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Table of Contents
CASE REPORT
Year : 2021  |  Volume : 18  |  Issue : 1  |  Page : 41-43

Tubercular meningitis presenting with cortical laminar necrosis


1 Department of Neurology, Apollo Speciality Hospital, Nellore, Andhra Pradesh, India
2 Department of Radiology, Apollo Speciality Hospital, Nellore, Andhra Pradesh, India

Date of Submission07-Sep-2020
Date of Acceptance05-Jan-2021
Date of Web Publication11-Feb-2021

Correspondence Address:
Dr. Manisha Sharma
Department of Neurology, Apollo Speciality Hospital, Pinakini Nagar, Nellore - 524 004, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/am.am_111_20

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  Abstract 

Cortical laminar necrosis (CLN) is a radiological and neuropathological finding which requires thorough evaluation for hypoxic, metabolic, infective, and toxic causes. Hypoxic, metabolic, and toxic etiologies for CLN have been frequently reported in past, but infective causes have never been systematically enumerated and limited literature is available for the same. We describe a case of tubercular meningitis (TBM) presenting clinically with focal visual seizures and radiologically as CLN. It was also challenging to rule out other etiologies for CLN before attributing it to TBM. To emphasize, CLN as a radiological finding needs an approach and detailed evaluation for etiological diagnosis.

Keywords: Cortical laminar necrosis, focal visual seizures, tubercular meningitis


How to cite this article:
Sharma M, Menon B, Manam G. Tubercular meningitis presenting with cortical laminar necrosis. Apollo Med 2021;18:41-3

How to cite this URL:
Sharma M, Menon B, Manam G. Tubercular meningitis presenting with cortical laminar necrosis. Apollo Med [serial online] 2021 [cited 2021 Apr 11];18:41-3. Available from: https://www.apollomedicine.org/text.asp?2021/18/1/41/309204


  Introduction Top


Cortical laminar necrosis (CLN) is similar to infarction physiologically as both indicate cytotoxic edema, but neuropathologically, CLN has delayed selective neuronal necrosis of a particular layer of the gray matter giving it a characteristic gyral or curvilinear pattern on brain imaging. CLN is a consequence of generalized hypoxia rather than a local vascular abnormality. Therefore, it has been reported in conditions with depletion of oxygen or glucose as in anoxia, hypoglycemia, status epilepticus, ischemic stroke, and less common in immunosuppressive therapy and polychemotherapy. It is also considered an indicator of poor prognosis.[1] We present here a case of tubercular meningitis (TBM) presenting with CLN. There is a paucity of literature on infective causes of CLN. It was challenging to rule out other differentials in this case, so it will throw an approach to evaluate the radiological finding of CLN.


  Case Report Top


A 35-year-old male, known case of hypertension, presented with a 2-day history of sudden onset difficulty in vision in form of episodes of moving of surroundings and flashes of light from one direction to another. Each episode lasted for 30 s to 1 min. Frequency of such episodes was once every 10–15 min with full recovery in between. There was no history of associated focal motor activity, impaired awareness, or loss of consciousness. The next day, he had sudden-onset paresthesias in the left lower limb without any motor deficit. Magnetic resonance imaging (MRI) of the brain [Figure 1] was done which was showing TI hypointense, T2 isointense, and fluid-attenuated inversion recovery hyperintense signal in a gyral pattern in right parieto-occipital cortices with diffusion restriction and corresponding apparent diffusion coefficient fall. Magnetic resonance angiography (MRA) of the brain showed short segment mild-to-moderate stenosis involving cavernous segment of the right internal carotid artery (ICA) and there was focal mild stenosis of M1 segment of the right middle cerebral artery (MCA). T1 + contrast images showed abnormal leptomeningeal enhancement in the right temporoparietal and right medial temporal region along with parenchymal enhancement in the right medial temporal region. Electroencephalogram was a normal study. The patient was started on dual antiplatelets, antiepileptics, and supportive treatment. On routine blood investigations, he was found diabetic though no episode of hypoglycemia was reported during the hospital stay. Chest X-ray was showing cavitary lesion in the upper lobe of the right lung. Sputum examination confirmed active pulmonary tuberculosis. Lumbar puncture was done which was showing proteins: 324 mg%, glucose: 32 mg%, and cells: 150 with 80% lymphocytes and tubercular polymerase chain reaction was positive. He was started on antitubercular therapy.
Figure 1: Magnetic resonance imaging of the brain axial images shows TI hypointense signal (a) with diffusion restriction (b) and corresponding apparent diffusion coefficient fall (c) in a gyral pattern in right parieto-occipital cortices. T1 + contrast images (d and e; arrow) show abnormal leptomeningeal enhancement in the right temporoparietal and right medial temporal region along with parenchymal enhancement in the right medial temporal region. Magnetic resonance angiography brain (f) showed short segment mild-to-moderate stenosis involving a cavernous segment of the right internal carotid artery and there was focal mild stenosis of the M1 segment of the right middle cerebral artery

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  Discussion Top


In the context of the present case, CLN can be assumed to be because of focal seizures, an independent cerebral infarction, or atypical presentation of central nervous system (CNS) tuberculosis in the absence of toxic, metabolic, and hypoxic events.

In our patient, there is a history suggestive of focal sensory (visual) seizure activity which persisted for 2 to 3 days but with a normal interval in between seizure episodes and none of the episode lasted more than 1 min. This ruled out focal status epilepticus. Seizure semiology corresponded with occipitoparietal location of the CLN. CLN has been reported in multiple case reports in generalized and prolonged focal status epilepticus with or without associated impairment of metabolic parameters. The mechanisms proposed for this association are an increase in cerebral metabolic demand resulting in hypermetabolic neural necrosis and excitotoxic injury mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA receptors.[2]

There is no case reported prior considering any association of focal seizures without status epilepticus with CLN. It will be difficult to comment upon whether focal seizure activity caused CLN or CLN is the structural cause for focal seizure. Advanced studies including positron-emission tomography/single-photon emission computed tomography might helped in localizing focal areas of impaired glucose or oxygen metabolism done in the ictal or interictal state.[3]

CLN has been reported in cerebral infarcts as the most vulnerable third cortical layer is selectively involved in mild ischemic insults. It follows a chronological pattern on MRI. T1-weighted images are most sensitive. Tissue edema due to acute infarct causes early cortical low signal intensity on T1-weighted images followed by a high signal which generally begins to appear about 2 weeks after the ictus, which becomes prominent at 1–2 months and begins to fade at 3 months, although it could persist up to 11 months.[1],[4] MRA of the brain in our case was showing right ICA and right M1 focal stenosis, but the extension of infarct in the occipital region rules out the causative association between the two and there is no territorial or watershed involvement. Hence, it is unlikely that this radiological presentation is a consequence of independent cerebral infarction.

Infection as a cause of CLN has been stated in past but rarely enumerated or published. One case reported CLN with dengue encephalitis.[5] Cerebral infarction has been reported in 15%–57% of TBM patients. Infarcts involve mainly perforators and terminal cortical branches common being lateral lenticulostriate arteries, medial lenticulostriate arteries, and perforators from the posterior cerebral artery. Large arteries of Circle of Willis may be affected. Mechanisms proposed are vasculitis and vasospasm both common in the territory of MCA.[6] Vasculitis or vasospasm of a particular artery cannot explain the radiological picture and it was also not demonstrated on imaging. However, atypical presentations are quite common with CNS tuberculosis. The presence of leptomeningeal and parenchymal enhancement on MRI of the brain put suspicion of infective etiology for CLN which was diagnosed by cerebrospinal fluid analysis.

To conclude, the present case put an emphasis on approach based evaluation of radiological finding of CLN for hypoxia, hypoglycemia, seizures, infarction, infection, and immune or chemotherapy drugs.

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.
Samain JL, Haven E, Gille M, Mathys P. Typical CT and MRI features of cortical laminar necrosis. JBR-BTR 2011;94:357.  Back to cited text no. 1
    
2.
Donaire A, Carreno M, Gómez B, Fossas P, Bargalló N, Agudo R, et al. Cortical laminar necrosis related to prolonged focal status epilepticus. J Neurol Neurosurg Psychiatry 2006;77:104-6.  Back to cited text no. 2
    
3.
Sarikaya I. PET studies in epilepsy. Am J Nucl Med Mol Imaging 2015;5:416-30.  Back to cited text no. 3
    
4.
Komiyama M, Nishikawa M, Yasui T. Cortical laminar necrosis in brain infarcts: Chronological changes on MRI. Neuroradiology 1997;39:474-9.  Back to cited text no. 4
    
5.
Garg RK, Rizvi I, Ingole R, Jain A, Malhotra HS, Kumar N, et al. Cortical laminar necrosis in dengue encephalitis-A case report. BMC Neurol 2017;17:79.  Back to cited text no. 5
    
6.
Tai MS, Viswanathan S, Rahmat K, Nor HM, Kadir KA, Goh KJ, et al. Cerebral infarction pattern in tuberculous meningitis. Sci Rep 2016;6:38802.  Back to cited text no. 6
    


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This article has been cited by
1 Editorial
Raju Vaishya,SatishKumar Agarwal
Apollo Medicine. 2021; 18(1): 1
[Pubmed] | [DOI]



 

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