Inspection of muscle bulk and contour is the silent first step of the motor exam — the part that happens before you touch the patient and that often declares the diagnosis. A scaphoid hollow above the patient’s clavicle. A sunken thenar eminence. A calf that looks too large for the leg. The shape of the muscles tells you, in some patients, what the rest of the exam is going to find. The skill is in noticing.

This page covers the inspection of muscle bulk, the patterns of atrophy and hypertrophy, and what each pattern means at the bedside. The page complements the strength testing and motor unit pages; here the focus is on what the muscles look like at rest, before any voluntary movement has been requested.

What Determines Normal Bulk

Muscle bulk reflects the balance of synthesis and degradation of muscle fibers, modulated by activity, hormonal status, and nutrition. The bulk of a muscle depends on:

• The number of functional motor units: each motor unit innervates many muscle fibers, and loss of motor units (anterior horn cell disease, severe peripheral neuropathy) directly reduces muscle bulk.
• The size of each muscle fiber: fiber atrophy from disuse, denervation, steroid excess, malnutrition, or aging reduces the size of individual fibers.
• Replacement of muscle by fat or fibrous tissue: in some dystrophies, especially Duchenne, the muscle volume may be preserved or even increased while the actual contractile tissue is reduced — pseudohypertrophy.
• Sex, age, body habitus, and activity: men have larger muscles than women on average; older adults have less bulk than younger ones; a sedentary patient has less bulk than an athlete. These baseline differences inform interpretation of bedside findings.

How to Inspect Bulk Systematically

The patient should be undressed enough that you can see the muscles. Stand back and look. The first impression is often the most useful one.

Standard sites to inspect:

• Shoulder girdle: deltoid, trapezius, supraspinatus and infraspinatus fossae (the latter visible posteriorly), pectoralis major, latissimus dorsi.
• Upper arm: biceps and triceps.
• Forearm: flexor and extensor masses.
• Hand: thenar eminence, hypothenar eminence, first dorsal interosseous (visible from the dorsum of the hand), other interossei (sunken spaces between metacarpals), and the lumbricals.
• Pelvic girdle: gluteal mass.
• Thigh: quadriceps and hamstring mass.
• Lower leg: gastrocnemius and soleus, tibialis anterior.
• Foot: extensor digitorum brevis on the dorsum, intrinsic foot muscles, and the high-arched (pes cavus) or flat foot, which are clues to chronic neurological disease.
• Face: temporalis (a sunken hollow above the zygoma), masseter, facial muscles (visible asymmetry), tongue, sternocleidomastoid.

Compare each muscle group with the contralateral side. Asymmetry in adults is usually pathological (a slight dominance of the writing-hand musculature is normal but should not be marked).

Atrophy

Atrophy is a reduction in muscle bulk. It can be classified by mechanism and by distribution.

Patterns by Mechanism

• Denervation atrophy: from loss of innervation (anterior horn cell disease, severe peripheral nerve injury, chronic radiculopathy). Often dramatic and accompanied by fasciculations and weakness in the same distribution.
• Disuse atrophy: from prolonged immobilization (cast, bed rest, hemiplegia). Develops over weeks; less severe than denervation atrophy for similar duration. The reflexes are preserved (because there is no denervation).
• Atrophy from primary muscle disease: dystrophies, inflammatory myopathies, metabolic myopathies. The distribution follows specific muscle groups characteristic of each disease. Sensation is preserved.
• Atrophy from systemic disease: malnutrition, malignancy (cachexia), advanced renal or hepatic disease, hyperthyroidism, prolonged corticosteroid use. Usually generalized.
• Sarcopenia: age-related loss of muscle mass, often present in healthy older adults. Distinguished from pathological atrophy by its symmetry, its generalized distribution, and its slow progression.

Patterns by Distribution

Specific Patterns to Recognize

The Wasted Hand

A wasted hand can localize precisely:

• Thenar atrophy with preserved hypothenar bulk: median neuropathy (carpal tunnel in chronic disease). The first lumbrical may also be wasted.
• Hypothenar atrophy with first dorsal interosseous wasting: ulnar neuropathy (especially at the elbow). Preserved thenar bulk distinguishes this from a median lesion.
• Wasting of all hand intrinsics (thenar + hypothenar + interossei): C8-T1 root or lower brachial plexus lesion, syringomyelia involving the cervical cord, or distal motor neuron disease (Hirayama disease in young men, monomelic amyotrophy; or ALS).
• Split hand sign (selective wasting of thenar eminence and lateral hand with relative sparing of hypothenar): highly suggestive of ALS, where there is preferential involvement of certain motor neuron pools.

The Wasted Shoulder Girdle

• Scapular winging: detailed in the CN XI page. Trapezius winging (CN XI) is distinct from serratus anterior winging (long thoracic nerve). Each has a distinctive resting pattern of the scapula.
• Bilateral shoulder girdle atrophy: facioscapulohumeral dystrophy (FSHD) — winging, atrophy of pectoralis major (with preserved deltoid), characteristic “Popeye” appearance of forearms. Limb-girdle dystrophy. Polymyositis and dermatomyositis. ALS.
• Asymmetric shoulder girdle wasting: brachial neuritis (Parsonage-Turner), thoracic outlet syndrome, brachial plexopathy.

The Wasted Lower Leg

• Distal wasting with pes cavus and hammer toes: chronic peripheral neuropathy, classically Charcot-Marie-Tooth disease. The combination is so characteristic that a single look at the feet often makes the diagnosis. The wasting follows a length-dependent pattern with the small intrinsic foot muscles affected first.
• “Inverted champagne bottle” leg: distal wasting with a relatively preserved proximal thigh, classical for CMT.
• Calf atrophy: S1 radiculopathy, distal myopathy (Welander, Miyoshi), neuropathy.
• Tibialis anterior atrophy: L5 radiculopathy, peroneal nerve palsy, sciatic neuropathy.

Bulbar Atrophy

The tongue is the most informative bulbar muscle. A normal tongue has smooth, rounded contours; a denervated tongue is shrunken, hollow, and scalloped. Bilateral tongue atrophy with fasciculations is essentially diagnostic of motor neuron disease (ALS or progressive bulbar palsy) or, in younger patients, Kennedy disease. The temporalis and masseter can also show atrophy in motor neuron disease and in chronic trigeminal disease, producing characteristic facial sunkenness above the cheekbones and at the angle of the jaw.

Hypertrophy and Pseudohypertrophy

The opposite finding — increased muscle bulk — can also be diagnostic.

True Hypertrophy

Increased muscle bulk from increased contractile tissue. Causes:

• Exercise: the most common cause; asymmetric in pitchers, tennis players, and others with one-sided sports.
• Myotonic disorders: myotonia congenita (Thomsen and Becker) produces generalized muscular hypertrophy (“herculean” appearance), reflecting continuous low-grade contraction of the affected muscles.
• Anabolic steroid use: dramatic generalized hypertrophy out of proportion to training history.

Pseudohypertrophy

Increased muscle bulk from replacement of muscle by fat and fibrous tissue. The classical site is the calf in Duchenne and Becker muscular dystrophies, where the calf appears bulky but is weak — the contractile tissue has been replaced. The deltoid and tongue can also show pseudohypertrophy in some dystrophies. The bedside test is to feel the muscle: pseudohypertrophic muscle has a doughy or rubbery consistency rather than the firmness of normal muscle, and is weak when tested.

Quantifying Bulk

For research and longitudinal tracking, muscle bulk can be measured with calipers or with imaging (CT or MRI volumetrics, ultrasound). At the bedside, the classical method is circumference measurement at standardized sites:

• Mid-arm circumference (at the midpoint between acromion and olecranon).
• Mid-thigh circumference (at the midpoint between greater trochanter and joint line of knee).
• Calf circumference (at the maximum widest point).

Compare side to side and document. A difference of more than about 1 cm in arm or calf circumference, or more than 1.5-2 cm in the thigh, is meaningful in most patients. Smaller differences may still be significant if the patient is asymmetrically active.

Distinguishing Denervation Atrophy from Disuse

This distinction matters because the implications are very different. Denervation atrophy is a sign of nervous system disease; disuse atrophy is a sign of immobility. Several features help distinguish them:

🔍 Did You Know?

The “split hand” sign in ALS — selective preferential wasting of the thenar eminence and the first dorsal interosseous, with relative sparing of the hypothenar eminence — reflects a peculiar selective vulnerability of certain motor neuron pools to the disease process. The thenar muscles and first dorsal interosseous, which are involved in fine grip and pinch, share an inferred selective sensitivity that hypothenar muscles do not. The pattern was not appreciated as a diagnostic sign for decades; it is now recognized as one of the most useful single bedside findings in distinguishing ALS from other causes of hand weakness.

Special Inspection Findings

Pes Cavus and Hammer Toes

The high-arched foot with hammer toes is the chronic structural signature of distal lower-extremity neuropathy. The intrinsic foot muscles weaken over years, the long flexors and extensors become unopposed, and the result is the characteristic foot deformity. CMT is the prototype, but any chronic distal neuropathy (hereditary spastic paraplegia with peripheral involvement, Friedreich ataxia, sometimes diabetic neuropathy) can produce it. The deformity tells you the disease has been present for many years, often since childhood.

Scapular Winging Patterns

Scapular winging is described in detail on the CN XI page. The key distinction is between trapezius winging (CN XI, scapula displaced laterally and downward) and serratus anterior winging (long thoracic nerve, medial border of scapula lifts off the chest wall when the patient pushes against a wall).

Wasted Tongue with Fasciculations

The tongue in motor neuron disease is shrunken, wrinkled like a raisin, and conspicuously fasciculating. The combination of bilateral tongue atrophy, fasciculations, dysarthria, and dysphagia is essentially diagnostic of bulbar motor neuron disease in an adult. Kennedy disease shows additional features: perioral fasciculations (chin twitching), proximal limb weakness, gynecomastia, and androgen insensitivity.

Calf Pseudohypertrophy

A young boy with large calves and difficulty climbing stairs has Duchenne muscular dystrophy until proven otherwise. The calves look full and rounded but are weak on testing. Becker muscular dystrophy presents with a similar picture but later (childhood or adulthood) and less severely. Calf pseudohypertrophy in an older patient suggests Becker, limb-girdle dystrophy (some types), or rarely amyloid myopathy.

Pitfalls and Pearls

• Inspect before you touch. Bulk findings are most reliable when the patient is at rest, fully exposed, and not yet flexing or tensing muscles.
• Compare sides. Asymmetry is the easiest finding to detect and often the most diagnostic.
• Wasting + fasciculations + weakness = anterior horn cell disease until proven otherwise. Look for the combination across multiple body regions to clinch ALS.
• Wasting + sensory loss + areflexia = peripheral neuropathy. The sensory component is the distinguishing feature.
• Pseudohypertrophy of the calves in a young boy = Duchenne until proven otherwise. Send a CK and obtain genetic testing.
• Pes cavus and hammer toes signal chronic distal neuropathy. Family history and a careful look at parents’ feet may make the diagnosis of CMT before any testing.
• Bilateral tongue atrophy with fasciculations is ALS or Kennedy disease. Check the rest of the patient: brisk reflexes argue for ALS, perioral fasciculations and proximal weakness with gynecomastia argue for Kennedy.
• Split hand pattern is highly specific for ALS. Selective thenar and first dorsal interosseous wasting with preserved hypothenar bulk is one of the most useful single bedside signs.
• Hand intrinsics wasted + brisk arm reflexes + leg spasticity = ALS or cervical myelopathy with motor neuron involvement. Differentiation is by imaging and EMG.
• FSHD is recognizable at a glance. The combination of scapular winging, pectoralis atrophy with preserved deltoid (“Popeye” arms), facial weakness, and asymmetric onset is highly characteristic.
• The temporalis fossa is hollow in chronic CN V denervation — most commonly from myotonic dystrophy, occasionally from trigeminal motor nerve injury.

References

1. Campbell WW. DeJong’s The Neurologic Examination. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2013. Chapter 29.
2. Wilbourn AJ. The split hand syndrome. Muscle Nerve. 2000;23(1):138.
3. Bushby K, Finkel R, Birnkrant DJ, et al. Diagnosis and management of Duchenne muscular dystrophy. Lancet Neurol. 2010;9(1):77-93.
4. Amato AA, Russell JA. Neuromuscular Disorders. 2nd ed. McGraw-Hill; 2016.
5. Reilly MM, Murphy SM, Laurá M. Charcot-Marie-Tooth disease. J Peripher Nerv Syst. 2011;16(1):1-14.
6. Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 7th ed. Philadelphia: Wolters Kluwer; 2017.