acute motor axonal neuropathy in hiv infection

SCIENTIFIC LETTER Acute Motor Axonal Neuropathy in HIV Infection Shruti Jadhav & Mukesh Agrawal & Surbhi Rathi Received: 13 April 2012 / Accepted: 27 June 2013 / Published online: 21 September 2013 # Dr. K C Chaudhuri Foundation 2013 To the Editor: Acute motor axonal neuropathy (AMAN)—a variant of Guillian Barre Syndrome (GBS) without sensory involvement has been rarely reported in HIV-infected adults and perhaps never in HIV-infected children. An 11-y-old girl presented with sudden weakness of lower limbs that gradually progressed over three days to involve upper limbs. She had dysentery 20 d back. One year back, she had an attack of Herpes Zoster and was diagnosed to have HIV1 and HIV2 co-infection on ELISA with CD4 count of 853 cells/mm 3 . Both parents had asymptomatic HIV infection. Child was undernourished, weighing 25 kg i.e., < 3rd centile. She had symmetric flaccid quadriparesis with truncal weakness and depressed tendon reflexes. Higher functions and sensory examination were normal. Weakness worsened over next week with complete loss of power in lower limbs but no respiratory or bulbar involvement. CSF and spinal MRI was normal. Stool was negative for poliovirus. Diagnostic tests for C. jejuni were not available. CD4 count was 542 cells/mm 3 . Nerve conduction velocity revealed pure motor axonal neuropathy without demyelination. Patient was treated with intravenous immunoglobulin, following which disease progression stopped but no im- provement was noted in muscle power till discharge after one month. Peripheral neuropathies are not uncommon in HIV- infected population, caused by direct viral invasion, immu- nological dysregulation or antiretroviral drugs, though clinico-pathological spectrum may vary with severity of immunosuppression [1, 2]. Inflammatory demyelinating neuropathies are usually seen during acute seroconversion, while distal sensory neuropathies are common with progressive immunosuppression [3]. Neurological complications are sug- gested to be more common in HIV2 than HIV1 infection, perhaps due to longer survival or higher neurotropism [4]. Present case had combined infection. AMAN is more common in young adults, often following C. jejuni infection. Present case had history of dysentery but confirmation of C. jejuni infection was not possible. Clinical presentation of AMAN in HIV-infected population is same as in others, except longer and severe course or higher recurrence [5]. Diagnosis is supported by nerve conduction studies. Treatment is similar to that in HIV sero- negative patients with intravenous immunoglobulins and plasmapheresis being equally effective in hastening recovery, if initiated early. References 1. Araujo AP, Nascimento OJ, Garcia OS. Distal sensory polyneuropathy in a cohort of HIV-infected children over five years of age. Pediatrics. 2000;106:E35. 2. Wulff EA, Wang AK, Simpson DM. HIV-associated peripheral neuropathy: Epidemiology, pathophysiology and treatment. Drugs. 2000;59:1251–60. 3. Ferrari S, Vento S, Monaco S, Cavallaro T, Cainelli F, Rizzuto N, et al. Human immunodeficiency virus–associated peripheral neuropathies. Mayo Clin Proc. 2006;81:213–9. 4. Moulignier A, Lascoux C, Bourgarit A. HIV type 2 demyelinating encephalomyelitis. Clin Infect Dis. 2006;42:e89–91. 5. Millogo A, Sawadogo A, Lankoandé D, Sawadogo AB. Guillain- Barré syndrome in HIV-infected patients at Bobo-Dioulasso Hospital (Burkina Faso). Rev Neurol (Paris). 2004;160:559–62. S. Jadhav (*) : M. Agrawal : S. Rathi Department of Pediatrics, TN Medical College and BYL Nair Hospital, Mumbai 400008, Maharashtra, India e-mail: [email protected] Indian J Pediatr (February 2014) 81(2):193 DOI 10.1007/s12098-013-1171-z

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SCIENTIFIC LETTER

Acute Motor Axonal Neuropathy in HIV Infection

Shruti Jadhav & Mukesh Agrawal & Surbhi Rathi

Received: 13 April 2012 /Accepted: 27 June 2013 /Published online: 21 September 2013# Dr. K C Chaudhuri Foundation 2013

To the Editor: Acute motor axonal neuropathy (AMAN)—avariant of Guillian Barre Syndrome (GBS) without sensoryinvolvement has been rarely reported in HIV-infected adultsand perhaps never in HIV-infected children.

An 11-y-old girl presented with sudden weakness of lowerlimbs that gradually progressed over three days to involveupper limbs. She had dysentery 20 d back. One year back, shehad an attack of Herpes Zoster and was diagnosed to haveHIV1 and HIV2 co-infection on ELISA with CD4 count of853 cells/mm3. Both parents had asymptomatic HIV infection.

Child was undernourished, weighing 25 kg i.e., < 3rdcentile. She had symmetric flaccid quadriparesis with truncalweakness and depressed tendon reflexes. Higher functionsand sensory examination were normal. Weakness worsenedover next week with complete loss of power in lower limbsbut no respiratory or bulbar involvement.

CSF and spinal MRI was normal. Stool was negative forpoliovirus. Diagnostic tests for C. jejuni were not available.CD4 count was 542 cells/mm3. Nerve conduction velocityrevealed pure motor axonal neuropathy without demyelination.

Patient was treated with intravenous immunoglobulin,following which disease progression stopped but no im-provement was noted in muscle power till discharge afterone month.

Peripheral neuropathies are not uncommon in HIV-infected population, caused by direct viral invasion, immu-nological dysregulation or antiretroviral drugs, thoughclinico-pathological spectrum may vary with severity ofimmunosuppression [1, 2]. Inflammatory demyelinatingneuropathies are usually seen during acute seroconversion,while distal sensory neuropathies are commonwith progressive

immunosuppression [3]. Neurological complications are sug-gested to be more common in HIV2 than HIV1 infection,perhaps due to longer survival or higher neurotropism [4].Present case had combined infection.

AMAN is more common in young adults, often followingC. jejuni infection. Present case had history of dysentery butconfirmation of C. jejuni infection was not possible. Clinicalpresentation of AMAN in HIV-infected population is sameas in others, except longer and severe course or higherrecurrence [5]. Diagnosis is supported by nerve conductionstudies.

Treatment is similar to that in HIV sero- negative patientswith intravenous immunoglobulins and plasmapheresisbeing equally effective in hastening recovery, if initiatedearly.

References

1. Araujo AP, Nascimento OJ, Garcia OS. Distal sensory polyneuropathyin a cohort of HIV-infected children over five years of age. Pediatrics.2000;106:E35.

2. Wulff EA, Wang AK, Simpson DM. HIV-associated peripheralneuropathy: Epidemiology, pathophysiology and treatment. Drugs.2000;59:1251–60.

3. Ferrari S, Vento S, Monaco S, Cavallaro T, Cainelli F, Rizzuto N,et al. Human immunodeficiency virus–associated peripheral neurop-athies. Mayo Clin Proc. 2006;81:213–9.

4. Moulignier A, Lascoux C, Bourgarit A. HIV type 2 demyelinatingencephalomyelitis. Clin Infect Dis. 2006;42:e89–91.

5. Millogo A, Sawadogo A, Lankoandé D, Sawadogo AB. Guillain-Barré syndrome in HIV-infected patients at Bobo-Dioulasso Hospital(Burkina Faso). Rev Neurol (Paris). 2004;160:559–62.

S. Jadhav (*) :M. Agrawal : S. RathiDepartment of Pediatrics, TN Medical College and BYL NairHospital, Mumbai 400008, Maharashtra, Indiae-mail: [email protected]

Indian J Pediatr (February 2014) 81(2):193DOI 10.1007/s12098-013-1171-z

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