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Semester 3 > Case 7 - Basal Ganglia Lecture > Flashcards

Case 7 - Basal Ganglia Lecture Flashcards

1
Q

what is meant by hypokinetic

A

too little movement

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2
Q

what is meant by hyperkinetic

A

too much movement
often abnormal involuntary movements

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3
Q

what can both of these be caused by

A

basal ganglia dysfunction

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4
Q

what is the input nucleus

A

the striatum made up of the caudate and putamen

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5
Q

what is the D1 pathway

A

this pathway projects directly to the globus pallius media - contains GABA which is the main inhibitory neurotransmitter and that projects directly to the GPm D1 dopamine receptors

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6
Q

what are the output regions of the basal ganglia

A

the globus pallidus media along with the substantia nigra pars reticulate

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7
Q

where does the indirect pathway project

A

to the GPl and then to the output region, the medial globus pallidus via another GABA transmission pathway to the sub thalamic nucleus which then projects back using glutamate to the medial globes pallidus

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8
Q

features of the striatum

A

comprises the caudate and putamen
input region of the basal ganglia

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9
Q

what are medial spiny neurones

A

dendritic spines

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10
Q

what do medium spiny neurones do

A

vastly increase surface area and are 96% of striata neurones

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11
Q

medium spiny neurones are ……..ergic

A

GABAergic ± neuropeptides

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12
Q

what are internueones

A

don’t project outside of the striatum

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13
Q

features of interneurones

A

GABAergic
Cholinergic (large aspiny neurones)

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14
Q

where does striatal input come form

A

corticostriatal pathway and nigrostriatal pathway

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15
Q

features of the corticostriatal pathway

A

glutamaterguc
inout from the whole cerebral cortex

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16
Q

features of the nigrostrital pathway

A

dopaminergic
from substantia nigra pars compatacta
projects to the striatum
interaction of dopamine and glutamate which controls the level of activity in the striatum
dopamine regulates and fine tunes the output of the basal ganglia

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17
Q

what do dopamine and glutamate interact to do

A

modulate synaptic strength

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18
Q

what are the neuropeptides in the direct pathway

A

dynorphin and substance P

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19
Q

what are the neuropeptides in the indirect pathway

A

enkephalin

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20
Q

what is the dynorphin precursor

A

PPE-B

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21
Q

what is the enkephalin precursor

A

PPE-A

22
Q

where does the D1 receptor mainly act

A

on g-alpha-s subunits - excitatory and activates adenyl cyclase which leads to cAMP formation

23
Q

where does the D2 receptor mainly act

A

on inhibitory G protein subunits which inhibits adenylyl cyclase and leads to less activation of cAMP

24
Q

diagram of basal ganglia organisation

A
25
Q

what does the D2 pathway involve

A

The suppression of unwanted movements

26
Q

what does the D1 pathway involve

A

the facilitation of wanted movements

27
Q

what is the action of dopamine in resting conditions

A
28
Q

what are the actions of dopamine in active movement

A
29
Q

What is the hyper direct pathway

A

additional role in inhibitory control
parallel loops subserving different functions
dorsolateral to ventromedial gradient in terms of function

30
Q

where is the hyper direct pathway from

A

the cortex to the STN

31
Q

what happens if there is a loss of dopamine in the direct pathway

A

reduced excitation

32
Q

what happens if there is a loss of dopamine in the indirect pathway

A

reduced inhibition

33
Q

diagram demonstrating the basal ganglia in Parkinson

A
34
Q

is there an increase or decrease of enkephalin in parkinsons

A

increase in enkephalin

35
Q

is there an increase or decrease of dynorphin in parkinsons

A

decreased production of dynrophin

36
Q

what is the net result

A

is there is less inhibition of the output regions of the basal ganglia via the direct pathway and there is too much excitation via the indirect pathway

37
Q

what does this therefore lead to

A

the output from the basal ganglia is increased - increased inhibition of the brainstem and spinal cord and increased inhibition of the motor part of the thalamus

this leads to reduced excitatory output from the thalamus and reduced excitation of the cortex which leads to less movement

38
Q

what is the pathophysiology of Parkinsonism

A

relative overactivity of the indirect pathway
suppression of movement which leads to bradykinesia and rigidity

impaired motor learning - loss of LTP

subthalamic overactivity - lesions of STN alleviates experimental Parkinsonism and effects of lesion surgery?

39
Q

what are the cognitive disturbances linked too in PD

A

changes in dopamine handling in basal ganglia loops
later dementia related to cortical Lewy body pathology

40
Q

impulsive behaviour in PD:n

A

pathological gambling, hypersexuality and compulsive eating

linked to more severe dopaminergic deficit in ventral (limbic) striata areas

41
Q

depression and anxiety in PD

A

related to monoamine cell loss in the brainstem
dopamine agonists may improve depression in PD

42
Q

what are hyperkinetic choreiform disorders

A

huntinngtons disease
Levodopa induced dyskinesia
dystonia
tic disorders

43
Q

what is Chorea

A

rapid, multifocal irregular movements
flitting between various muscle groups and body parts
motor impersistence

44
Q

what is the pathophysiology of chorea

A

imbalance between direct and indirect pathways
relative overactivity of direct pathway - excessive movement
under activity of indirect pathway - no suppression of unwanted movement

45
Q

what is Huntington’s disease

A

expanded CAG repeats in Huntington Gene (chromosome 4p16.3)
complete penetrance with over 40 repeats
anticipation, greater expansion with male transmission

46
Q

what is the pathophysiology of Huntingtons

A

selective loss of D2 receptor bearing indirect pathway neurones –> involuntary movements

later loss of direct pathway neurones –> hypokenetic movement disorder

47
Q

what is the cortical pathology in HD

A

loss of neurones in layers V and VI

48
Q

what is the striatal pathology

A

degeneration in caudate and indirect pathway D2 receptor bearing MSNs

49
Q

diagram for the basal ganglia in HD

A
50
Q

what is Tourette syndrome

A

tic disorder, usually onset age of less than 20
rapid, repetitive stereotyped movements or vocalisations
frequent comorbin neuropsychiatric illness

51
Q

what is the pathophysiology of touettes

A

loss of cholinergic and GABAergic striata interneurones
increased striata dopamine D2 receptor binding in patients with TS compared to controls

52
Q

what are the therapies used in tic disorders

A

antidopaminergic therapy - tetrabenzine
antipsychotic agents - haloperidol, sulphide (block D2 receptor)
alpha receptor agonists - clonidine

Semester 3 (94 decks)

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