
addition of DA (decrease risk of dyskinesias)

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20
Q

risks of using ergot derivatives

A

valvular heart disease

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21
Q

MAO-B inhibitors

A
  • selegiline is commonly used
    inhibit oxidative metabolism of dopamine and doesn’t require dietary restrictions
    delay need for other parkinsons drugs
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22
Q

side effects of COMT inhibitors

A

liver dysfunction

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23
Q

side effects of MAO inhibitors

A

interactions with other drugs (anti-dep, tyramine food and opioids)

24
Q

side effects of amantadine

A

hallucinations

25
Q

side effects of anticholinergics

A

hallucinations

26
Q

side effects of DA

A

hallucinations, sleep attacks, orthostatic dizziness, compulsive behaviors

27
Q

surgical treatment of PD

A

DBS
- response to dopaminergic meds is the best predictor of success

  • patients less than 80
    globus pallidus or subthalmic nucleus

PD related dementia is a contraindication

28
Q

benefits of DBS

A

reduces on-off

can reduce dose of levodopa

29
Q

progressive supra-nuclear palsy (PSP)

A
  • No tremor
  • poor response to L-dopa
    (+)lunging, fast walking, bumping, frontal lobe dementia
30
Q

corticobasal degeneration

A
  • no tremor
  • poor response to L-dopa
    (+) rest of PD signs
31
Q

in general how does PD and parkinsons plus syndromes differ?

A

plus syndroms have a more rapid progression of symptoms

32
Q

other name for Wilson’s disease

A

hepato-lenticular degeneration

33
Q

Wilson’s disease

A

autosomal recessive disease
onset during childhood
treatable
CU (overload in liver and CNS- basal ganglia)

34
Q

findings in Wilson’s disease

A 
kayser-fleischer rings
wing beating tremor
risus sardonicus
easy bruising
anemia
HSM
35
Q

treatment of Wilson’s disease

A
  • removal of excess copper with chelators such as D-penicillamine
  • prevent Cu accumulation using oral zinc
  • liver transplant
36
Q

dx of Wilson’s disease

A

serum ceruloplasmic level
24 hours copper
LFTs
biopsy

37
Q

huntingtons disease

A
  • choreiform movement
  • psychiatric problems
  • autosomal dominant inheritance
  • dementia is inevitable w/ loss of executive function
38
Q

when is memory loss seen in Huntington’s dementia?

A

late

39
Q

pathology of Huntington’s disease

A
  • accumulation of a mutant huntingtin protein–> reduction of GABA
40
Q

treatment options in Huntington’s disease

A

tetrabenazine is a dopamine depleter useful for treating the chorea

causes depression, Parkinsonism, QT prolongation at higher doses

41
Q

sydenhams chorea “st vitus dance”

A

autimmune destruction of basal ganglia
results from childhood infection with group a beta hemolytic strep
females younger than 18 most common

42
Q

athetosis

A

writhing movements

mainly due to CP

43
Q

dyskinesia

A

tardive dyskinesis
due to drugs (exposure greater than 6 weeks to DA)
tics on steroids

44
Q

hemiballismus

A

throwing of the limbs on one side of the body

usually die to cva involving subthalmic nucleus

45
Q

dystonia

A
  • repeated patterned twisting and sustained movements that might be rapid or slow
  • start before 20
  • children (distal)
  • adults (cranial-cervical)
  • primary: focal
  • secondary: generalized (wilsons, toxins)
46
Q

monoclonus

A

simple jerky movements that are not coordinated or supressable

47
Q

tics

A

go away at night

  • dopamine excess
    tx: DA
48
Q

resting tremor

A

occurs at rest and improves with movement

- body is supported by gravity

49
Q

action tremor

A

worsens as patient attempts to initate and continue activity

50
Q

intention tremor

A

increase in amplitude as finger reaches the target

51
Q

task-specific tremor

A

emerges during a specific activity

52
Q

postural tremor

A

worsens when limbs held away from body

53
Q

essential tremor

A

most common pathologic tremor

  • 50% cases autosomal dominant
  • bilateral, postural, action
  • most ob in hand and wrists (head, LE, voice can be affected)
54
Q

cerebellar tremor

A

action (intention) tremor

  • seen w/ MS, trauma, stroke
  • caused by alcoholism
55
Q

physiologic tremor

A

postural, action tremor not usually visible

56
Q

parkinsonian tremor

A

pill rolling-> forarm (pron/supin)–> elbow flexion/extension
- usually a combo of action and rest

Clin Med-Neuro (8 decks)

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