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Year : 2019  |  Volume : 8  |  Issue : 5  |  Page : 1794-1797  

Guillain Barre syndrome with pulmonary tuberculosis: A case series from a tertiary care hospital

Department of Medicine, RPGMC Tanda, Kangra, Himachal Pradesh, India

Date of Web Publication31-May-2019

Correspondence Address:
Dr. Tarun D Sharma
Assistant Professor, RPGMC Tanda, Kangra, Himachal Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jfmpc.jfmpc_161_19

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Introduction: Guillain-Barre syndrome (GBS) is post-infectious autoimmune polyradiculopathy which characteristically presents with a monophasic illness with CSF albumino-cytological dissociation with partial or complete recovery. The incidence of GBS is about 1 to 2/100,000 per year.[1] Subtypes are described based on electrophysiological patterns, the most common being acute inflammatory demyelinating polyneuropathy (AIDP) and rarer ones being acute motor axonal neuropathy (AMAN), and acute motor and sensory axonal neuropathy (AMSAN). Tuberculosis is prevalent in India with various neurological manifestation including tuberculoma, brain abcess, pott's spine, and radiculomyelopathy.[2] Five cases have been published of tuberculosis and GBS.[3],[4],[5],[6],[7] The main underlying pathophysiological mechanism is aberrant immune activation due to molecular mimicry against ganglioside in myelin. Although tuberculosis is mainly T-cell-mediated chronic disease, still there are cases reported with tuberculosis with GBS. Here we are going to present four cases of pulmonary tuberculosis presented with GBS. Materials and Methods: This study describes clinical profile of four patients who presented with concomitant pulmonary tuberculosis and GBS over a period of 4 years in a tertiary hospital. Diagnosis was made according to Brighton criteria and alternative diagnosis were ruled out by clinical examination, serological markers, and MRI imaging of the spine. All patient underwent thorough investigation including HIV 1, 2, anti-CMV, anti-EBV to rule out other possible triggers of GBS, NCV, CSF study along with sputum AFB culture. ZN staining and CECT thorax were also done to support the diagnosis. Results: Of total four cases, 3 were male and 1 was female who presented with weight loss, anorexia, cough with or without hemoptysis, and acute progressive LMN quadriparesis in which there was typical albumin-cytological dissociation in CSF. Nerve conduction studies were suggestive of AIDP in two patients, AMAN in one patient, and AMSAN in the fourth one. An exhaustive investigation for triggers of GBS were performed for all patients who were treated with IVIG and two of them completely recovered and rest of two did not recover completely after 6 weeks of follow-up. Conclusion: In pulmonary tuberculosis, patients with polyneuropathy demands urgent search for GBS as there has been case reports in literature though the association between tuberculosis and GBS is not clear.

Keywords: Guillain--Barre syndrome, nerve conduction studies, polyneuropathy, tuberculosis

How to cite this article:
Malakar S, Sharma TD, Raina S, Sharma KN, Kapoor D. Guillain Barre syndrome with pulmonary tuberculosis: A case series from a tertiary care hospital. J Family Med Prim Care 2019;8:1794-7

How to cite this URL:
Malakar S, Sharma TD, Raina S, Sharma KN, Kapoor D. Guillain Barre syndrome with pulmonary tuberculosis: A case series from a tertiary care hospital. J Family Med Prim Care [serial online] 2019 [cited 2020 May 27];8:1794-7. Available from:

  Case Series Top

Case 1

A 46-year-old female patient presented with undocumented weight loss, cough, and anorexia for 1 month and acute onset weakness of bilateral lower limb followed by weakness of truncal muscles and upper limb for 12 days. It was ascending, without any bladder bowel or sensory symptoms. There was no involvement of cortex, cerebellum, or higher mental function. There were no preceding upper respiratory or diarrheal illness. Her sputum was positive for M. tuberculosis [Figure 1]. Her chest X- ray [Figure 2] showed fibrosis and old healed lesion of past tuberculosis. She had a past history of ATT intake 16 years ago for sputum positive pulmonary tuberculosis.
Figure 1: ZN staining showing AFB

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Figure 2: Chest X-ray fibrosis and old healed lesion

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On examination, she had generalized areflexia. Nerve conduction studies (NCS) was suggestive of AIDP and CSF protein was 122 mg/dL without any cellularity. Her HIV status was negative. She was treated with IVIG, although recovery was incomplete in 3 months of follow-up. But she was cured of pulmonary TB.

Case 2

A 32-year-old male presented with cough, hemoptysis for 18 days and bilateral lower limb weakness for 2 days which was distal to start with gradually progressed to involve hip muscles. On examination, there was acute flaccid paraplegia. There were patchy sensory loss and left seventh LMN CN palsy without any autonomic or bladder bowel involvement. His NCV was suggestive of AIDP and CSF protein was 158 mg/dL with three lymphocytes. His sputum was negative but sputum was positive by gene expert for tuberculosis. He was treated with intravenous immunoglobulin and CAT 1 ATT and completely recovered neurologically by 6 weeks.

Case 3

A 52-year-old male patient with past history of sputum positive tuberculosis presented with progressive shortness of breath and cough with sputum production for last 3 months. But for last 5 days he complained of sudden onset weakness of bilateral lower limb followed by truncal and upper limb weakness. On examination, his right sided chest shows signs of volume loss with bronchial breath sound with coarse crepitations which was confirmed by CT chest [Figure 3]. On nervous system examination, his higher mental examination were normal with generalized areflexia. Chest X-ray was suggestive of right sided fibrosis lung. NCS [Figure 4] was suggestive of AMAN. And his CSF protein was also raised without cellularity done on day 11th of symptom onset. Patient's weakness started improving on itself. Patient was treated with CAT 2 ATT.
Figure 3: CECT chest showing active lesions

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Figure 4: NCS showing CMAP reduced, SNAP normal suggestive of AMAN

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Case 4

A 39-year-old male patient presented with progressive cough for 2 months with anorexia and weight loss. There was no history of hemoptysis. His father was diagnosed to have pulmonary tuberculosis 1 year ago and was a defaulter.

Apart from chronic cough he presented with low back pain and leg paresthesias and weakness for last 15 days. He had transient bladder involvement. On examination, his lower limb power was 0/4 with areflexia. He underwent MRI [Figure 5] lumbosacral spine which revealed marked enhancement of thickened nerve roots in conus medullaris and cauda equina. He was diagnosed to be sputum positive pulmonary tuberculosis. Earlier MRI findings were explained on the basis of tuberculosis until his CSF showed albumin-cytological dissociation. To confirm the diagnosis, his GQ1b was sent which came out to be positive. He was treated with IVIG and showed marked improvement and was concomitantly treated with ATT.
Figure 5: Marked contrast enhancement and thickened nerve roots in cauda and conus region

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  Discussion Top

The association has mostly been reported with pulmonary tuberculosis. All previously reported cases had features suggesting tuberculosis prior to the onset of weakness. With high prevalence of pulmonary tuberculosis, it is likely that GBS may also be prevalent but is unrecognized or treated as possible tuberculous radiculitis, and therefore it is imperative to know the likely association of this communicable disease with this highly treatable immune condition. The subtype of GBS described in this series [8] follow the same distribution as in the rest of the world: AIDP is the most common (73.8%), followed by AMAN (13.4%) and AMSAN (4.6%). The AMSAN variant is very rare and has a worse prognosis and delayed recovery. Peripheral neuropathies in association with TB infection are very uncommonly reported except polyneuropathy related to isoniazid and ethambutol toxicity, apart from these toxic forms, reports are in form of acute or chronic demyelinating polyneuropathy.[9] The exact pathogenesis of GBS associated with TB remains obscure but it is believed to be due to a molecular mimicry leading to the immunological attack of peripheral nerves. This concept of molecular mimicry is further supported by studies showing clinical improvement after receiving immunomodulatory agents. The antigens production mechanism would be caused by the liberation of tuberculosis bacillus proteins or by the liberation of cytokines, mainly tumor necrosis factor alpha, both related to the action of tuberculosis treatment.[10] A cell-mediated delayed hypersensitivity reaction to, or invasion of the nerve roots by tubercle bacilli would seem to be the likely explanation of the neuropathy.[11] In our study, two patients had complete recovery, one had partial and last had incomplete recovery. Only three patients received IVIG. Since tuberculosis in India has high prevalence and tuberculosis is primarily diagnosed at primary healthcare level, hence it is very important for primary care physicians to be very alert when a patient presents with neurological illness that too pure motor along with symptoms of tuberculosis and these cases are not wrongly attributed to tuberculosis. These cases are very rare and physician must be very alert when any patient presents with acute pure motor weakness along with respiratory symptoms.

Declaration of patient consent

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

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Yuki N, Hartung HP. Guillain-Barre syndrome. N Engl J Med 2012;366:2294-304.  Back to cited text no. 1
Kocen RS, Parsons M. Neurological complications of tuberculosis: Some unusual manifestations. Q J Med 1970;39:17-30.  Back to cited text no. 2
Canham M, Iseman MD. Guillain Barre syndromerelated to pulmonary tuberculosis. Ann Am Thorac Soc 2014;11:855-7.  Back to cited text no. 3
de la Torre RG, Moris G, Martinez DP, Montes IC. Guillain-Barre syndrome, tuberculosis and inflammatory bowel disease: A multiple association. Int Arch Med 2010;3:15.  Back to cited text no. 4
Soehardy Z, Yuhanisa A, Thein SS, Rohana AG, Fauzi AR, Norlinah MI, et al. AMSAN variant of Guillain Barre syndrome progressing tochronic inflammatory demyelinating polyneuropathy in a patient with Marfan's syndrome and pulmonary tuberculosis. Med J Malaysia 2005;60:655-6.  Back to cited text no. 5
Taha AA, Tee KH. Guillain-Barre syndrome associated with pulmonary tuberculosis. BMJ Case Rep 2012;13:2012. doi: 10.1136/bcr-01-2012-5484.  Back to cited text no. 6
Vyravanathan S, Senanayake N. Guillain-Barre syndrome associated with tuberculosis. Postgrad Med J 1983;59:516-7.  Back to cited text no. 7
Kalita J, Misra UK, Goyal G, Das M. Guillain-Barre syndrome: Subtypes and predictors of outcome from India. J Peripher Nerv Syst 2014;19:36-43.  Back to cited text no. 8
Shin SS, Hyson AM, Castañeda C, Sánchez E, Alcántara F, Mitnick CD, et al. Peripheral neuropathy associated with treatment for multidrug-resistant tuberculosis. Int J Tuberc Lung Dis 2003;7:347-53.  Back to cited text no. 9
Fernández-Fúnez A, Gómez Garrido J, Alamillo A, Sáez L. Demyelinating polyneuropathy as the Honest form of lymph node tuberculosis. Paradox response in an immunocompetent patient. Med Clin 2007;129:78-9.  Back to cited text no. 10
Akhtar J. Acute inflammatory demyelinating polyradiculoneuropathy associated with mycobacterium tuberculosis. EC Neurol 2018;10:855-9.  Back to cited text no. 11


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]


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