Basal Ganglia Dysfunction Flashcards
Function of the Basal Ganglia
Critical link b/w the idea of movement and the expression of movement
Indirect influence on motor action before the initiation of movement
Role in:
- Movement/Posture
- Perception and cognition
Function of BG in movement and posture
- Movement initiation and preparation
- Movement taht occur without external cues
- Movement execution time
- Response set
- Postural adjustment before distal movements
Role of BG in perception/Cognition
- Sensory integration
- spatial perception interpersonal/intrapersonal space
- behavior flexibility
- procedural learning (habits)
- complex learned tasks
Basal Gagnglia contains how many brain stem nuclei?
5
Dysfunction of the substantia nigra will lead to ________________
PD
Dysfunction of Caudate/Putamen will lead to _______________
HD
input/out of BG
input: cortex
output: thalamus
Name of the Pathways used by the BG to perform its function & function of each
Direct Pathway: thalamic excitation
Indirect Pathway: thalamic inhibition
Normal Function of the BG
Balance b/w Direct/Indirect Pathways
with thalamic disinhibition => cortical excitation
subthalamic disinhibition => decreased cortical excitation
Lesion of the direct pathway will lead to:
- loss of net thalamic excitation
- indirect pathway intact (thalamic inhibition)
- net effect: cortical inhibition
- ex: PD
Lesion of the Indirect pathway will lead to:
- Loss of net thalamic inhibition
- Direct pathway still intact: thalamic excitation
- net effect cortical excitation
- ex: HD, chorea, athetosis
Lesions of the BG will lead to
dyskinesia
no dysfunction of UMN/LMN systems (no paralysis or sensory changes)
no loss of will or knowledge needed to perform motor acts (they still know how to do something, but bdoy won’t cooperate)
Hypokinesia
lack of spontaneity
slowing of voluntary movements
Hyperkinesia
Involuntary spontaneous movements (chorea, ballismus, Tics, Athetosis)
example of Tics
Clearing throat all the time
eye twitch
Clinical Presentation of Bradykinesia
- fixed posture
- absent blink
- absent facial expression, gaunt
- no arm swing
- decreased gait speed, step length, cadence
- Drooling (end stage)
Cause of Pathology of BG
Primarily d/t deficity of specific neuronal cell death and resultant loss of neurotransmitters
Parkinson’s Disease vs Parkinsonism Syndrome
PD:
start out unilateral, rule everything else out, benefit from dopamine meds.
Parkinsonism syndrome:
Bilateral head trauma, don’t benefit from dopamine meds
Huntington Disease:
What happen?
causes?
Pathology
Gross wasting of caudate and putamen nuclei
loss of neurons in cerebral cortex (lead to dementia)
Etiology:
Mutation of huntington gene on chromosome 4
Autosomal dominant
Presentation of HD
Onset b/w 30-50 y.o.
First signs: Personality changes (aggression, withdrawal, short temper), dementia
Choreiform movements
late stage athetosis or dystonia
death in 10-15 years
Role of PT with HD patient during Early stages
Preventative/health and wellness (fall prevention/environment mods)
Restorative (balance training, core stability, HEP)
overall goal: Delay onset of mobility restriction
Role of PT with HD during middle stage
Preventative: Falls prevention and safety
Restorative: maintain mobility, core stability, ROM, amb/adl training, aquatics
Compensatory: home mods/AD (usually more of a hazard)
Overall Goal: maintain function/delay deterioration
Role of PT with HD during late stage
Restorative: ROM/postural exercises, chest PT
Compensatory: seating systems to maximize posture/comfort (dec. skin breakdown)
overall goal: limit impact of complications, education geared toward family member b/c patient can’t understand
outcome measures used with HD patients
DGI
TUG
6MWT (how many LOB)
Patient functional scale
ABC scale
