Inspection of the Motor System
Inspection is the first step of the motor examination and is undertaken before the examiner ever lays a hand on the patient. A great deal can be learned by observation alone, and the discipline of looking carefully — at posture, at muscle bulk, at the surface of the muscle for spontaneous movement — frequently narrows the differential before tone, power, or reflexes are formally assessed. The patient should be adequately exposed and observed at rest in good light, with the relevant limbs and muscle groups visible and symmetrically positioned so that the two sides can be compared.
Posture and Positioning
Note how the patient holds the body and limbs at rest. Asymmetry of resting posture is often the first clue to a lateralized lesion. A chronic spastic hemiparesis produces a characteristic attitude: the upper limb is adducted at the shoulder, flexed at the elbow, wrist, and fingers, while the lower limb is extended and the foot plantarflexed and inverted. The flexor-predominant posture of the arm and extensor-predominant posture of the leg reflect the selective distribution of weakness and the spasticity that accompany an upper motor neuron lesion. Other resting attitudes carry their own significance — for example, the wrist drop of a radial nerve palsy or the clawed posture associated with intrinsic hand-muscle weakness. Throughout inspection, compare one side with the other, since subtle asymmetry is more readily appreciated than an absolute abnormality.
Muscle Bulk
Examine the muscles for atrophy (wasting) and, less commonly, hypertrophy. Bulk is assessed by inspection and, when an asymmetry is suspected, by palpation and by measuring limb circumference at fixed bony landmarks on the two sides for comparison. Look systematically at the small muscles of the hands, the forearms, the shoulder girdle, the thighs, and the calves, and remember that handedness produces a normal, modest discrepancy in bulk between the dominant and non-dominant limbs.
- Neurogenic atrophy. Loss of the lower motor neuron supply — at the level of the anterior horn cell, nerve root, plexus, or peripheral nerve — produces denervation atrophy. The wasting conforms to the territory of the affected structure and is typically accompanied by weakness, hyporeflexia, and, often, fasciculations.
- Disuse atrophy. Prolonged immobilization, joint disease, or a painful limb leads to wasting in the absence of denervation. It is usually milder, more diffuse within the immobilized segment, and unaccompanied by fasciculations.
- Myopathic wasting. In many myopathies the atrophy is proximal and relatively symmetric, involving the pelvic and shoulder girdles, though the pattern varies with the specific disorder.
The distribution of atrophy is its most informative feature. Wasting of the intrinsic hand muscles, for instance, may localize to an ulnar or median neuropathy, a C8–T1 root or lower-trunk plexus lesion, or anterior horn cell disease, depending on which muscles are involved and what else accompanies the finding. In amyotrophic lateral sclerosis a recognized pattern is the “split hand,” in which the thenar eminence and first dorsal interosseous waste disproportionately while the hypothenar eminence is relatively spared. Atrophy may be generalized (as in cachexia or advanced motor neuron disease) or focal, and the distinction guides localization.
Hypertrophy and Pseudohypertrophy
True muscle hypertrophy — an increase in bulk from enlargement of muscle fibers — is uncommon and may follow sustained overuse or accompany certain myotonic and metabolic conditions. More clinically familiar is pseudohypertrophy, in which a muscle appears enlarged but is in fact weak because functioning muscle has been replaced by fat and connective tissue. The classic example is calf pseudohypertrophy in Duchenne muscular dystrophy, where the enlarged-appearing calves are weak rather than strong. Recognizing that an apparently bulky muscle is weak on testing is the key to identifying pseudohypertrophy.
Fasciculations
A fasciculation is a brief, involuntary contraction of a single motor unit — the muscle fibers supplied by one motor neuron — visible as a fine flicker or twitch beneath the skin. Fasciculations do not, on their own, move a joint. When pathologic, they reflect irritability of the lower motor neuron, most characteristically at the level of the anterior horn cell, and are a hallmark of motor neuron disease when they occur together with weakness and atrophy.
Because fasciculations are intermittent and easily missed, the examination requires patience and good technique:
- Inspect the fully relaxed muscle in good tangential lighting, which casts shadows that make surface flickers visible.
- Observe each region for an unhurried interval rather than glancing briefly, since fasciculations occur irregularly.
- Gentle percussion of the muscle, or brief voluntary contraction followed by relaxation, may provoke them.
- The tongue, examined at rest within the mouth (and not protruded, since protrusion produces normal tremulous movement that can be mistaken for fasciculation), is a sensitive site in suspected motor neuron disease.
Fasciculations must be interpreted in context and distinguished from related phenomena:
- Benign fasciculations are common in healthy people, often involving the calves, eyelids, or small hand muscles, and are not associated with weakness or atrophy. They are of no pathologic significance.
- Myokymia is a continuous, undulating, worm-like movement of muscle — a more sustained and rippling phenomenon than the discrete twitch of a fasciculation — and has its own set of causes.
Other Involuntary Movements Noted on Inspection
Inspection of the motor system also encompasses recognition of adventitious, involuntary movements. These should be observed and described — their distribution, rhythmicity, speed, and the circumstances under which they appear (at rest, with posture, or with action). The principal categories are tremor, chorea, dystonia, and myoclonus. A detailed treatment of their phenomenology and localization belongs to the study of movement disorders; at the stage of motor inspection the task is simply to recognize that an abnormal movement is present and to characterize it accurately for documentation and further evaluation.
Localizing Atrophy by Its Distribution
The pattern of wasting is one of the most useful localizing signs available on inspection alone. The following associations are broad guides and must always be interpreted alongside the rest of the examination.
| Pattern of atrophy | Likely localization |
|---|---|
| Focal wasting of intrinsic hand muscles | Ulnar or median neuropathy, or a C8–T1 root / lower brachial plexus lesion (pattern depends on which muscles are involved) |
| Proximal, relatively symmetric wasting (shoulder and pelvic girdles) | Myopathy |
| Wasting confined to one or more myotomes / dermatomyotomal segment | Nerve root (radiculopathy) or, when accompanied by fasciculations, anterior horn cell disease |
| Wasting in the territory of a single named peripheral nerve | Mononeuropathy |
| Distal, symmetric wasting (feet and hands, “length-dependent”) | Peripheral polyneuropathy |
| Widespread wasting with fasciculations across multiple regions | Anterior horn cell / motor neuron disease |
Documentation
Findings on inspection should be recorded plainly and in a way that another examiner can reproduce. Describe posture and any asymmetry; state where atrophy or hypertrophy is present and, where relevant, its measured circumference compared with the opposite side; note the presence, location, and provoking maneuvers for any fasciculations; and describe any involuntary movements by their character and distribution. Where bulk and surface findings are normal, this too is worth recording, since it anchors the subsequent assessment of tone and power.
Clinical Note
Fasciculations are most meaningful in context. When they accompany weakness and atrophy, they point to active denervation and raise concern for anterior horn cell disease such as amyotrophic lateral sclerosis. Isolated fasciculations in an otherwise normal muscle — without weakness or wasting — are usually benign and of no pathologic significance.
References
- Campbell WW, Barohn RJ. DeJong's The Neurologic Examination. 8th ed. Philadelphia: Wolters Kluwer; 2020.
- Ropper AH, Samuels MA, Klein JP, Prasad S. Adams and Victor's Principles of Neurology. 11th ed. New York: McGraw-Hill; 2019.
- Biller J, Gruener G, Brazis PW. DeMyer's The Neurologic Examination: A Programmed Text. 7th ed. New York: McGraw-Hill; 2017.
- O'Brien M. Aids to the Examination of the Peripheral Nervous System. 5th ed. Edinburgh: Saunders Elsevier (on behalf of the Medical Research Council); 2010.