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Medicine > Basal ganglia and parkinsons > Flashcards

Basal ganglia and parkinsons Flashcards

1
Q

what areas make up the basal ganglia

A

neostriatum
paleostriatum
subthalamic nucleus
substantia nigra

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2
Q

what is the basal ganglia

A

deep cerebral nuclei
primarily for motor control, also motor learning, executive functions, behaviours, emotions

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3
Q

what is the neostriatum

A

caudate nucleus
putamen

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4
Q

what is the paleostriatum

A

globus pallidus

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5
Q

what is special about the substantia nigra

A

filled with melanin
pars reticulata- GABAergic
pars compacta- dopaminergic

produce dopamine (dopaminergic neurons)

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6
Q

what is the function of the basal ganglia

A

smooth movement- basic patterns of movement
switching behaviour
reward systems
closely linked to thalamus, cortex and limbic system

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7
Q

what does the direct pathway vs indirect pathway of the basal ganglia motor look do
simple terms

A

direct- stimulate movement
indirect- inhibition of movement EXTRA STEP

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8
Q

how does the motor loop work

A

cortex
corpus striatum
basal ganglia-> thalamus
thalamus to cortex

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9
Q

what is the corpus striatum

A

caudate nucleus
putamen
globus pallidum

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10
Q

what is extra in the indirect loop

A

globus pallidus lateral is inhibited by neostriatum
therefore subthalamic nucleus is not inhibited and can stimulate the globus pallidus (medial) to inhibit the thalamus

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11
Q

what happens when you want to cause a movement to occur

A

cortex sends simulating input
stimulate inhibitory neurons
inhibit release of inhibitory NT from globus pallidus (medial)

removing inhibition of thalamus so thalamus is stimulated
therefore there is a POSITIVE STIMULATORY SIGNAL back to the cortex= MOVEMENT

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12
Q

where does dopamine come from

A

substantia nigra PARS COMPACTA
it tips the balance between indirect and direct pathway to cause movement.

two different receptors found in the neostriatum (caudate nucleus and putamen)
substantia nigra feeds into niastriatum

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13
Q

what is the pathway of the indirect path

A

cortex
neostriatum
globus pallidus (lateral)
subthalamus
globus pallidus (medial)
thalamus

extra step causes inhibitory signal coming out- inhibit thalamus and therefore inhibit movement.

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14
Q

what is the inhibitory neurotransmitter released by the neostriatum

A

GABA

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15
Q

what NT does the cortex release (excitatory), which is also released b the subthalamus in the indirect pathway

A

glutamate

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16
Q

what are the different dopamine receptors in the direct and indirect pathways

A

direct- D1 receptors– release of dopamine attaches and stimulation of direct pathway
indirect- D2 receptors

therefore tips the balance

17
Q

what are some clinical problems found in the basal ganglia

A

PARKINSONS
HUNTINGTONS
HEMIBALLISM
WILSON’S DISEASE

18
Q

describe clinical features of parkinsons disease

A

tremor at rest
rigidity (limbs>axial)
bradykinesia- slowness to INITIATE MOVEMENT
asymmetry
lossrighting reflex
30% cognitive decline
hypomimia (lack of facial expression)
glabellar tap
quiet speech
micrographia
pill rolling
trunk tilting to maintain balance
akinesia

19
Q

describe the pathophysiology of the basal ganglia in parkinsons disease

A

there is a degeneration of dopaminergic neurons of substantia nigra PARS COMPACTA
therefore loss of dopamine

no dopamine input
direct pathway not stimulated as much
no inhibition of the globus pallidus
therefore inhibitory signal to thalamus is greater
inhibits thalamus so signal to frontal cortex is reduced (movement occurs much slower)

also indirect pathway is no longer inhibited
strong inhibitory signal
etc.
stimulating globus pallidus medial which is inhibitory!- no inhibition coming from neostriatum
slow initiation of movement

20
Q

describe huntington’s disease
symptoms,
what is affected

A

autosomal dominant
CAG triplet repeat disease (>40 repeats) this causes mutant huntintin protein accumulates– becomes toxic and BREAKS DOWN CAUDATE NUCLEUS

causes CHOREA, BEHAVIOURAL DISORDERS, DEMENTIA
caudate nucleus wasting

hyperkinetc- forceful movements
hypotonia

21
Q

what is the triplet code affected in huntingtons

A

CAG triplet repeat

22
Q

describe the pathophysiology of the basal ganglia involved in huntingtons disease

A

dopamine not affected

neostriatum affected

specifically targets the INDIRECT pathway
-reduced outflow of inhibitory signal going to globus pallidus, inhibit signal from GP increased
-substantial inhibition of the subthalamus
-no input in GP medial
-reduced inhibitory outflow
-remove inhibition from thalamus
-powerful signal back to cortex

FORCEFUL MOVEMENTS
by knocking out smoothing of movement done by indirect pathway

23
Q

describe wilsons disease

A

abnormal recessive
abnormal copper accumultion
HEPATO-LENTICULAR DEGENERATION (liver and brain)

dystonia, ataxia, subcortical dementia
involuntary movements
copper transport protein abnormality
low serum copper and caeruloplasmin
KAYSER-FLEISHER RINGS

PENICILLAMINE treatment

24
Q

name an autosomal dominant an autosomal recessive disorder involving the brain

A

autosomal dominant- huntingtons
autosomal recessive- wilsons

25
Q

what are some treatments for parkinsons

A

levadopa (precursor)
with either:
-carbidopa
-benserazide

OR
-entacapone
-tolcapone

D1/D2 agoinsts

26
Q

describe side effects of levodopa

A

dyskinesia- may appear within 2 years
affect face and limbs

rapid FLUCTUATIONS
eg. hypokinesia, rigidity may worsen then improve
reflects fluctuating receptor dynamics
limited in effectiveness with time as neurodegeneration progresses

27
Q

what does the combination of levodopa with a dopa decarboxylase inhibitor allow

A

it allows for the dose to be lower
reduces peripheral system side effects (nausea, hypotension)

28
Q

what is the role of MAO inhibitors

A

protect dopamine from extraneuronal degradation

with levadopa it relieves symptoms and prolong life

29
Q

what is amantadine
what does it do and why is it not commonly used

A

antiviral drug
increases dopamine release- primarily responsible for its therapeutic effect

less effective than levadopa and bromocriptine
action declines with time

30
Q

name some acetylcholine antagonists and why they can be used

A

trihexyphenidyl (benzhexol)
orphenadrine
procyclidine

musc ach receptors exert inhibitory effect on dopaminergic nerves–lack of dopamine

31
Q

what other treatments are there that dont involve medications

A

neural transplantation
brain stimulation

32
Q

what is hemiballism and what symptoms does it give

A

subthalamic deficit
hyperkinetic
violent, involuntary movements

Medicine (54 decks)

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