The pattern of sensory loss is, in many cases, the single most localizing finding in clinical neurology. A patient with numbness from the umbilicus down has a cord lesion at T10. A patient with loss of pain and temperature on the left side of the face and the right side of the body has a lateral medullary stroke on the left. A patient with bilateral loss of pain and temperature in a cape distribution sparing the lower body has a central cord syrinx. None of these requires imaging to localize the lesion; the bedside pattern names the site.

This page assembles the major patterns of sensory loss and the lesions they point to. It is organized by anatomical level — peripheral nerve, root, plexus, cord, brainstem, thalamus, cortex — and within each level by the specific pattern. The aim is to give the trainee a mental atlas that can be consulted at the bedside when the question is “where is the lesion?”

Peripheral Nerve Patterns

Distal Symmetric Polyneuropathy (Stocking-and-Glove)

Length-dependent loss of sensation, beginning at the toes and progressing proximally up the legs, eventually involving the fingers and hands when the leg loss reaches the knees. The pattern is symmetric. Pinprick and temperature are often involved together (small-fiber or mixed disease), with vibration loss most prominent (large-fiber predominance) or all modalities affected. Common causes:

• Diabetes mellitus (the most common cause worldwide)
• Alcohol
• Vitamin B12 deficiency
• Uremia
• Hypothyroidism
• Chemotherapy (vincristine, paclitaxel, platinum agents, bortezomib)
• Hereditary (Charcot-Marie-Tooth and other hereditary sensorimotor neuropathies)
• Inflammatory (CIDP)
• Toxic (heavy metals, organic solvents, n-hexane)
• Paraprotein-associated (MGUS, multiple myeloma, POEMS)

Mononeuropathy

Discrete sensory loss in the territory of a single peripheral nerve, often combined with weakness of the muscles supplied by the nerve. Examples:

• Median nerve (carpal tunnel): numbness and tingling in the palmar thumb, index, middle, and half of the ring finger; weakness and atrophy of the thenar eminence.
• Ulnar nerve (cubital tunnel): numbness in the little finger and half of the ring finger; weakness of intrinsic hand muscles (Froment sign, weak abduction of the small finger).
• Radial nerve (spiral groove): wrist drop with sensory loss on the dorsum of the hand (radial side).
• Peroneal nerve (fibular head): foot drop with sensory loss on the lateral leg and dorsum of the foot.
• Lateral femoral cutaneous (meralgia paresthetica): numbness and burning in the anterolateral thigh; no motor involvement.

Mononeuropathy Multiplex

Multiple discrete mononeuropathies in different territories, often asymmetric, often painful. The pattern points to:

• Vasculitis (polyarteritis nodosa, granulomatosis with polyangiitis, rheumatoid arthritis)
• Diabetes (multiple cranial and peripheral mononeuropathies)
• HIV
• Leprosy (worldwide a leading cause)
• Sarcoidosis

Recognition is important because the underlying disease is usually treatable, often with steroids and immunosuppression.

Root and Plexus Patterns

Radiculopathy

Dermatomal sensory loss in the distribution of a single nerve root, usually with associated radicular pain and often with weakness of muscles supplied by the same root. The common radiculopathies and their distributions are listed in the Sensory Overview page. The key features:

• Pain in the dermatome, often shooting along the limb.
• Numbness or paresthesia in the same distribution.
• Weakness in muscles supplied by the root (e.g., L5 produces foot dorsiflexion weakness).
• Loss of the corresponding reflex (e.g., S1 root produces ankle jerk loss; C7 root produces triceps reflex loss).

The most useful localizing distinction is between an L5 and S1 radiculopathy, which are often confused: L5 produces dorsiflexion weakness (foot drop), numbness on the dorsum of the foot, and loss of the medial hamstring reflex; S1 produces plantar flexion weakness, numbness on the lateral foot and sole, and loss of the ankle jerk.

Plexopathy

Sensory and motor loss spanning multiple dermatomes and peripheral nerve territories, reflecting damage at the brachial or lumbosacral plexus. The pattern is wider than a single root or single nerve. Causes include traumatic plexus injury, idiopathic neuralgic amyotrophy (Parsonage-Turner), radiation plexopathy, infiltrative plexopathy from malignancy (lung apex, breast, pelvic), and inflammatory plexitis.

Brachial plexopathies are often distinguished by upper trunk patterns (C5-C6, Erb-Duchenne palsy: shoulder weakness and lateral arm sensory loss) vs lower trunk patterns (C8-T1, Klumpke: hand intrinsics weakness with medial hand sensory loss and Horner if T1 sympathetic involvement). Lumbosacral plexopathies cause patterns crossing several lumbar or sacral root territories.

Spinal Cord Patterns

The cord is the part of the nervous system where sensory localization rewards anatomy most generously. The patterns of cord disease are quite distinct and largely diagnostic of the location and the underlying pathology.

Complete Cord Transection

Loss of all sensation below a defined level, with bilateral motor weakness, bladder and bowel dysfunction, and (if above T1) loss of sympathetic outflow producing autonomic instability. The level is the cardinal feature; document it carefully.

Brown-Séquard Syndrome (Hemisection)

The most pathognomonic of all cord syndromes. Hemisection of the cord produces:

• Ipsilateral loss of dorsal column function below the level — vibration, joint position sense, and fine touch are lost on the same side as the lesion. The dorsal columns at this level carry information from the ipsilateral body, which has not yet decussated.
• Contralateral loss of pain and temperature below the level (typically with a level a few segments below the lesion). The spinothalamic fibers crossed at or near the level of entry, so the contralateral body is the side affected.
• Ipsilateral motor weakness below the level from corticospinal tract involvement.
• Ipsilateral loss of all sensation at the level itself from damage to dorsal root entry fibers.

The crossed pattern — ipsilateral dorsal column loss with contralateral spinothalamic loss — is unique to cord hemisection. Causes include traumatic injury, tumor (especially extramedullary, like schwannoma or meningioma), multiple sclerosis, and rarely vascular events.

Central Cord Syndrome

A central cord lesion (syringomyelia, central cord stroke, intramedullary tumor) damages the fibers crossing through the anterior white commissure to reach the spinothalamic tract. The result is a “suspended” sensory loss: bilateral loss of pain and temperature in a “cape” distribution across the shoulders, arms, and upper back, with sparing of the lower body and the face. Dorsal column function is typically preserved (the dorsal columns are not in the center of the cord). As the lesion expands, the laterally placed spinothalamic fibers can also be involved, but the medial fibers are affected first.

The classical cause is syringomyelia — a fluid-filled cavity within the central cord, often associated with Chiari malformation. The suspended dissociated sensory loss accompanied by motor weakness in the hands (corticospinal involvement of upper-extremity fibers, which are more medial) and intact lower-extremity function defines the picture. Acute central cord syndrome from hyperextension injury in the elderly with cervical spondylosis is the other common presentation: bilateral arm weakness greater than leg weakness, with variable sensory loss.

Anterior Cord Syndrome

The anterior spinal artery supplies the anterior two-thirds of the cord — the corticospinal tracts, the spinothalamic tracts, and the anterior horn cells — sparing the dorsal columns. Infarction produces:

• Bilateral loss of pain and temperature below the level (spinothalamic).
• Bilateral motor weakness below the level (corticospinal).
• Bladder and bowel dysfunction (sacral parasympathetics).
• Preserved dorsal column function: vibration and joint position sense are intact below the level.

The clinical signature is dissociated sensory loss — pain and temperature gone, vibration and proprioception preserved — combined with motor weakness. The most common cause is anterior spinal artery infarction, which can result from aortic dissection or surgery (the artery of Adamkiewicz supply), atheroma, or rarely embolic phenomena.

Posterior Cord Syndrome

A posterior cord lesion — most commonly tabes dorsalis or subacute combined degeneration from B12 deficiency, occasionally a posterior column infarct or compression — affects the dorsal columns selectively. The clinical picture:

• Loss of vibration and joint position sense below the level.
• Sensory ataxia and positive Romberg.
• Preserved pain and temperature.
• Preserved or mildly affected motor function.

The dissociation is the opposite of anterior cord syndrome — large-fiber sensations lost, small-fiber sensations preserved.

Transverse Myelitis

An inflammatory lesion of the cord at a defined level, producing variable combinations of motor weakness, sensory loss, and bladder dysfunction at and below the level. The sensory level is often striking and the most reliable bedside finding. Causes include multiple sclerosis, neuromyelitis optica, postinfectious myelitis, lupus, sarcoid, and infectious myelitis (viral, parasitic).

Conus Medullaris and Cauda Equina Syndromes

Lesions at the bottom of the cord present distinctively:

• Conus medullaris (L1-L2 cord level): bilateral, symmetric sacral sensory loss (the “saddle” anesthesia), early bladder and bowel dysfunction, often less prominent leg weakness, sometimes with both upper and lower motor neuron signs depending on which segments are affected.
• Cauda equina (multiple lumbar and sacral roots within the spinal canal below the conus): asymmetric leg weakness and sensory loss in the L4-S2 distributions, severe radicular pain, often urinary retention, areflexic lower extremities (lower motor neuron only, no upper motor neuron signs).

Either is a surgical emergency if compressive and presenting with bowel/bladder dysfunction. The most consistent and most missed feature is saddle anesthesia — always test perianal pinprick in any patient with new urinary or bowel symptoms with leg complaints.

Brainstem Patterns

Lateral Medullary Syndrome (Wallenberg)

The most clinically important brainstem sensory pattern. A lesion of the lateral medulla — typically from PICA occlusion or vertebral artery disease — produces ipsilateral facial pain and temperature loss with contralateral body pain and temperature loss, accompanied by ipsilateral Horner, ataxia, palatal weakness, and vertigo. The crossed sensory loss is the hallmark and is almost pathognomonic.

The anatomy: the spinal trigeminal tract carrying facial pain and temperature is interrupted on the side of the lesion (ipsilateral facial loss), while the spinothalamic tract carrying body pain and temperature has already crossed at the cord and now ascends on the side of the lesion (contralateral body loss).

Medial Lemniscus Lesions

A medial lemniscus lesion in the brainstem produces contralateral loss of vibration and joint position sense without pain and temperature loss (because the spinothalamic tract is anatomically separate). When combined with motor findings (corticospinal tract is nearby), the picture suggests a paramedian brainstem stroke.

Dissociated Facial Loss in Pontine Lesions

The principal sensory nucleus of the trigeminal nerve in the mid-pons handles touch and proprioception for the face. A small pontine lesion can selectively damage this nucleus, producing loss of facial touch with preserved facial pain (the spinal trigeminal tract carrying pain and temperature is not at the same level). This is the central analogue of the body’s dissociated sensory loss patterns.

Thalamic Patterns

Pure Sensory Stroke

A small lacunar infarct in the contralateral VPL nucleus of the thalamus produces a hemibody sensory loss without other findings — no motor weakness, no aphasia, no visual field defect. The pattern affects face, arm, and leg together. It is one of the classical lacunar syndromes.

Thalamic Pain Syndrome (Dejerine-Roussy)

After an initial period of hemisensory loss from a VPL infarct, some patients develop severe spontaneous burning pain in the previously numb hemibody, with marked hyperalgesia and allodynia. The pain is often resistant to standard analgesics; antidepressants (TCAs, SNRIs) and antiepileptics (gabapentin, pregabalin) are the standard treatments.

Cortical Patterns

Cortical Sensory Loss

A contralateral parietal cortex lesion typically produces hemibody loss of cortical sensations (two-point discrimination, stereognosis, graphesthesia, tactile localization) with relatively preserved primary modalities. Detailed in the Cortical Sensory Functions page.

The Cortical Hand Syndrome

A small primary somatosensory cortex stroke involving the hand area produces discrete sensory loss in the hand alone, often with the “useless hand” phenomenon — full strength but inability to perform skilled tasks because the patient does not know where the hand is in space without watching. The pattern can mimic a peripheral lesion but is distinguished by the involvement of all fingers (not a peripheral nerve distribution) and the dissociation between intact pinprick and impaired cortical functions.

Functional (Non-Organic) Sensory Loss

Functional sensory loss does not follow neuroanatomy and can be recognized by characteristic features:

• Midline-splitting on the trunk or face: a sharp boundary at the midline that does not respect the overlap of the contralateral dermatomes (which extend slightly across the midline in real anatomy).
• “Glove and stocking” distribution with a sharp proximal boundary: a complete loss to a defined level with an abrupt change to normal sensation. Real length-dependent neuropathy fades gradually.
• Loss that respects the hemibody but spares the genitals: a sensory midline split that does not extend across the perineum.
• Loss that includes the angle of the jaw: this region is C2-C3, not trigeminal.
• Fluctuation with attention: the deficit improves when the patient is distracted or worsens when they are focused on it.
• Sensory loss without functional consequence: a patient with “no feeling” in a limb who uses it normally for skilled tasks.
• Hoover sign positive: in a patient with apparent leg weakness, the absence of expected hip extension activation when the opposite leg is asked to flex against resistance — a sign of functional weakness.

The diagnosis of functional disorder is positive (made on characteristic features) rather than exclusionary. Patients with functional sensory loss often have a substantial improvement with reassurance, education, and physical therapy.

🔍 Did You Know?

The level of a cord lesion is often two or three segments below the bedside sensory level. The reason: the spinothalamic fibers ascend one to three segments in Lissauer’s tract before crossing the cord. A patient with a sensory level at T10 (the umbilicus) may have a cord lesion at T7 or T8. Imaging targeted at the level revealed by the sensory exam may miss the lesion; always image one to two segments above the sensory level for cord pathology.

Summary Table: Patterns and Localization

Pitfalls and Pearls

• The sensory level is often two to three segments below the cord lesion. Image above the level revealed at the bedside.
• Always test perianal sensation in patients with bowel or bladder symptoms. Saddle anesthesia is the cardinal sign of cauda equina or conus syndrome.
• Brown-Séquard hemisection is the most pathognomonic cord pattern. The crossed dissociated loss is unique.
• Syringomyelia produces a “cape” of pain and temperature loss with preserved touch — recognize the suspended pattern.
• Wallenberg gives ipsilateral facial loss and contralateral body loss, accompanied by ataxia, Horner, and palatal weakness.
• Cortical sensory loss with preserved primary sensation is parietal cortex disease. Look for stereognosis, two-point, graphesthesia, extinction.
• Pure sensory strokes from thalamic lacunes can present with isolated hemibody numbness without weakness or other findings.
• Length-dependent neuropathy fades gradually proximally. A sharp proximal boundary on a “stocking” suggests functional disease.
• Functional sensory loss is a positive diagnosis, made on characteristic features, not an exclusionary one. Treat with reassurance, education, and physical therapy.
• The combination of sensory ataxia, areflexia, and pseudoathetosis defines sensory neuronopathy. Pursue paraneoplastic and autoimmune causes — small-cell lung cancer in smokers, Sjögren in women with sicca symptoms.

References

1. Campbell WW. DeJong’s The Neurologic Examination. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2013. Chapter 36.
2. Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 7th ed. Philadelphia: Wolters Kluwer; 2017.
3. Goetz CG, ed. Textbook of Clinical Neurology. 3rd ed. Saunders; 2007.
4. Sghirlanzoni A, Pareyson D, Lauria G. Sensory neuron diseases. Lancet Neurol. 2005;4(6):349-361.
5. Stone J, Carson A. Functional neurological disorders: the neurological assessment as treatment. Pract Neurol. 2016;16(1):7-17.
6. Kim JS. Pure lateral medullary infarction: clinical-radiological correlation of 130 acute, consecutive patients. Brain. 2003;126(8):1864-1872.