PM&R

01 Neuroanatomy for Rehabilitation

A thorough understanding of motor and sensory neuroanatomy is the foundation of PM&R practice. Localizing lesions to upper motor neuron (UMN) versus lower motor neuron (LMN) pathways, understanding dermatomes and myotomes, and recognizing spinal cord tract organization are essential for accurate diagnosis, prognosis, and rehabilitation planning across stroke, spinal cord injury, traumatic brain injury, and peripheral nerve disorders.

Motor Pathways

The corticospinal tract (CST) is the primary motor pathway. It originates from the primary motor cortex (Brodmann area 4), premotor cortex (area 6), and supplementary motor area. Axons descend through the corona radiata, posterior limb of the internal capsule, cerebral peduncles, basis pontis, and medullary pyramids. At the cervicomedullary junction, ~85% of fibers decussate (pyramidal decussation) to form the lateral corticospinal tract, which controls voluntary distal limb movements contralaterally. The remaining ~15% continue ipsilaterally as the anterior corticospinal tract, controlling axial/proximal muscles bilaterally. The rubrospinal tract assists with upper extremity flexor tone. The reticulospinal tracts (pontine and medullary) modulate muscle tone, posture, and locomotion — pontine reticulospinal facilitates extensors; medullary reticulospinal facilitates flexors. The vestibulospinal tract maintains upright posture and balance via extensor facilitation.

Sensory Pathways

The dorsal column–medial lemniscus (DCML) pathway transmits proprioception, vibration, and fine (discriminative) touch. First-order neurons enter the spinal cord and ascend ipsilaterally in the fasciculus gracilis (lower body, below T6) and fasciculus cuneatus (upper body, above T6) to synapse in the medulla (nucleus gracilis and cuneatus). Second-order neurons decussate as the internal arcuate fibers and ascend in the medial lemniscus to the ventral posterolateral (VPL) nucleus of the thalamus. Third-order neurons project to the primary somatosensory cortex (S1, Brodmann areas 3, 1, 2). The spinothalamic tract (STT) transmits pain, temperature, and crude touch. First-order neurons synapse in the dorsal horn (laminae I, II, V); second-order neurons decussate within 1–2 spinal levels via the anterior white commissure and ascend contralaterally to the VPL thalamus.

UMN vs LMN Lesions

Dermatomes & Myotomes — Key Levels

02 Musculoskeletal Anatomy Essentials

PM&R physicians must understand musculoskeletal anatomy as it relates to functional impairment, biomechanics, and rehabilitation planning. Key areas include the shoulder complex, spine, hip, knee, and hand/wrist — the most common sites of musculoskeletal complaints encountered in rehabilitation practice.

Shoulder Complex

The shoulder has the greatest range of motion of any joint, achieved through four articulations: glenohumeral (primary), acromioclavicular, sternoclavicular, and scapulothoracic. The rotator cuff consists of four muscles: supraspinatus (abduction initiation, most commonly torn, suprascapular nerve C5–C6), infraspinatus (external rotation, suprascapular nerve C5–C6), teres minor (external rotation, axillary nerve C5–C6), and subscapularis (internal rotation, upper/lower subscapular nerves C5–C7). The mnemonic SITS captures the four muscles. The subacromial space is bounded superiorly by the acromion and coracoacromial ligament; narrowing causes impingement syndrome.

Spinal Anatomy

The vertebral column consists of 7 cervical, 12 thoracic, 5 lumbar, 5 fused sacral, and 3–4 coccygeal vertebrae. The intervertebral disc has an inner nucleus pulposus (gelatinous, high water content, shock absorption) and outer annulus fibrosus (concentric collagen lamellae). Disc herniations typically occur posterolaterally where the annulus is thinnest (posterior longitudinal ligament reinforces midline). In the lumbar spine, the L4–L5 and L5–S1 levels account for >90% of disc herniations. The spinal cord terminates as the conus medullaris at L1–L2 in adults; below this, the cauda equina (nerve roots L2–S5) traverses the thecal sac.

Brachial Plexus

The brachial plexus (C5–T1) is organized as: Roots → Trunks (upper C5–C6, middle C7, lower C8–T1) → Divisions (anterior and posterior) → Cords (lateral, posterior, medial — named by position relative to the axillary artery) → Branches (terminal nerves). Key terminal branches: musculocutaneous nerve (lateral cord → biceps, brachialis), axillary nerve (posterior cord → deltoid, teres minor), radial nerve (posterior cord → triceps, wrist/finger extensors), median nerve (lateral + medial cord → forearm flexors, thenar muscles), ulnar nerve (medial cord → intrinsic hand muscles, FDP to ring/small fingers).

Lumbosacral Plexus

The lumbar plexus (L1–L4) gives rise to the femoral nerve (L2–L4: quadriceps, hip flexion, knee extension, anterior thigh sensation) and obturator nerve (L2–L4: hip adductors, medial thigh sensation). The sacral plexus (L4–S3) gives rise to the sciatic nerve (the largest nerve in the body), which divides into the tibial nerve (plantarflexion, toe flexion, sole of foot sensation) and common peroneal (fibular) nerve (dorsiflexion, eversion, lateral leg and dorsum of foot sensation). The common peroneal nerve is highly vulnerable at the fibular head; injury causes foot drop.

03 The PM&R Evaluation & ICF Model

The PM&R evaluation is unique among medical specialties in its focus on function rather than solely on disease. The International Classification of Functioning, Disability, and Health (ICF), adopted by the World Health Organization in 2001, provides the conceptual framework that underlies all rehabilitation assessment and planning.

ICF Framework

Historical Terminology (Nagi Model / ICIDH)

The older Nagi model used related but distinct terms: Pathology (underlying disease) → Impairment (loss of function at organ level, e.g., weakness) → Functional Limitation (restriction in performing an activity, e.g., cannot walk) → Disability (inability to fulfill social role, e.g., cannot work). The WHO ICIDH (1980) used Impairment → Disability → Handicap. The ICF replaced this linear model with a biopsychosocial, interactive framework.

Functional Assessment

The PM&R evaluation systematically assesses: mobility (bed mobility, transfers, ambulation, wheelchair skills, community mobility), self-care (feeding, grooming, bathing, dressing upper/lower body, toileting), communication (expression, comprehension, reading, writing), cognition (orientation, attention, memory, problem-solving, safety awareness), psychosocial (adjustment, mood, motivation, social interaction), and vocational/avocational (work capacity, leisure, driving). Standardized outcome measures (FIM, Barthel Index, etc.) quantify these domains and track progress.

Rehabilitation Settings

04 Key Terminology & Abbreviations

Core PM&R Terminology

Essential Abbreviations

Manual Muscle Testing (MMT) Scale

05 Stroke Syndromes & Deficits

Stroke is the leading cause of adult disability and the most common diagnosis in inpatient rehabilitation facilities. Recognizing the vascular territory involved predicts the pattern of deficits and guides rehabilitation planning. Each stroke syndrome produces a characteristic constellation of motor, sensory, visual, language, and cognitive impairments.

Major Stroke Syndromes

Lacunar Stroke Syndromes

Lacunar infarcts are small (<15 mm) subcortical strokes caused by lipohyalinosis of small penetrating arteries, most commonly in the basal ganglia, thalamus, internal capsule, and pons. They account for ~25% of ischemic strokes.

06 Acute Stroke Rehab & Motor Recovery

Acute Rehabilitation Criteria

Stroke patients are candidates for inpatient rehabilitation facility (IRF) admission when they are medically stable, can tolerate at least 3 hours/day of multidisciplinary therapy (PT, OT, and often SLP), have identifiable functional goals, and require physician supervision. The IRF-PAI (Patient Assessment Instrument) documents admission function using Section GG (self-care and mobility items). CMS requires that 60% of IRF patients have qualifying diagnoses (the "60% rule"), including stroke as one of the 13 qualifying conditions.

Brunnstrom Stages of Motor Recovery (1–7)

The Brunnstrom stages describe the stereotyped sequence of motor recovery following stroke, from flaccidity through synergy patterns to isolated voluntary movement:

Post-Stroke Shoulder Pain

Hemiplegic shoulder pain affects 30–70% of stroke patients and is a major barrier to rehabilitation. Common causes include: subluxation (due to flaccid deltoid/rotator cuff muscles, gravitational pull on the humerus — most common early post-stroke), spasticity (subscapularis and pectoralis spasticity causing internal rotation/adduction contracture), adhesive capsulitis (frozen shoulder from immobility), complex regional pain syndrome (CRPS) type I (previously shoulder-hand syndrome — pain, edema, autonomic changes), rotator cuff injury, and brachial plexopathy. Management includes positioning (support the arm on a lapboard or armrest), ROM exercises, shoulder slings (controversial — may limit function), suprascapular nerve block, and spasticity treatment.

Stroke Rehabilitation Evidence-Based Interventions

Key evidence-based approaches include: constraint-induced movement therapy (CIMT) — restraining the unaffected limb to force use of the paretic limb for 6+ hours/day (requires some wrist/finger extension); body-weight-supported treadmill training; functional electrical stimulation (FES) for dorsiflexion and wrist extension; robotic-assisted therapy; mirror therapy for improving motor function and reducing pain/neglect; and task-specific repetitive practice (highest level of evidence for motor learning).

07 Spasticity Management

Spasticity is defined as a velocity-dependent increase in tonic stretch reflexes resulting from UMN lesion, manifesting as increased resistance to passive stretch. It is one of the most common and functionally limiting sequelae of stroke, SCI, TBI, MS, and cerebral palsy. Spasticity can be functionally helpful (aids standing/transfers in SCI) or harmful (causes pain, contracture, impaired hygiene, positioning difficulties).

Modified Ashworth Scale (MAS)

Oral Antispasticity Medications

Botulinum Toxin for Spasticity

Botulinum toxin (onabotulinumtoxinA [Botox], abobotulinumtoxinA [Dysport], incobotulinumtoxinA [Xeomin]) blocks acetylcholine release at the neuromuscular junction, producing focal, reversible chemodenervation. Onset 3–7 days, peak effect 2–6 weeks, duration 3–6 months. Injection is guided by EMG, electrical stimulation, or ultrasound. Maximum total dose of onabotulinumtoxinA per treatment session is typically 400–600 U. Common upper extremity targets: biceps (100–200 U), brachialis (50–100 U), brachioradialis (50–100 U), flexor carpi radialis (25–100 U), flexor carpi ulnaris (25–75 U), flexor digitorum superficialis (25–75 U per head). Common lower extremity targets: gastrocnemius (100–200 U per head), soleus (75–100 U), tibialis posterior (50–100 U).

Intrathecal Baclofen (ITB)

ITB delivers baclofen directly to the intrathecal space via a programmable pump, achieving effective CSF concentrations at 1/100th of the oral dose, thereby reducing systemic side effects. Indications include severe spasticity refractory to oral medications and botulinum toxin, particularly in SCI and CP. A screening trial (50–100 mcg bolus via lumbar puncture) is performed first; a ≥1-point reduction on the Ashworth Scale constitutes a positive trial. Maintenance doses typically range from 100–900 mcg/day. Pump reservoir requires refills every 1–6 months.

08 Dysphagia, Aphasia & Neglect

Dysphagia Assessment

Dysphagia occurs in 37–78% of acute stroke patients and is a major risk factor for aspiration pneumonia, malnutrition, and dehydration. Bedside assessment includes the water swallow test, oral motor exam, and cough/voice quality evaluation. Instrumental assessments are the gold standard:

The Penetration-Aspiration Scale (PAS) grades severity from 1 (material does not enter airway) to 8 (material enters airway, passes below vocal folds, and no effort made to eject — silent aspiration). Scores ≥6 indicate aspiration.

Aphasia Types

Hemispatial Neglect

Hemispatial neglect is failure to attend, perceive, or respond to stimuli on the contralesional side, most commonly left neglect from right (non-dominant) hemisphere lesions involving the right parietal lobe, temporoparietal junction, or frontal lobe. Types include: personal neglect (unawareness of contralesional body), peripersonal neglect (near space), extrapersonal neglect (far space). Associated findings: anosognosia (unawareness of deficit), anosodiaphoria (indifference to deficit), extinction (failure to detect contralesional stimulus during bilateral simultaneous stimulation). Assessment tools: line bisection, cancellation tasks, clock drawing. Treatment: visual scanning training, prism adaptation, limb activation strategies.

09 ASIA/ISNCSCI Classification

The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI), developed by the American Spinal Injury Association (ASIA), is the universal standard for classifying SCI severity. It determines the neurological level of injury and the completeness of injury through systematic motor and sensory examination.

ASIA Impairment Scale (AIS)

Neurological Level Determination

The neurological level of injury (NLI) is the most caudal segment with normal sensory and motor function on both sides. Sensory level is determined by testing light touch and pin prick at 28 dermatome key points (C2–S4/5) on each side, scored 0 (absent), 1 (impaired), or 2 (normal). Motor level is determined by testing 10 key muscles bilaterally (C5–T1, L2–S1), scored 0–5 using the MMT scale. The motor level is the most caudal level with at least grade 3 strength, provided all muscles above are grade 5.

Key Muscles for Motor Level Testing

Functional Expectations by SCI Level

10 Incomplete SCI Syndromes

Incomplete SCI syndromes result from partial spinal cord damage affecting specific tracts while sparing others. Each produces a characteristic pattern of motor and sensory deficits based on the anatomy of the affected region of the spinal cord cross-section.

11 Autonomic Dysreflexia & Cardiovascular

Cardiovascular Complications in SCI

Patients with SCI above T6 lose supraspinal sympathetic control, leading to: neurogenic shock (acute SCI — hypotension with bradycardia due to loss of sympathetic tone and unopposed vagal tone; treat with vasopressors and atropine), orthostatic hypotension (common in tetraplegia; manage with compression stockings, abdominal binder, midodrine, fludrocortisone, slow position changes), and loss of cardiac sympathetic innervation (T1–T4 — maximum HR limited to ~110–120 bpm, reduced cardiac output with exercise).

DVT/PE Prophylaxis in SCI

SCI patients have an extremely high DVT risk (40–80% without prophylaxis in the first 3 months). The highest risk period is 2–12 weeks post-injury. Standard prophylaxis: LMWH (enoxaparin 30 mg BID or 40 mg daily) initiated within 72 hours if no contraindication; combined with pneumatic compression devices and compression stockings. Duration: minimum 8 weeks for incomplete SCI, 12 weeks for complete SCI, or until mobilization. Screening with duplex ultrasound is recommended. IVC filter considered only if anticoagulation is contraindicated.

12 Neurogenic Bladder, Bowel & Skin

Neurogenic Bladder

Neurogenic Bowel

Pressure Injury Prevention

SCI patients are at extremely high risk for pressure injuries (formerly pressure ulcers/decubitus ulcers) due to sensory loss, immobility, moisture, and poor nutrition. Common sites: sacrum, ischial tuberosities (seated), trochanters, heels, occiput, and malleoli. Prevention strategies: pressure relief every 15–30 minutes in wheelchair (weight shifts), turning every 2 hours in bed, appropriate support surface (pressure-redistributing mattress), skin inspection daily, adequate nutrition (albumin, prealbumin), moisture management.

13 SCI Complications

Heterotopic Ossification (HO)

HO is the formation of mature lamellar bone in periarticular soft tissues, occurring in 10–53% of SCI patients, typically 1–4 months post-injury. Most common location: hip (most frequent), followed by knee, shoulder, elbow. Clinical presentation: localized swelling, warmth, decreased ROM, low-grade fever. Diagnosis: elevated alkaline phosphatase (earliest lab marker); triple-phase bone scan (most sensitive early imaging); X-rays show mature HO (delayed 2–4 weeks). Treatment: NSAIDS (indomethacin 75 mg/day for prophylaxis), etidronate disodium, ROM exercises (gentle — aggressive ROM may worsen), surgical resection (only after HO maturation, ~18 months; confirmed by normal alkaline phosphatase and "cold" bone scan). Radiation therapy is used for prophylaxis post-resection.

Syringomyelia (Post-Traumatic)

Post-traumatic syringomyelia occurs in 3–4% of SCI patients, may present months to years post-injury. A fluid-filled cavity (syrinx) develops within the spinal cord, typically extending rostrally from the injury site. Symptoms: ascending sensory level, new pain, increased spasticity, progressive weakness, loss of previously recovered function, new autonomic changes. Diagnosis: MRI (best imaging). Treatment: observation if asymptomatic; surgical shunting or untethering if progressive.

Respiratory Complications

Respiratory failure is the leading cause of mortality in acute SCI. The diaphragm is innervated by the phrenic nerve (C3, C4, C5 — "C3, 4, 5 keeps the diaphragm alive"). Injuries above C3 require mechanical ventilation. C3–C5 injuries may have partial diaphragm function. Intercostal muscles (T1–T12) and abdominal muscles (T6–T12) are needed for cough, forced expiration, and secretion clearance. SCI patients develop a restrictive ventilatory pattern with reduced vital capacity, reduced cough strength, and increased mucus retention. Management: assisted cough techniques (manual or mechanical insufflation-exsufflation), incentive spirometry, pulmonary toilet, possible phrenic nerve stimulation for high cervical SCI.

Thermoregulation

SCI patients with injuries above T6 have impaired thermoregulation (poikilothermia) below the level of injury due to loss of sympathetic control of cutaneous blood flow and sweating. They are susceptible to both hypothermia and hyperthermia. Environmental temperature management is essential.

Sexual Function & Fertility

UMN lesions (above S2–S4): reflex erections preserved, psychogenic erections lost; ejaculation impaired. LMN lesions (S2–S4): reflex erections lost, psychogenic may be preserved; ejaculation impaired. Fertility is significantly impaired in men with SCI due to ejaculatory dysfunction and poor semen quality. Treatment: PDE5 inhibitors (sildenafil) for erectile dysfunction; penile vibratory stimulation or electroejaculation for fertility.

14 TBI Classification & GCS

Traumatic brain injury (TBI) is a leading cause of death and disability worldwide, with approximately 2.87 million emergency department visits, hospitalizations, and deaths annually in the US. Classification is based on severity (GCS), mechanism (penetrating vs closed), pathology (focal vs diffuse), and associated complications.

Glasgow Coma Scale (GCS)

TBI Severity Classification

Post-Traumatic Amnesia (PTA)

PTA is the period of impaired continuous memory formation following TBI, from the moment of injury until the patient demonstrates consistent orientation and ability to form new memories. It is the single best predictor of long-term outcome after TBI. Assessment: Galveston Orientation and Amnesia Test (GOAT) — score ≥75 on two consecutive days indicates PTA resolution.

15 Rancho Los Amigos Scale & Recovery

Rancho Los Amigos Levels of Cognitive Functioning (Revised Scale, Levels I–X)

Agitation Management (Rancho Level IV)

Agitation in TBI (Rancho IV) is a transient phase of recovery, not a behavioral disorder. Environmental management is first-line: low stimulation, consistent staff, quiet room, minimize restraints (worsen agitation), establish predictable routines, redirect rather than confront. Pharmacological management when safety is at risk:

16 TBI Complications & Management

Post-Traumatic Seizures

Seizures after TBI are classified by timing: immediate (<24 hours — impact seizures), early (1–7 days), and late (>7 days — post-traumatic epilepsy). Risk factors for late seizures: penetrating injury, intracranial hemorrhage, depressed skull fracture, cortical contusion, early seizures, prolonged PTA.

Hydrocephalus

Post-traumatic hydrocephalus (communicating type, from impaired CSF absorption) occurs in 1–8% of TBI patients. Suspect when recovery plateaus or declines. Triad (similar to NPH): gait disturbance, cognitive decline, urinary incontinence. Diagnosis: CT/MRI showing ventriculomegaly out of proportion to atrophy; confirm with CSF tap test (improvement after removing 30–50 mL CSF). Treatment: VP shunt.

Neuroendocrine Dysfunction

Pituitary dysfunction occurs in 25–50% of moderate-to-severe TBI patients due to the pituitary's vulnerable location and blood supply. Anterior pituitary: GH deficiency (most common chronic deficiency), hypogonadism, hypothyroidism, adrenal insufficiency (most dangerous acutely). Posterior pituitary: diabetes insipidus (DI — polyuria, hypernatremia; common acutely, usually transient) and SIADH (hyponatremia — most common cause of hyponatremia in TBI). Screen with morning cortisol, TSH, free T4, testosterone/estradiol, IGF-1 at 3–6 months and 12 months post-injury.

Heterotopic Ossification in TBI

HO occurs in 10–20% of TBI patients, most commonly at the hip (most common), followed by elbow, shoulder, and knee. More common in patients with prolonged coma. Detection and management are identical to SCI-associated HO (see Section 13). The hip is at particular risk for development of clinically significant HO limiting ROM for sitting and ambulation.

Paroxysmal Sympathetic Hyperactivity (PSH)

Previously termed "sympathetic storming," "dysautonomia," or "diencephalic seizures." Occurs in 15–33% of severe TBI patients. Characterized by paroxysmal episodes of tachycardia, hypertension, tachypnea, hyperthermia, diaphoresis, and posturing (extensor or flexor). Episodes may be triggered by stimulation (noxious or non-noxious). Treatment: minimize triggers, beta-blockers (propranolol), bromocriptine, gabapentin, benzodiazepines, morphine, dantrolene. Intrathecal baclofen may be considered for refractory cases.

17 Concussion & Return to Activity

Sport-Related Concussion (mTBI)

Concussion is a mild TBI (GCS 13–15) caused by biomechanical forces. It is a functional rather than structural injury — standard neuroimaging is typically normal. Diagnosis is clinical. Core features: headache (most common symptom), dizziness, confusion, amnesia, balance problems, visual disturbance, sensitivity to light/noise, cognitive slowing, emotional lability. Loss of consciousness occurs in <10% of concussions. Symptoms typically resolve within 7–10 days in adults and 2–4 weeks in children.

Graduated Return-to-Sport Protocol (Consensus Statement on Concussion in Sport, 2023)

Minimum 24 hours at each step; if symptoms recur, drop back to previous asymptomatic stage. Children/adolescents: return to learn (school) before return to sport. No same-day return to play. Medical clearance required before full-contact practice.

Post-Concussion Syndrome

Persistent symptoms beyond expected recovery time (typically >2–4 weeks in adults). Symptoms: headache, dizziness, cognitive difficulties, fatigue, irritability, sleep disturbance, anxiety, depression. Risk factors: female sex, history of prior concussions, migraine history, psychiatric history, prolonged initial symptoms. Management: active rehabilitation (aerobic exercise below symptom threshold), vestibular therapy, vision therapy, cervicogenic headache treatment, cognitive behavioral therapy; avoid prolonged rest (>48 hours of strict rest is no longer recommended).

18 Low Back Pain & Spinal Disorders

Red Flags for Low Back Pain

Imaging Indications

Imaging is NOT indicated for acute non-specific low back pain (<6 weeks) without red flags. Indications for early imaging include: red flag symptoms (above), progressive neurological deficit, failure to improve after 6 weeks of conservative care. MRI is the modality of choice for evaluating disc herniation, spinal stenosis, infection, and malignancy. X-rays for suspected fracture, spondylolisthesis, or instability. CT when MRI is contraindicated.

McKenzie Classification (Mechanical Diagnosis and Therapy)

Cervical Radiculopathy & Myelopathy

Cervical radiculopathy presents with dermatomal arm pain, numbness, and weakness in a nerve root distribution (most common: C6 — thumb/index, C7 — middle finger). Special tests: Spurling test (head extension + lateral flexion + axial compression reproduces radicular symptoms), upper limb tension test (ULTT). Most cases (75–90%) resolve with conservative management (NSAIDs, PT, cervical epidural steroid injection).

Cervical myelopathy is a surgical condition caused by spinal cord compression (spondylosis, disc herniation, OPLL). UMN findings: gait instability (earliest finding), hand clumsiness, hyperreflexia, Hoffman sign, Babinski sign, Lhermitte sign (electric sensation with neck flexion). Surgery (decompression) is indicated for moderate-to-severe or progressive myelopathy.

Lumbar Spinal Stenosis

Narrowing of the spinal canal (central) or neural foramina (lateral/foraminal). Most common cause: degenerative spondylosis (age >60). Classic presentation: neurogenic claudication — bilateral leg pain/heaviness/weakness with walking or prolonged standing, relieved by sitting or forward flexion (opening the canal). Distinguish from vascular claudication (pain with exercise, relieved by standing still, normal spine flexion). The "shopping cart sign" (relief with forward flexion while pushing a cart) suggests spinal stenosis. Treatment: PT (flexion-based exercises), epidural steroid injections, surgical decompression/laminectomy for refractory cases.

19 Peripheral Nerve Injuries

Seddon Classification

Sunderland Classification (Expanded)

Common Peripheral Nerve Injuries

20 Upper Extremity Rehabilitation

Carpal Tunnel Syndrome (CTS)

CTS is the most common entrapment neuropathy, caused by compression of the median nerve at the wrist within the carpal tunnel (bounded by carpal bones and transverse carpal ligament). Presentation: numbness/tingling in median nerve distribution (thumb, index, middle, radial ring finger), pain worse at night (wakes patient), weak grip, thenar atrophy (late finding). Provocative tests: Tinel sign (tapping over carpal tunnel reproduces symptoms), Phalen test (sustained wrist flexion for 60 seconds reproduces symptoms; most sensitive clinical test), Durkan test (direct compression over carpal tunnel). Risk factors: pregnancy, diabetes, hypothyroidism, RA, obesity, repetitive wrist use.

Electrodiagnostic confirmation: prolonged median sensory distal latency (>3.5 ms over 14 cm) is the most sensitive NCS finding. Prolonged median motor distal latency (>4.2 ms) indicates more severe involvement. EMG may show fibrillations in APB (abductor pollicis brevis) in severe cases. Treatment: wrist splint in neutral (especially at night), activity modification, corticosteroid injection, surgical carpal tunnel release for moderate-to-severe or refractory cases.

Rotator Cuff Rehabilitation

Rotator cuff disorders represent a continuum: tendinopathy → partial tear → full-thickness tear. Supraspinatus is the most commonly affected tendon. Assessment tests: Neer test (passive forward flexion with scapula stabilized — impingement), Hawkins test (90° forward flexion then internal rotation — impingement), empty can test (Jobe — supraspinatus), external rotation lag sign (infraspinatus), lift-off test and belly press test (subscapularis). Rehabilitation phases: (1) pain control + protected ROM, (2) progressive ROM + scapular stabilization, (3) rotator cuff strengthening (internal/external rotation), (4) sport/work-specific training. Surgical repair is indicated for acute full-thickness tears in active patients and failed conservative management (≥6 months).

Lateral Epicondylitis (Tennis Elbow)

Tendinopathy of the common extensor origin, primarily ECRB (extensor carpi radialis brevis). Presentation: lateral elbow pain with gripping, wrist extension against resistance. Treatment: activity modification, counterforce brace (forearm strap), eccentric strengthening (wrist extensors), corticosteroid injection (short-term benefit but may impair long-term healing), PRP injection, surgical debridement (refractory cases).

21 Lower Extremity & Joint Replacement Rehab

Total Hip Arthroplasty (THA) Rehabilitation

The surgical approach determines post-operative precautions:

Rehabilitation milestones: weight-bearing as tolerated (typically), gait training with walker/crutches, stair training (up with good leg first, down with operated leg first — "up with the good, down with the bad"), hip strengthening (abductors, extensors), ROM exercises, ADL training with adaptive equipment (long-handled reacher, sock aid, shoe horn). DVT prophylaxis for 35 days post-operatively.

Total Knee Arthroplasty (TKA) Rehabilitation

Goals: achieve ≥0° extension and ≥120° flexion. Immediate WBAT with assistive device. Cryotherapy, CPM (continuous passive motion) use is controversial (recent evidence shows minimal benefit). Progressive rehabilitation: quad sets, SLR, AROM, progressive weight-bearing, stair training, stationary bike (when ≥90° flexion achieved). DVT prophylaxis for 14–35 days. Key complications: stiffness (may require manipulation under anesthesia if <90° flexion at 6–8 weeks), peroneal nerve palsy (from traction, positioning — foot drop), wound complications, instability.

Osteoarthritis Management (Non-Surgical)

Evidence-based approach: weight management (5% weight loss reduces knee OA symptoms significantly), aerobic and strengthening exercise, PT, NSAIDs (topical preferred for knee OA), acetaminophen, intra-articular corticosteroid injections (short-term relief), viscosupplementation (hyaluronic acid — modest benefit in knee OA), bracing (unloader knee brace for unicompartmental OA), assistive devices (cane in contralateral hand reduces hip joint loading by 25%).

22 Tendinopathy & Myofascial Pain

Tendinopathy

Modern understanding favors the term tendinopathy over "tendinitis" because histopathology typically shows degenerative changes (collagen disorganization, ground substance mucoid degeneration, neovascularization) rather than inflammatory infiltrate. Common tendinopathies: Achilles, patellar, rotator cuff (supraspinatus), lateral epicondyle (ECRB), de Quervain (APL/EPB at first dorsal compartment). Treatment principles: relative rest (not complete immobilization), eccentric exercise (strongest evidence — particularly for Achilles and patellar tendinopathy), load management, progressive tendon loading (heavy slow resistance training), NSAIDS (short-term only — may impair healing long-term), nitroglycerin patches (some evidence), PRP injection (mixed evidence), shockwave therapy (ESWT — evidence for calcific tendinopathy), avoid repeated corticosteroid injections (accelerate tendon degeneration).

Myofascial Pain Syndrome

Myofascial pain syndrome (MPS) is characterized by myofascial trigger points (MTrPs) — hyperirritable spots within a taut band of skeletal muscle that produce local and referred pain. Features: palpable taut band, exquisite spot tenderness, patient recognition of pain (jump sign), referred pain pattern, local twitch response with snapping palpation. Active trigger points cause spontaneous pain; latent trigger points cause pain only with compression. Common locations: upper trapezius (refers to temporal headache), levator scapulae, infraspinatus, quadratus lumborum, piriformis. Treatment: trigger point injection (lidocaine or dry needling), spray and stretch, manual therapy (ischemic compression, myofascial release), postural correction, stretching, addressing perpetuating factors (poor ergonomics, sleep disturbance, stress, vitamin D deficiency).

23 Nerve Conduction Studies

Nerve conduction studies (NCS) are the objective, quantitative component of the electrodiagnostic evaluation. They assess the integrity and function of peripheral nerves by applying electrical stimulation and recording the evoked responses. NCS evaluate both motor and sensory nerve fibers and can localize lesions to specific nerve segments.

Motor NCS

A compound motor action potential (CMAP) is recorded from a muscle after supramaximal stimulation of its motor nerve at two or more points along its course. Parameters measured: distal latency (time from distal stimulation to CMAP onset), amplitude (baseline to negative peak, reflects number of functioning motor axons), conduction velocity (distance between stimulation sites / difference in latencies; normal ≥50 m/s in upper extremity, ≥40 m/s in lower extremity), duration (temporal dispersion). A >50% drop in CMAP amplitude between distal and proximal stimulation sites indicates conduction block (focal demyelination — hallmark of neurapraxia).

Sensory NCS

A sensory nerve action potential (SNAP) is recorded after stimulating a sensory or mixed nerve. Can be performed orthodromic (stimulate distally, record proximally) or antidromic (stimulate proximally, record distally — larger amplitude, more commonly used). Parameters: onset latency, peak latency, amplitude (reflects number of functioning sensory axons), conduction velocity. SNAPs are critical for distinguishing pre-ganglionic (root) from post-ganglionic (plexus/nerve) lesions: in radiculopathy, the dorsal root ganglion (DRG) is proximal to the lesion, so the sensory axons distal to the DRG remain intact and SNAPs are preserved despite clinical sensory loss.

Late Responses

24 Needle EMG

Needle electromyography (EMG) assesses the electrical activity of muscle fibers and motor units by inserting a needle electrode into the muscle. It provides information about denervation, reinnervation, myopathy, and motor unit morphology that NCS alone cannot provide.

Insertional Activity

Normal insertional activity: brief burst of electrical activity with needle insertion/movement, lasting <300 ms. Increased insertional activity: sustained activity beyond normal duration; earliest sign of denervation (before fibrillations appear). Decreased insertional activity: seen in fibrotic or fatty-replaced muscle (chronic denervation, severe myopathy).

Spontaneous Activity

Motor Unit Analysis

Motor unit action potentials (MUAPs) are assessed during voluntary contraction for morphology (amplitude, duration, phases) and recruitment (firing pattern):

25 Electrodiagnostic Patterns by Condition

Characteristic EDX Patterns

Timing of Electrodiagnostic Studies

26 Cerebral Palsy & GMFCS

Cerebral palsy (CP) is a group of permanent disorders of movement and posture causing activity limitation, attributed to non-progressive disturbances that occurred in the developing fetal or infant brain. It is the most common cause of childhood physical disability, affecting 2–3 per 1,000 live births. Although the brain lesion is static, its musculoskeletal manifestations change with growth.

CP Classification by Motor Type

Gross Motor Function Classification System (GMFCS) — Levels I–V

Tone Management in CP

Treatment is goal-directed based on GMFCS level and specific functional limitations. Options: oral medications (baclofen, diazepam, dantrolene — limited by sedation/generalized weakness), botulinum toxin injections (focal spasticity, delayed need for surgery, commonly injected: gastrocnemius, hamstrings, hip adductors), intrathecal baclofen (generalized lower extremity spasticity, GMFCS III–V), selective dorsal rhizotomy (SDR) (sectioning posterior rootlets L1–S2 to reduce spasticity; best candidates: spastic diplegic CP, GMFCS II–III, age 4–8, good underlying strength), orthopedic surgery (muscle-tendon lengthening, tendon transfers, bony procedures for hip displacement/scoliosis).

Hip Surveillance in CP

Hip displacement is common in CP (1% in GMFCS I, up to 90% in GMFCS V). The migration percentage (MP) on AP pelvis X-ray quantifies femoral head uncovering. Screening protocol: AP pelvis X-ray at age 12–24 months, then annually for GMFCS III–V, every 1–2 years for GMFCS II. MP >30% warrants referral to orthopedics; MP >40–50% typically requires surgical intervention (soft tissue releases, varus derotation osteotomy, pelvic osteotomy).

27 Spina Bifida & Brachial Plexus Injury

Spina Bifida (Myelomeningocele)

Myelomeningocele is the most severe form of spina bifida, involving herniation of the spinal cord and meninges through a vertebral defect. It is the most common neural tube defect compatible with life. Associated conditions: Arnold-Chiari II malformation (virtually 100% — cerebellar tonsillar herniation through foramen magnum), hydrocephalus (80–90% require VP shunt), tethered cord (can present with new neurological decline during growth), and latex allergy (up to 65% sensitization — use latex-free precautions for ALL procedures).

Functional Expectations by Lesion Level

Obstetric Brachial Plexus Injury

If no biceps function by 3 months, microsurgical nerve repair (nerve grafting, nerve transfer) should be considered. Active ROM exercises, splinting, and positioning are mainstays of conservative management.

28 Muscular Dystrophies & Developmental Milestones

Muscular Dystrophies

Developmental Milestones

29 Amputation Levels & Pre-Prosthetic Management

Lower Extremity Amputation Levels

Pre-Prosthetic Management

Pre-prosthetic care begins immediately post-operatively: wound care and monitoring for healing (especially critical in vascular amputees with diabetes and peripheral vascular disease), edema control and limb shaping (figure-of-eight elastic wrapping, rigid removable dressings, or shrinker socks to shape the residual limb into a conical shape for optimal socket fit), desensitization (tapping, rubbing, weight bearing on residual limb to reduce hypersensitivity), ROM exercises (prevent hip flexion/abduction contracture in transfemoral, knee flexion contracture in transtibial — prone positioning helps), strengthening (emphasis on hip extensors/abductors in AKA, knee extensors in BKA), single-leg balance and transfers, and psychological support (grief, body image, adjustment).

Phantom Limb Pain

Phantom limb pain occurs in 50–80% of amputees; distinguished from phantom limb sensation (non-painful awareness of the absent limb, nearly universal) and residual limb pain (pain in the remaining stump). Mechanisms include peripheral (neuroma formation), spinal (dorsal horn sensitization), and cortical (maladaptive neuroplasticity / cortical reorganization) factors. Management:

30 Prosthetic Components & Prescription

Transtibial Prosthetic Components

Socket: Patellar-tendon-bearing (PTB) — primary weight bearing on patellar tendon, medial tibial flare, anterior tibia protected; Total surface bearing (TSB) — distributes pressure over the entire residual limb using gel liner (modern standard). Suspension: Pin/shuttle lock (pin at end of gel liner locks into socket), suction (vacuum seal), sleeve suspension (neoprene or gel sleeve over socket and thigh), supracondylar cuff/strap. Foot/ankle units: SACH (Solid Ankle Cushion Heel) — simplest, durable, no moving parts, cushioned heel compresses to simulate plantarflexion; single-axis foot — allows plantarflexion/dorsiflexion, improves knee stability at heel strike; multi-axis foot — allows motion in all planes, good for uneven terrain; dynamic response/energy-storing feet (carbon fiber, Flex-Foot) — store energy during stance, release during push-off, best for active ambulators (K3–K4).

Transfemoral Prosthetic Components

Socket: Ischial containment (IC) — modern standard; ischial tuberosity inside the socket, narrow ML dimension, improved mediolateral control; Quadrilateral — older design, ischial tuberosity sits on posterior brim shelf. Knee units: Single-axis (manual lock) — most stable, for K1 patients; polycentric (multi-axis) — shortens in swing phase (cosmetic benefit), inherent stability; hydraulic/pneumatic — fluid resistance for smooth swing phase at variable cadences (K3+); microprocessor knee (C-Leg, Genium, Rheo Knee) — computer-controlled resistance, adapts to walking speed, improved stumble recovery, stair descent, ramp navigation; for K2–K4 patients.

Upper Extremity Prosthetics

Types: body-powered (cable-operated; harness converts shoulder motion to terminal device operation; most durable, provides proprioceptive feedback), myoelectric (EMG signals from residual muscles control electric motors; more cosmetic, stronger grip, but heavier and less durable), passive/cosmetic (no active function; cosmesis and light tasks), activity-specific (adapted for sports, work). Terminal devices: hook (voluntary opening or closing; excellent prehension, most functional) and hand (cosmetic advantage; weaker grasp).

31 Gait Deviations & K-Levels

Common Prosthetic Gait Deviations

Medicare K-Levels (Functional Classification)

32 Spasticity Injections & Neurolysis

Botulinum Toxin Injection — Dosing by Muscle

OnabotulinumtoxinA (Botox) dosing guidelines for common spasticity targets (doses are for onabotulinumtoxinA; conversion: 1 U Botox ≈ 3–5 U Dysport ≈ 1 U Xeomin):

Maximum total dose per treatment session: typically 400–600 U onabotulinumtoxinA for adults (some experts use up to 800 U for large adults with diffuse spasticity). Injection localization methods: EMG guidance, electrical stimulation, ultrasound (increasingly preferred for superficial muscles). Re-injection interval: ≥12 weeks minimum.

Phenol & Alcohol Neurolysis

Phenol (5–7% aqueous solution) and alcohol (45–100% ethanol) produce chemical neurolysis — protein denaturation and nerve destruction, reducing spasticity. Advantages: immediate effect, longer duration (3–12+ months), lower cost than botulinum toxin, no dose ceiling. Disadvantages: painful injection, risk of dysesthesias (especially with mixed sensorimotor nerves), fibrosis with repeated injections. Best targets: motor nerve branches with minimal sensory component — musculocutaneous nerve (elbow flexion spasticity), obturator nerve (hip adductor spasticity — most common target), tibial nerve branches to gastrocnemius (equinovarus). Phenol motor point blocks inject the motor point (NMJ entry zone) directly within the muscle.

33 Intrathecal Baclofen & Guided Procedures

Intrathecal Baclofen Pump

The ITB pump system consists of a programmable titanium pump (implanted subcutaneously in the abdominal wall) and an intrathecal catheter threaded into the spinal subarachnoid space (tip typically at T10–T12 for LE spasticity, C5–C7 for UE + LE spasticity). The pump delivers continuous baclofen to the CSF at a programmable rate.

ITB Trial Protocol

Post-implant: starting continuous dose is typically 2× the effective bolus trial dose per 24 hours (e.g., 50 mcg bolus → 100 mcg/day). Dose titrated over weeks to months. Pump refills required every 1–6 months depending on concentration and flow rate. MRI-conditional pumps are available.

Fluoroscopic & Ultrasound-Guided Procedures

PM&R physicians commonly perform image-guided procedures:

34 Therapeutic Modalities

Thermal Modalities

Electrotherapy

Traction

Cervical traction: mechanical or manual; angle determines which disc space is opened (neutral = upper cervical; flexion = lower cervical). Sustained traction: 25–30 lb for 15–20 minutes (disc herniation). Intermittent traction: 5–10 seconds on/off cycles. Contraindications: ligamentous instability, RA (atlantoaxial instability), fracture, malignancy, acute disc herniation with progressive neurological deficit, spinal cord compression. Lumbar traction: force must exceed ~50% body weight to separate vertebral segments (typically 60–100 lb); limited evidence for efficacy.

35 Orthotic Prescribing

Lower Extremity Orthoses

Spinal Orthoses

36 Wheelchair Prescription & Seating

Manual vs Power Wheelchair

Seating & Positioning

Proper seating is essential for posture, skin protection, and function. Key principles: seat width = widest point of hips + 1–2 inches; seat depth = posterior buttock to popliteal fossa − 2–3 inches (avoid popliteal pressure); seat height = allow proper footrest clearance and transfer height. Cushion selection for pressure redistribution: foam (basic, lightweight, inexpensive; limited lifespan), gel (good pressure distribution; heavy), air (ROHO — excellent pressure redistribution; requires maintenance, can bottom out if under-inflated), alternating pressure (powered; best for highest-risk patients). Tilt-in-space maintains hip/knee angles while tilting the entire seating system posteriorly for pressure relief and positioning (essential for patients unable to do weight shifts independently). Recline opens the seat-to-back angle for pressure relief, catheterization access, and spasm management, but creates shear forces on the skin.

Wheelchair Driving Interfaces

37 Functional Outcome Measures

Functional Independence Measure (FIM)

The FIM is the most widely used functional assessment in rehabilitation, measuring the burden of care across 18 items in 6 domains. Each item is scored 1–7; total score ranges from 18 (complete dependence) to 126 (complete independence). FIM score change during rehabilitation admission is the primary measure of rehabilitation effectiveness.

FIM Scoring Scale

FIM Items (18 Total)

Barthel Index

An older ADL measure, scored 0–100 (0 = complete dependence, 100 = independence). Ten items: feeding (10), bathing (5), grooming (5), dressing (10), bowels (10), bladder (10), toilet use (10), transfers (15), mobility/walking (15), stairs (10). A score ≥60 generally indicates potential for discharge home with some assistance. Simpler than FIM but less sensitive to change.

Other Key Outcome Measures

38 Classification Systems (All)

This section consolidates all major classification systems used in PM&R practice for rapid reference. Each is fully enumerated with all grades/levels.

ASIA Impairment Scale (AIS)

Modified Ashworth Scale

Brunnstrom Stages of Motor Recovery

Rancho Los Amigos Levels of Cognitive Functioning

Glasgow Coma Scale

GMFCS Levels (Cerebral Palsy)

K-Levels (Medicare Functional Classification for Amputees)

Seddon / Sunderland Classification of Nerve Injury

39 Medications Master Table

Antispasticity Agents

Neuropathic Pain Medications

Neurogenic Bladder Agents

Bowel Medications

40 Abbreviations Master List

41 Risk Factors & Comorbidities

Comorbidities Affecting Rehabilitation Outcomes

Risk Factors for Common Rehabilitation Conditions

Metabolic Equivalents (METs) for Activity Prescription