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Table of Contents    
Year : 2011  |  Volume : 59  |  Issue : 6  |  Page : 904-906

Segmental myoclonus and marked ataxia in a patient of pulmonary tuberculosis

1 Department of Neurology, Malabar Institute of Medical Sciences, Calicut, Kerala, India
2 Department of Paediatrics, Malabar Institute of Medical Sciences, Calicut, Kerala, India
3 Department of Radiology, Malabar Institute of Medical Sciences, Calicut, Kerala, India
4 Department of Pathology, Malabar Institute of Medical Sciences, Calicut, Kerala, India

Date of Submission12-Jun-2011
Date of Decision15-Jun-2011
Date of Acceptance04-Aug-2011
Date of Web Publication2-Jan-2012

Correspondence Address:
V V Ashraf
Department of Neurology, Malabar Institute of Medical Sciences, Calicut, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.91376

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How to cite this article:
Ashraf V V, Praveenkumar, Sureshkumar E K, Anand R, Kuruvilla S, Girija A S. Segmental myoclonus and marked ataxia in a patient of pulmonary tuberculosis. Neurol India 2011;59:904-6

How to cite this URL:
Ashraf V V, Praveenkumar, Sureshkumar E K, Anand R, Kuruvilla S, Girija A S. Segmental myoclonus and marked ataxia in a patient of pulmonary tuberculosis. Neurol India [serial online] 2011 [cited 2020 Aug 6];59:904-6. Available from:


Myoclonus is rarely associated with the pathology of cerebellum. [1] We report segmental myoclonus and ataxia in a child with pulmonary tuberculosis.

An 8-year-old boy was admitted with fever and cough of 1-month duration and unsteadiness of gait, tremor of hands and spontaneous, intermittent, nonrhythmic jerking of lower limbs and trunk of 2-day duration. Three weeks before, he was admitted at another facility with a 1-week history of fever with cough and was diagnosed to have right lung consolidation and received parentral antibiotics. On examination at this admission he had significant coordination impairment with marked symmetric intention tremor involving both upper limbs and was unable to stand due to severe trunkal ataxia. He had intermittent jerky movements involving leg and later involving the trunk muscles [video].-

Rest of the neurological examination was normal.

Abnormal laboratory tests were hemoglobin 9.2 g/dl, high ESR 120 mm/hr, and microcytic anemia on peripheral smear. Chest X-ray showed right middle lobe collapse consolidation and right mediastinal lesion [Figure 1]a. Ultrasound of abdomen showed minimal hepatomegaly. Magnetic resonance imaging (MRI) of brain revealed patchy lesions over both cerebellar hemispheres, hypointense on T1-weighted images and hyperintense on T2-weighted images and fluid attenuated inversion recovery (FLAIR) images [Figure 1]b and c. There was no enhancement on contrast. Cerebrospinal fluid (CSF) analysis was normal. Short-term video-EEG monitoring revealed normal background rhythm and no epileptiform discharges associated with myoclonic jerks. Somatosensory evoked potential (SSEP) of upperlimb and lowerlimb were within normal range. Surface electromyography of quadriceps femoris and hamstring muscles revealed repetitive irregular discharges with no apparent reciprocities. He underwent thoracoscopy and biopsy of the mediastinal lesion. At thoracoscopy there was a large superior mediastinal mass which on probing ruptured and drained thick pus. Histopathology revealed fragmented lymphnode with extensive area of caseation and granulomas composed of epitheloid histocytes and lymphocytes, features suggestive of caseating tuberculous lymphadenitis [Figure 1]d. AFB staining of the drained cheesy material was strongly positive for Mycobacterium tuberculosis. He was put on antituberculous treatment. His ataxia and myoclonus improved completely in 2 weeks time.
Figure 1: (a) MRI brain axial flair image showing patchy hyperintensities in cerebellum, (b) MRI brain sagittal flair image showing hyperintense signal in the cerebellar vermis, (c) Chest X-ray revealing right middle lobe collapse with right hilar lesion, (d) Histopathology of the hilar lymph node revealing extensive caseation and granulomas composed of epitheloid histiocytes and lymphocytes

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Symptomatic myoclonus has been associated with lesions at various locations of neuroaxis. There have been several reports of patients with symptomatic myoclonus in whom the most notable pathology is in the cerebellum. Frequently, ataxia was the associated feature in these patients. Most commonly reported pathology was nonlocalizing and included anoxic necrosis, degenerative diseases, and paraneoplastic syndrome. [1] There have been reports of myoclonus in patients with cerebellar tumor and cerebellitis. [2],[3] Myoclonus associated with cerebellar pathology may be due to increased excitability of the cerebellar output. [4] In our patient neurophysiological studies were not suggestive of cortical myoclonus. [5]

Cerebellar involvement in a patient with pulmonary tuberculosis can be due to tuberculomas, tuberculous meningitis, or cerebellitis. MRI and CSF findings in our patient were not suggestive of the first two possibilities. Differential diagnosis between cerebellitis and demyelination (confining to cerebellum) may at times be difficult. Bilateral diffuse hemispheric abnormalities represent the most common imaging presentation in cerebellitis. [6] Acute cerebellitis is characterized by an acute or subacute onset of cerebellar ataxia following an infection or vaccination. [7] In this patient the MRI features can go with cerebellitis. We are not aware of any previous reports of cerebellitis due to tuberculosis. Our patient had good clinical improvement with antituberculous treatment, however, we did not do repeat MRI to document the status of the lesions observed.

  References Top

1.Marsdon CD, Harding AE, Obeso JA, Lu CS. Progressive myoclonic ataxia (the Ramsay Hunt syndrome). Arch Neurol 1990;47:1121-25.  Back to cited text no. 1
2.Mink WJ, Caruso AP, Pomeroy LS. Progressive myoclonus in a child with deep cerebellar mass. Neurology 2003;61:829-31.  Back to cited text no. 2
3.Costa B, Tacconi P, Pinn L, Cannas A, Fiaschi A. Segmental myoclonus in a young man who had localized encephalitis in childhood. Ital J Neurol Sci 1989;10:357-9.  Back to cited text no. 3
4.Tijssen MA, Thom M, Ellison DW, Wilkins P, Barnes D, Thompson PD, et al. Cortical myoclonus and cerebellar pathology. Neurology 2000;54:1350-6.  Back to cited text no. 4
5.Ragothaman M, Kulkarni G, Ashraf VV, Pal KP, Chickabasavaiah Y, Shankar SK, et al. Elemental mercury poisoning probably causes cortical myoclonus. Mov Disord 2007;22:1964-8.  Back to cited text no. 5
6.De Bruecker Y, Claus F, Demaerel P, Ballaux F, Sciot R, Lagae L, et al. MRI findings in acute cerebellitis. Eur Radiol 2004;14:478-83  Back to cited text no. 6
7.Horowitz MB, Pang D, Hirsch W. Acute cerebellitis: Case report and review. Pediatr Neurosurg 1991-1992;17:142-5.  Back to cited text no. 7


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