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deanne's - NEURO (neuroscience) > 4.3 - motor pathways pt2 (basal ganglia) > Flashcards

4.3 - motor pathways pt2 (basal ganglia) Flashcards

1
Q

components and structures of

- Diencephalon? *4

A
  1. Thalamus (all diff thalamic nuclei)
  2. Hypothalamus (all diff hypothalamic nuclei)
  3. Epithalamus (pineal gland)
  4. Subthalamus (part of basal ganglia)
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2
Q

components & struct’s

- Limbic Lobe?

A
  1. cingulate gyrus
  2. uncus & olfactory cortex
  3. parahippocampal gyrus & hippocampus
  4. subcallosal gyrus
  5. septal nuclei
  6. amygdala
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3
Q

diff btw-

corticospinal vs corticobulbar

  • what kind of pathway?
  • orig.
  • term.
A

both

Q- what kind of pathway?
A
both direct motor output
both pyramid tracts

Upper motor neurons (UMNs) are the main source of voluntary movement.

Q orig.
A
corticospinal - cortex (homunculas - 1. dorso/lateral precentral gyrus = arm/hand 2. para/central lobule = leg)
corticobulbar - cortex (homunculus - ventral/lateral precentral gyrus)

Q term.
A
corticospinal - term. on lower motor neurons and interneurons in the spinal cord, controlling movements of the limbs and trunk.
corticobulbar - project to cn. motor nuclei in the brainstem

corticobulbar tract:
is composed of the upper motor neurons of the cranial nerves. The muscles of the face, head and neck are controlled by the corticobulbar system, which terminates on motor neurons within brainstem motor nuclei.

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4
Q

types of HYPERkinetic dyskinesia ? *2

charicterised by?
due to?

A
  1. hemiballismus
  2. huntington’s disease

characterised by
-increased motor activity

due to
-REDUCED inhibition of VENTRAL THALAMUS by
GPi & SNr (vs incr inhib of same for parkinsons)

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5
Q

types of HYPOkinetic dyskinesia ? *1

charicterised by?
due to?

A

parkinson’s disease

characterised by
- impairment in the initiation of movement

due to
- INCREASED inhib. of ventral thalamus (by GPi & SNr)

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6
Q

damage to the basal ganglia give rise to

disturbances of _ & disorders of _

A

_disturbance of mus. tone (rigidity)

_disorders of movement (dyskinesias)

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7
Q

hemiballismus:

A

involuntry
flailing movement of proximal limb
rotatory nature
distal limb movements generally CHOREIFORM

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8
Q

hemiballismus

type of disorder?
due to?

which weakens…?
results in?
symptoms can be reduced by?

A

hemiballismus is a type of
-hyperkinetic dyskinesia

due to
- vascular leisions
of
-subthalamic nucleus (on the contralateral side of the body)

this weakens
-the influence of the indirect pathway

resulting in

  • over excitation of motor cortex
  • over exuberance of movement

symptoms can be reduced by
- lesioning the GP & ventral thalamus

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9
Q

hemibalismus

explain disrupted pathway..

A 
due to
- loss of output from the subthalamic nucleus (STN)
weakens 
-the indirect pathway
making it more difficult to 
-inhibit unwanted movements
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10
Q

huntington’s disease

explain disrupted pathway

A

motor impairment
due to
atrophy of the striatum (caudate nucl. + putamen)

reduction of input to the GPe (globus pallidus externus)

weakens both direct and indirect pathway more..
-the indirect pathway
making it more difficult to
-inhibit unwanted movements
&
-causing desired movements to be exuberant

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11
Q

parkinson’s disease

explain the disrupted pathway…

A 
reduced dopaminergic drive from 
SNc (substantia nigra compacta)
weakens
- direct pathway
making it more difficult to
- facilitate desired movement
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12
Q

hemibalismus

basal ganglia effected?

A

output from STN (subthalamic nucleus)

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13
Q

huntington’s

basal ganglia effected?

A

red. of input to GPe

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14
Q

parkinson’s

basal ganglia effected?

A

red. dopaminergic drive from SNc (substantia nigra compacta)

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15
Q

basal ganglia function

mn= file sender

A

basal ganglia facilitate behavior & movement that are required
and
inhibit inappropriate movents

  1. search files
  2. select file, send file to motor cortex
  3. same time temporary block on unwanted movements
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16
Q

basal ganglia consists of ? *5

A
  1. CN (caudate nucleus) -head, body, tail
  2. Pt (putamen)
  3. GP (globus pallidus) incl’s GPi & GPe internus & externus
  4. STN (subthalamic nucleus)
  5. SNc & SNr (substantia nigra - compacta & reticulata)
17
Q

basal ganglia

- striatum =

A

caudate + putamen = striatum

18
Q

basal ganglia

- lentiform *mn= wifi

A

putamen + globus pallidus (ext & int) = lentiform

19
Q

what’s the disease?
inherited autosomal dominant disorder involving progressive dementia and choreiform movements

symptoms appear btw age 30-50

A

huntington’s disease

20
Q

whats the disease?
involuntary, flailing movements of the proximal limb, often of roatory nature. Distal limb movements are generally choreiform

A

Hemiballismus

21
Q

whats the disease?

bradykinesia (slowness of movement)
akinesia (difficulty initiating movement)
rigidity
tremor
postural instability
masked facies (lack of facial emotion)
involves degeneration of dopaminergic neurons in the SNc (substantia nigra compacta)
which project to the caudate nucleus & putamen
this strengthens the influence of the indirect pathway

The GPi (globus pallidus internus) and the SNr (substantia nigra reticulata) inhibit the
ventral thalamus more strongly
which reduces exitation of motor cortex
and causes poverty of movement

A

parkinson’s disease

22
Q

what is?
L-Dopa therapy for parkinsons
effectiveness?

A

Leva-Dopa therapy provides
-and extra substrate for dopamine production in the remaining SNc (substantia nigra compacta) neurons

effectiveness
wanes as the disease continues to progress

23
Q

what population has much higher risk of developing

parkinson’s disease?

A

meth addicts

methamphetamine/ anphetamine overstimulates dopamine production, and withdrawal leads to retarded production (less production of dopamine)

24
Q

explain deep brain stimulation for parkinsons disease

A

and implanted electrode that activates the
indirect pathway (GPi & STN subthalamic nucleus)
can dramatically reduce the
-tremors
-rigidity
- and reliance on L-Dopa

25
Q

basal ganglia circuitry

A

direct pathway
cerebral cortex —> striatum (< —SNc ) —> GPi & SNr —> thalamus —> motor cortex —> descending tract

indirect pathway
striatum —> GPe (externus) –>STN —> GPi & SNr

  • substantia nigra compacta SNc
  • globus pallidus (internus, externus) GP
  • subthalamic nucleus STN
26
Q

basal ganglia vs cerebellum

  1. basal ganglia receive input form _
  2. basal ganglia have _ connections with_
  3. basal ganglia receive NO direct projections from_
  4. basal ganglia DO receive direct projections from _
A
  1. basal ganglia receive input form ENTIRE NEOCORTEX (not just sensorimotor regions)
  2. basal ganglia have FEW connections with BRAINSTEM NUCLEI
  3. basal ganglia receive NO direct projections from SPINAL CORD
  4. basal ganglia DO receive direct projections from CEREBRAL CORTEX
27
Q

state direct pathway (basal ganglia)

A

C-P (striatum) to GPi
then to ventral thalamus
via ansa lenticularis

signals form the striatum

  • REDUCE the inhibition of ventral thalamus
  • and INCREASE movement
28
Q

state indirect pathway (basal ganglia)

A

striatum to GPe
to STN to GPI
then to ventral thalamus

this pathway exerts the strongest influene on the GPi

signals from the striatum DISINHIBIT the
-exitatory rojection of the STN to the GPi
which INCREASE the inhibition of the thalamocortical projection
and REDUCE MOVEMENT

deanne's - NEURO (neuroscience) (16 decks)

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