4.6 Parkinsonism, Movement Disorders & Functional Neurologic Disorder
Key Takeaways
- Parkinsonism is a clinical syndrome of bradykinesia plus tremor, rigidity, or postural instability; idiopathic Parkinson disease shows asymmetric resting tremor, robust levodopa response, and asymmetric onset; atypical parkinsonisms (PSP, MSA, CBD) show early postural instability, poor levodopa response, and atypical features.
- Rehabilitation in Parkinson disease targets freezing of gait, postural instability, falls, hypophonia, and deconditioning through cueing strategies (visual/auditory), LSVT BIG/LOUD, dual-task training, and aerobic exercise (which may modify disease progression).
- Functional neurologic disorder (FND) produces genuine neurologic symptoms not explained by structural disease; diagnosis is one of positive clinical features (inconsistency, internal variability, suggestibility), and management is multidisciplinary CBT/physio, not 'diagnosis of exclusion.'
- Levodopa-related motor fluctuations (wearing off, on-off, dyskinesia) require rehab timing of therapy and gait training around medication cycles.
Parkinsonism, Movement Disorders & Functional Neurologic Disorder
Parkinsonism and movement disorders are Domain C conditions (movement disorders/parkinsonism plus functional neurologic disorder). The physiatrist manages gait, falls, voice, and deconditioning while neurology handles diagnosis and pharmacology.
Parkinsonism: Idiopathic vs Atypical
| Feature | Idiopathic Parkinson Disease | Atypical (PSP, MSA, CBD) |
|---|---|---|
| Onset | Asymmetric | Often symmetric |
| Tremor | Resting, asymmetric | May be absent; action/postural |
| Postural instability | Late | Early falls (PSP especially within first year) |
| Levodopa response | Robust | Poor/minimal |
| Autonomic involvement | Variable | Prominent (MSA: dysautonomia, cerebellar) |
| Progression | Slower | More rapid |
Multiple system atrophy (MSA) features autonomic failure (orthostatic hypotension, urinary) plus parkinsonism or cerebellar signs; progressive supranuclear palsy (PSP) shows vertical gaze palsy and early falls; corticobasal degeneration (CBD) shows asymmetric apraxia and cortical signs.
Rehabilitation in Parkinson Disease
Bradykinesia + Rigidity + Postural Instability ──► Freezing, Falls, Deconditioning, Hypophonia
│
└── Cueing (visual/auditory) + LSVT BIG/LOUD + Aerobic Exercise + Dual-Task Training
- Freezing of gait: external cueing—auditory (metronome, "1-2-3"), visual (laser cane, floor stripes), or mental strategies ("stepping over")—overcomes freezing episodes. Turning is the highest-risk task; train with wider arcs.
- Balance and falls: balance and dual-task training, reactive stepping practice, and tai chi reduce falls; postural instability responds less to levodopa, requiring exercise.
- LSVT BIG / LOUD: intensive, high-amplitude movement and voice programs improve amplitude, gait, and speech intelligibility.
- Aerobic exercise: accumulating evidence suggests disease-modifying potential; aim for moderate-to-vigorous aerobic activity several times weekly.
- Hypophonia/speech: LSVT LOUD and speech therapy.
- Cognition/depression: screen and manage; deep brain stimulation candidates require multidisciplinary assessment.
Levodopa & Motor Fluctuations
Patients on levodopa develop wearing off, "on-off" fluctuations, and dyskinesia. Rehabilitation should time mobility training during the medication "on" state when feasible and educate on wearing-off patterns. Falls may cluster in "off" periods.
Functional Neurologic Disorder (FND)
FND produces genuine neurologic symptoms (motor, sensory, gait, seizures) that are inconsistent with recognized neurologic disease. The modern diagnosis is positive, based on clinical features of internal inconsistency and suggestibility—not exclusion after exhaustive workup:
| Positive FND Signs | Example |
|---|---|
| Hoover sign | Hip extension weakness returns when testing contralateral flexion |
| Tremor entrainment / variability | Tremor frequency tracks tapping task or is distractible |
| Functional (non-epileptic) seizures | No EEG correlate; eyes-closed resistance, pelvic thrusting |
| Gait inconsistency | Walking pattern inconsistent; "knees buckling," without falls |
| Splitting of sensory loss | Sensory pattern non-anatomic, midline-split |
Management is multidisciplinary: an explained, de-stigmatized diagnosis, physiotherapy with movement retraining (graded, expectation-based), cognitive behavioral therapy, and treatment of comorbid depression/anxiety. Outcomes are best when early, active, and coordinated; "diagnosis of exclusion" framing or dismissing symptoms worsens prognosis.
Non-Motor Symptoms & Multidisciplinary Care
Parkinson disease is far more than motor: non-motor symptoms—constipation, orthostatic hypotension, urinary urgency, depression/anxiety, cognitive impairment progressing to dementia, REM sleep behavior disorder, and psychosis—often dominate quality of life and may precede motor onset. Orthostatic hypotension is exacerbated by levodopa and dopaminergic agents; manage with hydration, compression, midodrine/fludrocortisone, and medication review. Psychosis (often visual hallucinations) is treated by reducing dopaminergic/anticholinergic burden and adding pimavanserin or a low-dose atypical antipsychotic (quetiapine), avoiding high-potency agents that worsen parkinsonism.
Exercise as Disease Modification
Accumulating evidence suggests aerobic exercise (and possibly forced, high-intensity cycling and tai chi) may modify disease progression beyond symptomatic benefit, hypothesized through neuroplasticity and neurotrophic mechanisms. Recommendations increasingly favor moderate-to-vigorous aerobic activity, balance training, and skill-based exercise, individualized to capacity and fall risk, sustained long-term.
Deep Brain Stimulation & Rehabilitation Implications
DBS (subthalamic nucleus most commonly) reduces motor fluctuations and dyskinesia but does not improve axial/postural symptoms and may not help cognition. Rehabilitation around DBS includes preoperative cognition screening (dementia is a relative contraindication), postoperative medication adjustments (often reduced levodopa), and gait/balance training. The physiatrist collaborates with neurosurgery and neurology to optimize function and screen for complications (infection, mood changes, stimulation-induced side effects).
FND: Prognostic Factors & Pitfalls
| Favorable Prognostic Factors | Poor Prognostic Factors |
|---|---|
| Short symptom duration | Long symptom duration |
| Acceptance of diagnosis, engagement | Rejection of diagnosis, doctor-shopping |
| Active physiotherapy + CBT | Lack of multidisciplinary treatment |
| Treating comorbid mood/anxiety | Ongoing litigation alone (variable) |
| Identifiable precipitant (injury, stress) | Severe comorbidity / fixed beliefs |
Pitfalls: dismissing symptoms as "imagined" or "not real" worsens outcomes; equally, over-investigating reinforces disease conviction. The diagnosis is communicated with empathy and clarity, framed as a software (functional network) problem rather than absence of illness. Physiotherapy using normal movement retraining, expectation of recovery, and graded exposure is evidence-based; combining with CBT addresses maintaining factors. Co-existing organic disease is common and must be treated alongside the functional overlay.
A 72-year-old presents with symmetric onset of parkinsonism, vertical gaze palsy, and recurrent falls within the first year of symptoms, with minimal levodopa benefit. Which is most likely?
Which rehabilitation strategy is most effective for freezing of gait in Parkinson disease?
A patient develops a gait disorder with knees buckling without falling, a tremor that entrains to a tapping task, and a positive Hoover sign, with normal imaging. Which is most consistent?