Workshop 5 BSG/PD Flashcards

1
Q

Upper Motor Neuron Cell Bodies situated where?

A

Pre-Central Gryus- Motor Cortex

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2
Q

LMNs located?

A

ventral horn of the gray matter
Motor nucluei of cranial nerves in the brainsteam

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3
Q

BSG Def

A

group of subcortical nuclei, base of forebrain

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4
Q

BSG and Cerebellum are Diff to other motor system as

A

they modulate movement
other functions in addition to modulating motor control

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5
Q

Damaged BSG leads to

A

damaged in primary motor structures

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6
Q

BSG Functions-

A

Dont directly LMNS
Regulate activity of UMNs
Prevenet UMNs from iniating unwanted movements
Prepare motor cirucits for initation
Regulate transition from 1 pattern to another of voluntary movements

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7
Q

BG Anatomy

A

Striatum(forebrain)
Dorsal Stratium
Caudate Nuclues & Ventral Straitum=Nucleus Accumbens)

Globus Pallidus: Base of forebrain:
Internal, External Segment

Subthalamic Nucleus

Susbtantia nigra

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8
Q

Functional Classification Intrinsic Nuclei:

A

Globus Pallidus(external)
Subthalamic Nucleus
Substantia nigra

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8
Q

Functional Classification Intrinsic Nuclei:

A

Globus Pallidus(external)
Subthalamic Nucleus
Substantia nigra

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9
Q

Functional Classification- Striatum(Input Nuclei)

A

Caudate Nucleus
Putamen
Nucleus Accumbens

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10
Q

BSG Functions

A

-Modulate and Regulate Activity
Goal Directed Movement
Motor Learning
Motor Pattern Selection

Fine tuning the starting and stopping voluntary movements
Preventing unwanted movements
Procedural Learning ie: complex patterns/sequences of movement
Planning and controlling movement intensiitees an directions
eye movements
cognition
emotions

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11
Q

Motor Loops

A

BG work with other CNS regions to modulate movements both before and during their execution
Actions effected via body movements and Oculomotor

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12
Q

Putamen

A

acts as a reservoir for learning motor programs
assembles an approipiate motor sequence for desired movements
info is sent to the Supplementary Motor Area

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13
Q

Damage to the Substania Nigra

A

inhibition of the direct pathways and dishibition of the indirect pathway

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14
Q

Functional Classification Output Nuclei:

A

Globus Pallidus (internal)
Subthalamic Nucleus
Substania Nigra

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15
Q

BG: Functional Connections Step by Step

A

Cerebral Cortex, Thalamus, Limbic System send excitatory information to input nuclei
Information is processed and sent to the intrinsic nuclei
Input Nuclei process & pass info output nuclei
Output Nuclei send info to thalamus
Thalamus relays info to motor cortex

16
Q

Resting State

A

Globus Pallidus Internal inhibits the motor thalamic neurons hence no output to upper motor neurons in the motor cortex

17
Q

Direct Pathway:

A

Reduced Inhibition of Thalamic Neurons
Increased Thalamic Output to Cortex
Increased Motor Cortex Output
Increased Motor Activity in Corticospinal tract
Increased Movement

18
Q

Indirect Pathway

A

Increased Inhibition of Thalamic Neurons
Reduced thalamic Output to Cortex
Inhibition of Motor Cortex
Reduced Motor activity in corticospinal tract
Reduced Movement

19
Q

Role of the Substantia Nigra

A

Turns up the Direct and Turns Down the Indirect
Less Thalamic Inhibition
Increased thalamic Output to Motor Cortex
Increased Activity in the Motor Cortex
Increased Output in the Corticospinal Tract
Increased Movement

20
Q

Motor learning involves what structures?

A

Prefrontal (cognitive)
Head of Caudate Nucleus receives projections from the prefrontal cortex and appears to participate in motor learning

21
Q

Limbic Loop role?

A

giving motor expression to emotions
High in dopamine

22
Q

PD Etiology

A

idiopathic degeneration of the dopamine producing cells in the substantia nigra resulting in reduced dopamine production

23
Q

PD Initial Motor Stages

A

Akinesia
Bradykinesia
Rigidity
Resting tremor
Decreased mm power
Impaired automatic postural responses to position and movement

24
Q

PD: Advanced Motor Manifestations

A

Festinating Gait
Montonous/Weak Voice
Micrographia
Dysphagia

25
Q

PD Non-Motor Symptoms

A

Constipation
Sleep-related Disorders
Erectile Dysfunction
Anosmia

26
Q

PD Stage 1

A

Mild, uni-lateral symptoms which don’t interfere with quality of life

27
Q

PD Stage 2

A

Symptoms worsen become bi-lateral. Daily activities become more difficult and take more to complete

28
Q

PD Stage 3

A

Individual loss balances, move more slowly and falls are common. Ssx impair daily activites

29
Q

PD Stage 4

A

Symptoms are severe: assistance needed for walking and performing daily activities

30
Q

PD Stage 5

A

Individual is unable to walk and needs full time assistance with living

31
Q

PD Diagnosis

A

Clinically no lab tests

32
Q

PD DD’s

A

Alzheimers
Cardio-embolic stroke
Neurological manifestations of vasuclar dementia

33
Q

PD: Treatment/Management:

A

Gold Standard: Levodopa and Carbidopa

34
Q

How long do these medications lasts for?

A

4-6years

35
Q

Mechanism of Levodopa

A

Resembles a dopamine precursor, taken orally crosses the blood-brain barriers. Taken up by dopaminergic and converted to dopamine

36
Q

Levodopa Brand Name:

A

none-
found in combination with carbidopa

37
Q

Mechanism of Action for Carbidopa

A

Doesnt cross the brai barrier, added to levodpa before it crosses the brain.
Reduces the risk of side effects from levodopa such as vommitng and nausea