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Table of Contents    
LETTER TO EDITOR
Year : 2020  |  Volume : 68  |  Issue : 2  |  Page : 512-514

Tuberculous Meningitis Presenting with Nonconvulsive Status Epilepticus and Transient Diffusion Restriction: A Rare Case


Department of Neurology, Kitano Hospital, Tazuke Kofukai Medical Research Institute, 2-4-20 Ohgimachi, Kita-ku, Osaka, Japan

Date of Web Publication15-May-2020

Correspondence Address:
Yuwa Oka
Department of Neurology, Kitano Hospital, Tazuke Kofukai Medical Research Institute, 2-4-20 Ohgimachi, Kita-ku, Osaka 530-8480
Japan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.283759

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How to cite this article:
Oka Y, Tabu H, Matsumoto S. Tuberculous Meningitis Presenting with Nonconvulsive Status Epilepticus and Transient Diffusion Restriction: A Rare Case. Neurol India 2020;68:512-4

How to cite this URL:
Oka Y, Tabu H, Matsumoto S. Tuberculous Meningitis Presenting with Nonconvulsive Status Epilepticus and Transient Diffusion Restriction: A Rare Case. Neurol India [serial online] 2020 [cited 2020 May 26];68:512-4. Available from: http://www.neurologyindia.com/text.asp?2020/68/2/512/283759




Sir,

The estimated mortality due to tuberculous meningitis in India is 1.5 per 100,000 population.[1] Central nervous system tuberculosis such as tuberculous meningitis accounts for approximately 10% of all tuberculosis cases.[1]

To the best of our knowledge, only two cases of tuberculous meningitis presenting with nonconvulsive status epilepticus have been published to date.[2],[3] We present here such a rare report not only presenting with SE but also reversible hyperintensity on diffusion weighted imaging (DWI).

In this report, we present the case of a 61-year-old Indian woman who was admitted to our hospital with a history of fever and fatigue of one week duration. Her history included haemodialysis for over a year due to chronic renal failure. The family history was non-revealing. She had never been treated for tuberculosis. On day nine after her admission, treatment for tuberculosis with isoniazid, rifampicin and ethambutol was started, since interferon-γ serum assay had yielded positive results. On day 10, she showed deterioration in consciousness. On day 12, her level of consciousness deteriorated to a comatose state and our department was consulted. Physical examination revealed meningeal irritation with a stiff neck. She was unable to cooperate with neurological testing. Tremor-like clonic movements were observed in the upper extremities.

Routine blood tests revealed: white blood cell count, 5400/μL; and C-reactive protein level, 0.29 mg/dL. The patient showed negative results for human immunodeficiency virus. In cerebrospinal fluid (CSF) study, the opening pressure was 22.5 cmCSF, the leukocyte count was 255/μL (52% polymorphonuclear neutrophils), the protein level was 405.7 mg/dL, and the glucose level was 10 mg/dL (corresponding blood glucose level, 99 mg/dL). CSF tuberculous DNA polymerase chain reaction (PCR) showed negative results, but nested PCR assay yielded a positive result. Adenosine deaminase level was 32.4 IU/L. Tuberculous meningitis (TBM) was diagnosed, and pyrazinamide was added to treatment. Magnetic Resonance Imaging (MRI) of the brain revealed mild ventricular dilation. No diffusion restriction was evident at this point in time.

Electroencephalography (EEG) showed left frontal 2.5- to 3-Hz repetitive focal sharp wave activity compatible with nonconvulsive status epilepticus (NCSE) [Figure 1]. Treatment with levetiracetam was started. On day 19, she became responsive to simple questions, although intermittent unresponsiveness was observed. At this time, cranial MRI revealed hyperintensity on DWI and a low apparent diffusion coefficient (ADC) bilaterally in the thalamus and frontal cortex and the left insula [Figure 2]a and [Figure 2]b. Fluid-attenuated inversion recovery (FLAIR) imaging showed no significant hyperintensity [Figure 2]c. On day 26, restricted diffusion had improved [Figure 2]d,[Figure 2]e,[Figure 2]f. Seizure-induced hyperexcitability was suspected.[4] The patient's level of consciousness was improved at that time. Epileptic activity on EEG ceased with anticonvulsant treatment [Figure 3]. On day 100, she managed to communicate in an ordinary manner but required a wheelchair for mobility.
Figure 1: EEG on day 12- EEG showed left frontal 2-5- to 3-Hz repetitive focal sharp wave activity compatible with NCSE

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Figure 2: (a.c) Neuroimaging on day 19. Hyperintensity on DWI (a) and a low ADC (b) bilaterally in the thalamus and frontal cortex and in the left insula suspecting seizure-induced hyperexcitability. FLAIR imaging showed no significant hyperintensity (c). (d-f) Neuroimaging on day 26. DWI hyperintensity and low ADC had improved (d and e). FLAIR imaging showed no difference (f)

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Figure 3: EEG on day 91. After anticonvulsant treatment, persistent EEG activity ceased with the recovery of consciousness. She managed to communicate in an ordinary manner but needed a wheelchair for mobility

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In this case, a patient with TBM presented with NCSE. The frequency of status epilepticus in TBM patients is reportedly 7.6%.[5] However, only 2 cases of TBM presenting with NCSE have been reported.[2],[3] In TBM patients who present with an altered mental state, NCSE may have been undiagnosed. In addition, MRI changes attribute to status epilepticus in 11.6% of cases.[4] MRI abnormalities during status epilepticus indicate the presence of hyperperfusion of the epileptic lesion. MRI findings may mimic those of acute ischemic stroke by showing DWI hyperintensity with a corresponding low ADC.[6] Reversible hyperintensity on DWI has been reported for patients with status epilepticus.[6] Like in our case, transient diffusion restriction may be a clue to suspect NCSE. Since TBM patients with seizures are associated with worsened outcome at six months[5], prompt diagnosis and treatment are important. EEG and neuroimaging should be considered when patients show fluctuations in the level of consciousness.

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

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Murthy JMK. Tuberculous meningitis: The challenges. Neurol India 2010;58:716-22.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Arman F, Kaya D, Akgün Y, Kocagöz S. Tuberculous meningitis presenting with nonconvulsive status epilepticus. Epilepsy Behav 2011;20:111-5.  Back to cited text no. 2
    
3.
Narayanan JT, Murthy JMK. Nonconvulsive status epilepticus in a neurological intensive care unit: Profile in a developing country. Epilepsia 2007;48:900-6.  Back to cited text no. 3
    
4.
Milligan TA, Zamani A, Bromfield E. Frequency and patterns of MRI abnormalities due to status epilepticus. Seizure 2009;18:104-8.  Back to cited text no. 4
    
5.
Misra UK, Kumar M, Kalita J. Seizures in tuberculous meningitis. Epilepsy Res 2018;148:90-5.  Back to cited text no. 5
    
6.
Lansberg MG, O'Brien MW, Norbash AM, Moseley ME, Morrell M, Albers GW. MRI abnormalities associated with partial status epilepticus. Neurology 1999;52:1021-7.  Back to cited text no. 6
    


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