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A rare presentation of reversible ALS in HIV infection
G Model
HIVAR-114; No. of Pages 3 HIV & AIDS Review xxx (2015) xxx–xxx
Contents lists available at ScienceDirect
HIV & AIDS Review journal homepage: www.elsevier.com/locate/hivar
Case Report
A rare presentation of reversible ALS in HIV infection Aju Abraham John *, Suryanarayana Sharma, B.K. Madhusudhan, Rohan Mahale, Mahendra Javali, R. Srinivasa Ramaiah Medical College, India
A R T I C L E I N F O
Article history: Received 19 January 2015 Received in revised form 15 February 2015 Accepted 16 February 2015 Available online xxx Keywords: Motor neuron disease Amyotrophic lateral sclerosis Reversible ALS HIV infection HAART
A B S T R A C T
Amyotrophic lateral sclerosis (ALS) is the most common type of motor neuron disease (MND) [1]. It is usually associated with an irreversible course, and treatable causes of ALS are rare. Here, we present a case report of a 35-year-old male, with progressive weakness and wasting of muscles in all four limbs with fasciculation and electro diagnostic features compatible with a diagnosis of probable ALS. He was later diagnosed to have HIV infection and initiated on anti-retroviral therapy. On 6 months follow-up, he had a weight gain of 8 kg and electro diagnostic studies revealed near total normalization of the neurogenic pattern. Reversible ALS like illness in HIV infection has been documented in literature but most of them are diagnosed cases of HIV infection. This case identifies the importance of identifying reversible causes of ALS and near total response to treatment in a patient who presented to us with MND features as the only manifestation of HIV infection. ß 2015 Polish AIDS Research Society. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.
1. Introduction Amyotrophic lateral sclerosis (ALS) is the most common type of motor neuron disease (MND) that primarily affects the motor neuron cell population involving spinal cord or bulbar motor neurons and pyramidal tracts resulting in progressive weakness and wasting of muscles [1]. ALS is mostly associated with an irreversible course and treatable causes are rare. Mulder et al. has reported from a study of two decades of more than two thousand patients with MND, many cases had an initial diagnosis of ALS but later improved [2].
2. Case report A 35-year-old male patient was admitted with a history of progressive asymmetric weakness of limbs of three months duration. Initially it was noticed in the left lower limb which progressed to other limbs in a span of 1 month and predominantly involved the proximal group of muscles. Patient had also noticed fasciculation of muscles in his right arm since 2 months. He had easy fatigability and weight loss of approximately 10 kg in
* Corresponding author at: M.S. Ramaiah Institute of Neurosciences, New Bel Road, Mathikere, Bangalore 560094, Karnataka, India. Tel.: +91 8022183125; mobile: +91 9900136112. E-mail address: [email protected] (A.A. John).
6 months. He denied symptoms suggestive of cranial nerve involvement, sensory symptoms, bowel and bladder sphincter impairment and sexual dysfunction. He also denied history of any systemic illness, exposure to toxins, multiple blood transfusions, drug abuse and high risk sexual behavior. He was a manual laborer by occupation. General physical examination and vital signs were normal. Neurological examination revealed a normal higher mental functions and cranial nerves exam. Fasciculations were observed on the right deltoid, wasting of bilateral deltoids, trapezius and quadriceps (Left>Right) with a normal tone (Fig. 1A and B). Upper limbs power were graded 3/5 in proximal group bilaterally, 4/5 in right and 4-/5 in left lower limb proximal muscle groups. All deep tendon reflexes were brisk with jaw jerk present, normal abdominal reflexes and bilateral plantar flexor. Other systems examination was normal. Blood investigations of complete blood counts, renal functions, liver functions and electrolytes were normal. CSF analysis for cell count, cell type, protein, glucose, chloride, TB-PCR, VDRL, cryptococcal antigen and Indian ink preparation was normal. Serum vitamin levels was more than 2000 pg/ml, TSH was 2.294 uIU/ml and creatinine kinase was 92 IU/L. Angiotensin converting enzyme levels (19 U/L), markers for malignancy like Alfa feto protein (1.48 IU/ml), Prostrate specific antigen (0.49 ng/ml), Carcino embryionic antigen (0.8 ng/ml) and serum PTH (23.7 pg/ml) were normal. Nerve Conduction Study was normal except for mildly reduced CMAP amplitude in right common peroneal nerve, with a normal SNAP. EMG revealed
http://dx.doi.org/10.1016/j.hivar.2015.02.004 1730-1270/ß 2015 Polish AIDS Research Society. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.
Please cite this article in press as: A.A. John, et al., A rare presentation of reversible ALS in HIV infection, HIV & AIDS Review (2015), http://dx.doi.org/10.1016/j.hivar.2015.02.004
G Model
HIVAR-114; No. of Pages 3 A.A. John et al. / HIV & AIDS Review xxx (2015) xxx–xxx
2
Fig. 1. Wasting of bilateral deltoid muscles (A and B), EMG of 1st dorsal interossei and deltoid muscles (C and D).
fasciculations, positive sharp waves, early recruitment and delayed interference pattern in both deltoids, biceps, dorsal interossei, left quadriceps and para-spinal muscles (Fig. 1C and D). Right lower limb EMG was normal. MRI of brain and spinal cord was normal. He was diagnosed as a case of probable ALS as per El-Escorial criteria [3]. Further investigation revealed the patient to be HIV-1 positive by ELISA and Western blot. At time of diagnosis he had a low CD4 count of 184 cells/mL and HIV type-1 RNA quantification by RT-PCR assay was 101,767 copies/ml. HIV RNA level in CSF was not done in this patient. He was started on Lamivudine 150 mg, Zidovudine 300 mg and Nevirapine 200 mg (HAART) twice daily along with co-trimoxazole and patient tolerated the medications well with no side effects. On 6 months follow-up his symptoms improved significantly, had a weight gain of 8 kg and Electroneuromyography test revealed a normal insertional and spontaneous activity with normal interference pattern (Fig. 2). CD4 count was 317 cells/mL and HIV-1 viral load by RT-PCR assay was not detectable at 6 months follow-up. 3. Discussion A viral etiology of MND has been hypothesized for more than five decades. Poliovirus selectively infects motor neurons in the
spinal cord and brainstem and a persistent polio virus infection as a cause of ALS was proposed 5 decades earlier [4]. HIV-associated MND was initially reported in 1985 by Hoffman et al. in fourth year of AIDS epidemic, who described a 26-year-old patient with both upper and lower motor neuron signs [5]. In the next 20 years, at least 22 more cases of ALS like syndrome in HIV infected patients have been reported [6]. MND syndrome can occur in several forms with HIV infection and may be indistinguishable from the classical sporadic ALS, which is a progressive disorder of lower and upper motor neurons, culminating in progressive weakness, respiratory failure and finally death [6]. These associations are not proven epidemiologically and it is not certain if HIV is a risk factor for either ALS or other MND [7]. According to WHO an estimated 0.8% of adults aged 15–49 years are living with HIV infection. Moulignier et al. identified six patients with HIV-1 infection in a large series of 1700 patients who were diagnosed to have an ALS like disorder. It gave an incidence of ALS as 3.5 per 1000 in HIV infected patients versus 0.4–1.76 per 100,000 in general population. These cases differed from the patients of sporadic ALS in relatively younger age, more rapid progression of symptoms and at least partial clinical recovery following HAART. [1] In contrast to other occasional reports, a study by Ashok Verma et al. of two cases with HIV and
Please cite this article in press as: A.A. John, et al., A rare presentation of reversible ALS in HIV infection, HIV & AIDS Review (2015), http://dx.doi.org/10.1016/j.hivar.2015.02.004
G Model
HIVAR-114; No. of Pages 3 A.A. John et al. / HIV & AIDS Review xxx (2015) xxx–xxx
3
The responsiveness to antiretroviral treatment and the viral load reduction and CD4+ T-cell count improvement and immune reconstitution, suggest an indirect association of MND and HIV infection [9]. Subrata Chakrabarti et al. has reported a case of 33-year-old male with ALS as a sole neurological manifestation of HIV but he was diagnosed with the infection 7 years earlier and treatment with HAART did not produce any significant improvement [10]. Our patient presented with neurological symptoms as sole manifestation of HIV infection and significantly improved with antiretroviral therapy. 4. Conclusion The exact causative role of HIV in ALS is not known at present. Recognition of these HIV-related motor neuron syndromes is important because they may respond to treatment. Such cases also raise issues like – if sporadic ALS is a result of a virus infection or due to autoimmune causes. Our case demonstrates a remission of MND, following HAART defined by definite clinical improvement and normal ENMG studies with improvement of CD4 counts and reduction in plasma viral load at 6 months follow-up. It also illustrates the importance of identifying reversible causes of ALS and response to treatment in a patient who presented with motor neuron disease features as the only manifestation of HIV, with no other neurological or systemic symptoms and later diagnosed to have HIV infection. Financial disclosure None declared. Conflict of interest Fig. 2. EMG showing normal insertional/spontaneous activity (A) and normal interference pattern (B).
None declared. Acknowledgements
features of MND, one showed partial recovery and the other did not show neurological recovery following effective HAART [8]. Factors predicting therapeutic response are onset at a younger age, rapid progression and abnormal CSF. The unresponsive form may be the sporadic ALS that occurs by chance in an HIV-infected person [7]. Our case presented with symptoms and signs of motor neuron disease. Once all secondary causes of motor neuron disease were ruled out, he was diagnosed as having probable ALS as per El Escorial criteria with HIV infection. On initiation of HAART there was a progressive improvement clinically at 6 months follow-up with a reduction in plasma viral load and improvement in CD4 counts. In the study by Moulignier et al., five of the six patients were seen before effective antiretroviral therapy was available and poorer control of the plasma HIV-1 viral load. Since that period they have not observed ALS-like illness in treated patients who are HIV-1 positive. It may probably be due to suppression of CNS viral replication, suppression of plasma viral load which reduced further CNS seeding or an improvement of the patient’s immune system that reduced HIV-associated neurologic complications [1]. The mechanism of death of motor neurons in HIV infected persons is not known. It is not a neurotropic virus and rarely infects neurons, but infection occurs predominantly in microglial cells within the CNS. Primary nervous system involvement in HIV infection may be due to viral proteins that are neurotoxic or by cytokines and chemokines, as a consequence of the HIV disease.
I thank Dr. Anish Metha, Dr. Kiran Buddharaju and Dr. Abhinandhan K.S. for all the support and help in preparation of this manuscript. References [1] A. Moulignier, A. Moulonguet, G. Pialoux, W. Rozenbaum, Reversible ALS-like disorder in HIV infection, Neurology 57 (2001) 995–1001. [2] D.W. Mulder, F.M. Howard Jr., Patient resistance and prognosis in amyotrophic lateral sclerosis, Mayo Clin. Proc. 51 (9) (1976) 537–541. [3] R.B. Daroff, G.M. Fenichel, J. Jankovic, et al. 6th ed., Bradley’s Neurology in Clinical Practice, vol. 2, 2012, p. 1881. [4] D.C. Poskanzer, H.M. Cantor, G.S. Kaplan, The frequency of preceding poliomyelitis in amyotrophic lateral sclerosis, in: Motor neuron disease: research on amyotrophic lateral sclerosis and related disorders, Grune & Stratton, New York, (1969), pp. 286–290. [5] P.M. Hoffman, B.W. Festoff, L.T. Giron Jr., R.M. Garruto, F.W. Ruscetti, Isolation of LAV/HTLV-III from a patient with amyotrophic lateral sclerosis, N. Engl. J. Med. 313 (1985) 324–325. [6] A. Verma, M. Shri Kant, Spectrum of motor neuron diseases with HIV-1 infection, Ann. Indian Acad. Neurol. 9 (2006) 103–109. [7] L.P. Rowland, et al., HIV-related neuromuscular diseases: nemaline myopathy, amyotrophic lateral sclerosis and bibrachial amyotrophic diplegia, Acta Myol. XXX (2011) 29–31. [8] A. Verma, J.R. Berger, ALS syndrome in patients with HIV-1 infection, J. Neurol. Sci. 240 (2006) 59–64. [9] B. Jubelt, J.R. Berger, Does viral disease underlie ALS? Lessons from the AIDS pandemic, Neurology 57 (2001) 945–946. [10] S. Chakrabarti, K. Pan, K. Mondal, et al., Amyotrophic lateral sclerosis as sole neurological manifestation of human immunodeficiency virus, J. HIV Hum. Reprod. 2 (1) (2014).
Please cite this article in press as: A.A. John, et al., A rare presentation of reversible ALS in HIV infection, HIV & AIDS Review (2015), http://dx.doi.org/10.1016/j.hivar.2015.02.004
HIVAR-114; No. of Pages 3 HIV & AIDS Review xxx (2015) xxx–xxx
Contents lists available at ScienceDirect
HIV & AIDS Review journal homepage: www.elsevier.com/locate/hivar
Case Report
A rare presentation of reversible ALS in HIV infection Aju Abraham John *, Suryanarayana Sharma, B.K. Madhusudhan, Rohan Mahale, Mahendra Javali, R. Srinivasa Ramaiah Medical College, India
A R T I C L E I N F O
Article history: Received 19 January 2015 Received in revised form 15 February 2015 Accepted 16 February 2015 Available online xxx Keywords: Motor neuron disease Amyotrophic lateral sclerosis Reversible ALS HIV infection HAART
A B S T R A C T
Amyotrophic lateral sclerosis (ALS) is the most common type of motor neuron disease (MND) [1]. It is usually associated with an irreversible course, and treatable causes of ALS are rare. Here, we present a case report of a 35-year-old male, with progressive weakness and wasting of muscles in all four limbs with fasciculation and electro diagnostic features compatible with a diagnosis of probable ALS. He was later diagnosed to have HIV infection and initiated on anti-retroviral therapy. On 6 months follow-up, he had a weight gain of 8 kg and electro diagnostic studies revealed near total normalization of the neurogenic pattern. Reversible ALS like illness in HIV infection has been documented in literature but most of them are diagnosed cases of HIV infection. This case identifies the importance of identifying reversible causes of ALS and near total response to treatment in a patient who presented to us with MND features as the only manifestation of HIV infection. ß 2015 Polish AIDS Research Society. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.
1. Introduction Amyotrophic lateral sclerosis (ALS) is the most common type of motor neuron disease (MND) that primarily affects the motor neuron cell population involving spinal cord or bulbar motor neurons and pyramidal tracts resulting in progressive weakness and wasting of muscles [1]. ALS is mostly associated with an irreversible course and treatable causes are rare. Mulder et al. has reported from a study of two decades of more than two thousand patients with MND, many cases had an initial diagnosis of ALS but later improved [2].
2. Case report A 35-year-old male patient was admitted with a history of progressive asymmetric weakness of limbs of three months duration. Initially it was noticed in the left lower limb which progressed to other limbs in a span of 1 month and predominantly involved the proximal group of muscles. Patient had also noticed fasciculation of muscles in his right arm since 2 months. He had easy fatigability and weight loss of approximately 10 kg in
* Corresponding author at: M.S. Ramaiah Institute of Neurosciences, New Bel Road, Mathikere, Bangalore 560094, Karnataka, India. Tel.: +91 8022183125; mobile: +91 9900136112. E-mail address: [email protected] (A.A. John).
6 months. He denied symptoms suggestive of cranial nerve involvement, sensory symptoms, bowel and bladder sphincter impairment and sexual dysfunction. He also denied history of any systemic illness, exposure to toxins, multiple blood transfusions, drug abuse and high risk sexual behavior. He was a manual laborer by occupation. General physical examination and vital signs were normal. Neurological examination revealed a normal higher mental functions and cranial nerves exam. Fasciculations were observed on the right deltoid, wasting of bilateral deltoids, trapezius and quadriceps (Left>Right) with a normal tone (Fig. 1A and B). Upper limbs power were graded 3/5 in proximal group bilaterally, 4/5 in right and 4-/5 in left lower limb proximal muscle groups. All deep tendon reflexes were brisk with jaw jerk present, normal abdominal reflexes and bilateral plantar flexor. Other systems examination was normal. Blood investigations of complete blood counts, renal functions, liver functions and electrolytes were normal. CSF analysis for cell count, cell type, protein, glucose, chloride, TB-PCR, VDRL, cryptococcal antigen and Indian ink preparation was normal. Serum vitamin levels was more than 2000 pg/ml, TSH was 2.294 uIU/ml and creatinine kinase was 92 IU/L. Angiotensin converting enzyme levels (19 U/L), markers for malignancy like Alfa feto protein (1.48 IU/ml), Prostrate specific antigen (0.49 ng/ml), Carcino embryionic antigen (0.8 ng/ml) and serum PTH (23.7 pg/ml) were normal. Nerve Conduction Study was normal except for mildly reduced CMAP amplitude in right common peroneal nerve, with a normal SNAP. EMG revealed
http://dx.doi.org/10.1016/j.hivar.2015.02.004 1730-1270/ß 2015 Polish AIDS Research Society. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.
Please cite this article in press as: A.A. John, et al., A rare presentation of reversible ALS in HIV infection, HIV & AIDS Review (2015), http://dx.doi.org/10.1016/j.hivar.2015.02.004
G Model
HIVAR-114; No. of Pages 3 A.A. John et al. / HIV & AIDS Review xxx (2015) xxx–xxx
2
Fig. 1. Wasting of bilateral deltoid muscles (A and B), EMG of 1st dorsal interossei and deltoid muscles (C and D).
fasciculations, positive sharp waves, early recruitment and delayed interference pattern in both deltoids, biceps, dorsal interossei, left quadriceps and para-spinal muscles (Fig. 1C and D). Right lower limb EMG was normal. MRI of brain and spinal cord was normal. He was diagnosed as a case of probable ALS as per El-Escorial criteria [3]. Further investigation revealed the patient to be HIV-1 positive by ELISA and Western blot. At time of diagnosis he had a low CD4 count of 184 cells/mL and HIV type-1 RNA quantification by RT-PCR assay was 101,767 copies/ml. HIV RNA level in CSF was not done in this patient. He was started on Lamivudine 150 mg, Zidovudine 300 mg and Nevirapine 200 mg (HAART) twice daily along with co-trimoxazole and patient tolerated the medications well with no side effects. On 6 months follow-up his symptoms improved significantly, had a weight gain of 8 kg and Electroneuromyography test revealed a normal insertional and spontaneous activity with normal interference pattern (Fig. 2). CD4 count was 317 cells/mL and HIV-1 viral load by RT-PCR assay was not detectable at 6 months follow-up. 3. Discussion A viral etiology of MND has been hypothesized for more than five decades. Poliovirus selectively infects motor neurons in the
spinal cord and brainstem and a persistent polio virus infection as a cause of ALS was proposed 5 decades earlier [4]. HIV-associated MND was initially reported in 1985 by Hoffman et al. in fourth year of AIDS epidemic, who described a 26-year-old patient with both upper and lower motor neuron signs [5]. In the next 20 years, at least 22 more cases of ALS like syndrome in HIV infected patients have been reported [6]. MND syndrome can occur in several forms with HIV infection and may be indistinguishable from the classical sporadic ALS, which is a progressive disorder of lower and upper motor neurons, culminating in progressive weakness, respiratory failure and finally death [6]. These associations are not proven epidemiologically and it is not certain if HIV is a risk factor for either ALS or other MND [7]. According to WHO an estimated 0.8% of adults aged 15–49 years are living with HIV infection. Moulignier et al. identified six patients with HIV-1 infection in a large series of 1700 patients who were diagnosed to have an ALS like disorder. It gave an incidence of ALS as 3.5 per 1000 in HIV infected patients versus 0.4–1.76 per 100,000 in general population. These cases differed from the patients of sporadic ALS in relatively younger age, more rapid progression of symptoms and at least partial clinical recovery following HAART. [1] In contrast to other occasional reports, a study by Ashok Verma et al. of two cases with HIV and
Please cite this article in press as: A.A. John, et al., A rare presentation of reversible ALS in HIV infection, HIV & AIDS Review (2015), http://dx.doi.org/10.1016/j.hivar.2015.02.004
G Model
HIVAR-114; No. of Pages 3 A.A. John et al. / HIV & AIDS Review xxx (2015) xxx–xxx
3
The responsiveness to antiretroviral treatment and the viral load reduction and CD4+ T-cell count improvement and immune reconstitution, suggest an indirect association of MND and HIV infection [9]. Subrata Chakrabarti et al. has reported a case of 33-year-old male with ALS as a sole neurological manifestation of HIV but he was diagnosed with the infection 7 years earlier and treatment with HAART did not produce any significant improvement [10]. Our patient presented with neurological symptoms as sole manifestation of HIV infection and significantly improved with antiretroviral therapy. 4. Conclusion The exact causative role of HIV in ALS is not known at present. Recognition of these HIV-related motor neuron syndromes is important because they may respond to treatment. Such cases also raise issues like – if sporadic ALS is a result of a virus infection or due to autoimmune causes. Our case demonstrates a remission of MND, following HAART defined by definite clinical improvement and normal ENMG studies with improvement of CD4 counts and reduction in plasma viral load at 6 months follow-up. It also illustrates the importance of identifying reversible causes of ALS and response to treatment in a patient who presented with motor neuron disease features as the only manifestation of HIV, with no other neurological or systemic symptoms and later diagnosed to have HIV infection. Financial disclosure None declared. Conflict of interest Fig. 2. EMG showing normal insertional/spontaneous activity (A) and normal interference pattern (B).
None declared. Acknowledgements
features of MND, one showed partial recovery and the other did not show neurological recovery following effective HAART [8]. Factors predicting therapeutic response are onset at a younger age, rapid progression and abnormal CSF. The unresponsive form may be the sporadic ALS that occurs by chance in an HIV-infected person [7]. Our case presented with symptoms and signs of motor neuron disease. Once all secondary causes of motor neuron disease were ruled out, he was diagnosed as having probable ALS as per El Escorial criteria with HIV infection. On initiation of HAART there was a progressive improvement clinically at 6 months follow-up with a reduction in plasma viral load and improvement in CD4 counts. In the study by Moulignier et al., five of the six patients were seen before effective antiretroviral therapy was available and poorer control of the plasma HIV-1 viral load. Since that period they have not observed ALS-like illness in treated patients who are HIV-1 positive. It may probably be due to suppression of CNS viral replication, suppression of plasma viral load which reduced further CNS seeding or an improvement of the patient’s immune system that reduced HIV-associated neurologic complications [1]. The mechanism of death of motor neurons in HIV infected persons is not known. It is not a neurotropic virus and rarely infects neurons, but infection occurs predominantly in microglial cells within the CNS. Primary nervous system involvement in HIV infection may be due to viral proteins that are neurotoxic or by cytokines and chemokines, as a consequence of the HIV disease.
I thank Dr. Anish Metha, Dr. Kiran Buddharaju and Dr. Abhinandhan K.S. for all the support and help in preparation of this manuscript. References [1] A. Moulignier, A. Moulonguet, G. Pialoux, W. Rozenbaum, Reversible ALS-like disorder in HIV infection, Neurology 57 (2001) 995–1001. [2] D.W. Mulder, F.M. Howard Jr., Patient resistance and prognosis in amyotrophic lateral sclerosis, Mayo Clin. Proc. 51 (9) (1976) 537–541. [3] R.B. Daroff, G.M. Fenichel, J. Jankovic, et al. 6th ed., Bradley’s Neurology in Clinical Practice, vol. 2, 2012, p. 1881. [4] D.C. Poskanzer, H.M. Cantor, G.S. Kaplan, The frequency of preceding poliomyelitis in amyotrophic lateral sclerosis, in: Motor neuron disease: research on amyotrophic lateral sclerosis and related disorders, Grune & Stratton, New York, (1969), pp. 286–290. [5] P.M. Hoffman, B.W. Festoff, L.T. Giron Jr., R.M. Garruto, F.W. Ruscetti, Isolation of LAV/HTLV-III from a patient with amyotrophic lateral sclerosis, N. Engl. J. Med. 313 (1985) 324–325. [6] A. Verma, M. Shri Kant, Spectrum of motor neuron diseases with HIV-1 infection, Ann. Indian Acad. Neurol. 9 (2006) 103–109. [7] L.P. Rowland, et al., HIV-related neuromuscular diseases: nemaline myopathy, amyotrophic lateral sclerosis and bibrachial amyotrophic diplegia, Acta Myol. XXX (2011) 29–31. [8] A. Verma, J.R. Berger, ALS syndrome in patients with HIV-1 infection, J. Neurol. Sci. 240 (2006) 59–64. [9] B. Jubelt, J.R. Berger, Does viral disease underlie ALS? Lessons from the AIDS pandemic, Neurology 57 (2001) 945–946. [10] S. Chakrabarti, K. Pan, K. Mondal, et al., Amyotrophic lateral sclerosis as sole neurological manifestation of human immunodeficiency virus, J. HIV Hum. Reprod. 2 (1) (2014).
Please cite this article in press as: A.A. John, et al., A rare presentation of reversible ALS in HIV infection, HIV & AIDS Review (2015), http://dx.doi.org/10.1016/j.hivar.2015.02.004