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Neuroanatomy > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

What is Parkinson’s Disease?

A

a progressive degenerative disease caused by death of dopaminergic neurons primarily in the substantia nigra pars compacta

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2
Q

What does PD actually begin with?

A

loss of noradrenergic input into the dorsal motor nucleus of X
loss of noradrenergic neurons of the locus coeruleus

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3
Q

What is seen in the SNc with normal aging?

A

a loss of dopaminergic neurons (50% decrease ages 20-60)

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4
Q

Besides the SNc, what is another area that experiences a decline in DA?

A

mesolimbic system.

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5
Q

What is the mesolimbic system?

A

it includes projections from the ventral tegmental area to the amygdyla,
nucleus accumbens,
prefrontal cortex,
and hippocampus via medial forebrain bundle (MFB)

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6
Q

With continued development of Parkinson’s, there is a continued decline and loss of connections within the PFC, limbic cortex, and hippocampus. what symptoms does this cause?

A

loss of cognitive skills
memory loss
higher associative cognitive functioning

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7
Q

What are cardinal signs of Parkinsons?

A
  • resting tremor
  • bradykinesia
  • rigidity
  • postural instability
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8
Q

What is resting tremor characterized by?

A

4-6 Hz resting “pill rolling” tremor which begins in peripheral extremities but progresses proximally

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9
Q

What are the 3 components of bradykinesia?

A

Hypokinesia
Bradykinesia
Akinesia

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10
Q

Hypokinesia?

A

paucity of movement

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11
Q

Bradykinesia?

A

slow movement

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12
Q

Akinesia

A

problem initiating movement

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13
Q

What is rigidity?

A

increased muscle tone and resistance to movement

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14
Q

What are the two types of rigidity common in PD?

A

Lead pipe- continuous rigidity making joints stiff

Cog-wheel- interposition of rigidity and breaking of rigidity when limbs are passively moved

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15
Q

What is postural instability in PD?

A

slowing of postural reflexes.

posture and rigidity make pt more unstable and increased risk of falling

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16
Q

What are the gait abnormalities associated with PD?

A

slow shuffle
no arm swing
retropulsion (stepping backward)
festinating gait (rapid short steps)

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17
Q

2 other S/S with PD?

A

Dysarthria and dysphagia

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18
Q

What are 6 nonmotor impairments common in PD?

A
  • cognitive decline (up to 80%)
  • postural hypotension
  • hallucinations
  • autonomic changes
  • fatigue and sleepiness
  • pain
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19
Q

in most cases there is no known cause of the degeneration of DA neurons, but some cases might have what involved?

A

environmental or genetic causes

20
Q

What are a few pharmacological management approaches to PD?

A
  • replacement therapy
  • dopamine agonists
  • blocking enzymatic breakdown of DA
  • anticholinergic interventions
21
Q

What is used in replacement therapy for PD?

A

Levodopa (L-Dopa)
Levorotatory 3, 4 dihydroxyphenylanaline
(metabolic precursor to DA because it cannot cross BBB)

22
Q

Why is L-Dopa rapidly metabolized peripherally? how can we fix this?

A

because there are a large # of DA neurons in the gut area.

typically co administered with carbidopa

23
Q

what is carbidopa?

A

blocker of DOPA decarboxylase

24
Q

What is the combination of carbidopa and L-Dopa called?

A

SinemetTM

25
Q

What does the use of L-Dopa require?

A

intact DA neurons (therefore with the progression of the disease, L-Dopa becomes less effective because it might have intact dopaminergic neurons,

26
Q

What might pts on L-Dopa experience?

A

On-Off sudden shifts of symptoms late in therapy

27
Q

How do we get extension of the action of L-DOPA?

A

sustained release Sinemet-CR

28
Q

What symptom could be caused by an effect of dosing of L-DOPA and the rapid metabolism of it?

A

considerable dyskinesias

29
Q

Why might L-DOPA accelerate DA neuron cell death?

A

increased free radicals or metabolic stress.

this is why some neurologists might suggest shifting medications

30
Q

What are some advantages of DA receptor agonists rather than L-Dopa?

A
  • no requirement for DA neurons, so there longer effect over the course of the disease
  • slower rate of metabolism (longer half life effectiveness)
  • more selective action (D1 or D2)
  • less dyskinesias
  • not accelerate SNC cell death
31
Q

What are adverse reactions of DA agnoists and L- DOPA?

A

dyskinesias- choreoform movements
abnormal thinking- hold onto false beliefs
hallucinations
addictive behaviours
constipation - due to action on DA neurons of enteric nervous system

32
Q

What is used for PD that is inhibiting the DA metabolism?

A

Monoamine oxidase inhibitors (MAOI)

Catechol-O-methyl transferase inhibitors (COMT)

33
Q

What is one of the oldest therapies for PD?

A

anticholinergic agents (before L-DOPA

34
Q

Why would blocking muscarinic receptors reduce PD symptoms?

A

because there is a large # of cholinergic striatal interneurons and PPN afferents to the substantia nigra

35
Q

What is wrong with anticholinergic agents?

A

strong autonomic adverse reaction

36
Q

What is amantadine?

A

used for PD

antiviral that may also effect catecholamine pathways

37
Q

Why would anti depressants be used in pts with PD?

A

other than MAOI, probably have no direct effect per se but used for depression symptoms

38
Q

why are newer NMDA receptor antagonists being used?

A

slow cell degeneration (apoptosis)

39
Q

What is a surgical approach for PD?

A

pallidotomy- lesion of the GPi. use stereotaxic device to localize GP and stabilize pt.

40
Q

what does a pallidotomy do?

A

reduces tremor and rigidity but not other symtpoms

41
Q

What is a ventrolateral thalamotomy?

A

lesion of the VL nucleus

42
Q

What is deep brain stimulation?

A

involves the implantation of leads to different brain regions along with implanted pacemaker unit

43
Q

What does the deep brain stimulator target?

A

thalamus, subthalamus, GPi

44
Q

Which intervention does the PD pt show remarkable improvement?

A

deep brain stimulation

improve in tremor and other symptoms (but sometimes there are behavioral adverse reactions)

45
Q

What is fetal nigral ttransplation?

A

adverse reactions noted in young pts.

Neuroanatomy (14 decks)

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