Clincial Correlation: Movement Disorders


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)


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)



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


Most common cause=Huntington’s disease


distally pre-dominant


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


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


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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