Neurological manifestation of leprosy

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WHO leprosy peripheral nerve impairment neurological manifestations

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PMID: 39322926

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PMID: 37850518

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https://www.who.int/news-room/fact-sheets/detail/leprosy

Neurological manifestations of leprosy

Leprosy (Hansen disease), caused by Mycobacterium leprae, has a marked predilection for peripheral nerves, particularly Schwann cells. Nerve damage results from direct infection plus immune-mediated inflammation, especially during lepra reactions. It is a major cause of preventable sensory, motor, and autonomic disability.

1. Peripheral neuropathy

Typical pattern

Usually involves cool, superficial peripheral nerves.
Nerves may be thickened, tender, or both.
Distribution varies by type:
- Tuberculoid leprosy: focal, asymmetric neuropathy near skin lesions.
- Lepromatous leprosy: more diffuse, bilateral, usually symmetric polyneuropathy.
- Pure neuritic leprosy: peripheral nerve involvement without visible skin lesions.

Commonly affected nerves are:

Ulnar nerve at the elbow
Common peroneal nerve at the fibular neck
Posterior tibial nerve behind the medial malleolus
Median nerve at the wrist
Radial cutaneous nerve
Facial nerve

2. Sensory impairment

Loss of sensation is often the earliest and most characteristic neurological feature.

Hypoesthesia or anesthesia over skin lesions
Loss of pain and temperature sensation, followed by touch and pressure sensation
Paresthesia, tingling, numbness, or burning neuropathic pain
Loss of protective sensation in hands and feet

Consequences:

Repeated unnoticed trauma or burns
Painless ulcers, especially plantar ulcers
Secondary infection and osteomyelitis
Bone resorption and deformity

A hypopigmented or erythematous patch with definite sensory loss is a WHO cardinal sign of leprosy. WHO fact sheet

3. Motor neuropathy

Motor involvement causes weakness and muscle wasting in the distribution of affected nerves.

Nerve affected	Main motor deficit	Resulting deformity
Ulnar nerve	Interossei weakness, impaired finger abduction/adduction	Clawing of ring and little fingers
Median nerve	Thenar weakness, loss of thumb opposition	Thenar wasting, thumb deformity
Common peroneal nerve	Loss of ankle dorsiflexion	Foot drop, high-stepping gait
Posterior tibial nerve	Intrinsic foot-muscle weakness	Claw toes, unstable foot
Facial nerve	Weak eye closure	Lagophthalmos, exposure keratitis
Radial nerve	Wrist extensor weakness	Wrist drop, less common

Textbook examination emphasizes assessment of eye closure, finger abduction, thumb opposition, wrist extension, and ankle dorsiflexion for functional nerve impairment. Harrison's Principles of Internal Medicine, 22nd ed., section “Diagnosis.”

4. Autonomic dysfunction

Damage to autonomic fibers produces:

Anhidrosis or reduced sweating in affected skin
Dry, scaly, fissured skin
Loss of hair over lesions
Vasomotor changes
Dry eyes when facial/trigeminal involvement occurs

Dry, insensate skin is prone to cracks, wounds, and chronic ulceration.

5. Neuritis and lepra reactions

Neuritis is inflammation of peripheral nerves, presenting with:

Nerve pain and tenderness
New sensory loss
New weakness or paralysis
Rapid increase in nerve size
Sometimes edema around the nerve

It may occur:

At diagnosis
During multidrug therapy
After treatment completion

Silent neuritis means progressive sensory or motor loss without obvious nerve pain or tenderness. This is clinically important because irreversible paralysis can develop unnoticed.

Acute neuritis, new weakness, or recent sensory loss needs urgent specialist assessment because timely anti-inflammatory treatment can prevent permanent deficit.

6. Cranial nerve involvement

Cranial nerve involvement is less common than peripheral neuropathy. The main nerves affected are:

Facial nerve (VII): facial weakness and lagophthalmos
Trigeminal nerve (V): corneal hypoesthesia or anesthesia, impaired corneal protection, risk of corneal ulceration and blindness
Occasionally multiple cranial nerve palsies

A 2025 systematic review of reported cases found facial nerve involvement in 38.8% and trigeminal involvement in 28.6% of reported cranial neuropathy cases, but these figures come from selected case reports and should not be interpreted as population prevalence. Cranial-nerve review

7. Central nervous system involvement

Classically, leprosy is primarily a peripheral nervous system disease. Direct CNS involvement is rare, but case reports and limited cohorts describe:

Cervical myelopathy
Brachial plexus and spinal cord abnormalities
Brainstem involvement, including cranial nerve nuclei
Inflammatory CSF changes in rare cases

A systematic review found such CNS manifestations were uncommon and largely based on observational reports, imaging, pathology, and isolated cases. CNS systematic review

Clinical red flags

In a person with known or suspected leprosy, urgently evaluate:

New numbness or loss of sensation
New hand or foot weakness
Painful or tender thickened peripheral nerve
Foot drop, claw hand, or inability to oppose the thumb
Inability to close the eye fully
Red eye, eye pain, visual blurring, or corneal sensory loss
Plantar ulcer or painless recurrent injury

Summary: Leprosy neuropathy causes sensory loss, motor paralysis, autonomic skin changes, neuritis, and characteristic deformities. Peripheral nerve involvement is central to the disease, while cranial neuropathy and CNS disease are uncommon. Early recognition and treatment are key to preventing permanent disability.

Explain mononeuritis multiplex

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mononeuritis multiplex

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mononeuritis multiplex overview diagnosis causes vasculitic neuropathy

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https://pmc.ncbi.nlm.nih.gov/articles/PMC4357592/

Mononeuritis multiplex is a pattern of peripheral neuropathy in which two or more separate, noncontiguous peripheral nerves are damaged. It is also called multiple mononeuropathy.

Unlike a length-dependent polyneuropathy, which typically causes symmetric “stocking-glove” sensory loss, mononeuritis multiplex is asymmetric, patchy, and often stepwise.

Typical clinical picture

It usually presents acutely or subacutely with:

Painful burning, tingling, or numbness in the territory of one nerve
Focal weakness and muscle wasting
Loss of reflexes supplied by affected nerves
Later involvement of another unrelated nerve, often on the opposite limb

Example: A patient may first develop a painful right foot drop from common peroneal nerve involvement, then later develop numbness and weakness of the left hand from ulnar nerve involvement.

Commonly involved nerves include:

Common peroneal or tibial nerves in the legs
Ulnar nerve in the upper limb
Median or radial nerves
Occasionally cranial nerves

Why it occurs

The classic mechanism is vasculitis of the vasa nervorum, the small blood vessels supplying peripheral nerves.

Inflammation of these vessels causes narrowing or occlusion, resulting in nerve ischemia and axonal degeneration. Therefore, vasculitic mononeuritis multiplex is characteristically painful and causes abrupt motor and sensory deficits. Goldman-Cecil Medicine, section “Vasculitic Neuropathies.”

Causes

Category	Examples
Vasculitis	Polyarteritis nodosa, ANCA-associated vasculitis, eosinophilic granulomatosis with polyangiitis, rheumatoid vasculitis, cryoglobulinemic vasculitis
Connective-tissue disease	Rheumatoid arthritis, SLE, Sjögren syndrome
Metabolic	Diabetes mellitus, especially diabetic radiculoplexus neuropathy
Infections	Leprosy, HIV, hepatitis B/C, Lyme disease
Infiltrative or inflammatory disorders	Sarcoidosis, amyloidosis
Malignancy-related	Lymphoma, leukemic infiltration, paraneoplastic vasculitic neuropathy
Drug-related	Some chemotherapy or immune-checkpoint-inhibitor related neuropathies

Systemic vasculitis is a leading cause. Frameworks for Internal Medicine notes that more than half of cases are due to systemic vasculitic involvement of the vasa nervorum. Frameworks for Internal Medicine, p. 610.

Relation to leprosy

Leprosy can produce a mononeuritis multiplex-like pattern, particularly in tuberculoid or borderline disease:

One or several peripheral nerve trunks become enlarged and impaired.
Deficits are often asymmetric and correspond to involved nerves.
Sensory loss, weakness, autonomic dysfunction, and neuropathic ulcers may develop.
Lepra reactions can cause acute neuritis with rapid new nerve dysfunction.

This differs from lepromatous leprosy, which more often produces a diffuse and relatively symmetric neuropathy.

Diagnosis

Diagnosis is clinical, supported by:

Detailed neurological examination to map individual nerve territories.
Nerve-conduction studies and electromyography: typically demonstrate an asymmetric, multifocal axonal sensorimotor neuropathy.
Tests for the underlying cause, such as CBC, ESR/CRP, glucose/HbA1c, renal/liver function, ANA, ANCA, rheumatoid factor, complement, hepatitis and HIV testing, and tests directed by clinical suspicion.
Nerve with or without muscle biopsy if vasculitic neuropathy is strongly suspected and diagnosis remains uncertain.

Management principle

Mononeuritis multiplex is a neurological syndrome, not a diagnosis by itself. Treatment targets the cause:

Vasculitic neuropathy: urgent specialist-directed immunosuppression, commonly glucocorticoids with additional agents for severe disease.
Diabetes: glycemic management plus pain control and rehabilitation.
Leprosy: multidrug therapy; acute neuritis or lepra reaction may require prompt anti-inflammatory treatment under specialist supervision.
Infection or malignancy: cause-specific treatment.

Urgent assessment is needed for rapidly evolving weakness, foot drop, inability to use a hand, severe neuropathic pain, or eye-closing weakness, since timely therapy may limit permanent nerve loss.

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