4.6 Parkinsonism, Movement Disorders & Functional Neurologic Disorder

ABPMR Physical Medicine and Rehabilitation Board Exam Study Guide Exam

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1 Chapter 1: Introduction & Exam Overview

1.1 ABPMR Part I Exam Overview & Format 1.2 Board Review Strategy & Content Blueprint Breakdown

2 Chapter 2: Musculoskeletal Medicine

2.1 Shoulder & Upper Extremity Diagnostics 2.2 Knee, Hip & Lower Extremity Conditions 2.3 Spine Pathology, Radiculopathy & Myelopathy 2.4 Inflammatory Arthritis, Tendinopathies & Concussion 2.5 Bone Health, Osteoporosis & Metabolic Bone Disease 2.6 Thoracic Outlet Syndrome & Peripheral Nerve Entrapment 2.7 Fracture Rehabilitation & Immobilization Complications 2.8 Overuse Tendinopathies & Regenerative Medicine 2.9 Gait Analysis & Abnormal Gait Patterns

3 Chapter 3: Spinal Cord Injury Rehabilitation

3.1 ASIA Examination & Impairment Scale 3.2 Spinal Cord Injury Syndromes 3.3 Autonomic Dysreflexia & Acute Complications 3.4 Neurogenic Bladder, Bowel & Secondary Complications

4 Chapter 4: Stroke & Neuromuscular Rehabilitation

4.1 Stroke Vascular Syndromes & Acute Assessment 4.2 Stroke Motor Recovery & Hemiplegic Complications 4.3 Spasticity Assessment & Multimodal Management 4.4 ALS, GBS, CIDP & Neuromuscular Disease Rehab 4.5 Multiple Sclerosis & Demyelinating Disease Rehabilitation 4.6 Parkinsonism, Movement Disorders & Functional Neurologic Disorder

5 Chapter 5: Electrodiagnostics (EMG/NCS)

5.1 Nerve Conduction Studies Principles & Physics 5.2 Needle Electromyography & MUAP Analysis 5.3 Mononeuropathies & Radiculopathy Patterns 5.4 Neuromuscular Junction Disorders & Myopathies

6 Chapter 6: Traumatic Brain Injury

6.1 TBI Severity Classification, Glasgow Coma Scale, and Pathophysiology 6.2 Rancho Los Amigos Levels of Cognitive Functioning and Disability Rating Scale 6.3 Neurobehavioral Sequelae and Agitation Management 6.4 Concussion Evaluation, Vestibular-Ocular Dysfunction, and Return-to-Play/Work Protocols

7 Chapter 7: Chronic Pain & Interventional Spine

7.1 Fluoroscopic Spine Interventions 7.2 Opioid Stewardship & Controlled Substance Compliance 7.3 Complex Regional Pain Syndrome, Fibromyalgia & Myofascial Pain 7.4 Spinal Cord Stimulation & Intrathecal Therapy

8 Chapter 8: Amputee Rehabilitation & Prosthetics

8.1 Amputation Surgical Levels & Medicare K-Levels 8.2 Socket Designs & Suspension Systems 8.3 Prosthetic Feet & Microprocessor Knee Mechanisms 8.4 Post-Amputation Care, Residual Limb & Phantom Pain

9 Chapter 9: Pediatric Rehabilitation

9.1 Cerebral Palsy Classification & GMFCS 9.2 Spina Bifida & Myelomeningocele Management 9.3 Muscular Dystrophies & Neuromuscular Disease in Children 9.4 Pediatric Brachial Plexopathy & Congenital Disorders

10 Chapter 10: Prosthetics, Orthotics & Assistive Technology

10.1 Lower Limb Orthoses — AFOs & KAFOs 10.2 Spinal & Upper Extremity Orthoses 10.3 Upper Limb Prosthetics — Body-Powered vs Myoelectric 10.4 Wheelchairs, Seating Systems & Pressure Mapping

11 Chapter 11: Medical Rehabilitation & Outcomes

11.1 Dysphagia Assessment & Management 11.2 Neurogenic Bladder & Bowel Management 11.3 Pressure Injuries & Wound Management 11.4 Outcome Measures & Medical Complications 11.5 Cancer Rehabilitation & Oncologic Rehabilitation 11.6 Burns, Endocrine/Metabolic & Medical Complications Rehabilitation

12 Chapter 12: Cardiopulmonary Rehabilitation

12.1 Cardiac Rehabilitation Phases & Metabolic Equivalents 12.2 Pulmonary Rehabilitation & COPD Management

13 Chapter 13: Foundational Rehabilitation Concepts

13.1 Kinesiology, Biomechanics & Functional Anatomy 13.2 Rehabilitation Pharmacology & Medication Management 13.3 Research Methodology, Biostatistics & Evidence-Based Practice 13.4 Nutrition, Metabolism & Energy Expenditure in Rehabilitation 13.5 Diagnostic Procedures: Imaging, MSK Ultrasound, Urodynamics & Neuropsych Assessment

4.6 Parkinsonism, Movement Disorders & Functional Neurologic Disorder

Key Takeaways Explain This Topic AI

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.

Last updated: July 2026

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.