IM19.3-6 | Movement Disorder Clinical Evaluation — Summary & Reflection

KEY TAKEAWAYS

The structured clinical evaluation of movement disorders is a six-component procedural skill:

1. History — onset/progression (mode: acute/subacute/insidious), precipitating/aggravating/relieving factors (rest vs action, alcohol, sensory tricks, levodopa), associated symptoms (cognitive, psychiatric, autonomic, sleep, systemic), drug history (DRBAs), family history
2. General observation — gait on entry, posture, facial expression, spontaneous movements before formal examination
3. Tone — lead-pipe rigidity (velocity-independent) vs cogwheel (lead-pipe + tremor); Froment's manoeuvre to sensitise; contrast with spasticity (velocity-dependent, clasp-knife)
4. Bradykinesia — finger tapping (fatiguing is pathognomonic), hand movements, pronation-supination, foot tapping; score with MDS-UPDRS Part 3
5. Tremor characterisation — activation (rest/postural/intention), frequency, amplitude, distribution, modifying factors
6. Gait and postural stability — shuffling, reduced arm swing, en bloc turning, pull test

Rating scales: MDS-UPDRS Part 3 (parkinsonism), AIMS (tardive dyskinesia), BFMDRS (dystonia), Hoehn and Yahr (PD staging)

Diagnostic formulation = anatomical location + nature of process + probable cause:
- Hypokinesia + rigidity + rest tremor → nigrostriatal pathway → neurodegenerative (PD), drug-induced (DRBA), vascular, Wilson's
- Chorea → striatum/GPi → Huntington's (dominant, CAG), Sydenham's (post-streptococcal), drug-induced, metabolic
- Focal dystonia + sensory trick → motor circuit, focal → botulinum toxin
- Asymmetric PD onset → idiopathic; symmetric with DRBA exposure → drug-induced; early falls + vertical gaze palsy → PSP
- Young patient with movement disorder + liver disease → Wilson's disease (slit-lamp + ceruloplasmin + 24-h urine copper)

REFLECT

Reflect on the progression from information-gathering to formulation in Scenario A (Parkinson's disease formulation). You assembled approximately 12 distinct clinical findings (tremor quality, fatiguing finger tapping, cogwheel rigidity, micrographia, gait, postural stability, facial expression, blink rate, speech, asymmetry, duration, drug history) and synthesised them into a single anatomical-aetiological formulation. How did each piece of data contribute to excluding alternative diagnoses — and what would have changed the formulation if he had also had early falls from year 1, or if his tremor was purely postural? Now think about the role of the sensory trick in Scenario C. Why does touching the chin relieve cervical dystonia, and what does this phenomenon tell you about the pathophysiology of dystonia (maladaptive sensory-motor integration) — and why does the same trick not work for Parkinson's tremor? The answers lie in the differential circuit involvement of dystonia vs parkinsonism.