Differential diagnosis of neurological manifestations of Hansen's disease

by Patrícia D. Deps,

Department of Social Medicine, Post-Graduate Program in Infectious Diseases, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil.

Francisco Marcos B. Cunha,

Neurology Professor at the Federal University of Ceará, Fortaleza, Ceará, Brazil

and José Antônio Garbino.

Professor at Lauro de Souza Lima Institute,Bauru, São Paulo, Brazil.

In Brazil, diagnosis of Hansen's disease (HD) must be considered in patients presenting with sensory alterations such as paresthesias, tingling, burning, and/or sensory deficit corresponding to the area of a thickened nerve, associated or not with motor and/or autonomic deficits, with or without HD skin lesions.1

In a study of 161 patients with complaints related to the peripheral nervous system, single or multiple sensory-motor neuropathies - such as carpal tunnel syndrome, sensory neuropathy, and sensory and sensory-motor polyneuropathies - accounted for 69% of the cases included in other diagnoses, i.e. no diagnosis of HD. This highlights the importance of peripheral neuropathies in differential diagnoses between HD and other diseases with neurological manifestations, although all peripheral neuropathies should be evaluated for the possibility of HD. In this study, 16 patients (10%) were diagnosed with syringomyelia, narrow spinal canal and amyotrophic lateral sclerosis. Furthermore, it was found that central nervous system diseases should be evaluated in the differential diagnosis with HD.2

In another study of 481 patients with neurological complaints (sensory and/or motor), HD was confirmed in 320 (67%). In 161 patients (34%) not diagnosed with HD, underlying metabolic and deficiency pattern diseases were found, such as diabetes mellitus, hypothyroidism, uremia, secondary amyloidosis, alcoholic neuropathy, hereditary neuropathies (Charcot-Marie-Tooth I and II) (Figure 1), congenital insensitivity to pain, susceptibility to compression, neurofibromatosis type I, inflammatory and immune-mediated diseases (vasculitis, systemic lupus erythematosus, panarteritis nodosa, chronic inflammatory demyelinating polyneuropathy, monoclonal gammopathy), traumatic and compressive diseases with various presentations and topography, cervical syringomyelia, sequelae of transverse myelitis, true neurogenic thoracic outlet syndrome, cervical and lumbosacral radiculopathies), and drug side effects (isoniazid, chloroquine, antiretrovirals). Motor neurone diseases such as amyotrophic lateral sclerosis and non-neurological diseases such as palmar tendinopathy, camptodactyly (Figure 2), and osteoarthropathies were also found.3,4

Figure 1. Charcot-Marie-Tooth disase type I (demyelinating).

Figure 2. Camptodactyly.

For an etiologic investigation of peripheral neuropathies, a sequential approach of history taking and physical-neurological examination is essential. A detailed clinical history of the neuropathy being investigated, as well as the patients' past pathological and family history, are very helpful. Laboratory tests, electro-neurophysiological evaluation, and imaging are often indispensable to know the types of nerve fibers involved in the pathogenesis, as well as the anatomical and temporal patterns of the disease (see chapters 22 and 23 on complementary tests for HD). Histopathological evaluation of the affected nerve may be necessary to clarify the diagnosis of HD, especially when there is no etiological diagnosis by sputum smear and PCR.

Considerations on the differential diagnosis of primary neural Hansen’s disease with other peripheral neuropathies

Primary neural Hansen’s disease (PNHD) is uniquely characterized by the lack of clinical and laboratory identification of skin involvement, at least initially, when the abnormalities are restricted to the peripheral nervous system. It is therefore called primary neural HD, the pure neuritic form of HD or the pure neural form of HD (see chapter on neurological disorders).5

The prevalence of PNH can be overestimated when the identification of skin lesions in suspected cases is not properly performed, without adequate skin smears or poorly conducted skin biopsy.6,7 Thus, cases with unidentified skin lesions are diagnosed as PNH. Conversely, cases with nerve lesions of varied etiologies with no dermatological examination, when the respective differential diagnoses with PNH are not considered, end up being mislabeled as neural HD. A study of 162 patients with suspected PNH who underwent nerve biopsy confirmed the diagnosis in only 34 cases (21%).8

The most similar peripheral neuropathies requiring differential diagnoses.

The patient with distal mononeuropathy, multiple mononeuropathy or asymmetric polyneuropathy needs to be investigated, as extensively as possible, and HD should always be considered as one of the possible diagnoses.5,9

By assessing sensory, autonomic, motor, and deep reflex functions, one should identify whether the lesion has a cutaneous territory and/or peripheral nerve territory distribution. In the case of intracutaneous branch involvement, diagnosis of HD is virtually certain. When there is distribution in peripheral nerve territory, it is first necessary to identify the affected nerve or nerves individually. Next, the distribution of the lesion on each nerve should be investigated, which can be done by means of sensory changes and compromised muscles. This is a very important detail, because some neuropathies affect nerves in preferential topographies. For example, the most common neuropathy of the median nerve is carpal tunnel syndrome, while HD affects this nerve both distally and proximally. Another important point to be considered concerns the fibers that are preferentially involved: sensory (tactile, thermal, and painful); motor and neurovegetative. Even in peripheral nerve trunk lesions, HD affects the finer fibers initially and the involvement of vibratory sensitivity and kinetic postural motor fibers and deep reflexes occurs later. On the other hand, compressive neuropathies tend to block the thicker and more myelinated fibers first, such as those of the vibratory and kinetic-postural sensitivities and motricity.


There are several clinical entities that present with isolated and multiple mononeuropathies (see Table 2 and Figure 3). These entities are important in the differential diagnosis of the paucibacillary forms. The mononeuropathies with the greatest similarities to HD are ulnar tunnel syndrome and fibular nerve mononeuropathy in the retrofibular tunnel.10,11 Cross-leg fibular syndrome and other mononeuropathies affecting cutaneous nerves may be confused with the neural involvement of tuberculoid HD,12 but their acute nature and spontaneous improvement help differentiate them from the neuropathy of HD. Nerve tumors present difficulties in differentiation with the nerve abscesses of the tuberculoid forms.8,13

Figure 3. Posterior interosseous nerve compressive syndrome in the left hand. Patient is unable to make the "OK" sign.

Carpal tunnel syndrome is considered the most common chronic compressive neuropathy (Figure 4). It leads to compression of the median nerve and in advanced cases can present intense thenar atrophy.14

Figure 4. Carpal tunnel syndrome. Atrophy in the thenar region.

Multiple mononeuropathies

Multiple mononeuropathy imposes a complex differential diagnosis with vasculitic neuropathies (also as polyneuropathy), arteritis, and neuropathies due to a wide range of primary or secondary immune-mediated collagen diseases, such as systemic lupus erythematosus and Sjöegren's syndrome (sensitive axonal mononeuropathy), and infectious diseases such as hepatitis B and C and HIV infection (see Table 2).15

Among the immune-mediated neuropathies, multifocal motor neuropathy may be confused with HD neuropathy, but the fact that it preserves the sensory fibers is an important differential factor. Lewis-Sumner syndrome or MADSAM (multifocal acquired demyelinating sensory and motor neuropathy) is a mixed inflammatory neuropathy, which is difficult to diagnose because it also progresses with sensory involvement. The predominance of motor manifestations and the topography of the findings, i.e., polyradicular involvement, aids in the differential diagnosis, as does the presence of persistent conduction block.

Hereditary neuropathy with susceptibility to pressure presents as an asymmetrical neuropathy with focal accentuation at sites of compression, often involving the same nerves as HD. Its initial clinical manifestation may be sensory and, as it develops, myelinic involvement almost always predominates over axonal.16 Conduction studies show reduced conduction velocity at many of the natural sites of anatomical narrowing. Most of the time, the anamnesis can reveal the hereditary character of this neuropathy.


Acute Brachial Plexus Neuritis

Also known as brachial nerve amyotrophy or Parsonage-Turner syndrome (Figure 5), acute brachial plexus neuri is a neurological dysfunction of unknown cause, often preceded by viral upper airway infections. There may be an immune system-mediated mechanism against the nerve fibers of the brachial plexus. Pain is of sudden onset, intense and acute. It has a stabbing character, often starting at night, located in the scapular waist, usually unilateral, and may radiate to the neck and the side of the arm, lasting from hours to weeks, followed by weakness and/or muscle atrophy, and partial anesthesia of the limb. The prognosis is favorable and rarely causes dysfunctional disability.2,17

Figure 5. Brachial neuritic amyotrophy or Parsonage-Turner syndrome. A. Posterolateral view shows amyotrophy of the levator scapulae, supraspinatus and infraspinatus muscles. Patient will have difficulty abducting shoulder.

Neurogenic Thoracic Outlet Syndrome

Another plexopathy that should be considered is neurogenic thoracic outlet syndrome, also known as scalene (cervico-brachial) syndrome. That motor impairment predominates in the median nerve and sensory impairment predominates in the ulnar nerve makes identification of this syndrome much easier.18 The anterior and middle scalene muscles are of great importance in the cervical region, since the levels of origin of the brachial plexus and the subclavian artery pass between them (Figure 6). Intense cervicobrachialgia is generated when the scalene anterior muscle clamps the brachial plexus and subclavian artery against the scalene medius muscle. Pain, numbness, and tingling appear in the cervical region radiating to the shoulder and upper limb mainly in the morning, culminating in weakness of the arm and hand muscles and a decrease in the radial pulse when performing the Adson maneuver.19,20

Figure 6. A. Amyotrophy of the first interosseous space. B. MRI of the cervical spine showing invagination of the odontoid process.


Distal polyneuropathies should be considered in the differential diagnosis of multibacillary forms of HD. These polyneuropathies are defined as having diffuse peripheral nerve involvement and bilateral, symmetrical, and length-dependent distribution, that is, compromising nerve fibers more distally than proximally (Figure 7). Therefore, the nerves of the lower limbs are initially compromised.

The most relevant polyneuropathies in the differential diagnosis of HD neuropathy are diabetes mellitus, AIDS, systemic lupus erythematosus, familial amyloid polyneuropathy, intoxication by arsenic and other metals, genetic neuropathies, and the ethylic-charential one. Chronic consumption of alcoholic beverages causes thiamine deficiency, which in synergistic action can cause neuropathic pain.21 There are cases of peripheral neuropathies associated with low body levels of micronutrients, especially copper, iron, selenium, and zinc.22

Figure 7. Cervical radiculopathy. Atrophy of the wrist and hand muscles. MRI (sagittal cut): cervicoarthrosis, rectification of the spine and narrow cervical spinal canal.

Diabetes mellitus polyneuropathy

Diabetes mellitus is the most common cause of polyneuropathy in general and it can present in several ways. Although it also affects the motor part, distal diabetic polyneuropathy is predominantly sensory and its distribution is symmetrical, affecting primarily the distal segments of the longest nerves. The patient complains of acute, subacute, or chronic burning pain in the podotactiles or legs, and skin hyperesthesia and paresthesias may also occur. These symptoms can be excruciating, without remission, and with nocturnal exacerbation. In addition, it can also range from a decrease in tactile, thermal, pain, and vibration sensitivities to a complete abolition of deep reflexes. Clinically, diabetic polyneuropathy differs from HD neuropathy because it is length dependent, that is, it affects long fibers more intensely, predominantly in the lower limbs, and the motor deficit is symmetrical and diffuse, being initially subclinical.23–25 In HD endemic areas these diseases can coexist.

Systemic lupus erythematosus polyneuropathy

This polyneuropathy appears as a sensory or motor disorder of the peripheral nerves, with variable duration, characterized by symmetry of symptoms and distal distribution. In general, it is related to disease activity. It may account for 60% of lupus neuropathies in late disease.26,27

HIV infection and AIDS

The mechanisms of damage to the peripheral nervous system include the action of the virus itself, immunological alterations, the use of antiretroviral drugs, and opportunistic infections. There are several forms of presentation of peripheral neuropathies linked to HIV infection, such as, in sequence: inflammatory demyelinating polyneuropathies; distal symmetrical sensory-motor polyneuropathy; mononeuritis and multiple mononeuritis; progressive polyradiculopathies; ganglioneuritis and autonomic neuropathies; toxic neuropathies having as often related drugs: ddC (zalcitabine), ddI (didanosina), d4T (estavudina), isoniazida, e metronidazol. Ascending neuromuscular weakness, associated with metabolic acidosis, and secondary to side effects of antiretroviral drugs, mainly d4T.2,28–30

Chemotherapy-induced peripheral neuropathy

Chemotherapy-induced peripheral neuropathy (CIPN) is considered a challenge in medical practice because of the increasing incidence of cancer in the population and the impact of cancer treatments on increasing patient survival. CIPN is a clinical syndrome that can resemble HD neuropathy. It is common in the extremities of the limbs, with ‘glove and sock’ neuropathy being most common. A sensory neuropathy predominates, with the most common complaints being burning, followed by tingling, numbness, and paresthesia, and to a lesser extent neuropathic pain. Complaints can arise during chemotherapy and persist for years.31 In a follow-up study of childhood cancer, approximately 48% of the children had some type of CIPN, predominantly sensory, with marked reduction in quality of life.32 The chemotherapy drugs most implicated in CIPN are: oxaliplatin, cisplatin, paclitaxel, bortezomib, vincristine, combination of cisplatin and paclitaxel.33

Heavy metal poisoning

With growing environmental contamination by various metals, it is important to know their toxic effects on human health, and those that can result in peripheral neuropathies (Table 1).

Inorganic mercury poisoning can cause peripheral nervous system disorders and psychosis. The authors Letz et al. in 2000 demonstrated that peripheral neuropathy was observed 30 years after occupational exposure to mercury, with tremor of the extremities and alteration in the motor conduction speed of the peroneal and ulnar nerve.34

Organic mercury intoxication (contaminated fish) affects the dorsal root and trigeminal ganglion causing CNS dysfunction, polyneuropathy, paresthesias, and tremors of the extremities. Minamata syndrome is a severe mercury intoxication involving the CNS with manifestations such as visual changes, sensory disturbances, cerebellar ataxia, and dysarthria.35

Lead poisoning can lead to a clinical picture that resembles the peripheral motor neuropathy of HD, including paralysis of the extensors of the hands and fingers and equinus foot, with asymmetric nerve damage associated with paresthesias.36–38

Neurotoxicity from inorganic arsenic can cause severe acute poisoning one to two days after exposure, presenting with nausea, vomiting, and diarrhea. In the initial phase, sensory neuropathy with neuropathic pain and symmetrical distal polyneuropathy with sensory losses of ‘glove and boot’ distribution sets in. This is followed by abolition of reflexes and marked weakness, which may progress to severe Guillain-Barré Syndrome. Chronic exposure to inorganic arsenic can cause peripheral neuropathy that is predominantly sensory, with few symptoms, but with decreased conduction velocity on electroneuromyography (ENMG).39

Thallium is a highly toxic chemical element used as a component in pesticides and rodenticides that has been banned from several countries. Intoxication is characterized by alopecia (1-2 weeks after intoxication) and peripheral neuropathy similar to inorganic arsenic intoxication.36,40

In general, metal intoxication goes along with symptoms linked to the central nervous system: irritability, lethargy or agitation, headache, and dizziness.29,30

Guillain-Barré syndrome (GBS - acute inflammatory demyelinating polyneuropathy)

GBS presents with weakness or paralysis in more than one limb, usually symmetrical. In many cases there is neural lymphocytic infiltration with demyelination and subsequent axonal degeneration. There is early tendon areflexia and elevated cerebrospinal fluid protein without pleocytosis. Overall, weakness is most evident in the legs and is progressive in character, affecting both short and long nerves. It reaches full involvement in about two weeks. It can be fatal because of the potential to cause respiratory failure and dysregulation of the autonomic nervous system.2,42

Chronic inflammatory demyelinating polyneuropathy

Chronic inflammatory demyelinating polyneuropathy (CIDP) is an autoimmune disease of unknown etiology. CIDP may present in a typical or atypical form, with only half of patients expressing the typical phenotype exhibiting symmetrical sensory and motor symptoms over a period of eight weeks or more. The remainder, with an atypical phenotype, may present with predominantly focal, sensory, motor, distal, or asymmetric symptoms. Because it is a chronic demyelinating inflammatory neuropathy, this atypical form can be confused with HD.43 Diagnosis of CIDP is made after the condition has developed over a period of 8 weeks or more. It differs from acute inflammatory demyelinating polyneuropathy (Guillain-Barré Syndrome), which has an acute, monophasic onset and a self-limited course. Patients may present with a progressive worsening of their clinical condition (progressive course) or may evolve with periods of acute worsening (flare-ups) alternating with periods of stabilization (remission).44

Table 1. Characteristics of lead, inorganic arsenic, thallium, and mercury poisoning.

Legend. NS - nervous system; NP - neuropathic pain; GBS - Guillain-Barré syndrome; PNRP - polyneuroradiculopathy; GI - gastrointestinal; ANS - autonomic nervous system; MCV - motor conduction velocity; HgO - organic mercury; HgI - inorganic mercury. Urine - 24-hour urine test.

Hereditary neuropathies (selected)

Familial amyloid polyneuropathy (FAP) 1 and 3

These are autosomal dominant disorders that occur in the 30-40 year-old age group.42 Fibrillar amyloid protein deposits in the peripheral nerve around the blood vessels, and in the sensory and autonomic ganglia, appear to contribute to nerve damage resulting in a sensory polyneuropathy which, in the initial phase, is length dependent in most cases. Peripheral neuropathy has sensorimotor symptoms with small fiber involvement, resulting in an inability to perceive mechanical and thermal trauma. FAP also has the following clinical features: a family history of neuropathy and or cardiomyopathy, neuropathic pain, orthostatic hypotension, diarrhea, constipation or alternating bowel rhythm, dysphagia, neuromyopathy, and severe weight loss.45 Painless trauma can lead to chronic infections and osteomyelitis. There are no changes in deep tendon reflexes. Autonomic dysfunction reduces quality of life. Compression of the median nerve by amyloid deposition can lead to carpal tunnel syndrome in some patients.

Regarding genetic classification, FAP presents the TTR (transthyretin) V30M forms (Val30Met mutation) and the non-V30M type, with FAP-TTR V30M progressing more slowly (10-15 years) than non-V30M.45 TTR gene sequencing is available and should be requested whenever the neuropathy shows these characteristics.

Acute intermittent porphyria

An inherited disorder usually autosomal dominant with incomplete penetrance, occasionally autosomal recessive. Rare before puberty. Results from failure of heme synthesis with accumulation of porphyrins and their precursors. The neuropathy is predominantly motor due to axonal degeneration. Acute or subacute onset, with asthenia of the proximal muscles, more frequent in the arms than in the legs. It may be asymmetric and focal. Tendon reflexes are initially exaggerated, but later may be absent. It may involve cranial and sensory nerves. Neuropathy will rarely occur without abdominal symptoms being present: colicky pain, nausea, vomiting, and constipation. There is sympathetic overactivity.2

Genetically-determined or developmental myelopathies


In syringomyelia (Figures 8 and 9), a cavity is formed in the central canal of the spinal cord, with expansion of this canal, of the spinal substance, and of the brainstem due to changes in the cerebrospinal fluid circulation. It can be caused by Chiari malformation, tumor growth in the spinal cord, infections, after trauma, or have no identified cause (idiopathic). It affects more the cervical and upper thoracic spinal cord, generating asymmetric segmental weakness and atrophy of the hands and arms. There is damage to the fibers that will form the lateral spinothalamic tracts. Loss of thermal and pain sensitivity in the corresponding dermatomes: "hypoesthesia of suspended distribution". Loss of muscle strength in the upper or lower limbs, depending on the site of involvement. Proprioception and touch are preserved. Symptoms depend on the extent of spinal cord involvement.2,42

Figure 8. Syringomyelia. A. Atrophy of the interosseous muscles of the hands. B. Atrophy of interosseous muscles in the hands. Right hand with radial-median-ulnar claw and in the left hand radial claw.

Figure 9. Syringomyelia. MRI sagittal cut showing enlargement of the spinal canal in the cervical and thoracic region.

Myelopathy with monomelic amyotrophy or Hirayama disease

Hirayama disease is most prevalent in young men in Asia. There are few reports from the Americas. In this clinical condition there is a hypodevelopment of the spinal dura mater, a posterior dural ‘detachment’ in the cervical and upper thoracic region during flexion movements of the neck (Figure 10). It leads to compression and ischemia, focal and asymmetric, of the motor neurons in the anterior horn of the spinal cord, i.e. it causes paralysis without causing loss of sensation. These clinical findings differentiate this condition from HD and syringomyelia, which always present with sensory loss.

MRI studies of the cervical spine in flexion can show the posterior venous plexus engorged with intense enlargement compared to the neutral position.46

Figure 10. Distal juvenile muscular atrophy of the upper limb or Hirayama's disease. A. Atrophy of the forearm and hand and palmar interosseous muscles. A and B. Hands showing atrophy of the left tenar and hypotenar regions with clawing of the 2nd to 5th fingers.

Table 2 summarizes the different diagnoses of neurological diseases according to the classification of peripheral neuropathies and the forms of HD. The differential diagnosis with PNH may assume any form of peripheral neuropathy, and the investigation propedeutics should be carried out according to the approach to neuropathies in general.

Table 2. Clinical entities presenting with isolated and multiple mononeuropathies.

Legend. Forms of Hansen’s disease: T = Tuberculoid; BT = Borderline Tuberculoid; BB = Borderline borderline; BV = Borderline Virchowian; V = Virchowian


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