Clincial Correlation: Movement Disorders

Parkinson’s

occurs at any age, but highest in 50/60s

;

Hallmarks for disease:

RESTING tremor -pill rolling tremor

Bradykinesia (slowness of mvmt, absence of automatic mvmts)

Rigidity

Loss of postural reflexes

most affected side has a reduced arm swing

don’t swallow saliva well-can drool-produce a normal amount just can’t swallow what have

;

Pathology of Parkinson’s

loss of dopaminergic neurons in the substntia nigra (motor)

Loss of cholinergic neuorns in cortex (cognitive)

Loss of cholinergic neurons in brainstem (postural loss)

Loss of serontonergic neurons in brainstem (affective)

Parkinson’s treatment

aim is to replace dopamine for motor symptoms

;

1. Dopamine itself doesn’t cross BBB

2. A precursor of dopamine, L-DOPA does cross BBB

3. Most of orally administered L-DOPA is decarboxylated to dopamine outside the BBB

4. Orally administered L-DOPA can be combined with a DOPA decarboxylase inhibitor

New treatment for Parkinson’s

1. Fetal mesencephaic tissue transplantation

2. Deep brain stimulation of STN or GP

3. New drugs involved in catabolism of L-DOPA

4. Trophic factors ; anti-apoptotic agents

;

Gait freezing: tx: turn automatic function into a voluntary fx–> i.e. shine a light on ground-have step over line-makes it a voluntary task

Parkinson’s Etiology
combo of environmental (agrichemicals) and genetic factors (suspectible genes)

 

Chorea

definition: relatively rapid non-sterotypic mvmt that flows from one body part to another

 

Most common cause=Huntington’s disease

 

distally pre-dominant

Ballism

chorea that affects the proximal extremities & is of large amplitude

 

 

Hemiballism or Hemichorea
ballism/chorea affecting one side of the body
Chorea pathology

lesion in Subthalamic nucleu

 

 

Huntington’s Disease

autosomal dominant (with age dependent onset)

 

Genetics: have an expanded trinucleotide repeat

 

 

Huntington’s disease patholgy
initial degeneration of enkephalin/GABA medium spiny stiral neurons that project to GPe
Huntington’s disease clincial features

1. typical onset after child-bearing years

2. generalized chorea

3. dementia

4. pre-symptomatic diagnosis possible

Dystonia

definition: twisting (around an axis) slwo & sustained abnormal mvmts of trunk & extremities or cranial musculature

 

variety of lesions in CNS and PNS can cause-most common=PUTAMEN LESION

 

 

Idiopathic Torsion Dystonia (DYT1 dystonia)

an example of generalized dystonia

 

-autosomal dominant

-defect gene (DYT) is on chromosome 9

-Genetic abnormality is a trinucleoitide (GAG) deletion

-Pentrance of the gene is much less in comparison to Huntington’s diesease

-No clear CNS structural abnormality

-Pallidal stimulation may improve

RNA interference to silence the abnormal gene is being researched

Dystonia clinical features

Begins in childhood

 

Lower extremities affected first

 

generatlization ultimately occurs

Tardive dyskinesia & akanthisia are mvmt disorders caused by the use of dopamine-blocking agents-Pathology=

no strucutral CNS abnormality

 

is the result of aberrations of receptor function

Clincal Features of Tardive Dyskinesias
involuntary mvmts of tongue & mouth
Clincial features of Akanthisia

is an incessant desire to keep in motion

 

movements consist of= fidgeting, marching in place, moving the extremities, speaking incessantly

 

induced by Dr-results from med

Tyrettes

starts in childhood

 

overtime ticks change, but at nay time they are the same

 

to be diagnosed-must have phonic AND motor ticks

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