Sports Medicine, Physical Medicine & Rehabilitation, Electrodiagnostics (EMG/NCS) & Concussion

Because standard non-contrast head CT is normal in uncomplicated concussion and exposes children to ionizing radiation, the Pediatric Emergency Care Applied Research Network (PECARN) rules guide selective neuroimaging in children presenting with GCS 14-15 after minor head trauma. In children at least 2 years of age, head CT is indicated if high-risk features exist (GCS 14, altered mental status, or clinical signs of basilar skull fracture such as hemotympanum, Battle sign, raccoon eyes, or CSF otorrhea/rhinorrhea), and observation versus CT is weighed for intermediate features (history of loss of consciousness, vomiting, severe headache, or severe mechanism of injury). In infants less than 2 years of age, non-frontal scalp hematomas (parietal, temporal, or occipital), palpable skull fracture, loss of consciousness greater than 5 seconds, or failure to act normally per parents additionally warrant evaluation. While 85-90% of concussions resolve within 10-28 days, persistence of headache, vertigo, cognitive fatigue, and irritability beyond 4 weeks defines Post-Concussion Syndrome, managed with targeted vestibular physical therapy, subsymptom-threshold aerobic exercise (Buffalo Concussion Treadmill Protocol), cognitive behavioral therapy, and non-sedating headache prophylaxis (amitriptyline or topiramate).

Repetitive concussive and subconcussive head impacts sustained over years of contact sports (American football, boxing, ice hockey, soccer heading, or military blast exposure) predispose to Chronic Traumatic Encephalopathy (CTE), a progressive neurodegenerative tauopathy that can only be definitively diagnosed postmortem. Gross neuropathological examination reveals generalized cerebral cortical atrophy (most pronounced in the frontal and temporal lobes), atrophy of the hippocampus, amygdala, and mammillary bodies, pallor of the substantia nigra, ventriculomegaly, and a fenestrated cavum septum pellucidum. Microscopically, the pathognomonic signature of CTE is the perivascular accumulation of hyperphosphorylated tau protein (neurofibrillary tangles and astrocytic tangles) concentrated specifically at the depths of the cortical sulci around small blood vessels—a distribution distinct from Alzheimer disease (which begins in the transentorhinal/hippocampal cortex without perivascular sulcal depth predilection and features prominent beta-amyloid neuritic plaques). Clinically, CTE presents years to decades after retirement from contact sports with an insidious triad of behavioral/mood dysregulation (explosive impulsivity, aggression, depression, suicidality), cognitive decline (executive dysfunction and episodic memory loss progressing to dementia), and late parkinsonian motor features.

A foundational localization principle in electrodiagnostic medicine is the preservation of the Sensory Nerve Action Potential (SNAP) in spinal nerve root lesions (radiculopathies) despite clinical dermatomal numbness. The cell body of the first-order peripheral sensory neuron resides in the Dorsal Root Ganglion (DRG) within the intervertebral foramen, sending a central axon proximally through the dorsal root into the spinal cord and a peripheral axon distally into the limb. Intervertebral disc herniations and foraminal osteophytes compress the dorsal root proximal (pre-ganglionic) to the DRG. Because the peripheral sensory axon remains connected to its trophic cell body in the DRG, it does NOT undergo Wallerian degeneration; consequently, a pure cervical or lumbar radiculopathy exhibits completely NORMAL sensory nerve conduction studies (normal SNAP amplitude) even when the patient has complete anesthesia in that dermatome! Conversely, any lesion located distal (post-ganglionic) to the DRG—such as a brachial or lumbosacral plexopathy, thoracic outlet syndrome, or peripheral mononeuropathy—severs the peripheral sensory axon from the DRG cell body, causing Wallerian degeneration and a reduced or absent SNAP amplitude.

Needle EMG inserts a concentric recording electrode directly into skeletal muscle to evaluate electrical activity at rest and during voluntary contraction. Normal muscle is electrically silent at rest (outside the endplate zone). In acute/ongoing neurogenic denervation (radiculopathy, ALS, axonal neuropathy, or inflammatory polymyositis with muscle fiber necrosis), the resting muscle membrane becomes unstable and fires spontaneous single-fiber Fibrillation potentials and Positive Sharp Waves (and fasciculations arising from motor neurons). After chronic denervation and collateral sprouting (reinnervation, where surviving motor axons adopt orphaned muscle fibers), voluntary contraction produces giant, High-Amplitude, Long-Duration, Polyphasic Motor Unit Action Potentials (MUAPs) with Decreased (neurogenic) recruitment. Conversely, in primary Myopathies (muscular dystrophies, steroid myopathy, polymyositis), random loss of individual muscle fibers within each motor unit shrinks the territory of the motor unit, producing Small-Amplitude, Short-Duration, Polyphasic MUAPs coupled with Early recruitment (many motor units must fire simultaneously just to generate weak force). Finally, Repetitive Nerve Stimulation (RNS) differentiates neuromuscular junction disorders: Myasthenia Gravis (postsynaptic nicotinic AChR autoantibodies) shows a classic Decremental CMAP response (greater than 10% drop in amplitude) during slow (2-3 Hz) repetitive stimulation, whereas Lambert-Eaton Myasthenic Syndrome (presynaptic P/Q-type voltage-gated calcium channel autoantibodies in small cell lung cancer) shows low baseline CMAP amplitude that exhibits a dramatic Incremental response (greater than 60-100% facilitation) after 10 seconds of maximal isometric exercise or high-frequency (20-50 Hz) stimulation.

Focal peripheral nerve entrapments must be distinguished from cervical radiculopathies by the distribution of motor weakness, sensory sparing, and absence of neck pain or paraspinal EMG denervation. Along the median nerve pathway, Pronator Teres Syndrome (compression between the two heads of the pronator teres in the proximal forearm by repetitive forceful pronation) differs from carpal tunnel syndrome by causing aching proximal volar forearm pain reproduced by resisted pronation, weakness of the flexor pollicis longus (FPL) and flexor digitorum profundus (FDP) to digits 2/3, AND sensory loss over the central thenar palm (because the palmar cutaneous branch is compressed proximal to its takeoff). Anterior Interosseous Nerve (AIN) Syndrome (Kiloh-Nevin syndrome, compression of the pure motor branch of the median nerve by the Gantzer muscle or fibrous bands) causes isolated motor weakness of the FPL, index/middle FDP, and pronator quadratus with ZERO sensory loss; when asked to make an OK sign, the patient cannot flex the thumb IP joint or index DIP joint, producing a flat pinch sign instead of a circle. Along the radial nerve, Posterior Interosseous Nerve (PIN) Syndrome (compression within the arcade of Frohse in the supinator muscle) causes pure motor weakness of finger metacarpophalangeal extension and thumb extension (finger drop) with ZERO sensory loss and preserved wrist extension (though the wrist deviates radially during extension because extensor carpi radialis longus arises proximal to the supinator while extensor carpi ulnaris is paralyzed). Conversely, Neurogenic Thoracic Outlet Syndrome (compression of the lower trunk C8-T1 of the brachial plexus by a cervical rib or hypertrophied scalene muscles within the interscalene triangle) presents with medial forearm numbness (medial antebrachial cutaneous nerve) and pan-intrinsic hand atrophy affecting both median (thenar) and ulnar (hypothenar/interossei) muscles simultaneously (Gilliatt-Sumner hand).

In the lower extremity, Meralgia Paresthetica results from mechanical compression of the Lateral Femoral Cutaneous Nerve (L2-L3)—a purely sensory nerve that courses under or through the lateral attachment of the inguinal ligament just medial to the anterior superior iliac spine (ASIS). Classic triggers include obesity, pregnancy, tight utility belts or body armor, diabetes mellitus, and prone surgical positioning. Patients experience burning pain, tingling, and numbness strictly localized to the anterolateral thigh, exacerbated by hip extension and relieved by sitting (hip flexion), with completely normal quadriceps/hip strength and a normal patellar reflex (differentiating it from L2-L4 femoral neuropathy or L3 radiculopathy). Obturator neuropathy (after pelvic/hip surgery, obturator hernia, or prolonged lithotomy positioning) causes sensory loss over the medial thigh and weakness of hip adduction with normal knee extension and preserved patellar reflex. Piriformis syndrome occurs when hypertrophy or spasm of the piriformis muscle in the greater sciatic foramen compresses the sciatic nerve (which pierces or passes directly through the piriformis muscle belly in ~15% of individuals), causing deep gluteal buttock pain radiating down the posterior thigh that worsens with sitting and is reproduced by the FAIR test (Flexion, Adduction, and Internal Rotation of the hip).

In adult and adolescent runners (especially females due to an increased quadriceps Q-angle from a wider pelvis and genu valgum), Patellofemoral Pain Syndrome (runner's knee) is the most common cause of chronic anterior knee pain. Dynamic lateral maltracking of the patella within the femoral trochlear groove results from weakness of the hip abductors (gluteus medius) and hip external rotators—which allows excessive femoral internal rotation and dynamic knee valgus during single-leg stance—combined with imbalance of the vastus medialis obliquus (VMO). Patients report dull, aching peripatellar or retropatellar pain exacerbated by descending stairs, squatting, running on inclines, or sitting for prolonged periods with the knees flexed (theater sign). Physical examination demonstrates a positive patellar grind test (Clarke sign: retropatellar pain when the examiner compresses the superior pole of the patella distally while the patient contracts the quadriceps) without joint effusion or ligamentous instability; first-line therapy is targeted physical therapy strengthening the hip abductors/external rotators and quadriceps. Conversely, Lateral knee pain in long-distance runners or cyclists localizes to Iliotibial (IT) Band Friction Syndrome, where the distal IT band repeatedly snaps over the lateral femoral epicondyle at ~30 degrees of knee flexion (positive Ober test for IT band tightness; tenderness 2 cm superior to the lateral joint line). Medial knee pain situated 4-5 cm inferior to the medial joint line over the anteromedial proximal tibia—classic in older obese women with underlying knee osteoarthritis or runners with tight hamstrings—defines Pes Anserine Bursitis (at the conjoined insertion of Sartorius, Gracilis, and Semitendinosus—mnemonic Say Grace Before Tea).

In the foot and ankle, Plantar Fasciitis (degenerative microtearing and collagen necrosis of the plantar aponeurosis origin at the medial tubercle of the calcaneus) presents with sharp, stabbing inferior heel pain that is worst during the first few steps out of bed in the morning (post-static dyskinesia) or after prolonged sitting, improves slightly with warming up, and worsens again by the end of the day. Risk factors include pes planus or pes cavus, obesity, prolonged standing on hard surfaces, and tight Achilles tendons. Examination reveals pinpoint tenderness at the anteromedial calcaneal tubercle worsened by passive dorsiflexion of the great toe (Windlass test); plain radiographs are unnecessary initially (inferior calcaneal heel spurs are incidental reactive findings and are NOT the source of pain), and treatment consists of plantar fascia and calf stretching, silicone heel cups/orthotics, night splints, and NSAIDs (avoiding repeated corticosteroid injections which risk plantar fascia rupture and fat pad atrophy). Achilles Tendinopathy presents with pain and fusiform thickening 2-6 cm proximal to the calcaneal insertion (the hypovascular watershed zone) treated with eccentric calf-loading exercises (Alfredson protocol); fluoroquinolone antibiotics (ciprofloxacin, levofloxacin) and glucocorticoid injections predispose to acute Achilles tendon rupture (audible pop, inability to plantarflex, palpable defect, and positive Thompson calf-squeeze test). Finally, Metatarsal (2nd/3rd shaft) and Tibial Stress Fractures occur in military recruits, marathon runners, and female athletes with the Female Athlete Triad / Relative Energy Deficiency in Sport (RED-S: low energy availability with or without disordered eating, functional hypothalamic amenorrhea, and low bone mineral density); because plain radiographs are falsely negative in the first 2-3 weeks, MRI (or triple-phase bone scan) is the gold-standard sensitive modality.

Voiding function requires coordinated pontine micturition center integration of sacral parasympathetic detrusor contraction (pelvic splanchnic nerves S2-S4 via M3 muscarinic receptors), lumbar sympathetic internal sphincter tone (hypogastric nerve T11-L2 via alpha-1 and beta-3 receptors), and somatic external sphincter relaxation (pudendal nerve S2-S4). Spinal cord lesions ABOVE the sacral micturition center (suprasacral lesions above T12/L1, or multiple sclerosis) produce an Upper Motor Neuron (Spastic / Hyperreflexic) Neurogenic Bladder characterized by Detrusor Hyperreflexia and Detrusor-Sphincter Dyssynergia (DSD—the detrusor contracts involuntarily against a simultaneously contracting external urethral sphincter). This generates dangerously high intravesical pressures that cause vesicoureteral reflux, hydronephrosis, and renal failure; management combines Clean Intermittent Catheterization (CIC every 4-6 hours) with antimuscarinic agents (oxybutynin, tolterodine, solifenacin), beta-3 agonists (mirabegron), or intravesical botulinum toxin A injections to relax the detrusor. Conversely, lesions OF the sacral cord (conus medullaris S2-S4) or cauda equina roots produce a Lower Motor Neuron (Flaccid / Areflexic) Neurogenic Bladder characterized by detrusor areflexia, large bladder capacity, high post-void residual volume (greater than 300-500 mL), and overflow incontinence; management is strictly Clean Intermittent Catheterization (avoiding antimuscarinics, which worsen retention). Parallel principles govern neurogenic bowel: UMN bowel (hypertonic anal sphincter) is managed with a scheduled daily bowel program using digital rectal stimulation (activating the gastrocolic/rectocolic reflex) and bisacodyl/glycerin suppositories, whereas LMN bowel (flaccid anal sphincter) requires firm stool-bulking fiber and manual digital disimpaction.

Following the initial 1-to-6-week phase of Spinal Shock (complete flaccid areflexia and loss of the bulbocavernosus reflex below the acute cord injury), upper motor neuron spasticity emerges as spinal interneuronal arcs reorganize. While mild extensor spasticity can assist standing transfers, severe spasticity causes painful spasms, contractures, and impaired hygiene. First-line oral pharmacotherapy for spinal spasticity is Baclofen, a structural GABA analog that acts as a presynaptic and postsynaptic GABA-B receptor agonist in the dorsal horn of the spinal cord to hyperpolarize motor neurons (rapid discontinuation of oral or intrathecal baclofen causes life-threatening withdrawal: hyperthermia, rhabdomyolysis, status epilepticus, and multiorgan failure, requiring urgent restoration of baclofen and IV benzodiazepines). Alternative agents include Tizanidine (a central alpha-2 adrenergic agonist related to clonidine that causes dry mouth, sedation, and hypotension), Diazepam, Botulinum toxin type A/B (for focal limb spasticity), and Dantrolene (which acts peripherally on skeletal muscle sarcoplasmic reticulum ryanodine RyR1 channels to block calcium release; preferred in cerebral/stroke spasticity because it causes less central sedation, though it carries a black-box risk of idiosyncratic hepatotoxicity). Finally, two common subacute SCI complications below the level of injury are Deep Vein Thrombosis (requiring low-molecular-weight heparin prophylaxis) and Heterotopic Ossification (ectopic lamellar bone formation within periarticular soft tissues, most commonly around the hip joint, presenting 1-4 months post-SCI with warm, swollen, erythematous joint stiffness, elevated serum alkaline phosphatase, and early uptake on triple-phase bone scan; treated with indomethacin or etidronate/bisphosphonates and gentle range of motion).

Pressure injuries develop over bony prominences (sacrum, coccyx, greater trochanters, heels in supine patients; ischial tuberosities in wheelchair users) when sustained external pressure exceeds capillary closing pressure (~32 mmHg), causing tissue ischemia and necrosis that begins deep at the bone-muscle interface and extends superficially. The National Pressure Injury Advisory Panel (NPIAP) classifies ulcers into six categories: Stage 1 (intact skin with localized non-blanchable erythema over a bony prominence); Stage 2 (partial-thickness loss of dermis presenting as a shallow open ulcer with a pink-red wound bed without slough, or an intact/ruptured serum-filled blister); Stage 3 (full-thickness skin loss extending into the subcutaneous adipose tissue, where fat is visible and undermining/tunneling may exist, but bone, tendon, and muscle are NOT exposed); Stage 4 (full-thickness skin and tissue loss with directly exposed or palpable bone, tendon, cartilage, or muscle, carrying a high risk of contiguous osteomyelitis requiring MRI or bone biopsy); Unstageable (full-thickness tissue loss in which the base of the ulcer is completely obscured by yellow/tan slough or black/brown necrotic eschar; the true stage—3 or 4—cannot be determined until the slough/eschar is debrided); and Deep Tissue Pressure Injury (intact or non-intact skin with a localized persistent deep red, maroon, or purple discoloration or blood-filled blister from deep shear damage). Note two critical management rules: (1) Stable, dry, intact black eschar on an ischemic heel without erythema, fluctuance, or drainage serves as a natural biological cover and should NOT be debrided until arterial inflow is evaluated and restored; and (2) Pressure ulcers do not reverse stages as they heal (a healing Stage 4 ulcer is documented as a healing Stage 4 ulcer, never down-staged to Stage 2).

Comprehensive post-stroke rehabilitation integrates physical therapy (gait, balance, mobility, and gross motor transfer training), occupational therapy (fine motor upper-extremity coordination, adaptive equipment, and Activities of Daily Living—bathing, dressing, toileting, grooming, feeding, plus Instrumental ADLs like cooking and managing finances), and speech-language pathology (aphasia therapy, cognitive-linguistic rehabilitation, and dysphagia evaluation). Up to 50% of acute stroke patients develop neurogenic oropharyngeal dysphagia, with a high incidence of silent aspiration (entry of liquid or food below the true vocal cords without triggering a protective cough reflex). Every acute stroke patient must remain strictly NPO (nothing by mouth, including oral aspirin) until passing a bedside nursing water swallow screen; patients who fail screening undergo gold-standard instrumental evaluation via a Modified Barium Swallow Study (Videofluoroscopic Swallowing Study, VFSS) or Fiberoptic Endoscopic Evaluation of Swallowing (FEES) to guide chin-tuck maneuvers and thickened liquid diets. In the hemiplegic upper extremity, early flaccidity of the rotator cuff (especially supraspinatus) allows gravitational downward traction of the humeral head, causing Glenohumeral Subluxation and Complex Regional Pain Syndrome type I (shoulder-hand syndrome); prevention requires supporting the hemiplegic arm on a wheelchair lap tray or pillow and strictly avoiding pulling on the paretic arm during bed transfers or using overhead pulley exercises.