Bilateral Lower Limb Sensory Motor Neuropathy as the Initial Manifestation of Borderline Tuberculoid Leprosy: A Diagnostic Challenge

Abstract

Leprosy primarily affects the skin and peripheral nerves, with neuropathy usually accompanying skin lesions. Rarely, neural involvement may precede cutaneous manifestations, leading to diagnostic delay. We report the case of a 36-year-old male presenting with bilateral lower limb sensory motor neuropathy initially attributed to Vitamin B12 deficiency. Despite normalization of B12 levels, symptoms persisted, and subsequent skin changes led to biopsy confirmation of borderline tuberculoid leprosy. This case emphasizes considering Hansen’s disease in patients with unexplained neuropathy, particularly in the endemic regions, even before overt skin lesions appear.

INTRODUCTION

Leprosy results from infection with Mycobacterium leprae. It is a chronic granulomatous disease primarily affecting the skin and peripheral nerves.[1,2] Neuropathy is predominant feature, usually associated with hypoesthetic skin lesions.[3] In atypical presentations, neural involvement may precede or overt skin lesions, resulting in delay in diagnosis, as nutritional, metabolic, or idiopathic neuropathy will be considered before leprosy.[3]

Borderline tuberculoid (BT) leprosy represents an immunologically unstable form, often characterized by early nerve involvement and granulomatous inflammation.[1] We describe the case of BT Hansen’s disease presenting initially as bilateral lower limb sensory motor neuropathy, mimicking Vitamin B12 deficiency.

CASE REPORT

A 36-year-old male software engineer presented with complaints of pricking sensation over both lower limbs for 4 months. The symptoms involved the right leg up to mid-thigh and the left leg up to the ankle. There was no weakness, upper limb involvement, or bowel/bladder disturbance.

Initial evaluation showed nerve conduction studies (NCS) revealed bilateral lower limb sensorimotor axonal neuropathy and serum Vitamin B12 was low (150 pg/mL). MRI of the brain and Doppler studies of the bilateral lower limbs were normal. He was diagnosed with Vitamin B12 deficiency-related neuropathy and treated accordingly.

Despite correction of Vitamin B12 (1560 pg/mL after supplementation), over the next 2 months, he developed progressive numbness associated with difficulty in walking and scaling of the skin.

General examination revealed thickened nontender bilateral ulnar nerves and common peroneal nerves and other systemic examination was within the normal limits. Local examination revealed bilateral lower limb ichthyosis, extending up to mid-thigh on the right and ankle on the left. Sensory examination showed reduced pain and touch sensations in L4–1 dermatomes bilaterally, with normal motor power (5/5).

Routine investigations, including complete blood count, renal and liver function tests, and thyroid profile, were within the normal limits. Antinuclear antibody by indirect immunofluorescence and LIA-15 panel were negative. MRI lumbosacral spine and sacroiliac joints were unremarkable.

Slit-skin smear was negative for acid-fast bacilli. Skin biopsy from ichthyotic patch of the right thigh showed perivascular and perineural granulomatous inflammation composed of epithelioid cells, lymphocytes, and occasional Langhans-type giant cells, consistent with BT Hansen’s disease [Figures 1-3]. Wade–Fite stain was negative for M. leprae.

Figure 1.

Histopathological image of skin biopsy showing periadnexal chronic inflammatory infiltrate

Figure 3.

Histopathological image of skin biopsy showing perineural inflammatory infiltrate

Figure 2.

Histopathological image of the skin biopsy showing granulomas with multinucleated giant cells

The patient was started on WHO multidrug therapy (MDT) for paucibacillary leprosy, along with prednisolone 10 mg once daily for mild Type 1 reaction and Gabapentin and Amitriptyline for neuropathic pain. Emollients were advised for ichthyosis. The patient showed gradual symptomatic improvement on the follow-up.

DISCUSSION

Leprosy manifests across a spectrum from tuberculoid (TT) to lepromatous (LL) forms, with borderline types occupying the intermediate spectrum.[4] BT leprosy lies near the TT end and is immunologically unstable, with strong cell-mediated immunity, granulomatous inflammation, and low bacteriological index.[1]

BT leprosy typically presents with a few well-demarcated hypopigmented or erythematous skin lesions associated with marked sensory loss, reflecting early asymmetric nerve involvement.[1,5] Peripheral nerves such as ulnar, median, radial cutaneous, lateral popliteal, and posterior tibial nerves may show thickening and tenderness, while early detection of subclinical neuropathy is crucial to prevent irreversible damage.[6,8]

Neuropathy in BT leprosy presents with negative symptoms (hypoesthesia, anesthesia, and anhidrosis) and occasionally positive symptoms (paraesthesia, neuropathic pain, and hyperhidrosis).[7] Although pure neuritic leprosy is common in India, mononeuritis multiplex is more typical.[3] Rarely, as in this patient, neuropathy precedes skin lesions, leading to misdiagnosis as nutritional or idiopathic neuropathy.[3,9] This diagnostic challenge is compounded in regions where Vitamin B12 deficiency is prevalent.

Our patient’s initial sensory motor neuropathy progressing to scaly patches with nerve thickening highlights the importance of detailed dermatoneurological examination. Skin biopsy confirmed BT leprosy, even with negative slit-skin smears.[1,6,10] Prompt WHO-recommended MDT, corticosteroids for mild reactions, and symptomatic management for neuropathic pain can prevent disability.[3,6,9]

Although peripheral nerve involvement is a hallmark of BT leprosy, it classically manifests as predominantly sensory neuropathy, owing to the early involvement of superficial cutaneous nerve fibres. Motor involvement is generally mild or absent in early BT disease and usually occurs late, secondary to severe neuritis, nerve compression, or repeated lepra reactions. Consequently, the presence of a sensory motor axonal neuropathy at initial presentation, as seen in our patient, is distinctly uncommon in BT leprosy and contributes to diagnostic difficulty. Most reported cases of BT leprosy describe asymmetric sensory deficits or mononeuritis multiplex rather than a length dependent or bilateral sensory motor neuropathy.[6,7]

Motor fiber involvement is typically associated with advanced disease, chronic inflammation, or LL forms, where diffuse nerve infiltration and immune-mediated injury are prominent. Because of strong cell-mediated immuvnity in BT Hansen’s disease, bacillary load is usually low. This leads to localized granulomatous inflammation rather than widespread axonal damage. The presence of early motor involvement in this case may be because of intense focal neuritis or subclinical immune-mediated nerve injury before overt cutaneous manifestations. This atypical presentation is similar to metabolic or nutritional neuropathies, particularly Vitamin B12 deficiency, thereby making the diagnosis of Hansen’s disease challenging, specifically in the absence of classical skin lesions.

Hence, alternate diagnosis should always be considered in chronic peripheral neuropathy unresponsive to initial therapy, with leprosy always in consideration in the endemic areas. This should prompt thorough nerve and skin assessment, with histopathology for confirmation, to enable early intervention and prevent permanent nerve damage.[3,7]

CONCLUSION

In cases of peripheral neuropathy, which are unresponsive to conventional therapy, leprosy should always be considered in the differential diagnosis. This is of paramount importance, especially in India and other endemic regions. Early diagnosis and initiation of treatment are crucial to prevent disability. This case emphasizes the fact that BT Hansen’s disease can initially present as neuropathy, which can be masked by nutritional causes, leading to delay in the diagnosis and initiation of treatment.[8]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.