Motor Control Disorders Flashcards

1
Q

what are the basal ganglia and cerebellum do?

A

regulate planning and execution of movement

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2
Q

what is the basal ganglia?

A

a series of interconnected structures in the brain

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3
Q

describe basal ganglia circuitry…

A

parallel direct and indirect pathways

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4
Q

what is the direct pathway of the basal ganglia?

A

facillitates movement by focusing and amplifying circuits involved in movement.
the direct pathway is activated by dopamine binding to D1 receptors

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5
Q

what is the indirect pathway of the basal ganglia?

A

the indirect pathway aims to inhibit movement via inhibitory cascade in the putamen to gpe and gpi
this pathway is inhibited by dopamine binding to D2 receptors on neurons

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6
Q

what is parkinsons disease?

A

a progressive movement disorder that occurs mainly in the elderly

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7
Q

what are the symptoms of parkinsons?

A
tremor at rest
akinesia
bradykinesia 
rigid
mask expression
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8
Q

what are the causes of parkinsons disease?

A

most are idiopathic (meaning the cause is unknown)

there are some rare hereditary forms and ennvironmental factors can also contribute

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9
Q

what is the ‘case of the frozen addicts’?

A

heroin addicts in the 80s developed severe PD following treatment with a heroin substitute called MPTP
within the body the MPTP was converted into the toxic substance MPP+ (by dopamine) and this was taken up by dopamine transport systems and killed DA neurons

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10
Q

what are the key pathophysiological traits of parkinsons disease?

A

losing neurons from substantia nigra and losing dopaminergic input to the basal ganglia

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11
Q

how can we harness the DA pathway to treat PD?

A

must consider: DA synthesis, metabolism, receptors, and DA uptake and transport

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12
Q

why cant we treat PD patients with dopamine?

A

it is too large and cannot cross the BBB

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13
Q

what is the first line treatment for PD?

A

L-DOPA, and the decarboxylation occurs rapidly and lead to synaptic flooding of exogenous DA

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14
Q

what are the side effects of L-DOPA?

A

dyskinesia (involuntary writhing movements)
on-off effect (rapid fluctuatons between symptomatic and non-symptomatic states)
acute side effects (occuring short term following beggining of drug intake)

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15
Q

what are the key components in dopamine metabolism?

A

DA is broken down via two pathway: the Monoamine oxidase pathway and the catechol-o-methyl transferase inhibition pathway

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16
Q

what are two further treatments for PD?

A

deep brain stimulation

neural transplantation

17
Q

what is Huntington’s disease?

A

a progressive neurodegenerative disease that present a midlife onset and life expectancy of 15-20 years, following diagnosis

18
Q

how is huntingtons caused?

A

via genetic and inherited in an autosomal dominant fashion

there is a mutation in the huntington gene affecting number of CAG repeats (36+ = disease)

19
Q

what are the symptoms of huntingtons disease?

A

motor (including chorea, slurred speech, dystonia, dysphagia)
cognitive impairment (including impaired executive function)
psychiatric/behavioural (including anxiety and depression)

20
Q

what is the pathology of huntingtons?

A

cell loss in caudate and putamen
GABAergic spiny neurons most at risk (these are inhibitory neurons)
an overactivation of the direct pathway

21
Q

what is hemiballismus?

A

a rare movement disorder characterised by involuntary violent fliniging motions

22
Q

what causes hemiballismus?

A

lesions to the subtahalmic nucleus of the basal ganglia

23
Q

what is the pathophysiology of hemiballismus?

A

loss of excitatory neurons in the GPI

24
Q

what are the treatment options for huntingtons disease and hemiballismus?

A

use of anti-dopaminergic drugs, including dopamine receptor antagonists and VMAT inhibitors