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523 - Neuroscience - Exam 3 > 01_Basal Ganglia > Flashcards

01_Basal Ganglia Flashcards

1
Q

What are the components of the Basal Ganglia?

A
  1. Caudate nucleus
  2. Putamen
  3. Globus pallidus (interna and externa)
  4. Subthalamic nucleus
  5. Substantia nigra (pars reticulate and pars compacta)

The nucleus accumbens is considered by some to be a 6th nucleus of the basal ganglia

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1
Q

caudate + putamen = ?

A

striatum or neostriatum

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2
Q

caudate + putamen + globus pallidus = ?

A

corpus striatum

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3
Q

putamen + globus pallidus = ?

A

lenticular nucleus

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4
Q

The basal ganglia include a collection of (white or gray) matter nuclei in the diencephalon and mesencephalon (midbrain)?

A

Gray matter

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5
Q

What are the four parallel channels of the basal ganglia?

A

Occulomotor, Prefrontal, Limbic and Motor Channels

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6
Q

What pathological evidence (effects from lesions) suggests that the basal ganglia play an important role in motor control (motor channel)

A

persons with lesions of the basal ganglia who demonstrate abnormalities such as tremor, rigidity, difficulty in initiating voluntary movements, bradykinesia, ballismus, and choreoathetoid movements

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7
Q

What are the respective roles of the four channels of the basal ganglia? Occulomotor channel Prefrontal channel Limbic channel Motor channel

A

a. control of eye movements (occulomotor channel)
b. cognitive functions (prefrontal channel)
c. emotional functions (limbic channel)
d. motor control (motor channel)

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8
Q

How does electrical stimulation of basal ganglia nuerons cause movement?

A

The basal ganglia have no direct connections to the motor neurons in the spinal cord. Therefore, stimulation of basal ganglia neurons does NOT directly cause movements.

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9
Q

Though the basal ganglia plays a role in cognitive functions and emotion, it is known best for its role in performing which function?

A

The basal ganglia is best known for its function in motor control

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10
Q

How does the motor channel of the basal ganglia play a role in the formulation of GENERAL motor plans?

A

It determines which general plans are appropriate for movement and which general motor combinations are available to achieve a motor goal.

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11
Q

How does the dysfunction of the motor channel loop (in the formulation of GENERAL motor plans) manifest itself clinically?

A

Dysfunction of the loop decomposes behavior into isolated motor acts (similar to cerebellar dysfunction).

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12
Q

How does the motor channel of the basal ganglia play a role in the execution of SPECIFIC motor plans?

A

The basal ganglia determine how much scaling of motor effort is required for movement and when the quality of the movement is appropriate for automatization.

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13
Q

How does the motor channel of the basal ganglia play a role in the scaling of motor intensity?

A

This function involves helping bring about a smooth integration of programmed movement and postures that make up the learned motor acts.

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14
Q

How does the dysfunction of the motor channel loop (in the scaling of motor intensity) manifest itself clinically?

A

Dysfunction of the motor loop results in movement of inappropriate rates, amplitudes and duration.

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15
Q

How does the motor channel of the basal ganglia play a role in the automatic execution of learned motor plans?

A

This function involves the automatization of learned motor acts such as handwriting.

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16
Q

How does the dysfunction of the motor channel loop (in the automatic execution of learned motor plans) manifest itself clinically?

A

Dysfunction means that much more mental effort must be applied during skilled movement, because all learned acts must proceed under voluntary guidance.

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17
Q

The basal ganglia have output to which structure?

A

The basal ganglia have output to the motor cortex, which, in turn, controls the activity of extrapyramidal upper motor neuronal pathways (as well as the pyramidal or corticospinal tract).

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18
Q

What are the main inputs to the basal ganglia? What are other significant inputs?

A

The main inputs to the basal ganglia are to the Caudate and Putamen (striatum). The main inputs come from the cortex and thalamus and are excitatory (glutamatergic). Significant inputs also come from the substantia nigra pars compacta and are dopaminergic.

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19
Q

What are the main outputs of the basal ganglia?

A

The main outputs from the basal ganglia are from the globus pallidus interna and the substantia nigra pars reticulata. The main output pathways are inhibitory (GABAergic) and project to the thalamus (ventral lateral and ventral anterior), the reticular formation, and the superior colliculus.

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20
Q

Which neurons located in the striatum also play an important role in basal ganglia function?

A

Acetylcholinergic neurons in the striatum also play important roles in basal ganglia function.

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21
Q

The main anatomical/functional circuitry in the basal ganglia is separated into two which pathways?

A
  1. The Direct Pathway of the Basal Ganglia (excitatory pathway) 2. Indirect Pathway (Subthalamic Nucleus Circuit, inhibitory pathway)
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22
Q

What is the primary function of the substantia nigra circuit within the basal ganglia?

A

The substantia nigra circuit helps modulate activity in the direct and indirect pathways

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23
Q

What is the result of the direct pathway of the basal ganglia (excitatory pathway) on the thalamus and in the motor, prefontal and limbic channels?

A

-Caudate/putamen disinhibition of the thalamus -in the motor channel this will mean increased movement -in the prefrontal channel it will mean increased cognitive function -in the limbic channel, it will mean increased emotions.

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24
Q

What does caudate/putamen disinhibition of the thalamus lead to?

A

increased thalamic excitation of the cortex and increased cortical output

25
Q

What is the result of the indirect pathway of the basal ganglia (inhibitory pathway) on the subthalamic nucleus and in the motor, prefontal and limbic channels?

A

-caudate/putamen disinhibition of the subthalamic nucleus -in the motor channel this will mean decreased movement -in the prefrontal channel it will mean decreased cognitive function -in the limbic channel, it will mean decreased emotions

26
Q

What does caudate/putamen disinhibition of the subthalamic nucleus lead to?

A

globus palidus interna/substantia nigra pars reticulata inhibition of the thalamus (thereby decreasing thalamic excitation of the cortex and decreasing cortical output)

27
Q

Where do axons arising from neurons in the substantia nigra pars compacta synapse?

A

on neurons of the direct and indirect pathways in the caudate and putamen.

28
Q

What is the neurotransmitter of the axons named the nigrostriatal pathway?

A

dopamine

29
Q

Which neurons are excited and inhibited by the Substantia Nigra Pars Compacta Circuit?

A

-excites caudate/putamen neurons of the direct pathway (these neurons have the D1 receptors) -inhibits caudate/putamen neurons of the indirect pathway (these neurons have the D2 receptors).

30
Q

While lesions of the basal ganglia do not produce paralysis, unilateral damage to the basal ganglia will produce which type of dyskinesias? (Unilateral or contralateral)

A

Contralateral dyskinesias (abnormal movements)

31
Q

What does Bradykinesia refer to and how is it caused?

A

Bradykinesia - (slowed movements) also see hypokinesia (decreased amount of movement) and akinesia (absence of movement) - caused by increased inhibitory output of the basal ganglia to the thalamus (decrease in the direct pathway or increase in the indirect pathway)

32
Q

What are the common symptoms of the following basal ganglia pathology? –Athetosis

A

Athetosis - twisting movements of the limb, face and, trunk. -It is associated with Huntington’s disease, perinatal hypoxia involving the basal ganglia, antipsychoitic medications, anitemetic medications, Levadopa

33
Q

What are the common symptoms of the following basal ganglia pathology? –Chorea

A

Chorea – (means dance), continuous involuntary movements that have a fluid or jerky quality, but constantly vary. Can range from fidgeting or restless movements to frantic “break dancing”. - Associated with Huntington’s disease, perinatal hypoxia involving the basal ganglia, antipsychoitic medications, anitemetic medications, Levadopa, infarct or focal lesion of the basal ganglia, systemic lupus erythematosus.

34
Q

What are the common symptoms of the following basal ganglia pathology? –Ballismus

A

Ballismus – Movements of proximal limb muscles with larger-amplitude and more flinging quality than chorea. - Usually it is unilateral due to a unilateral lesion to the contralateral subthalamic nucleus. Lesion of the subthalamic nucleus decreases inhibition of the thalamus

35
Q

What are the common symptoms of the following basal ganglia pathology? –Tremor

A

Tremor – Rhythmic or semirhythmic oscillating movements. - Can be classified as resting (Parkinson’s), postural, or intention, can have many causes.

36
Q

What are the common symptoms of the following basal ganglia pathology? –Rigidity

A

Rigidity – Increased resistance to passive movement of a limb. Rigidity caused by basal ganglia disorders is referred to as plastic, waxy, or lead-pipe; meaning that it is fairly continuous throughout attempts to move the limb.

37
Q

What are the common symptoms of the following basal ganglia pathology? –Dystonia

A

Dystonia – Sustained assumption of abnormal, often distorted, positions of the limbs trunk or face. Can be generalized or focal. Associated with basal ganglia dysfunction.

38
Q

What is the main pathology of ideopathic Parkinson’s disease?

A

Main pathology is an unexplained degeneration of dopaminergic neurons in the substantia nigra that project to the striatum (caudate and putamen).

39
Q

What are the four cardinal features of PD?

A

tremor, rigidity, bradykinesia and postural instability

40
Q

What are some typical characteristics of tremors associated with Parkinson’s?

A

-Present at rest; often (but not always) disappears upon voluntary movement; increases with emotional stress -Present in hands, feet, and head -Frequency is 6-7 Hz -Described as a pill-rolling, resting tremor, but some patients have action tremor (tremor during movement rather than at rest)

41
Q

What are some typical characteristics of rigidity associated with Parkinson’s?

A

-Increased tone in all muscles. -May be uniform throughout the range of motion imposed by examiner (lead-pipe rigidity). -May be interrupted by series of brief relaxations (cog-wheel rigidity).

42
Q

What are some typical characteristics of bradykinesia associated with Parkinson’s?

A

-Probably the major disabling feature of PD -Sometimes an inability to initiate movements (akinesia) -Slowness of movements once initiated (slow dressing) -Difficulty crossing barriers (going through doorways) -Poverty of movement -Micrographia (handwriting is slow and becomes small & illegible) -Mask face or lack of facial expression -Slow finger dexterity (makes ADLs slow and difficult) -Slow gait (small steps, shuffling; tendency for gait to freeze, induced by walking through narrow confines, coming up to a chair, or meeting a minor obstacle) -Decreased arm swing

43
Q

What are some typical characteristics of postural instability associated with Parkinson’s?

A

-poor balance control; tendency to fall; loss of balance may be expressed as retropulsion or propulsion

44
Q

Besides the most common idiopathic cases of Parkinson’s, what are six additional causes of the disease?

A

-Encephalitis lethargica (early 20th century Europe and America, Oliver Sacks, L-DOPA) -MPTP (contaminant of synthetic heroin, 1982, tool for producing animal models of PD) -Head trauma (e.g., pugilistic Parkinson’s) -Prolonged use of antipsychotic drugs AKA neurolepic drugs (other movement disorders include akathesia (patient moves about continuously), acute dystonic reaction (facial grimacing and occasional torticollis); and tardive dyskinesia (repeated involuntary choreoathetoid movements and involuntary sucking, lip smacking, lateral jaw movements and darting protrusion of the tongue)) -Poisoning with manganese or carbon monoxide -Some pesticides used in farming (e.g., rotenone and paraquat)

45
Q

What are four pharmacological agents (or classes of agents) used to treat PD?

A
  • Monoamine oxidase inhibitors
  • Dopamine agonist drugs
  • Non-steroidal anti-inflammatory agents
  • Levodopa (L-DOPA)
46
Q

How do monoamine oxidase inhibitors work?

A

(e.g., Seligiline) prevent the breakdown of dopamine so the brain content of dopamine remains high (dopamine is a monoamine).

47
Q

How do dopamine agonist drugs work?

A

(e.g., Mirapex and Requip). These drugs mimic the effects of dopamine, stimulating dopamine receptors directly without having to be converted to dopamine to be effective.

48
Q

What is the main idea behind Levodopa (L-DOPA)?

A

Dopamine (the missing neurotransmitter in PD) does not cross the BBB so it cannot be given to patients directly. L-DOPA is a precursor that can cross and is later converted to dopamine by an enzyme DOPA decarboxylase in the substantia nigral neurons. Period of maximum response for the drug is about 2-5 years.

49
Q

~90% of L-DOPA is converted to dopamine outside the CNS where it is not effective. What drug combines L-DOPA with a DOPA decarboxylase inhibitor to prevent the conversion of L-DOPA to dopamine in the blood?

A

Sinemet-Sinament allows more L-DOPA to cross the BBB and be converted to dopamine on the brain-side of the BBB where it is useful.

50
Q

Whare are some signs (dyskinesias) that may indicate that the useful window for using L-DOPA has passed?

A

-head bobbing -lip smacking -tongue thrusting -leg writhing -hand clasping -trunk twisting

51
Q

What are two surgical treatments for PD?

A

Deep brain stimulation (DBS) and surgical lesions-ablations)

52
Q

Some of the key points to know regarding deep brain stimulation as a treatment for Parkinson’s:

A

-Electrical stimulation is continuous and reduces the discharge of action potentials of cells to rebalance control messages throughout the movement control centers of the brain -an electrode placed in the thalamus and globus pallidus to help treat disabling tremor and dyskinesias -an electrode placed in the subthalamic nucleus helps reduce most of the main motor features of PD (postural instability does not improve)

53
Q

What is a thalamotomy?

A

thalamotomy – surgery to destroy a small area of the thalamus to treat tremor

54
Q

What is a pallidotomy?

A

surgery to destroy a small area of the globus pallidus to treat akinesia

55
Q

Huntington’s Disease occurs in clusters of families and is characterized by which four features?

A

A. heritability (autosomal dominant; each child of affected parent has a 50% chance of getting HD) B. chorea uncontrolled rapid, dance-like movements C. dementia: schizophreniform psychosis D. death after 15-20 yrs

56
Q

Other signs and symptoms of Huntington’s disease include:

A

A. absent mindedness B. irritability C. depression D. fidgeting (choreiform movements which increase and worsen) E. clumsiness F. speech becomes slurred at first, then incomprehensible and ceases altogether as facial expressions become distorted and grotesque G. mental functions decline; ability to reason disappears (schizophreniform psychosis); about 50% of HD patients acquire manic depression H. HD patient is almost always moving while awake

57
Q

What causes Huntington’s Disease?

A

A. loss of cholinergic and GABA-ergic neurons in the striatum (caudate & putamen); thought to cause choreiform movements B. loss of cortical cells thought to cause impaired cognitive functions and dementia

58
Q

What is Ballism or Hemiballism?

A

Extrapyramidal motor disorder characterized by violent flinging of one extremity (hemiballism) or both extremities (ballism).

59
Q

What causes Ballism or Hemiballism?

A

Caused by vascular infarct, hemorrhage or tumor of the subthalamic nucleus.

60
Q

What are some treatment options available for Ballism?

A

-May be treated with dopamine-blocking drugs or with GABA-mimicking drugs. -Surgical treatment involves lesion of a selected part of the thalamus.

523 - Neuroscience - Exam 3 (5 decks)

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