Sensory loss

Sensory loss is an objective reduction or absence of one or more sensory modalities found on examination, with or without symptoms. It is often reported as numbness, but may be found without complaint (for example the insensate diabetic foot). The work is to map the deficit, localise the lesion, treat reversible causes, and protect insensate areas from injury.

Clinical relevance. Loss of protective sensation leads to unnoticed burns, pressure injury, ulcers, joint destruction and amputation. Sudden or level-defined loss may signal stroke, cord compression or Guillain Barré syndrome.

Anatomy. Fine touch, vibration and joint position travel in large myelinated fibres, ascend ipsilaterally in the dorsal columns and cross in the medulla. Pain, temperature and crude touch travel in small fibres, cross within one or two spinal segments and ascend in the contralateral spinothalamic tract. The combination of modalities lost therefore localises the lesion.

Patterns of loss.

• Length dependent glove and stocking loss: polyneuropathy.
• Single nerve territory or dermatome: mononeuropathy or radiculopathy.
• Patchy, asymmetric, non length dependent with severe proprioceptive loss and ataxia: sensory neuronopathy (ganglionopathy).
• Transverse sensory level on the trunk: cord lesion.
• Ipsilateral loss of vibration and position with contralateral loss of pain and temperature: hemicord lesion (Brown Sequard syndrome).
• Cape distribution loss of pain and temperature with preserved vibration and position (dissociated loss): central cord lesion (syringomyelia).
• Loss of pain and temperature with preserved dorsal column function: anterior spinal artery infarct.
• Saddle distribution: conus medullaris or cauda equina.
• Ipsilateral face with contralateral body loss of pain and temperature: lateral medullary syndrome.
• Contralateral hemisensory loss of all modalities: thalamus, internal capsule or cortex.
• Impaired stereognosis, graphaesthesia, two point discrimination and sensory extinction with intact primary modalities: parietal cortex.
• Non-anatomical, shifting or midline splitting: functional.

Loss of protective sensation is defined as inability to feel a 10 g monofilament at one or more plantar sites.

History. Onset and speed, symmetry, distribution, painless injuries, burns and ulcers, falls and imbalance in the dark or when washing the face, dropping objects, weakness, bladder, bowel and sexual dysfunction, autonomic symptoms, neck and back pain, preceding infection, vaccination, and constitutional symptoms.

Background and drugs. Diabetes, alcohol, diet and bariatric surgery, nitrous oxide use, thyroid, kidney and liver disease, HIV, syphilis, leprosy contact, cancer, connective tissue disease, monoclonal gammopathy, family history of neuropathy or foot deformity, and occupational toxins. Neurotoxic drugs: platinum agents, taxanes, vincristine, bortezomib, thalidomide, isoniazid, metronidazole, nitrofurantoin, linezolid, dapsone, stavudine, amiodarone and excess pyridoxine.

Examination

• Test each modality in a distal to proximal order and in each limb and the trunk: light touch (cotton wool), pinprick, temperature, vibration (128 Hz tuning fork at toe, ankle, knee, finger), joint position, and the 10 g monofilament at plantar sites.
• Mark the upper edge of any level, the dermatomal or nerve boundary, and the midline.
• Cortical sensation: stereognosis, graphaesthesia, two point discrimination, extinction.
• Romberg test, gait, power, tone, reflexes (absent in neuropathy, brisk distal to a cord lesion), plantar responses, Lhermitte sign, anal tone and perianal sensation when a cord or cauda equina lesion is possible.
• Feet and hands: ulcers, callus, deformity (Charcot foot: warm, swollen, deformed), burns, trophic change, pulses.
• Cranial nerves including facial sensation and corneal reflex, thickened nerves, hypopigmented anaesthetic skin patches, and signs of vasculitis (livedo, purpura, nailfold infarcts).

Red flags

• Sudden loss in a vascular pattern, or with weakness, speech or visual symptoms
• Sensory level, saddle anaesthesia, bladder or bowel dysfunction
• Ascending loss with weakness and reduced reflexes over days
• Rapid progression over weeks, or severe asymmetric painful loss (vasculitis)
• Numb chin or facial numbness (can indicate malignancy or skull base disease)
• Painless wounds, burns or foot ulcers, or a warm swollen insensate foot
• Weight loss, fever, cancer or immunosuppression

Special groups. Pregnancy: carpal tunnel syndrome and meralgia paraesthetica. Children: hereditary sensory neuropathies, spinal dysraphism and tethered cord. Older adults: vitamin B12 deficiency, cervical myelopathy and diabetes. Region specific: leprosy, HIV neuropathy, tropical neuropathies and neurosyphilis.

Peripheral nerve, generalised

• Diabetic neuropathy, impaired glucose tolerance
• Vitamin B12, folate, thiamine, pyridoxine (deficiency and excess) and copper deficiency
• Alcohol related, uraemic, hypothyroid and liver disease neuropathy
• Leprosy, HIV, syphilis, hepatitis B and C, Lyme disease, diphtheria
• Amyloidosis, paraproteinaemic neuropathy, POEMS syndrome, paraneoplastic neuropathy
• Guillain Barré syndrome, chronic inflammatory demyelinating polyneuropathy, vasculitic neuropathy, connective tissue disease neuropathy
• Hereditary: Charcot Marie Tooth disease, hereditary sensory and autonomic neuropathies, Fabry disease, porphyria
• Toxic and drug induced neuropathy including heavy metals (arsenic, lead, thallium, mercury)
• Sensory neuronopathy: Sjogren syndrome, paraneoplastic (anti-Hu), pyridoxine toxicity, cisplatin

Focal peripheral

• Mononeuropathy (carpal tunnel, ulnar, radial, peroneal, lateral femoral cutaneous), mononeuritis multiplex
• Radiculopathy, plexopathy, mental neuropathy (numb chin), trigeminal sensory neuropathy
• Traumatic or iatrogenic nerve injury

Spinal cord

• Compression (tumour, disc, abscess, haematoma), cervical spondylotic myelopathy
• Multiple sclerosis, transverse myelitis, neuromyelitis optica
• Subacute combined degeneration (B12, nitrous oxide), tabes dorsalis, HIV and HTLV-1 myelopathy
• Syringomyelia, spinal cord infarction, dural arteriovenous fistula
• Cauda equina syndrome, tethered cord

Brainstem, thalamus and cortex

• Stroke (lateral medullary, thalamic, parietal, lacunar), transient ischaemic attack
• Tumour, abscess, demyelination, cerebral venous thrombosis
• Migraine aura, focal seizure

Other

• Functional sensory loss
• Anaesthetic effect (spinal or regional block, local anaesthetic, ciguatera or shellfish toxin)
• Reduced sensation from ischaemia, compartment syndrome or cold injury

Reasoning. Define the pattern and the modalities lost, localise the lesion, decide the urgency from speed of onset and weakness, and then test for reversible systemic causes. Examine feet in every diabetic patient.

First line. Glucose and HbA1c, full blood count and film, urea, creatinine, electrolytes, calcium, magnesium, liver function, thyroid stimulating hormone, vitamin B12 with methylmalonic acid when 200 to 300 ng/L, folate, ESR and C reactive protein, serum protein electrophoresis with immunofixation and free light chains, HIV, syphilis, and hepatitis B and C serology.

Imaging. Emergency MRI brain with diffusion weighted sequences for a vascular pattern. Emergency MRI of the whole spine for a sensory level, saddle loss or bladder dysfunction (skip lesions occur). MRI cervical spine for suspected myelopathy, and MRI brain and spine for demyelination. In a sensory ganglionopathy MRI may show dorsal column T2 hyperintensity.

Neurophysiology. Nerve conduction studies and electromyography for large fibre neuropathy, entrapment, radiculopathy and plexopathy; sensory nerve action potentials are reduced or absent in neuronopathy. Studies are normal in pure small fibre neuropathy, which needs skin biopsy for intraepidermal nerve fibre density or quantitative sensory testing.

Targeted tests. Antinuclear antibody, anti-Ro and anti-La, ANCA, rheumatoid factor, complement, cryoglobulins; paraneoplastic antibodies (anti-Hu, anti-CV2) with CT chest, abdomen and pelvis; aquaporin-4 and MOG antibodies; HTLV-1 serology; heavy metal levels; slit skin smear and nerve or skin biopsy for leprosy and amyloid; genetic testing after counselling. Lumbar puncture (after imaging) for Guillain Barré syndrome (raised protein with normal cell count, often absent in the first week), inflammatory neuropathy, myelitis and infection.

Foot risk grading in diabetes. No loss of protective sensation and normal pulses: low risk. Loss of protective sensation or absent pulses or deformity: moderate risk. Previous ulcer, amputation, renal replacement therapy or Charcot foot: high risk.

Limitations. Monofilament testing alone misses early disease. Vibration thresholds fall with age. Normal MRI does not exclude demyelination or infarction in the first hours.

Time critical causes

• Acute ischaemic stroke (onset within 4.5 hours, haemorrhage excluded): alteplase 0.9 mg/kg IV (maximum 90 mg), 10 percent as a bolus over 1 minute and the remainder over 60 minutes, or tenecteplase 0.25 mg/kg IV as a single bolus (maximum 25 mg); blood pressure under 185/110 mmHg before and under 180/105 mmHg for 24 hours after treatment; aspirin 300 mg orally daily when thrombolysis is not given; thrombectomy referral for large vessel occlusion.
• Cord compression with neurological signs: dexamethasone 16 mg orally or IV daily (or 10 mg IV then 4 mg every 6 hours) with gastric protection, flat bed rest, and emergency neurosurgical or oncology referral.
• Guillain Barré syndrome: intravenous immunoglobulin 0.4 g/kg daily for 5 days, with forced vital capacity monitored twice daily.
• Cauda equina syndrome: emergency MRI and surgical decompression.

Treat the cause

• Vitamin B12 deficiency with neurological signs: hydroxocobalamin 1 mg IM on alternate days until no further improvement (up to 3 weeks), then 1 mg every 2 months; never give folic acid alone first. Stop nitrous oxide.
• Alcohol related neuropathy: abstinence, thiamine 100 mg orally three times daily (500 mg IV every 8 hours for 3 days when Wernicke encephalopathy is possible), nutrition.
• Diabetes: glycaemic control without very rapid correction.
• Hypothyroidism: levothyroxine 1.6 micrograms/kg orally daily (start at 25 to 50 micrograms in older adults and in heart disease).
• Isoniazid: pyridoxine 10 mg orally daily as prophylaxis, and 50 to 100 mg daily if neuropathy has developed.
• Neurosyphilis: benzylpenicillin 18 to 24 million units IV daily in divided doses for 10 to 14 days.
• Leprosy: multibacillary disease takes rifampicin 600 mg once monthly (supervised), clofazimine 300 mg once monthly (supervised) and 50 mg daily, and dapsone 100 mg daily for 12 months. Paucibacillary disease takes the same three drugs at the same doses for 6 months. Doses are reduced in children. Nerve function impairment and reactions: prednisolone 40 mg orally daily reduced gradually over several months, with nerve function checked monthly. Specialist care.
• Chronic inflammatory demyelinating polyneuropathy: intravenous immunoglobulin 2 g/kg over 2 to 5 days, or prednisolone 1 mg/kg daily (maximum 60 to 80 mg), under specialist care. Vasculitic neuropathy: prednisolone 1 mg/kg daily with cyclophosphamide or rituximab, by specialists.
• Compressive entrapment: splinting, avoidance of provoking posture, injection or surgical release by specialist decision.
• Cervical myelopathy with progressive signs: urgent spinal surgical referral.
• Syringomyelia, tethered cord and spinal tumour: neurosurgery.

Protection of insensate areas (for every patient with loss of protective sensation)

• Daily inspection of feet (mirror or helper), well fitting closed shoes, no barefoot walking, cotton socks, protection from heat sources, testing bath water with the elbow or a thermometer (under 37 degrees Celsius), and avoidance of hot water bottles and heaters.
• Podiatry, callus care and therapeutic footwear. Review frequency rises with risk: annually for low risk, every 3 to 6 months for moderate risk, and every 1 to 3 months for high risk.
• Active foot ulcer or suspected Charcot foot (warm, swollen, deformed insensate foot): multidisciplinary foot service within 1 working day, offloading with a total contact cast or removable walker, and urgent X-ray and MRI.
• Infected ulcer: antibiotics by severity and cultures, with urgent vascular assessment when pulses are absent.
• Falls prevention, balance training and occupational therapy for proprioceptive loss. For hands: care with sharp objects, hot items and tools.

Functional sensory loss. Positive diagnosis with explanation, physiotherapy and occupational therapy, and psychological input.

Monitoring. Repeat sensory examination and monofilament testing at every foot review, HbA1c every 3 months in diabetes, vitamin B12 at 3 months after replacement, and nerve function monthly in leprosy.

Referral and escalation. Immediate: stroke, cord compression, Guillain Barré syndrome, cauda equina syndrome. Neurology within 2 weeks for rapid, asymmetric, painful or severe sensory loss, and for sensory neuronopathy. Diabetes foot service, podiatry and vascular surgery for ulcers and ischaemia. Dermatology and infectious disease for leprosy. Haematology for paraproteinaemia.

Admission criteria. Acute stroke or transient ischaemic attack with high risk features, Guillain Barré syndrome, cord compression, infected diabetic ulcer with systemic features, suspected Charcot foot with ulcer, or unsafe self care.

Discharge and safety netting. Review in 2 to 4 weeks. Return for new weakness, spreading loss, loss of bladder or bowel control, speech or visual change, a new wound, or a red, hot or swollen foot.