Other Signs & Eponyms

The bedside neurologic examination is studded with named signs, each a compact maneuver that, when correctly performed and correctly interpreted, points to a particular pathway or mechanism. The value of an eponymous sign lies not in the name but in what it localizes. This page assembles the well-established bedside signs that are not given their own chapter elsewhere, grouped by the function each one interrogates: corticospinal release phenomena, meningeal irritation, root and peripheral-nerve provocation, sensory and demyelinating signs, and the neuromuscular and metabolic signs. The plantar (Babinski) response and the functional or non-organic signs are addressed in full on their own dedicated pages and are therefore only cross-referenced here, not repeated. Throughout, the recurring lesson is that a sign localizes a lesion or implicates a mechanism; the disease itself is named by the clinical context.

Upper Motor Neuron / Release Signs

These signs reflect loss of cortical inhibition over reflexes and posture — the disinhibited spinal and segmental machinery that emerges when the corticospinal tract is damaged. They are most informative when asymmetric, since minor symmetric responses occur in normal individuals.

• Hoffmann sign. The examiner stabilizes the patient's middle finger and sharply flicks the nail of its distal phalanx into flexion; a positive response is reflex flexion (adduction) of the thumb and, often, the index finger. It indicates an exaggerated finger-flexor reflex from a corticospinal lesion rostral to the C5–C6 segment, most commonly cervical spondylotic myelopathy. A unilateral or clearly asymmetric Hoffmann is the meaningful finding; a faint bilateral response can occur in hyperreflexic but otherwise normal people.
• Trömner sign. A variant eliciting the same finger-flexor reflex by flicking or tapping the volar surface of the fingertip (typically the middle finger) upward rather than flicking the nail downward. A positive response is the same reflex flexion of the thumb and fingers and carries the same significance as Hoffmann — an upper motor neuron sign suggesting a corticospinal lesion above the lower cervical cord.
• Pronator drift. With the arms held outstretched in front, palms upward (supinated), and the eyes closed, the affected arm slowly drifts downward while the forearm rotates into pronation. The pronation is the key feature: corticospinal control biases the upper limb toward its antigravity flexor and pronator muscles, so a subtle corticospinal lesion unmasks itself as drift with pronation before frank weakness is detectable on confrontation testing. It is one of the most sensitive signs of mild pyramidal (upper motor neuron) hemiparesis. (Pronator drift is covered in greater depth on its own page.)

Meningeal Irritation

These signs reflect reflex protective contraction in response to stretch of inflamed or chemically irritated meninges and nerve roots. They support a diagnosis of meningitis or subarachnoid hemorrhage when present, but all three are insensitive — their absence does not exclude meningeal irritation, particularly in the very young, the elderly, the immunosuppressed, or the obtunded.

• Nuchal rigidity. Resistance to passive flexion of the neck, with the patient supine. The neck resists the chin being brought toward the chest, whereas passive rotation and lateral movement are comparatively preserved — a pattern that distinguishes meningeal rigidity from generalized cervical spine stiffness.
• Kernig sign. With the patient supine and the hip flexed to 90 degrees, the examiner attempts to passively extend the knee. Resistance to extension and pain in the posterior thigh and back constitute a positive sign, reflecting stretch of the inflamed lumbosacral roots and meninges.
• Brudzinski sign. Passive flexion of the neck provokes involuntary reflex flexion of the hips and knees — the patient draws the legs up to relieve traction on the irritated meninges. Several variants exist, but the neck (nape) sign is the classically taught form.

Root and Nerve Provocation

These maneuvers mechanically provoke a compressed or irritated nerve root or peripheral nerve, reproducing the patient's characteristic symptoms in the appropriate distribution. A positive test is reproduction of the radicular or neuropathic symptom, not merely local discomfort.

• Spurling sign. The examiner extends and laterally flexes the patient's neck toward the symptomatic side and applies gentle downward axial compression on the head. Reproduction of radicular pain or paresthesia radiating into the ipsilateral arm indicates cervical radiculopathy, as the maneuver narrows the neural foramen onto the affected root.
• Straight-leg raise (Lasègue sign). With the patient supine and the knee extended, the examiner passively flexes the hip by raising the leg. Reproduction of radicular pain radiating down the posterior leg, typically between 30 and 70 degrees of elevation, indicates lower lumbosacral (L5/S1) root irritation, most often from a herniated disc. The crossed straight-leg raise — radicular pain in the symptomatic leg provoked by raising the contralateral, asymptomatic leg — is less sensitive but considerably more specific for a clinically significant disc herniation. The reverse straight-leg raise (femoral stretch test), performed with the patient prone and the knee flexed and hip extended, stretches the upper lumbar roots and tests for an L2–L4 radiculopathy.
• Tinel sign. Light percussion over a compressed or regenerating peripheral nerve elicits tingling or an electric sensation radiating into that nerve's sensory territory. Percussion over the median nerve at the volar wrist reproducing paresthesia in the thumb, index, and middle fingers supports carpal tunnel syndrome; the sign can be applied over any superficial entrapment site.
• Phalen sign. The patient holds both wrists in sustained, maximal flexion (commonly by pressing the dorsal surfaces of the hands together) for up to a minute. Reproduction of numbness or tingling in the median distribution supports carpal tunnel syndrome, as wrist flexion raises pressure within the carpal tunnel.

Sensory and Demyelinating Signs

These signs interrogate the integrity of myelinated conduction and of balance, but they do not all converge on a single pathway: Lhermitte localizes to the cervical posterior columns, Uhthoff reflects heat-sensitive conduction block in previously demyelinated tracts, and Romberg exposes balance that depends on vision because proprioceptive and/or vestibular input is impaired. (Lhermitte, Uhthoff, and Romberg are treated together in greater depth on a dedicated page; they are summarized here for completeness within this compendium.)

• Lhermitte sign. Neck flexion provokes a transient electric-shock or buzzing sensation that travels down the spine and often into the limbs. It localizes to irritation of the demyelinated or otherwise affected cervical dorsal columns and is non-specific as to cause: multiple sclerosis, cervical spondylotic myelopathy, vitamin B12 deficiency (subacute combined degeneration), radiation myelopathy, and certain chemotherapies (e.g., cisplatin) can all produce it.
• Uhthoff phenomenon. A transient worsening of neurologic symptoms — classically blurring or dimming of vision in a previously affected eye — provoked by a rise in body temperature from exercise, fever, or a hot environment. It reflects reversible, temperature-sensitive conduction block in previously demyelinated pathways: most famously the optic nerve, but motor and sensory tracts can re-declare their deficits the same way. Cooling restores conduction and the deficit resolves. Recognizing it as a pseudo-relapse spares an unnecessary relapse work-up.
• Romberg sign. The patient stands with the feet together, first with the eyes open and then closed. A positive sign is steadiness with the eyes open but swaying or falling once vision is removed, indicating that balance was depending on vision because proprioceptive and/or vestibular input is inadequate — most often dorsal-column proprioceptive loss (sensory ataxia), though vestibular failure can also unmask it. Romberg is not a test of cerebellar function: the patient with cerebellar ataxia is unsteady with the eyes open as well, so removing vision adds little.

Neuromuscular and Metabolic Signs

This group spans the disordered excitability of nerve and muscle in metabolic states and the patterns of weakness produced by myopathy and segmental cord lesions.

• Chvostek sign. Tapping over the facial nerve just anterior to the ear elicits an ipsilateral twitch of the facial muscles. It reflects the heightened neuromuscular excitability of hypocalcemia, but its specificity is low — a minor twitch is present in a substantial fraction of normocalcemic individuals — so it must be interpreted with caution.
• Trousseau sign. A sphygmomanometer cuff is inflated above systolic pressure on the upper arm and held for up to three minutes; in hypocalcemia this provokes carpopedal spasm — flexion of the wrist and metacarpophalangeal joints with extension of the interphalangeal joints and adduction of the thumb. It is more specific for latent tetany than the Chvostek sign.
• Beevor sign. When the supine patient flexes the neck or attempts a partial sit-up, the umbilicus deviates upward because the lower rectus abdominis is weaker than the upper. Upward umbilical movement localizes weakness to the lower abdominal muscles and implies a cord or segmental lesion at approximately the T9–T10 level; it is also described in some neuromuscular disorders affecting the abdominal wall, such as facioscapulohumeral muscular dystrophy.
• Gowers sign. Rising from the floor, the patient cannot lift the trunk against gravity using the hip and knee extensors alone and instead "climbs up" the legs — placing the hands on the thighs and walking them upward to push the trunk erect. It signifies proximal lower-limb (pelvic-girdle) weakness and is classically associated with the muscular dystrophies, though it occurs in any cause of significant proximal myopathy.