10.1 Diagnosis: Muscular Disorders

10.1 Diagnosis: Muscular Disorders

Muscular complaints are among the most common reasons patients enter a chiropractic office, yet NBCE Part II rewards candidates who can separate a straightforward mechanical strain from a systemic myopathy or a central sensitization syndrome. Within the Neuromusculoskeletal Diagnosis domain (20% of the 255-question exam), muscular vignettes usually offer a handful of clues — onset, distribution of weakness versus pain, skin findings, medication history, and laboratory values — and ask you to name the most likely diagnosis or identify the finding that demands medical referral before continued manual care.

Muscle Strain: The Mechanical Baseline

A muscle strain (pulled muscle) is traumatic tearing of muscle fibers, most often at the musculotendinous junction. Strains follow acute overload: sprinting, heavy lifting, an unexpected eccentric load, or a slip on ice that forces the hamstrings to decelerate the body. The history is focal, the timeline is acute, and the patient can usually point to one muscle belly or tendon insertion.

Strains are classified by severity:

On examination, strain pain is reproducible: palpation over the injured tissue, passive stretch of the muscle, and resisted activation all provoke the same localized discomfort. Deep tendon reflexes and sensation remain intact unless a concurrent nerve injury exists. Creatine kinase (CK) may rise mildly after a large tear but does not reach the levels seen in inflammatory myopathy or rhabdomyolysis. Imaging is unnecessary for most Grade I–II injuries; MRI confirms a Grade III rupture when surgical consultation is being considered.

Inflammatory Myopathies

A myopathy is primary disease of muscle itself, as opposed to neuropathy (nerve), radiculopathy (nerve root), or neuromuscular junction disorders. Part II emphasizes autoimmune inflammatory myopathies because their proximal weakness pattern overlaps with what patients describe as difficulty exercising, yet the treatment pathway is entirely different from manual therapy for a strain.

Polymyositis

Polymyositis features subacute, progressive, symmetric proximal weakness: hip flexors, quadriceps, shoulder girdle, and neck flexors. Patients report trouble climbing stairs, rising from a low chair, or reaching overhead. Deep tendon reflexes are typically preserved. Muscle pain may be present but objective weakness is the dominant finding — a key distinction from fibromyalgia.

Laboratory hallmarks include markedly elevated CK, elevated aldolase, and AST/ALT elevation from muscle breakdown (not primary hepatocellular disease). Autoimmune serology may show ANA positivity; myositis-specific antibodies include anti-Jo-1 (antisynthetase syndrome, associated with interstitial lung disease and mechanic's hands), anti-SRP, and anti-Mi-2. Electromyography (EMG) shows a myopathic motor-unit pattern: short-duration, low-amplitude, polyphasic potentials.

Dermatomyositis

Dermatomyositis shares the proximal weakness and laboratory profile of polymyositis but adds pathognomonic skin findings:

• Heliotrope rash — violaceous or dusky erythema of the upper eyelids, sometimes with periorbital edema
• Gottron papules — flat-topped violaceous papules over the extensor surfaces of metacarpophalangeal (MCP) and interphalangeal (IP) joints
• Shawl sign (erythema over upper back/shoulders), V-sign (anterior neck/upper chest), periungual telangiectasias, and mechanic's hands in antisynthetase overlap

When a Part II vignette mentions violaceous eyelids or knuckle papules with shoulder weakness, think dermatomyositis before polymyositis. Both require rheumatology referral; dermatomyositis carries an increased association with underlying malignancy in adults over 40, especially when the rash precedes weakness.

Inclusion body myositis (IBM)

Inclusion body myositis is an inflammatory myopathy of adults over 50 with a distinctive pattern: both proximal and distal weakness, often asymmetric, with prominent finger-flexor and quadriceps involvement. Patients may drop objects or fall because of knee buckling. CK is only mildly elevated compared with polymyositis. IBM responds poorly to immunosuppression — a clue in answer choices that mention steroid failure.

Fibromyalgia and Fibromyalgia-Like Presentations

Fibromyalgia is a central sensitization syndrome, not an inflammatory myopathy. Diagnostic features include:

• Widespread pain for at least three months, affecting both sides of the body, above and below the waist, and the axial skeleton
• Fatigue, non-restorative sleep, and cognitive disturbance ("fibro fog")
• Frequent comorbidities: tension headache, irritable bowel symptoms, mood disturbance, temporomandibular discomfort
• Normal CK, normal ESR, normal CRP
• Normal strength on formal manual muscle testing despite the patient's report of exhaustion
• Generalized tenderness or multiple tender points without objective inflammation

The classic Part II trap pairs fibromyalgia with polymyositis: both may complain of diffuse aching and fatigue, but only inflammatory myopathy produces measurable proximal weakness and markedly elevated CK. Fibromyalgia patients hurt everywhere yet move individual joints through full range when asked one joint at a time; polymyositis patients cannot generate normal force on hip flexion or shoulder abduction testing.

Toxic and Metabolic Myopathies

Statin-associated myopathy ranges from benign myalgias without CK elevation to severe weakness and rhabdomyolysis (CK often >10,000 U/L, myoglobinuria, dark urine, risk of acute kidney injury). Symptoms typically begin weeks to months after starting or dose-escalating a statin. Weakness is often symmetric and proximal. Discontinue the offending agent and obtain CK; coexisting hypothyroidism, intense exercise, and interacting medications (fibrates, macrolide antibiotics) increase risk.

Hypothyroid myopathy, alcohol-related myopathy, and electrolyte disturbances (hypokalemia, hypophosphatemia) appear less frequently but follow the same principle: diffuse or symmetric weakness plus laboratory clues outside the normal strain profile.

Differential Summary

Red Flags and Chiropractic Management Boundaries

Refer before aggressive manual care when you encounter progressive symmetric proximal weakness, CK more than five to ten times normal, heliotrope rash or Gottron papules, dysphagia or dysphonia with weakness (bulbar involvement), fever with muscle pain, dark urine after exertion, or weakness accompanied by sensory loss and reflex changes (think neuropathy or radiculopathy instead).

Uncomplicated Grade I–II strains are appropriate for conservative care: relative rest, ice in the acute phase, gradual reloading, and correction of biomechanical contributors. Inflammatory and toxic myopathies require medical co-management; high-velocity manipulation into acutely inflamed or systemically weakened muscle is inappropriate.

Exam-Style Pearls

Expect stems that pair difficulty climbing stairs + CK of 3,200 U/L (polymyositis), violaceous eyelids + shoulder weakness (dermatomyositis), or widespread tender points + normal labs and normal strength (fibromyalgia). A statin started six weeks ago with diffuse aching and CK of 2,400 U/L is statin myopathy, not fibromyalgia. A weekend athlete who felt a pop in the hamstring with ecchymosis and focal weakness on knee flexion testing has a strain until proven otherwise.