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Year : 2017 | Volume : 5 | Issue : 1 | Page : 41 - 43  


Case Reports
A Case report of Tubercular meningitis initially presenting as transient paraparesis

Madoori Srinivas1, Dikshitha2

1Professor, 2Post graduate, Department of Pediatrics, Chalmeda Anand Rao institute of medical sciences and hospital, Karimnagar

Corresponding Author:

Dr. Madoori Srinivas

Email: madoorisrinivas@gmail.com

SUMMARY:

Tuberculosis is the worlds leading cause of death from a single infectious agent and is caused by mycobacterium tuberculosis. Central nervous system tuberculosis is most serious complication of tuberculosis in children. Central nervous system tuberculosis in children presents commonly as tubercular meningitis, post-tubercular meningitis hydrocephalus, and much more rarely as space occupying lesions known as tuberculomas. Compression of spinal cord can result in paralysis, and the extent of which depends on the level and area of cord involvement. Tuberculosis of dorsal or dorsolumbar spine causes paraplegia which is the presenting feature of TB spine and incidence is 16-35% and it is rare without spine involvement. Incidence of paraparesis is about 0.9% which is rare and it occurs at a later stage of the disease. Here we report a case of 3yrs old male child with tubercular meningitis who initially presented with transient paraparesis.

Keywords: TBM, Paraparesis, Neck stiffness, Children

INTRODUCTION:

Tuberculosis has been declared as a global emergency in 1993 and it is one of the most devastating and widespread infections in the world. (1) It is the most common childhood diseases in developing countries. Tuberculosis is described with different names like kings evil, phthisis, Rajyakshma, tapedic etc, and it appears to be a disease as old as human history(1). It has been described in India as early as 3000BC and in Rig-Veda it is described as Yakshama (1). Central nervous system tuberculosis is most serious complication of tuberculosis in children (2). Approximately 10% cases of tuberculosis have CNS involvement (2). Many symptoms and sequelae of TBM are the result of an immunologically directed inflammatory response to infection (2). Neurotuberculosis is represented by different and possibly concomitant forms, of which the most frequent are TBM and tuberculoma. (2)

CASE REPORT:

A 3 year male child presented with history of high grade fever and difficulty in walking. Child presented with fever for 2 days, insidious onset, high grade, continuous, associated with chills and rigors and relieved on medication. The child developed weakness in the lower limbs after 1 day of fever and was unable to walk. There was no history of trauma, seizures, weight loss or loss of appetite. There is no history of contact with tuberculosis. No history of trauma. No history of recent vaccination or any injection. He was born at full term through normal vaginal delivery without any perinatal problems. Child was immunized till date. The Neuro Psychomotor development of the patient was globally normal. The child was born to non consanguinous parents, second in order of birth, with other sibling normal. No family history of similar complaints and neurological disorders.

On examination child was irritable and febrile with temperature 101o F. The tone, and reflexes were normal and the power was grade 3 in both lower limbs while it was normal in the upper limbs, and plantars showed flexor response.

The diagnosis of Gullian Barre Syndrome was considered and child was treated accordingly.

The investigations showed normal complete blood picture and 8-10 pus cells on urine examination. So the child was started on ceftrioxone and amikacin and other symptomatic treatment.

On the 2nd day of treatment the child developed neck stiffness and he was drowsy. There were no signs of raised ICT. The Fundus examination was normal. The CT scan of Brain showed hypodensities along bilateral occipital projection. In view of neck stiffness and drowsiness, CSF analysis was done which showed 156 cells out of which 95% were neutrophils; CSF glucose was less than 2/3rd of the blood glucose that is 35mg/dl while blood glucose was 84 mg/dl. CSF proteins were normal (42mg/dl) and ADA was slightly elevated (14 U/L). With CSF analysis report, diagnosis was considered as pyogenic meningitis and the child was treated with IV ceftrioxone and ampicillin. As the child was 3 yrs old, to prevent complications due to Hemophilous influenza meningitis IV Dexamethasone was given. The weakness of the lower limbs subsided on the 3rd day and the child was able to walk properly without any external support.

After 1 week of antibiotics the child was still febrile, the neck stiffness reduced slightly probably, due to dexamethasone and he developed increased work of breathing and decreased breath sounds on right side. Chest X-ray showed right pleural effusion (fig1). CECT of Chest showed peripherally enhancing loculated moderate right pleural effusion. Pleural fluid tapping was done and was straw colored. It was sent for analysis and it showed 3500 cells with 95% neutrophils. The pleural fluid glucose was 36mg/dl, protein 5.5gm/dl and ADA 55 U/l suggesting It to be exudate fluid and most probably tuberculosis. The sputum examination was done which was negative for 3 samples. HIV testing was done and it was nonreactive. Anti tubercular therapy with Isoniazid, Rifampicin, Pyrizinamide and Ethambutol was started and the child responded to the therapy. The fever subsided within 1 week of ATT and then the pleural effusion almost cleared within 3 months of therapy. Now the child is on continuation phase with Isoniazid and Rifampicin and is doing well.

DISCUSSION:

Tuberculosis of central nervous system is most devastating condition especially in children. Approximately 10% of cases of tuberculosis have CNS involvement. Many of the symptoms and sequelae are a result of immunologically directed inflammatory response to infection. (2) Infection usually begins with inhalation of infected droplet of aerosolized sputum generated by cough of individuals with active tuberculosis (2). Further course depends on the immune status of the child. (2) Caseous contents of a tuberculide located on the meninges containing a large amount of mycobacterial antigen along with dead and living bacteria leaks into CSF and this leads to tubercular meningitis. (2) Before most children have signs and symptoms of meningeal irritation, they experience the prodromal stage characterized by malaise and myalgia. (3) Around 25% of patients show neck stiffness. Approximately 80% of children have low grade fever with night time sweats. 10% of adults and 50% of children give a past history of infection with tuberculosis. (3-5) In our case the child presented with high grade fever and paraparesis. So initially he was treated as GBS. But the paraparesis resolved in 3 days. Paraparesis may be probably due to spinal arachnoiditis. The child developed neck stiffness on the 2nd day of treatment in our case.

Any focal neurological deficit may occur in the limbs, ranging from monoplegia to quadriplegia (3). The incidence of paraplegia is about 0.9%. (6) Generally paraplegia and paraparesis are associated with pott spine or may occur in the later stages of tuberculosis but do not occur in early stages. (2) In the present case child developed paraparesis initially. Abnormal movement disorders may occur like choreoform or hemi ballistic movements, athetosis, tremors and myoclonic jerks have all been described. (3) Seizures may be the presenting feature of patients with tuberculomas or tuberculous abscesses. (3) CSF examination is the mainstay of diagnosis of TBM. (3) Usually, there is a lymphocytic reaction, with raised protein levels. (3) In the initial stages of the infection, CSF may be show polymorphonuclear leukocytes predominance but soon these are replaced predominantly by lymphocytes. (3) There is gradual decrease in the glucose level in the CSF, less than 50% of the serum levels, but it is never as low as in pyogenic meningitis. (3) In our case there was neutrophilic predominance so he was treated as pyogenic meningitis. Later child failed to improve and suddenly developed pleural effusion.

Adenosine deaminase (ADA) is an enzyme that catalyses the deamination of adenosine forming inosine in the process. ADA activity increases in cell mediated immune response during T-cell differentiation and proliferation. (7) Various studies have been conducted demonstrating CSF-ADA estimation can differentiate TBM from normal subjects or other infectious meningitis. (7) They found that the sensitivity of CSF ADA activity was 85% and the specificity of CSF ADA activity was 88%. (7)

Definitive diagnosis of TBM depends on detection of tuberculous bacilli in CSF either by smear examination or bacterial culture. (3) Culture of CSF for detection of mycobacterium tuberculosis is time consuming. Cytology gives overlapping results. CT scan and MRI are of less value. (3) Contrast-enhanced MR scanning is superior to CT Scans in assessing meningeal and parenchymal abnormalities, (3) Isoniazid, Rifampicin, Pyrizinamide and Ethambutol are recommended as a 4-drug regime to commence treatment. (3) With rapid development of pleural effusion, high ADA levels in CSF (14 U/L) and pleural fluid (55 I/U), High protein (5.5 gm/dl) in pleural fluid, child was suspected to have tuberculosis and was started on ATT. Cough was not predominant symptom in our case unlike other cases of tuberculosis. The child improved with the ant tubercular therapy and the pleural effusion also cleared with ATT.

If microbiologic confirmation can not be made, then the diagnosis of tuberculosis meningitis may be difficult. (8) Thus it is recommended that empiric treatment should be started without waiting for confirmation of microbiologic examination. (8)

There is a difference of opinion on duration treatment. Some say it is for 6-9 months and other say that it should be given for 18 months. (9, 10) The use of corticosteroids in CNS tuberculosis remains a controversial issue. (3) Much of the neurologic sequelae of TBM is considered to be due to an over exuberant host-inflammatory response that causes tissue injury and brain edema.

Systamic steroids reduce the inflammation and are used as an adjunctive treatment of tuberculosis meningitis. (8)

Our case presented with transient paraparesis in early stages. Because of the unusual course, and progression of TBM, we are reporting the case.

CONCLUSION:

Central nervous system tuberculosis is most serious complication of tuberculosis in children. It may be presented with varied symptomatology, so TBM must be excluded if the child presents with neurological symptoms.

REFERENCES:

  1. Vimlesh Seth, SK Kabra. History of tuberculosis. In: Essentials of tuberculosis in children, 4th edition 2011: 3-7.
  2. Seth V, Udani PM, Aneja S et al. Neurotuberculosis and Osteoarticular tuberculosis. In Essentials of tuberculosis in children, 4th edition 2011: 150-213.
  3. Chatterjee S. Brain tuberculomas, tubercular meningitis, and post-tubercular hydrocephalus in children. J Pediatr Neurosci 2011;6:96-100.
  4. Garg RK. Tuberculosis of the central nervous system. Postgrad Med J. 1999;75:133-40.
  5. StlaƟ PN, Unal A, Forta H et al. Tuberculous meningitis in adults: Review of 61 cases. Infection 2003;31:387.
  6. RK Puri, HPS Sachdev, PM Udani. Neurotuberculosis. In: Tuberculosis in children, 1st edition 1994; 1: 143-187.
  7. Gautam N, Aryal M, Bhatta N et al. Comparative study of cerebrospinal fluid Adenosine deaminase activity in patients with meningitis. Nepal Med Coll J2007;9(2):104-6.
  8. Marx GE, Chan ED. Tuberculous Meningitis: Diagnosis and Treatment Overview. Tuberculosis Research Treatment 2011;2011:Article ID 798764, 9 pages, 2011. doi:10.1155/2011/798764.
  9. Donald PR, Schoeman JF, Van Zyl LE et al. Intensive short course chemotherapy in the management of tuberculous meningitis. Int J Tuberc Lung Dis 1998;2:704-11.
  10. Misra UK, Kalita J, Srivastava M et al. Prognosis of tuberculous meningitis: A multivariate analysis. J NeurolSci 1996;137:57-61.





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