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Neuroscience > Module E-07 > Flashcards

Module E-07 Flashcards

1
Q

Describe development of Basal ganglia

A

The first neurons generated in the cerebral periventricular zone migrate short distances. They aggregate as subcortical islands of gray matter (basal ganglia or basal nuclei) in the cerebral white matter.

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2
Q

Caudate and Putamen together are called_______

A

Striatum

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3
Q

Globus Pallidus and Putamen together are called______

A

Lentiform nucleus

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4
Q

Structures taht modulate motor cortex with Basal ganglia

A
  1. Striatum: Caudate, putamen, ventral striatum 2. Globus pallidus: External (lateral) part (GPe), internal (medial) part (GPi) 3. Subthalamic nucleus 4. Substantia Nigra: Pars reticulata (SNr) and pars compacta (SNc)
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5
Q

How do basal ganglia modulate the motor activity of the frontal cortices?

A

• Basal ganglia receive inputs from cerebral cortex • Basal ganglia modulate thalamus • Thalamus regulates motor cortex • Through the thalamus, basal ganglia participate in the initiation and control of voluntary movement

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6
Q

The substantia nigra projects to the ______ to release _______

A

striatum; dopamine

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7
Q

What is the effect of the dopamine released by substantia nigra on striatum?

A

Dopamine regulates basal gangliar function, thus indirectly regulating cortical control of movement

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8
Q

What is the effect of basilar output onto thalamus

A
  • Basal gangliar output inhibits the thalamus, thereby suppressing an excitatory thalamocortical projection. - The degree of thalamic inhibition therefore dictates modulation of cortex-dependent motor activity. - Because lesions affecting the basal ganglia disturb basal gangliar output and hence cortical activity, movement often suffers.
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9
Q

Corticostriatal fibers release ________ to excite striatal neurons

A

glutamate

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10
Q

What region of the Substantia nigra a) releases neurotransmitter on to striatal cells, b)What neurotransmitter is released , c) what is the effect of the neurotransmitter and d) on which receptor does the neurotransmitter bind?

A

a) Pars compacta (SNc) b) Dopamine c) excitatory or inhibitory d) D1 (excitatory), D2 (inhibitory)

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11
Q

The substantia nigra receives inhibitory ______ signals from the striatum

A

GABAergic

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12
Q

GABAergic output from the MEDIAL (internal) part of the globus pallidus (GPi) inhibits cells _________________

A

GABAergic output from the medial (internal) part of the globus pallidus (GPi) inhibits cells of the ventral anterior and ventral lateral thalamic nuclei

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13
Q

Thalamic cells excite the motor cortex via the release of _______

A

glutamate

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14
Q

What is the effect of striatum on globus pallidus internal?

A

– Suppresses activity in the GPi – Decreased output from the GPi increases thalamic activity – Increased thalamic activity increases cortical activity to facilitate movement

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15
Q

What is the effect of Globus Pallidus on Thalamus?

A

-secretes GABA to suppress thalamic output

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16
Q

Describe Direct Basal Gangliar Motor Loop

A
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17
Q

What is the effect of Subthalamic nucleus on Globus Pallidus medial?

A

Releases Glutamate to activate GPi and increase GABA release and thereby suppression of thalamus

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18
Q

Describe the Indirect Basal Gangliar Motor Loop

A
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19
Q

Effect of Direct circuit on movement

A

o Striatal output suppresses activity in the GPi

o Decreased output from the GPi increases thalamic activity

o Increased thalamic activity increases cortical activity to facilitate movement

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20
Q

Effect of INDirect circuit on movement

A

o Striatal output suppresses activity in the GPe

o Decreased output from the GPe increases output from the Sth

o Increased output from the Sth increases activity within the GPi

o Increased activity within the GPi inhibits the thalamus o Decreased thalamic output decreases cortical activity, thereby diminishing movement

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21
Q

Role of Striatal Dopamine in movement

A

Tonically released dopamine arising from the substantia nigra optimizes the output of the two basal gangliar circuits to normalize movement

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22
Q

Normal Role of Basal Ganglia in Voluntary Movement

A
  • Normal initiation and maintenance of voluntary motor activity depends on basal gangliar output
  • Normal basal gangliar activity regulates motor cortices to optimize communications between upper and lower motor neurons
  • Optimized communication between upper and lower motor neurons depends on delicately balanced activities of direct and indirect basal gangliar components

o Unbalanced influences of the direct and indirect pathways on the GPi (and hence the thalamus) yield either hypo- or hyperkinesis

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23
Q

What defect causes Hypokinesis in Parkinson’s disease?

A

pathologically diminished release of striatal dopamine secondary to degeneration of the dopaminergic nigrostriatal tract

– The net effect is increased inhibition of the thalamus, leading to decreased cortical activity and hypokinesis

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24
Q

Effect of Diminished dopamine on the Direct pathway

A

o Diminished activation of excitatory D1 receptors reduces striatal output within the direct basal gangliar pathway

o Diminished striatal output disinhibits the GPi

o The overly active GPi suppresses the thalamus

o Decreased thalamic activity decreases cortical output, suppressing movement

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25
Q

Effect of Diminished dopamine on the INDirect pathway

A

o Decreased stimulation of inhibitory striatal D2 receptors disinhibits striatal cells contributing to the indirect pathway

o Increased activity of striatal cells inhibits cells in the GPe

o Decreased activity in the GPe disinhibits the Sth

o Increased excitatory output from the Sth increases activity within the GPi

o Increased activity within the GPi suppresses thalamic activity

o Decreased thalamic activity reduces cortical excitation

o Reduced cortical activity once again diminishes voluntary movement

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26
Q

What causes drug induced Parkinsonism?

A

– Antipsychotic drugs like Phenothiazines, (DA receptor blockers)

– Depletors of DA stores (e.g., reserpine)

– Toxic contaminants (MPTP)

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27
Q

What produces MPTP?

A

a contaminant produced during improper preparation of a synthetic narcotic

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28
Q

How does MPTP induce Parkinsonism?

A

by damaging nigral mitochondria

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29
Q

What receptors do phenothiazines block ?

A

D2 receptors

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30
Q

How do phenothiazines cause drug induced Parkinsonism?

A

by limiting dopamine-mediated inhibition of striatal neurons of the indirect pathway

31
Q

How does reserpine cause Drug-induced Parkinsonism?

A

may diminish striatal dopaminergic transmission to affect both the direct and indirect pathways

32
Q

What is Vascular Parkinsonism?

A

Strokes interrupting the nigrostriatal pathway that may cause parkinsonism, affecting both direct and indirect pathways

33
Q

Other Parkinsonian Conditions

A
  • Drug-induced
  • Vascular – Strokes disrupting nigrostriatal pathway
  • Traumatic – Multiple blows to the head can damage the midbrain, yielding a syndrome with parkinsonian features
  • Postencephalitic – Viral encephalitis can lead to nigral degeneration
  • Neoplastic – Tumors can disturb the nigrostriatal system
34
Q

What pathways are affected in Vascular Parkinsonism?

A

affecting both direct and indirect pathways

35
Q

What is Dementia Pugilistica?

A
  • a parkinsonian syndrome brought about due to multiple blows to the head as in boxers
  • The midbrain flexes during traumatically induced acceleration of the forebrain, which can tear small mesencephalic blood vessels and shear axons
  • The dura forming the tentorial notch may also interact unfavorably with the nearby midbrain during excessive cranial acceleration
  • Cumulative effects of blows to the head may damage nigral (and other) cells
36
Q

What is degenrated that leads to Postencephalitic Parkinsonism?

A
  • due to degeneration of the SNc
  • caused by Encephalitis Lethargica
37
Q

What causes Neoplastic Parkinsonism?

A

Neoplasia can impact the substantia nigra or its output pathway to the striatum

38
Q

What is Huntington’s disease?

A

an autosomal dominant condition with Hyperkinesis that tends to strike younger adults

39
Q

What is the first presentation of Huntington’s Disease and what is usually the early indicator of onset?

A

first present as emotional dysregulation (disinhibition, impulsivity, emotional lability, etc.), motor system failure may be the sole early indicator of onset

40
Q

Describe the progression of Huntington’s

A
  • Facial/oral musculature is often affected early (uncontrolled grimacing, eyebrow-raising and lingual protrusion)
  • The hands are often the next body parts to show choreatic activity, often assuming a piano-playing posture
  • Progression of the disease is highly variable, but life-expectancy is approximately two decades after diagnosis
41
Q

Which pathway is effected in Huntington’s that causes the HyperKinesis?

A
  • Destruction of striatal neurons (bilaterally) expressing D2 receptors
  • Reduced inhibition of thalamus via indirect pathway
  • Increased cortical activity, leading to hyperkinesis
42
Q

Which pathway is mainly affected in Huntington’s?

A

Indirect pathway

43
Q

Name 4 other Choreatic Disorders

A

1) Sydenham Disease
2) Drug induced Chorea
3) Hyperballismus
4) Athetosis

44
Q

What causes Sydenham Disease?

A

It is an autoimmune disease that arises months after rheumatic fever causing choreatic movements

45
Q

age of onset of Sydenham disease

A

between 5 and 15 years

46
Q

Recovery time for Sydenham’s Disease

A

Recovery tends to be complete within about 6 weeks

47
Q

What drugs result in Drug induced Chorea?

A

Treatment with l-dopa (for Parkinson disease) or some anticonvulsants may produce chorea consequent to altered transmission within the basal ganglia

48
Q

What is Athetosis?

A

Slow continuous writhing (athetoid) movements can reflect striatal or thalamic injury

49
Q

What is Hemiballismus?

A

Flinging and rotational movements of the limbs that arise from contralateral subthalamic injury

50
Q

Whta causes Hemiballismus?

A

reflects unilateral stroke related injury to the subthalamus

51
Q

What is damaged in Hemiballismus?

A
  • excitatory output to the GPi decreases
  • Decreased excitation of the GPi disinhibits the thalamus, yielding increased cortical excitation
  • Increased cortical activity may produce contralateral ballismus
52
Q

Whta lesion usually occur with Parkinson’s disease?(besides the Nigral dopaminergic cells)

A
  • Catecholaminergic cells are generally vulnerable
    • The pontine locus coeruleus, which contains noradrenergic neurons, readily degenerates
    • Even peripheral noradrenergic cells, such as those providing sympathetic inputs to the heart, degenerate, yielding orthostatic hypotension and hence increased vulnerability to injurious falls
53
Q

Mean age of diagnosis for Parkinson’s

A

55 years

54
Q

Treatments for Parkinson’s disease

A
  1. Front line therapy: L-dopa and carbidopa
  2. Agonists of Striatal Dopamine Receptors
  3. Drugs that Enhance Striatal Dopamine Release
  4. Inhibitors of Dopamine Metabolism (MAO-B and COMT inhibitors)
  5. Anticholinergics
  6. Ablative Surgical Treatments
  7. Deep Brain Stimulation
55
Q

What are the Front line therapies for Parkinson’s?

A
  • Oral l-dopa increases dopamine synthesis in surviving neurons of the SNc
  • Carbidopa reduces peripheral metabolism of l-dopa (peripheral decarboxylase inhibitor)
  • Treatment with l-dopa/carbidopa becomes less effective over several years

– Responses also variable over hours (patients may benefit from transgastric catheterization)

56
Q

Why does treatment with I-dopa and carbidopa become less effectuve over years?

A

the number of dopaminergic neurons in the SNc (the target of l-dopa) further declines

57
Q

Effect of Agonists of Striatal Dopamine Receptors

A
  • Agonists of D2 receptors interact with the indirect basal gangliar circuit
  • Agonists of both D1 and D2 receptors may beneficially interact with both the direct and indirect basal gangliar circuits
58
Q

Effect of Dopamine release enhancers

A

may reduce akinesia and rigidity

o The drug may promote the release of dopamine and/or block acetylcholine receptors (also weakly blocks NMDA receptors)

o Psychiatric side-effects reported

59
Q

What are the 2 enzymes that Dopamine metabolism inhibitor therapies Target

A

1) MAO-B
2) COMT

60
Q

Effect of MAO-B inhibitors

A

o suppress the breakdown of dopamine in the CNS

o It may improve responses or delay the need for other therapies

61
Q

Effect of COMT inhibitors

A

prolongs the longevity of the neurotransmitter, thereby promoting movement

(May be given in addition to l-dopa and carbidopa)

62
Q

Effect of Acetylcholine in striatal pathway

A

Acetylcholine excites striatal neurons that express D2 receptors

ACh and dopamine exert opposing effects on striatal neurons expressing D2 receptors

63
Q

Effect of Muscarinic antagonists on striatal pathway

A

supress acetylcholine-mediated excitation of striatal neurons

64
Q

Effect of Anticholinergics

A
  • With decreased output from the striatum to GPe, output from the GPi decreases indirectly
  • Decreased output from the GPi increases the ability of the thalamus to excite the cortex and normalize motor function in Parkinson disease
  • Resting tremor appears to be preferentially vulnerable to muscarinic antagonists
65
Q

Side-effects of Anticholinergics

A

o Acutely, patients may be drowsy and confused

o Chronically, Parkinson disease-related dementia may be promoted

66
Q

What regions are targeted in surgical abaltion for Parkinson’s disease and why?

A
  • Subthalamus- reduce the excitatory inputs to the GPi, thereby disinhibiting the thalamus
  • Globus pallidus internal- directly reduces inhibitory input to the thalamus. The disinhibited thalamus is free to restore cortical excitation to reverse hypokinesia
67
Q

What is an undesirable side effect of surgical ablation of the subthalamic nuclei?

A

Ballismus

68
Q

What regions are targetted in deep brain stimulation therapy and what is the effect of each?

A
  • Thalamus - directly increases the excitatory output to the cortex
  • Globus pallidus - activation of local inhibitory neurons to decrease inhibitory output to the thalamus
  • Subthalamus - ?
69
Q

What is the Mean onset of Huntington’s disease?

A

40 years of age

70
Q

What is “boxcar ventricles”?

A

With degeneration of striatal cells and efferent tracts along with frontal cortices, lateral ventricular enlargement is seen

71
Q

Drugs used for Huntington’s Disease

A

1) Antidepressants
2) Antichoreatic (D2 antagonists and VMAT inhibitors)

72
Q

Effect of D2 antagonists

A

o The drugs disinhibit surviving striatal neurons forming part of the indirect loop, ultimately decreasing excitation of cortex to reduce chorea.

o The therapy requires surviving striatal neurons that express D2 receptors.

         Efficacy of the drugs declines as the disease progresses.
73
Q

Side effects of D2 antagonists

A

may adversely affect swallowing, speech, and gait

74
Q

Effects of Vesicular monoamine transporter (VMAT) inhibitors.

A

o Reduce the movement of dopamine into vesicles, thereby diminishing exocytosis.

o Reduced dopamine levels may disinhibit surviving striatopallidal cells within the indirect loop.

Neuroscience (32 decks)

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