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Flashcards in Basal Ganglia Deck (77):
1

5 major nuclei of the Basal Ganglia

1. caudate nucleus
2. putamen globus pallidus
3. subthalamus
4. substantia nigra
5. nucleus accumbens (thalamus, olfactory sections, amygdala)

2

Caudate nucleus + putamen

STRIATUM: dorsal striatum, corpus striatum
-Input from neocortex & many other sources but output only goes to BASAL GANGLIA

3

Putamen + Globus Pallidus

Lentiform nucleus (lenticular nucleus)
-both lens shaped

4

Functionally related nuclei to BG

1. subthalamus
2. substantia nigra (dopamine/parkinsons)

5

BG functions as action selection based off what?

dopamine rewards for correct selection

6

Cortex generates motor actions & actions are sent to _________ _________

Basal Ganglia! There, they pick correct action based off the dopamine reward system

7

BG: Refinement of cortically initiated motor activity through?

neocortex generates # of possible movement & BG selects correct based on dopamine. As result, there is a refine motor system: how strong/long you perform a movement!!!!

8

Refinement of cortically initiated motor activity through what 3 theories?

1. suppression of competing movements
2. regulation of associated motor movements
3. contribution to species specific learned motor control & built in reflex control

9

Supression of competing movements

extraneous to precise motor activity

10

Regulation of associated motor movements

am i reaching far enough?

11

Contribution to species specific learned motor control & built in reflex control

specific learned: birds singing, speaking
built in reflex control: breathing, heart rate

12

What 4 things is the BG NOT involved with?

1. movement initiation
2. direct projections to LMNs
3. UMN symptoms
4. Lesion induced paralysis

13

Innervation Pattern for BG Motor organization

symptom (involuntary movements) presence contralateral to lesion site

14

Where is damage for huntingtons chorea?

caudate nucleus

15

where is damage for parkinsons disease?

substantia nigra

16

Primary BG neurotransmitters

1. glutamate
2. dopamine
3. acetylcholine
4. GABA
5. Substance P & Enkephalin

17

Glutamate

+

18

Dopamine

+

19

GABA

-

20

Acetylcholine

+ and -

21

Substance P & enkephalin

-
Enkephalins prevent the release of substance p which inhibits ascending pain messages

22

Increase in enkephalins =

decrease in pain

23

Neurotransmitters can be excitatory, inhibitory, or both

Excitatory: causes more neural activation
Inhibitory: dampens the activation/suppresses activation

24

Inhibitory or facilitative parallel-running fivers forming multiple interconnecting loops:

these loops are net loops, one increases and one decreases

25

afferents

fibers running to the basal ganglia: motor cortex to striatum's medium spiny neurons

26

medium spinal neurons

slow fibers, glutamate-ergic fibers (+)

27

efferents

fibers from the BG to thalamus by way of Globus Pallidus

28

Efferents

inhibitory fibers from GP to motor cortex
GABAergic fibers (-) are fast fibers

29

Basal Ganglia circuitory loop

Cortex to Striatum to GP External to GP internal to Thalamus to Motor cortex

30

BG has how many circuits?

4!
-each loop w/ specific motor contributions

31

First (major Loop) direct path down middle

projections from sensorimotor & prefrontal cortex to striatum, internal GP, thalamus, and MC
-incorporation of integrated BG projections to the neocortex

32

Second loop

Bidirectional projections connecting striatum to substantia nigra

33

Third loop

GP external projections to subthalamic nucleus & proectsions back to internal GP

34

Fourth loop

Intralaminar and pontoreticular projections to the striatum (brainstem to the striatum)

35

Substantia Nigra

regions- pars compacta (melanin containing cells) & pars reticulata

36

Substantia Nigra Afferents

from striatum
-GABAergic striatal inhibitory projections

37

Substantia Nigra Efferents

to striatum via terminals containing dopamine
-dopamine inhibitory to striatal functioning
-parkinsonism

38

Physiology of BG circuitry

1.ascending feedback to motor cortex: input from motor cortex goes back to motor cortex
2. impacts of facilitation, inhibition, or disinhibition of BG
3. Effects of inhibitory and facilitatory neurotransmitters (glutamate, dopamine, GABA, acetylcholine, ennkephalin, & substance P) on cortical motor activity

39

Normal Physiological state

Motor cortical areas, intralaminar CM nucleus, pontine RF (glutamate)
-facilitatory (+) projections to neostriatum

40

Normal Physiological State

Neostriatum, SN and thalamocortical system
-inhibitory (-) projections to GP segments

41

Normal Physiological State

Subthalamic nucleus
-Facilitatory (+) projections to GP-INT

42

BG participation in what 3 things?

1. cognition
2. personality
3. motor learning

43

involvement of neurotransmitters in altered quality of motor functions in BG =

loss of adequate inhibitory control of MC leading to involuntary motor behavior

44

What 5 things happen from loss of adequate inhibitory control of motor cortex leading to involuntary motor behavior?

1. dyskinesia
2. bradykinesia
3. chorea
4. tremor
5. impaired postural positions

45

dyskinesia

dysfunctional movement, functioning is abnormal (involuntary)

46

bradykinesia

abnormally slow movement

47

chorea

dancing, jerky movements, typically in face/shoulders/hips

48

tremor

activated muscles, then others get activated

49

Signs of BG dysfunctionin

1. athetosis
2. heemiballism
3. chorea
4. tremor
5. dystonia

50

athetosis

slow, involuntary twisting of axial & speech muscles w/ hypertonia
-buccofacial muscles: dysarthria
-GP: suspected site w/ descending ascending projections

51

hemiballism

forceful, swinging, jerky, twisting, sudden movements of arms and legs on one side
-subthalamic nucleus: suspected site

52

chorea

rhythmic, quick & graceful looking involuntary movements
-distal extremities, muscles of face, tongue, & pharynx
*damage to Caudate Nucleus*

53

Sydenham chorea

postinfectious condidion appearing in childhood between ages 5-13 years after streptoccocal infection & fever

54

Huntington chorea

progressive neurologic condition w/ dementia, dysarthric speech, & personality changes

55

Tremor

constantly alternating motor activity in one or more parts of body
2 types: resting and intention

56

Resting tremor

degenerative changes in substantia nigra: parkinsons

57

Intention tremor

approaching voluntary movements (cerebellar lesions)

58

Associated symptoms w/ Tremors

masked face, infrequent blinking, slow movements, disequilibrium, stooped posture, dysarthai, and dysphasiz

59

4 diff types of dystonia

1. torticollis
2. musculorum deformans
3. myoclonus
4. Tics

60

Torticollis dystonia:

lateral fixation of neck (twisted neck)

61

Musculorum Deformans dystonia

sustained involuntary movements of axial and limb muscles/rare

62

Myoclonus Dystonia

repeated and isolated muscle contractions mostly involving small muscles (usually don't see this w/ large muscles)

63

Tics dystonia

common dyskinesic behaviors like throat clearing, sniffing, excessive blinking
-Gilles de la Tourette Syndrome releated to Hypersensitive dopaminergic receptors

64

tourettes syndrome related to?

hypersensitive dopaminergic receptors

65

BG Diseases

1. parkinsons
2. tardive dyskinesia
3. huntington chorea
4. wilson disease
5. progressive supranuclear palsy-brainstem celular degeneration

66

Parkinsons Disease

1. resting tremor
2. cogwheel musclar rigidity
3. limb bending
4. bradykinesia
5. loss of postural reflexes
6. paucity of facial expressions
7. shuffling gait

67

Treatment for Parkinsons

1. L-dopa
2. deep brain stimulation-intralaminar (CM) or subthalamic stimulation
3. pallidotomy or stn stimulation to reduce inhibitory output from GPM thereby facilitating movement

68

Tardive dyskinesia

involuntary movements of facial and lingual muscles from psychotropic drugs: drugs used to treat mental illness (behaviors, moods, and emotions)

69

Huntington Chorea

caudate degeneration leading to depletion of striatal, cholinergic, & GABAergic neurons
-disinhibition induced involuntary movements of chorea
-caudate nucleus & prefrontal cortical atrophy-suspected sites

70

Characteristics of Huntington Chorea

1. autosomal dominant disease: 50% chance of inheritance
2. Cognitive deficits dementia: forgetfulness, memory loss, personality changes
3. choreiform movements
4. dysarthria and dysphagia (eventual mutism)

71

Wilson Disease

HEPATOLENTICULAR DEGENERATION
-progressive disease (10-25 years onset)-autosomal recessive
-disorder of copper metabolism: degeneration of BG and cirrhosis of liver
-symptoms: muscular ridigity, tremor, dyarthria, and progressive dementia
-corneal pigmentation: kayser-fleisher ring***
-treatment: diet and medication

72

Progressive supranuclear palsy-brainstem cellular degeneration

initial: gaze palsy and impbalance
late: bradykinesia, impaired gait control, facial grimaces, dyarthria, and dysphagia
looks like parkinsons but no tremor
personality changes: socially withdrawn with possible cognitive impairments
:NO CURE: l-dopa for motor symptoms and botulinum toxin for involuntary eyelid closure

73

BG affects:

emotions, personality, & cognition: evidence from axonal connectivity and excitability

74

Projections to prefrontal cortex:

circuitry for higher mental functions

75

Ventromedial striatum:

connection to prefrontal lobe & limbic motor system

76

Cognitive disorders BG:

huntington, wilson, & parkinson

77

Neurotransmitter dysfunctions associated w/ psychiatrica illness w/ damage to BG

1. depression
2. parkinsonism
3. high suicide rate- huntingtons
4. depression and altered personality: altered dopaminergic projections: tourette syndrome and schizophrenia