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By Craig Brooker, M.D.
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Parkinsonism
Tremor
Myoclonus
Chorea
Tics
Dystonia
Stereotypies
RLS/PLMS
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Idiopathic Parkinson’s Disease
Dementia with Lewy Bodies
Multiple System Atrophy
Progressive Supranuclear Palsy
Corticobasal Degeneration
Vascular Parkinsonism
Post-Traumatic Parkinsonism
Secondary (Toxin, Meds, Metabolic)
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Indian Medicine
~2,500BC: Kampavata
“kampa” (shaking)
“vata” (lack of muscle
movement); tx’d w/
Mucuna plant, has Ldopa in it
1817 James Parkinson
“Essay on Shaking
Palsy”
Tretiakoff 1919 noted
loss of neurons of
substantia nigra
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Usually asymmetric
Cardinal Signs
Tremor (resting, “pill rolling”)
 Rigidity (cogwheel)
 Bradykinesia
 Postural instability/Gait abnormalities
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L-dopa responsive
Later findings: depression, dementia
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Often tremor
Sometimes just poor gait or falls
Usually > 70 yo; 1% of pop > 60yo; Only 4% of
parkinson’s patients dx’d <50yo
Males > females
+ family hx in 25%; 13 different “PARK” genes,
auto dom, recessive, & x-linked
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Exam: Do full neuro exam
(www.NeurologyExam.com)
Also look for decreased eye blinking, mask
face, clumsiness of alternating movement,
bradykinesia, slow talking, hypophonia,
cogwheeling rigidity, micrographia, difficulty
rising without pushing, freezing, stooped
posture, reduced arm swinging, shuffling gait,
en bloc turning, festination/retropulsion, & +
glabellar tap.
Also do tremor exam, expect pill rolling tremor
at rest > posturally or action, usu ok water
pouring (unlikely essential tremor)
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Conservative mgt ok until disability
Dopamine & its agonist:
L-dopa & carbidopa (sinemet); often therapeutic trial
 Ropinirole (Requip)
 Pramipexole (Mirapex)
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Some argue L-dopa sparing treatment early or
<60yo
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“Wearing off” phenomenon: increase
frequency
Decreased efficacy with time: increase dose
Dyskinesias: extra movements
L-dopa has most dyskinesias but is also most
effective
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Deep Brain Stimulation:
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subthalamic nucleus & Globus Pallidus
Only for patients responsive to L-dopa
Will never be more effective than L-dopa
Useful for patients who have SE on L-dopa (e.g. esp
dyskinesias)
Often reserved for those < 70yo or so & good surgical
candidates
Complications:
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Brain surgery
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Bleed
Infections acutely or chronically
Device needs adjustments esp early on, very specialized care
Some still require medications, though usu lesser dose
Can’t get MRIs after DBS
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“Differentiated” by hallucinations, usually
visual
Dementia may occur sooner than PD
Differentiation is somewhat arbitrary
May be L-dopa responsive
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Differentiated from PD:
early Autonomic failure (low BP)
 Poorly responsive to L-dopa
 Cerebellar signs and/or long tract signs
 Often little or no tremor
 Less cognitive problems usually
(Change in nomenclature: MSA now includes ShyDrager Syndrome, Olivo-ponto-cerebellar Syndrome,
and Striato-Nigral Syndrome)
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Differentiated from PD:
Vertical supranuclear palsy with down gaze
abnormalities
 Early falls
 Symmetric bradykinesia & rigidity; usu no tremor
 “pseudobulbar palsy” w/ dysarthria & dysphagia
 Dementia has frontal lobe features
 Poor response to dopamine
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Drugs: antipsychotics, metoclopramide, MPTP
Toxins: CO poisoning, cyanide, organic
solvents, manganese
Trauma: e.g. boxing (Mohammad Ali)
Structural effecting striatonigral pathways
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Hydrocephalus, tumor
Metabolic: Wilson’s, low parathyroid
Infections: encephalitis, PML, toxoplasmosis
Stroke: “vascular parkinsonism”
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Asymmetric but with poor response to L-dopa
Ideomotor Apraxia, Alien limb
Lack of tremor
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Common, usu family history
May start at very young age, but not always
Usu symmetric, postural and/or action
component >> resting
Often with more subtle head, jaw, voice
tremors
May be disabling, often respond to EtOH
No other features of parkinsonism
Tx: Propranolol, primidone; Gabapentin; DBS
(Thalamus)
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Usu symmetric in arms, may involve voice
Generally worse based on environmental
factors (e.g. social situations, stress, anxiety,
stimulants/caffiene, lack of sleep, alcohol
withdrawal, many different medications, etc)
Can otherwise be hard to differentiate from
essential tremor and they are often both
present
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Not a tremor
Sudden, shock-like muscle contractions
Focal, multifocal, or generalized
Usu not rhythmic
Epileptic or non-epileptic
Hypnic jerks (physiological)
Juvenile Myoclonic Epilepsy (pathological)
Anoxic injury
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Chorea: “Dance-like movement”
-excessive spontaneous movements
-irregular, random, brief, and abrupt
-non-repetitive
Usu distal predominance; may disguise in
other voluntary movements
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Causes:
-Post-infectious: Sydenham’s, Group A strep
mimicry; usu 1-8 mo after infection, self-limited
-Huntington’s, MRI: caudate atrophy
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Sx: chorea, psychosis, dementia, death
Dx: genetic testing, CAG repeat >38, autodom
MRI brain: caudate atrophy
Tx: symptomatic
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Chorea: tetrabenazine, neuroleptics
Psychosis: antipsychotics
No known disease modifying therapy
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Semi-voluntary (i.e. suppressible), rapid, nonrhythmic movements and/or sounds
Simple (e.g. blinking, grimacing, coughing) or
complex
May have OCD too
Tourette’s: vocal and motor tics
96% dx by age 11, most resolve by 18yo
Tx: Tetrabenazine to decrease dopamine (or
antipsychotics) or CBT for Tics
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Involuntary muscle contractions that cause
slow repetitive movements or abnormal
postures
E.g. writer’s cramp, cervical dystonia,
blepharospasm, musicians; Focal, generalized,
Usu idiopathic, rarely DYT1 or 2ndary
Tx: botox, Benztropine (anti-Ach), dopamine
sometimes useful, benzos; occasionally DBS
(Gpi)
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Repetitive, purposeless movements (no urge
unlike tics)
Mostly peds; esp with autism, MR,
Common: head nodding, rocking, arm
flapping, etc.
Etiology: believed psychological, self
reward/stim
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4 criteria for dx:
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Unpleasant sensation(“creeping, crawling, pulsing”)
Urge to move legs
Worse at night (while awake) or at rest
Improved by movement
Reversible causes: low ferritin (<50mg/dl),
SSRIs
Other causes: hereditary, idiopathic, 2ndary to
neuropathy
Tx: dopamine agonists, gabapentin
Complications: dopamine agonists (augmentation)
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Involuntary movements of legs during sleep
May be comorbid with RLS
Debatable as to whether it causes excessive
daytime sleepiness (EDS) unto itself
Not usually treated unless no other cause for
EDS can be found & patient is desperate
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Often a 1st sign of Parkinson’s
Incomplete loss of tone during REM
Classically, acting out dreams (usu being
chased or fighting)
Men > women
Diff Dx: “Pseudo-RBD” (i.e. OSA), 2ndary RBD
(SSRIs, EtOH withdrawal, sedative
withdrawal)
Tx: padded sleep environment, correct 2ndary
causes, consider clonazepam, gabapentin
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