Basal Nuclei Flashcards

1
Q

what does baseline activity allow for?

A
  • common throughout the nervous system, allows for increase and decrease in activity (activity never completely turned off)
  • allows for fine tuning
  • sensitivity
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2
Q

what does baseline activity allow for?

A
  • common throughout the nervous system, allows for increase and decrease in activity (activity never completely turned off)
  • allows for fine tuning
  • sensitivity
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3
Q

basal ganglia

A
  • directly effect UMN cortex through modulation.
  • determine appropriateness of actions, emotions, cognition: decide what behavior is most likely to be “Correct”
  • “basal nuclei” is more appropriate name, they are subcortical grey matter
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4
Q

basal ganglia

A
  • directly effect UMN cortex through modulation.
  • determine appropriateness of actions, emotions, etc.
  • “basal nuclei” is more appropriate name, they are subcortical grey matter
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5
Q

what forms striatum of basal nuclei?

A

caudate nucleus and putamen

  • note: caudate nucleus forms lateral wall of ventricle
  • called “striatum” because they have myelinated axons passing through causing them to look striated.
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6
Q

what forms lentiform nucleus?

A

putamen
+
globus pallidus (internal and external)

(have a lens like appearance together)

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7
Q

what is globus pallidus composed of?

A

GPe (external) or “lateral” segment

GPi (internal) or “medial” segment

  • globus pallidus lies just medial to putamen
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8
Q

substantia nigra involvement in basal ganglia?

A

pars compacta (SNc): releases dopamine

pars reticulata (SNr)

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9
Q

substantia nigra involvement in basal ganglia?

A

pars compacta (SNc): releases dopamine

pars reticulata (SNr)

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10
Q

Disinhibtion

A

= removal of an inhibitory effect by a stimulus

  • “inhibition of an inhibition”
  • inhibitory = gabaminergic
  • disinhibitory = glutamatergic
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11
Q

basal ganglia

A
  • directly effect UMN cortex through modulation.
  • determine appropriateness of actions, emotions, etc.
  • “basal nuclei” is more appropriate name, they are subcortical grey matter
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12
Q

what forms striatum of basal nuclei?

A

caudate nucleus and putamen

  • note: caudate nucleus forms lateral wall of ventricle
  • called “striatum” because they have myelinated axons passing through causing them to look striated.
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13
Q

what forms lentiform nucleus?

A

putamen
+
globus pallidus (internal and external)

(have a lens like appearance together)

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14
Q

what is globus pallidus composed of?

A

GPe (external) or “lateral” segment

GPi (internal) or “medial” segment

  • globus pallidus lies just medial to putamen
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15
Q

what portions of thalamus are involved in the in basal ganglia?

A

subthalamic nucleus

thalamus

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16
Q

substantia nigra involvement in basal ganglia?

A

pars compacta (SNc): releases dopamine

pars reticulata (SNr)

17
Q

what are the two paired circuits of the basal nuclei?

A
  1. Direct pathway: “yes” loop
  2. indirectly pathway: “no”/don’t loop
    - determine Motor, cognition and affect
    - there are two paired circuits in each hemisphere that run in a parallel manner
18
Q

where does output/input from basal nuclei come from? how do they influence the cortex?

A

input: from striatum (pyramidal cells and motor cx always project in through striatum)
output: globus pallidus internus and substantia nigra

final projection is into the thalamus. the thalamus ultimately influences the cortex (though this is technically not part of the basal nuclei )

19
Q

draw out direct and indirect pathways.

A

do it now.

and memorize it.

20
Q

direct loop: actions of ACH and dopamine

A

ACH: cholinergic neurons of striatum are inhibitory. ACH is released and ultimately results in decreased cortical activity of direct loop.

Dopa: released from SNc and binds D1 receptors: results in depolarization: facilitates cx through increasing thalamic activity (thalamus is disinhibited)

21
Q

indirect loop: actions of ACH and dopamine

A

ACH: cholinergic neurons of striatum are excitatory and decreases cortical activity of indirect loop

Dopa: released from SNc binds to D2: results in hyperpolarization: facilitates cx through increasing thalamic activity (subthalamic is disinhibited)

22
Q

what is role of substantia nigra compacta?

A

releases dopamine

  • Dopa depolarizes (excitatory) to D1 receptors of direct loop, results in facilitating cortex
  • dopa hyperpolarizes (inhibitory) to D2 receptors of indirect loop, thus facilitating cortex
  • this is what is damaged in Parkinson’s disease* thus increased cortical activity is lost with parkinson’s disease
23
Q

what does ACA supply to basal nuclei?

A

head of caudate

nucleus accumbens

24
Q

what does branches of MCA (lenticulostriate) supply of basal nuclei?

A

Lentiform (putamen and GP)

majority of caudate***

25
Q

what does branches of PCA supply?

A
  • substantia nigra
  • subthalamic nucleus

*** this is the most common place for stroke lesions, will produce hemiballismus symptoms = decrease in activity of the subthalamic nucleus of the basal ganglia, resulting in the appearance of flailing, ballistic, undesired movements of the limbs.

26
Q

what do pathologies of the basal nuclei usually present through?

A
  • movement disorders
  • not directly affecting strength, coordination or sensation
  • VOLUNTARY movmt systems are affected
  • will see abnormalities of tone (increased or decreased) depending on lesion
  • akinetic or hyperkinetic depending on lesion
27
Q

negative vs. positive signs

A
neg = reduced mvmt
pos = increased/inappropriate mvmt
28
Q

four different types of kinesias…

A
akinesia = no mvmt
hypokinesia = reduced mvmt
bradykinesia = slow mvmt
dyskinesia = inappropriate/incorrect mvmt
29
Q

tremor

A
  • oscillatory mvmt (4-6 Hz)

- greatest at rest, they are decreased with voluntary mvmt

30
Q

athetosis

A

slow writhing mvmt

31
Q

chorea

A

abrupt, rapid, jerking dance like (often distal limbs and orofacial mm)

32
Q

choreoathetosis

A

mixture of slow writhing mvmt and abrubt jerking.

33
Q

ballism

A

violent flinging

- usually unilateral = hemiballismus

34
Q

Parkinson’s disease cause

A
  • late onset disease (<50 y/o)
  • unknown cause
  • results in degeneration of SNc and loss of Dopa neurons
  • substantia nigra looks severely lesioned
  • results in decreased activity of cortical motor neurons - cx is inhibited
35
Q

Parkinson’s disease symtpoms: negatives and positives?

A

Negative signs:

  • hypokinesia/bradykinesia
  • Gait is small, shuffling steps
  • facial masking
  • loss of postural reflexes (flexed stooped posture)
  • late cognitive defects
  • difficulty initiating gait

Positive signs:
- Tremor that occurs at rest (pill rolling)

36
Q

Therapy for Parkinson’s disease

A
  • Replace missing L-dopa (effectiveness decreases over time)
  • replace missing cells of SNc via stem cell transplant (will eventually die just as predecessors did)
  • reduce the activity of indirect loop
37
Q

huntington’s disease cause?

A
  • earlier onset: age 30-40y/o
  • due to multiple CAG repeats on chromosome 4 “huntington protein”
  • autosomal dominante
  • results in degeneration of striatum (caudate) of indirect loop
38
Q

symptoms of huntington’s disease

A

positive changes:

  • hyperkenisias
  • choreoathetosis “huntingtono’s chorea”

negative symptoms:

  • dementia and cognitive changes (caudate is important part of “cognitive loops”)
  • psychoses (hallucinations and paranoia)
  • very little treatment. developes earlier than parkinson’s disease