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Neuroanatomy > Basal Ganglia > Flashcards

Basal Ganglia Flashcards

1
Q

What is basal ganglia made up of

A 
Caudate nucleus
Putamen
Globus pallidus (external/internal)
Substantia nigra (SNc/SNr--> compact/recticular)
Subthalamic Nucleus
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2
Q

What makes up the corpus striatum

A

Caudate nucleus and globus pallidus

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3
Q

what makes up the straitum

A

caudate nucleus and putamen

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4
Q

what makes up the lentiform nucleus

A

Putamen and globus pallidus

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5
Q

what are the segments of the globus pallidus

A

internal and external/medial and lateral segment

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6
Q

What are the parts of substantia nigra

A

Pars compacta–> contains dopaminergic neurons that contain melanin
Pars reticularis: contains gamma-aminobutyric acid (GABA)-ergic neurons

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7
Q

Where is the substantia nigra located

A

midbrain

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8
Q

Why is substantia nigra black

A

It releases dopamine, and a by product of dopamine in a healthy brain is melanin

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9
Q

What kind of dendrites do cells in the striatum have

A

Cells have ‘shiny dendrites’

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10
Q

What info does striatum recieve

A

recieves cortical afferents

mainly from M1 and S1 and projects efferents to GPi/SNr

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11
Q

Where does the globus pallidus lie

A

between putament and internal capsule (medial)

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12
Q

What are the 2 nuclei of globus pallidus

A
  • Lateral/external–> GPl/GPe

- Medial/Internal–> GPm/GPi

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13
Q

What does the GPi do

A

gathers many bits of information including movement-related activity from the striatum

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14
Q

What does the GPe do

A

Integrates info from GPi

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15
Q

GPm/GPi are functionally identical to what

A

SNR

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16
Q

what are most neurons in GP immunoreactive to

A

GABA–> therefore probably not NT

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17
Q

Where is the substantia nigra located

A

midbrain

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18
Q

What are the 2 sub-nuclei of SN

A
  • Substantia nigra reticular part–> SNr

- Substantia nigra compact part–> SNc

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19
Q

What do neurons in SNc produce

A

Dopamine

-carried to striatum and used there as a NT

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20
Q

Where do neurons in GPi/SNr project to

A

thalamus
superior colliculus
reticular formation of brainstem

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21
Q

Where is the subthalamic nucleus located

A

lies just medial to internal capsule and ventral lateral to thalamus

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22
Q

what are cells in subthalamic nucleus immunoreactive to

A

glutamate and may use it as a transmitter

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23
Q

What side does the basal ganglia circuitry occur

A

ipsilateral side of the brain–> hence basal ganglia affects function mediated by the ipsilateral motor cortex

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24
Q

what side does movement from circuitry occur on

A

Output/movements affected on contralateral side

Corticospinal tract crosses at medualla oblongata

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25
Q

Describe the connections of the basal ganglia

A

Fibres from cerebral cortex to striatum

  • striatum sends fibres to GP or to STN then to GP
  • GP sends fibres to ventral thalamus
  • thalamus sends fibres back to the principle motor areas of cerebral cortex
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26
Q

what is disinhibition

A

a decrease in inhibition

decreasing inhibition–> possibility of more excitation

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27
Q

What is the main purpose of direct pathway

A

increases motor activity

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28
Q

What is the main purpose of indirect pathway

A

decreases motor activity

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29
Q

What affect does the GPi normally have on thalamus

A

thalamus is normally under inhibition from the GPi

30
Q

Explain Direct pathway

A

Read notes

31
Q

Explain dopamine modulation of direct pathway

A

Read Notes

32
Q

Explain Indirect Pathway

A

Read notes

33
Q

Explain dopamine modulation of indirect pathway

A

Read notes

34
Q

what projection neurons use glutamate

A

projection neurons in cortex, subthalamic nucleus and VA/VL of thalamus

35
Q

What is the effect of glutamate

A

excitatory

36
Q

What projection fibres use GABA

A

projection fibres in striatum and both segments of GP

37
Q

what is the effect of GABA

A

inhibitory

38
Q

what is the overall effect of the dopaminergic modulation on the pathways

A

increase in motor activity

39
Q

what is the result of the cholinergic modulation on the pathways

A

decrease in motor activity

40
Q

What is the blood supply to the caudate nucleus

A

ACAp
MCAp
Look at pics!!!!!!!!!

41
Q

What is the blood supply to the putamen

A

ACAp
MCAp
Look at pics!!!!!!!!!

42
Q

What is the blood supply to the GP

A

AChA (anterior choroidal artery–> branch on internal carotid artery)
MCAp
Look at pics!!!!!!!!!

43
Q

What is the blood supply to the SN

A

PCAp
PcoAp
Look at pics!!!!!!!!!

44
Q

What is the blood supply to the STN

A

PCAp
PcoAp
Look at pics!!!!!!!!!

45
Q

define akinesia

A

loss or impairment of the power of voluntary movement; loss of ability to move muscles voluntarily

46
Q

Define dyskinesia

A

abnormality or impairment of voluntary movement; unwanted involuntary movement

47
Q

define bradykinesia

A

slowness of movement and is the cardinal manifestation of Parkinson’s disease; slow movement and an impaired ability to move body shiftly on command

48
Q

define rigidity

A

the quality or state of stiffness or inflexibility, abnormal stiffness of muscle not allowing it to bend or be bent

49
Q

What do lesions of the basal ganglia cause/affect

A

Don’t cause paralysis
-Affect the quality of movement–> disturbance in the initiation or cessation of motor activity
Result of a lesion is dyskinesia–> hypokinetic/hyperkinetic

50
Q

What are motor disturbances characterised by

A

involuntary movement
alterations in muscle tone
disturbances in body posture

51
Q

What are hypokinetic disorders

A
  • bradykinesia/hypokinesia–> slowness in beginning of movt, reduced ROM and force of movement
  • Reduced or absent emotional response
  • loss of balance
  • loss of postures associated with skilled motion
  • usually accompanied by muscular rigidity and tremor
52
Q

What are hyperkinetic disorders

A

hyperkinesia–> excessive motor activity, release of motor patterns at inappropriate times/continuously

53
Q

What do involuntary movements consist of

A 
choreiform movement
athetoid movement
ballismus disorders
dystonias
dyskinesias
54
Q

What does a lesion to subthalamic nucleus result in

A
  • Loss of excitatory STN projections= disinhibit thalamus
  • failure to surpress some cortical outputs
  • hyperkinetic disorder
55
Q

What does a lesion to SN result in

A

Loss of dopamine neurons–> can excite direct and inhibit indirect pathway
-hence decreased activity of direct and increased activity of indirect
-enhances output of GPi/SNr
inhibition of thalamus
decreased out–> bradykinesia/hypokinesia
-hypokinetic disorder

56
Q

Define Chorea

A

continuous series of rapid, idependent, jerky involuntary movements that are fragments of purposeful movement; associated with atrophy of striatum

57
Q

Define Dystonia

A

another type of involuntary movement where, in extreme form, joints are forced into a locked position for a long period by extreme contraction of antagonistic muscle groups

58
Q

define athetosis

A
  • uncontrolled writhing
  • One spontaneous movement blends into the next creating constant sinuous and purposeless motion
  • Usually involve hands and face
  • Movements are frequently combinations of alternating antagonistic motions such as supination/pronation
59
Q

define tics

A
  • type of uncontrollable compulsive behaviour
  • Like the movements of chorea, tics are quick fragments of a purposeful movement.
  • They differ from chorea in that they are endlessly repeated in a stereotyped manner
60
Q

What are S&S huntington’s disease

A

hereditory (autosomal dominant)–> chromosome 4
chronic progressive -chorea (jerking uncontrolled movt)
dystonic posturing
dementia
memory loss
psychological changes–> impulsiveness, moodiness, antisocial behaviour
-gradual physical, mental and emotional changes

61
Q

What are S&S of parkinsons disease

A 
resting tremor
rigidity
bradykinesia
mask-like face (expressionless)
slow festinating gait
systemic symptoms--> depression, dementia, autonomic symptoms (sweating, dysphagia, orthostatic hypotension)
62
Q

Is parkinsons disease a hypo/hyperkinetic disorder

A
  • hypokinetic
  • insufficient direct pathway output
  • excess indirect pathway output
63
Q

is huntington’s disease a hypo/hyperkinetic disorder

A
  • hyperkinetic
  • excess direct pathway output
  • insufficient indirect pathway output
64
Q

what is the pathology of parkinson’s disease

A
  • Decrease in the number of nerve cells in the substantia nigra pars compacta and pedunculopontine nucleus
  • Subsequent decrease in available dopamine
  • Loss of dopamine to the putame, reduces activity in motor areas of the cerebral cortex, decreasing voluntary movements.
  • Loss of pedunculopontine cells, combined with increased inhibition of the PPN, disinhibits the reticulospinal tracts, producing excessive contraction of postural muscles
65
Q

what is the pathology of huntingtons disease

A

• A hereditary disorder that causes degeneration in many areas of the brain

66
Q

what are the effects of huntington’s disease on the striatum and cerebral cortex

A

oAtrophy of the striatum
oCaused by faulty gene on chromosome 4
oAffects areas of the brain involved in emotions, intellect, and movement

67
Q

what are the effects of huntington’s disease on GABA neurons

A

• Loss of striatal GABAergic neurons
o GABAergic = inhibitory NT
o This overall reduction of inhibitory structures results in an overall increase in excitatory stimulus being passed through to the CST via the motor cortex.
o Therefore, causes an increase in motor activity (Hyperkinetic disorder)

68
Q

what is the effect of lesions of basal ganglia

A
  • do not cause paralysis, but affect the quality of movement: in that there is disturbance in the initiation or cessation of motor activity
  • The result of a lesion to the basal ganglia is unwanted involuntary movement - dyskinesia: hypokinetic or hyperkinetic.
  • Motor disturbances are characterised by involuntary movements, alterations in muscle tone, and disturbances in body posture
69
Q

what are different types of hypokinetic basal ganglia movement disorders

A 
o	Parkinson’s Disease
	Akinetic/Rigid Parkinson’s Disease
	Tremor-Dominant Parkinson’s Disease
o	Parkinson-Plus Syndromes
o	Parkinsonism
70
Q

what are different types of hyperkinetic basal ganglia movement disorders

A

what are different types of hypokinetic basal ganglia movement disorders

Neuroanatomy (18 decks)

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