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Movement Disorders

Neurology

QuestionAnswer
Action tremor: Most common; arise when attempting to maintain a fixed position; frequency is 7-13 Hz; Essential or physiologic
Essential tremor = resembles slower frequency physiologic tremor; essential or familial (auto dom); common in later life; extremities, head (titubation), or voice
Drug causes of physiologic tremor Amphetamines, theophylline, lithium and valproate.
Essential tremor Tx Firstline: BB: propranolol 60-240mg/day (CI in COPD; asthma; DM; bradycardia; AV conduction probs); Primidone 50/day - 125 TID (effective but sedating); Alprazolam for anxiety related; EtOH: temporary suppression
Ataxic (intention) tremor Absent at rest/start of movement; dysmetria
Ataxic tremor: Causes: Dz of cerebellum / connections (MS; tumors; infarct; ethanol-induced cerebellar degeneration)
Ataxic tremor: Tx: Meds usu ineffective; Weights; surgical lesions of ventrolateral thalamus may be effective in severe cases
Athetosis: slow writhing purposeless movements usu involving hands, tongue & face; usu in kids w/ cerebral palsy or result of kernicterus or hypoxia (poss later in life d/t hypoxia)
Chorea: Sx Involuntary, irregular jerky movements; can cause continuous movements.
Chorea: may be due to: untreated strep infxn (Sydenham chorea), PG (chorea gravidarum) or Huntington dz
Tics onset 2-13 yrs; tx Haldol/pimozide
Hemiballismus Violent flinging movements; Unilateral hemiballismus usu d/t infarct in contralateral subthalamic nucleus of Luys
Myoclonus = Shock-like contraction of a group of mx; irreg in rhythm/amplitude; may involve restricted grp mx or be generalized.
Myoclonus may result from: anoxic damage, spinal cord injury, uremia, hepatic encephalopathy or other rare neuro syndromes
Myoclonus Tx Clonazepam, Valproate (Both have limited efficacy)
Dystonia: Maintenance of a persistent extreme posture in one or more joints.
Generalized dystonia: dystonia musculorum deformans; a rare hereditary dystonia
Focal dystonias: torticollis (dystonia of the neck), writer's cramp & blepharospasm (dystonia of the mx’s involving eye closure).
Dystonia: Tx Botox injxn increasingly common & helpful; Surgical tx (torticollis) also available; Medical tx (benzos, anticholinergics, neuroleptics) generally unsatisfactory
Parkinson dz: epidemiology 500,000 in US; onset 40-70 yo; M=F
Parkinson dz: Sx Unilateral onset. Rest tremor/3-6 hz; pill rolling; cogwheeling; rigidity; bradykinesia; difficulty initiating movement. Masked facies; stooped posture, shuffling or festinating gait. Diminished postural reflexes & eye blinking rate. Micrographia
Parkinson dz: Pathology Degeneration & loss of pigmented cells in nigrostriatal pathway, raphe nuclei, locus ceruleus & motor nucleus of vagus; dramatic loss of DA-containing neurons
L-DOPA 80% of pts improve; Sinemet treats akinesia & is less effective in treating tremor.
L-DOPA MOA precursor of DA (which cannot cross BBB; L-DOPA can)
Dopamine agonists (Parlodel, Mirapex, Requip) MOA Act like DA; direct DA effect on striatal neurons; may allow for reduction in dose of Sinemet required & may decrease on-off phenomena
Amantidine MOA May increase DA release from presynaptic storage site at nerve terminals; weakly effective
Anticholinergic drugs (Artane, Cogentin) MOA: May be more effective for tx of tremor; AE = confusion, constipation, dry mouth, urinary retention
Selegiline MOA inhibits monoamine oxidase type B
Cabergoline MOA inhibits COMT
Huntington Dz presentation AD, onset 30-50 yo; Sx often begin w/ psych disorder (immaturity, impulsivity, depression); later apathy & dementia; Chorea, Athetosis; butterfly ventricles (caudate atrophy)
Huntington chorea due to: Decreased activity of acetylcholine & GABA neurons; increased activity of dopaminergic neurons
Huntington Tx For sx reduction only. Tetrabenazine or amantadine 25 TID for chorea. DA receptor blockers (haloperidol) for behaviors/dyskinesias; clozapine
Wilson dz Auto rec; onset 2nd-3rd decades; first sx: hepatic dysfn/cirrhosis; tremor/ bradykinesia, dysarthria, dysphagia; limbs rigid, facial mx fixed empty smile; arms: wing-beating tremor; Kayser-Fleischer (deep cornea)
Wilson: labs Serum ceruloplasmin (Cu carrying pro) very low; urine Cu high
Wilson: patho logy CNS changes: brownish discoloration of some basal ganglia; proliferation of protoplasmic astrocytes (Alzheimer Type II cells)
Wilson: Tx Should begin before neuro Sx onset; early tx prevents neuro sequela devt; eat low Cu foods; sulfurated potash with meals (prevent Cu absorption); chelator (d-penicillamine) to remove absorbed Cu
Wilson dz: Tx: foods to avoid liver; chocolate; mushrooms; shellfish; nuts
Tardive dyskinesia: cause Iatrogenic d/t LT neuroleptic tx (esp Haldol; also atypicals, poss metoclopramide, amphetamines, L-dopa); may be result of DA receptor supersensitivity
Tardive dyskinesia: Sx Abnormal BLM (tongue thrusting & chewing); head movements (turning & bobbing); poss also abnormal limb movements; Sx can fluctuate & may take mos-yrs to resolve (sometimes permanent)
Tardive dyskinesia: Tx stop the offending drug; many tx tried w/ marginal success
Tardive dyskinesia: most successful tx: achieved with DA-depleting agents (tetrabenazine); also Vitamin E?
Excess DA results in: dyskinesia and chorea
Dopamine deficiencies cause: Parkinsonian-like symptoms
Action of acetylcholine & DA: Act in opposite directions; adding DA is equivalent to blocking acetylcholine
CJD Sx usu later in life; rapidly progressive dementia, myoclonus, ataxia & somnolence; epileptiform pattern on EEG
MS epidemiology F>M; 350K in US (1M world); onset 20-40 yo; most present w/relapsing form; prevalence increases with distance from equator
MS S/S Optic (retrobulbar) neuritis; Transverse myelitis; Paresthesias; Ataxia; Weakness or incoordination; Spasticity; Cognitive impairment
MS: MRI findings multiple characteristic lesions or plaques: periventricular or subcortical U-fibers, corpus callosum lesions
MS: CSF findings evidence of oligoclonal bands or increased IgG index
MS: types of dx criteria Schumacher; Poser: Macdonald
MS: Goals of tx Tx whole dz; slow accumulation of disability; Reduce relapse rate & CNS inflam (lesions) & progression of brain atrophy (shrinkage); improve pt QOL (including cognitive)
MS Tx options Beta-interferon; SQ glatiramer; poss immunosupp adjuncts for aggressive/ breakthrough; corticosteroids (methylprednisolone) for relapse
Forms of MS: relapsing-remitting, primary progressive, secondary progressive
Tourette etiology / pathology Auto dominent; can be presentation of Wilson dz. Onset usually 2-15 yo
Recurrent episodes of vision change, diplopia, weakness & tingling in extremities that resolve MS
CJD S/S usu later in life; rapidly progressive dementia, myoclonus, ataxia & somnolence; epileptiform pattern on EEG
MS S/S Optic neuritis; Transverse myelitis; Paresthesias; focal neuralgia; Ataxia; Weakness/ incoordination; Spasticity; Cognitive impairment
Lhermitte’s sign = electrical sensation down body w/ neck flexion; seen in MS
MS pathophys immuno d/o assoc w/CNS Ig prodn & T-lymph alteration; poss viral etio
MS pattern of sxs affect multiple areas over time (if they don't, prob not MS)
Ataxic (intention) tremor Absent at rest/start of movement; dysmetria; Dz of cerebellum / connections (MS; tumors; infarct; ethanol-induced cerebellar degeneration)
Dystonia: Maintenance of a persistent extreme posture in one or more joints.
Focal dystonias: torticollis, writer's cramp, blepharospasm; tx Botox / surg
Huntington Dz presentation AD, varying age of onset; Sx often begin w/ psych disorder (immaturity, impulsivity, depression); later apathy & dementia; Chorea, Athetosis; butterfly ventricles (caudate atrophy)
Huntington chorea due to: DA excess state
Wilson dz Auto rec; onset 2nd-3rd decades; first sx: hepatic dysfn/cirrhosis; tremor/ bradykinesia, dysarthria, dysphagia; limbs rigid, facial mx fixed empty smile; arms: wing-beating tremor; Kayser-Fleischer (deep cornea)
Wilson: patho CNS changes: brownish discoloration of some basal ganglia; proliferation of protoplasmic astrocytes (Alzheimer Type II cells)
Tardive dyskinesia: Sx Abnormal BLM (tongue thrusting & chewing); head movements (turning & bobbing); poss also abnormal limb movements; Sx can fluctuate & may take mos-yrs to resolve (sometimes permanent)
Tardive dyskinesia: most successful tx: achieved with DA-depleting agents (tetrabenazine); also Vitamin E?
Action of acetylcholine & DA: Act in opposite directions; adding DA is equivalent to blocking acetylcholine
RLS can be primary, or secondary to: periph neuropathy, uremia, PG, Fe def
ALS: Dx criteria UMN & LMN sx in 3 regions; UMN: clinical; LMN: EMG; CK nml or high
Primary lateral sclerosis: path degeneration of lateral corticospinal tract
Primary lateral sclerosis clin findings usu legs before arms; leg weak/stiff; spasticity; ave duration >8 yrs; many pts develop LMN sx & transition to ALS
progressive muscular atrophy pure LMN dz; slower progress than ALS; often spares bulbar mx; CK very high
Wilson manifestations: hepatolenticular degen (impaired ceruloplasmin synth); presents in teen years (hepatitis); tremor, dysarthria, slow, hoarse, chorea
Parkinson: TRAP = Tremor, Rigidity, Akinesia, Postural instability
Most common genetic form of Parkinson: PARK8
Progressive demyelinating; brain, sp cord, optic n.; viral; F>M, peak 20-40yo MS
Entacapone is tx for: Parkinson dz
Entacapone side effect brown urine
Damaged areas in ALS corticospinal tracts, anterior horn cells, bulbar motor nuclei
Created by: Abarnard