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Neuroscience > Week 4 - The Basal Ganglia and Movement Disorders > Flashcards

Week 4 - The Basal Ganglia and Movement Disorders Flashcards

1
Q

why is the substantia nigra black?

A

breakdown products of dopamine

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2
Q

what are the basal ganglia structures and their primary and secondary subdivisions?

A
  1. striatum
    - dorsal striatum (caudate + putamen)
    - ventral striatum (nucleus accumbens + septum + olfactory tubercle)
  2. globus pallidus
    - external segment
    - internal segment (outer + inner portion)
    - ventral pallidum
  3. substantia nigra
    - pars compacta
    - pars reticulata (pars lateralis)
  4. subthalamic nucleus
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3
Q

which components of the substantia nigra are lateral and medial?

A

pars compacta is lateral

pars reticulata is medial

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4
Q

what is the most common neuron in the basal ganglia?

A

medium spiny stellate neuron

-cell bodies in caudate and putamen, dendrites in globus pallidus and substantia nigra (pars reticulata)

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5
Q

what are input, output, and intermediate structures of the basal ganglia, and what does this entail?

A

input: receive direct projections from cerebral cortex
- primarily striatum, but also subthalamic nuclei
output: project back to cerebral cortex via thalamus
- globus pallidus internal and substantia nigra pars reticulata
intermediate: modify activity of input and output structures
- substantia nigra pars compacta, subthalamic nuclei

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6
Q

what are the cortico-basal ganglia-thalamo cortical circuits?

A

the anatomical feature of basal ganglia participation in multiple loops with cerebral cortex

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7
Q

how is the cortico-basal ganglia like a bicycle?

A

cortex: pedals
input (striatum): front sprocket
output (pallidum): brake that’s “always on”
thalamus: rear sprocket
substantia nigra pars compacta: “oil” dopamine to keep chain moving
things are all connected by basal ganglia chain, and you need both sprockets working

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8
Q

are “direct” and “indirect” cortex messages usually excitatory or inhibitory for the “thalamus brake”?

A

direct: eventually inhibitory to brake, turning it “off” (disinhibition = release of brake)
indirect: eventually excitatory to brake, turning it “on”

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9
Q

what is the range of functions that can be influenced by these direct/indirect basal ganglia circuits?

A

largely determined by connections that basal ganglia have with different regions of cerebral cortex

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10
Q

how are the basal ganglia motor loops related?

A

each has its own parallel, segregated loop

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11
Q

what is the body movement loop?

  • cortical input
  • striatum
  • pallidum
  • thalamus
  • cortical targets
A

cortical input: motor, premotor, somatosensory cortex
striatum: putamen
pallidum: lateral globus pallidus, internal segment
thalamus: VLN and ventral anterior nuclei
cortical targets: primary motor, premotor, supplementary motor cortex

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12
Q

what is the oculomotor loop? when do they discharge more?

  • cortical input
  • striatum
  • pallidum
  • thalamus
  • cortical targets
A
  • cortical input: posterior parietal, prefrontal cortex
  • striatum: caudate (body); discharges most when activity of GABA-ergic increases
  • pallidum: globus pallidus, internal segment; substantia nigra pars reticulata; stops discharging when striatum starts, disinhibiting superior colliculus
  • thalamus: mediodorsal and ventral anterior nuclei
  • cortical targets: frontal eye field, supplementary eye field
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13
Q

what is the prefrontal loop?

  • cortical input
  • striatum
  • pallidum
  • thalamus
  • cortical targets
A
  • cortical input: dorsolateral prefrontal cortex
  • striatum: anterior caudate
  • pallidum: globus pallidus, internal segment; substantia nigra pars reticulata
  • thalamus: mediodorsal and ventral anterior nuclei
  • cortical targets: dorsolateral prefrontal cortex
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14
Q

what is the limbic loop?

  • cortical input
  • striatum
  • pallidum
  • thalamus
  • cortical targets
A
  • cortical input: amygdala, hippocampus, orbitofrontal anterior cingulate, temporal cortex
  • striatum: ventral striatum
  • pallidum: ventral pallidum
  • thalamus: mediodorsal nucleus
  • cortical targets: anterior cingulate, orbital frontal cortex
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15
Q

how do the basal ganglia participate in motor and non-motor function?

A

neurons in basal ganglia are very active in simple movements of limbs and in visually guided movements

  • location w/in basal ganglia determines precise properties that are observed
  • -some neurons are tuned for specific directions, some for specific sequences of movements, some for specific body parts
  • nearly all physiological properties can be explained by examination of connections of structure being recorded
  • -substantia nigra and globus pallidus neurons
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16
Q

what are 2 other types of basal ganglia circuits, other than direct/indirect?

A

hyperdirect: straight to excite STN (subthalamic nucleus)

striosomal path: excite anterior putamen –> inhibit substantia nigra pars compacta

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17
Q

are all inputs/outputs excitatory or inhibitory, and do they use glu or GABA?

A

all inputs are excitatory, use glutamate

all outputs are inhibitory, use GABA

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18
Q

what is the striosomal path most known for? how does it do this?

A

“habit learning” of basal ganglia with rewards
-neurons most involved are giant cholinergic interneurons (Tonically Active Neurons) in striatum, which interact w/ dopamine inputs from the SNpc at level of MSSNs

19
Q

what kind of relationships do TANs (tonically active neurons) and SNpc (substantia nigra pars compacta) neurons display to movements or body parts?

A

it’s not simple

  • neurons are activated by rewards or stimuli that predict occurrence of rewards
  • -modify activity of MSSNs based on this to form part of neural substrate underlying behavioral reinforcement
  • profound effects on properties of cells
20
Q

in the instructed saccade (rapid eye movement) task, what would reward drive?

A

visual patterns in both caudate cells and SNpc

21
Q

what is “neuroeconomics”?

A

the study of globus pallidus (internal) activation during rewarding strategies of card gambling

22
Q

what does basal ganglia damage most often produce, and what are the 2 types?

A

dyskinesia - diminished voluntary movements and/or increased involuntary movements

  • hyperkinetic - excessive movements
  • hypokinetic - reduced movements
23
Q

what are hyperkinetic disorders associated with, characterized by, and examples?

A

associated w/ abnormally low levels of BG output (which disinhibits the thalamus)

  • characterized by excessive motor activity in form of abnormal, involuntary, purposeless movements; difficulty continuing and stopping ongoing movement, abnormalities in muscle tone (hypertonia; muscle rigidity), and tremor
  • examples are chorea, athetosis, hemiballismus, dystonia, and tics
24
Q

what are hypokinetic disorders associated with, characterized by, and examples?

A

excessive inhibition of thalamus by BG (too much braking)

  • significant impairment in initiation of movement (akinesia), lack/reduction in amplitude and velocity of movement (bradykinesia)
  • accompanied by tremor, muscular rigidity, and postural abnormalities
  • examples are Parkinson’s
25
Q

what is chorea?

A

hyperkinetic disorder

  • quick, jerky, and purposeless movement of independent/discrete nature (fingers, grimacing, hips/shoulders)
  • resemble fragments of normal movement
  • involve mostly distal musculature of extremities
  • can become slower and more continuous (athetoid-like) if more frequent
  • can also occur as complication of long-term neuroleptic/dopamimetic drugs or exposure to Streptococci
26
Q

what is Sydenham’s corea?

A

AKA St. Vitus’ dance

  • caused by autoimmune RXN to childhood infection w/ group A beta-hemolytic streptococci
  • occurs in 25% of pts w/ acute rheumatic fever, 6 months later
  • more common in females, very rare in adults
  • symptoms for 2+ years, recovery in 2-6 mo. in 50% of cases
  • autoAb attack striatum
27
Q

what is Huntington’s disease?

A

AKA Huntington’s chorea

  • rare inherited AD where pts show progressive dementia and choreiform movements
  • appears first between 30-50 yo, associated w/ atrophy in neostriatum (esp. enkephalin-expressing neurons in caudate)
  • -HD kills ENK neurons in striatum, leading to unchecked D1 tone, keeping “thalamus brake off”
28
Q

what is Parkinson’s disease?

A

AKA paralysis agitans

  • progressive disorder that is very disabling and leads to dimentia
  • characterized by akinesia, bradykinesia, micrographia, tremor at rest, muscular rigidity, slow/shuffling gait, expressionless facies, dysautonomia, and other postural abnormalities
29
Q

what is akinesia?

A

difficulty initiating movement and paucity of volitional movement

30
Q

what is bradykinesia?

A

slow movements

31
Q

what is micrographia?

A

diminished range of movement

32
Q

what is expressionless facies?

A

loss of involuntary control over facial muscles

33
Q

in what diseases are there high order (extra motor) consequences of basal ganglia damage?

A

Huntington’s disease (almost always cognitive)
Sydenham’s chorea (emotional, behavioral, OCD)
Parkinson’s disease (common in advanced stages)
Wilson’s disease and Syndrome of the Corpus of Luys (almost always)

strong evidence that acute lesions lead to cognitive deficits, hallucinations, and even OCD

34
Q

what are non-genetic causes of basal ganglia lesions?

A

CO poisoning, wasp stings, adverse drug RXNs, high altitude sickness

35
Q

what are treatment choices for Huntington’s disease and Sydenham’s chorea? what are potential side effects?

A

block excess action of direct pathway via anti-dopaminergic or dopamine-depleting drugs (haldol, olanzapine, tetrabenazine)

  • for SC, also give antibiotics, immunomodulants, and maybe plasmapheresis
  • pts. may develop tardive dyskinesias with chronic treatment
36
Q

what are treatment choices for Parkinson’s? what are potential side effects?

A

L-DOPA (Sinemet) - metabolized to DOPA, and improves function short term, but disease continues to progress to need higher doses
-over decades, pts don’t respond, become immobilized, and die
Dopamimetics (Apomorphine, Bromocriptine, Pramipexole) - longer acting, show benefit for preventing further motor loss, but have stronger side effects, and are selective for D1/2 receptors
MAO-B/COMT inhibitors (Selegiline, Entacapone) - prevent degradation of DOPA
Anti-cholinergics (Benzhexol) - mild antiparkinsonian effect, best for tremor (to dampen unregulated DOPA release), but many other side effects

37
Q

why can’t you give dopamine to Parkinson’s patients?

A

it doesn’t cross BBB and isn’t well tolerated

38
Q

what is the pathophysiological model of Parkinson’s? why does L-DOPA treatment cause dyskinesis and hallucinations?

A

loss of dopamine (“great influencer”) leads to hyperreactive state b/c decreases drive to M1 (impaired/slowness of movements)

  • motor circuit: increases drive to M1, causing abnormal movements (decreased braking, increased excitement)
  • TE circuit: increases drive to TE causing visual hallucinations
39
Q

what are surgical treatments of Parkinson’s?

A
  1. take some out (pallidotomy/thalamotomy via surgical lesions)
  2. put some in (fetal nigral transplantations, embryonic stem cell transplantations, iPSC-derived dopaminergic cells)
  3. quiet down and wait (deep brain stimulation via pacemaking)
40
Q

how do pallidotomies and thalamotomies work to “fix” Parkinson’s?

A

small electrocoagulative or radiofrequency lesions are made in internal segment of globus pallidus or VLN of thalamus, respectively

  • pallido: improves functioning of motor system by reducing rigidity
  • thalamo: relieves tremor
41
Q

how does fetal nigral transplantation work to “fix” Parkinsons’?

A

suspensions of fetal nigral tissue are surgically placed into multiple sites of caudate and/or putamen

  • grafts survive, reinnervate denervated striatum, form synaptic connections w/ host neurons, release DOPA, and produce functional recovery
  • mild to moderate improvement in motor disturbances, W/O major side effects
42
Q

why is embryonic stem cell transplantation not as good as fetal nigral transplantation?

A

hard to maintain cell fate, so not as effective

43
Q

what happens when there is a subthalamic nucleus pacemaker installed?

A

when off, will have Parkinsonian defects

when on, can walk much faster, straighter, and w/o difficulty

Neuroscience (39 decks)

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