Journal of Postgraduate Medicine, Education and Research
Volume 57 | Issue 1 | Year 2023

Severe Tubercular Meningovasculitis Presenting as Fatal Brainstem Hemorrhage in a Young Female: A Rarity

Uma N Saikia1, Saikat Mitra2, Ritin Mohindra3, Ashish Bhalla4, Vikas Bhatia5, Sanjay Jain6

1,2Department of Histopathology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India

3,4,6Department of Internal Medicine, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India

5Department of Radiodiagnosis and Imaging, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India

Corresponding Author: Uma N Saikia, Department of Histopathology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India, Phone: +91 9876288554, e-mail:

How to cite this article: Saikia UN, Mitra S, Mohindra R, et al. Severe Tubercular Meningovasculitis Presenting as Fatal Brainstem Hemorrhage in a Young Female: A Rarity. J Postgrad Med Edu Res 2023;57(1):45-51.

Source of support: Nil

Conflict of interest: None


A 22-year-old female was admitted with a history of fever for 1.5 months. The fever was intermittent, documented up to 102°F and associated with an evening rise of temperature. History of holocranial headache for 1 month moderate in intensity was present with dizziness and blurring of vision was present. The patient had a loss of appetite and undocumented weight loss within this duration, with multiple episodes of nonbloody vomiting containing food. Presently she had altered mental status for 20 days with decreased responsiveness, irrelevant talks, and involuntary abnormal body movements. However, no history of any focal neurological deficit, loss of consciousness, or head trauma was present. There was no history of cough, chest pain, palpitations, shortness of breath, abdominal pain, or distention, nor was there any high-risk behavior, blood transfusion, recent travel, or contact with animals. A history of intake of alternative medication for vesicular lesions over the head and neck region 1 month before present admission was present. No other significant past or medical history. She was married for 17 months and had a history of fetal loss at 7 months period of gestation.

On admission, her Glasgow Coma Scale was 11/15. Blood pressure and pulse were normal, and the temperature recorded was 100.6°F. She was maintaining 96% oxygen saturation at room air. There was no pallor, icterus, clubbing, or cyanosis. Bilateral pitting pedal edema was noted; however, jugular venous pressure was not elevated. Generalized lymphadenopathy was noted. Central nervous system examination revealed neck rigidity and higher mental functions could not be assessed. The motor tone and power of all four limbs were normal. Cranial nerve examination revealed anisocoria and left eye ptosis. Fundus examination showed no papilledema, though choroid tubercles were noted. Bilateral coarse crackles were present on auscultation. Cardiovascular and per-abdominal examinations were essentially normal.

Lab Investigations

The detailed lab investigations are summarized in Table 1. She had anemia throughout her stay, with hemoglobin ranging from 10.5 to 8.9 gm/dL. At the initial presentation, she had leukocytosis and continued to have neutrophilia. The platelet count was essentially normal, ranging from 444 × 109 to 338 × 109/L. At presentation, she had hyponatremia though serum urea and creatinine levels were normal. The liver enzymes were initially normal with aspartate transaminase (AST)/alanine transaminase (ALT), ranging from 17/18 to 22/19 U/L. However, after starting antitubercular therapy (ATT), liver enzymes started rising and went up to 183/547 U/L. However, the bilirubin and alkaline phosphatase were normal. She had hypoalbuminemia with albumin of 125 mEq/L (norma1 35–145 mEq/L) and hypocalcemia ranging from 8.2 to 8.7 mg/dL with normal serum procalcitonin level. The serum and urine osmolality were normal. Enzyme-linked immunosorbent assay (ELISA) test for cytomegalovirus (CMV) immunoglobulin M (IgM) antibody, toxoplasma antibody [Immunoglobulin G (IgG) and IgM] and cysticercus antibody were negative. The human immunodeficiency virus (HIV), hepatitis B surface antigen (HBsAg), and hepatitis C virus (HCV) tests were also negative with normal blood cluster of differentiation 4 (CD4) subset count. The serology for antinuclear antibody and antineutrophil autoantibodies were also negative. The blood culture was sterile and gastric aspirate did not show any acid-fast bacilli. Cerebrospinal fluid (CSF) done outside showed only two cells/mm3 (all lymphocytes), CSF protein was 117 mg/dL, and CSF glucose was 18.2 mg/dL. A repeat CSF study showed 311 cells/mm3 with neutrophil predominance, elevated CSF protein (298 mg/dL), and low glucose (30 mg/dL). The CSF Ziehl–Neelsen (ZN) stain was negative though the GeneXpert detected mycobacterium tuberculosis (MTB), sensitive to rifampicin. The fungal culture, India ink preparation for cryptococcus and CSF toxoplasma polymerase chain reaction (PCR) were negative.1-6

Table 1: Routine laboratory investigations
Date 13/8/22 16/8/22 18/8/22 20/8/22 22/8/22 25/8/22
Hemoglobin (gm/dL) 10.5 8.8 9.2 9.6 10.0 8.9
Total leukocyte count 13,800 5,400 6,400 6,500 5,100 4,600
Differential (N/L/M) 94/1.2/4 87.3/6.4/5 86/6.8/7.1
Platelet count (×103) 444,000 279,000 324,000 319,000 410,000 338,000
Sodium/potassium 125/2.71/84 129/3.6/86 122/3.5/88 132/3.7/95 131/3.53/97 135/3.4/103
Urea/creatinine 47/0.43 27.9/0.45 19/0.45 35/0.41 33.5/0.75 49/0.54
AST/ALT/alkaline phosphatase 17/18/65 15.6/14.3/65 22/19 192/142 183/547/102 86/394
Bilirubin total/direct 0.57/0.10 0.57/0.36 0.69/0.21 0.67/0.23 0.5/0.29 0.78/0.31
Total protein/albumin 7.0/3.98 5.85/3.3 6.1/3.41 6.8/3.49 6.42/3.13 4.7/2.76
Calcium/phosphate 8.78/2.26 8.78/2.26 8.22/3.12

Radiology Investigations

Magnetic resonance imaging (MRI) was done on day 4 of admission. It showed bilateral basal ganglia infarcts with evidence of mild communicating hydrocephalus (Figs 1A and B). There was evidence of thick leptomeningeal exudates along the basal cisterns, perimesencephalic, and ambient cistern, as well as along the cranial nerves along with left-sided uncal herniation with medial displacement of the left uncus and parahippocampal gyrus (Figs 1C and D). Magnetic resonance angiography showed attenuation of the bilateral middle cerebral artery (MCA) and posterior cerebral artery (PCA) (right > left) (Fig. 1E). Postcontrast images showed thick pachymeningeal enhancement and multiple ring-enhancing lesions throughout the cerebral and cerebellar parenchyma along the grey-white junction (Figs 1F and G and Table 2).

Table 2: Other relevant investigations
Coagulogram (PT/PTI/INR/APTT) 13.3/100/0.98/30
Lactate dehydrogenase (U/L) 356
C-reactive protein (mg/L) 9.3
Serum osmolarity—265
Urine osmolarity—446
Spot urine potassium: 25.37 mmol/TV (25–125)
Urine chloride—146.5 mmol/TV (100–250)
Urine sodium—169
CMV IgM (17/08)—nonreactive
Ab (IgM and IgG) for toxoplasmosis by ELISA— negative
Ab (IgG) for cysticercosis by ELISA (16/08)— <1:800 (negative)
Antinuclear antibody—negative
C3: 109 C4: 15.6
HCV, HBsAg/HIV—nonreactive
Immunoglobulin profile—secretory (S) IgG—940 mg/dL (658–1837) S IgM—235 mg/dL (40–263)
S IgA—153 mg/dL (71–360)
CD4 + lymphocyte subset—WNL
Blood culture/sensitivity (C/S)—sterile
BACTEC culture—sterile
Extended sensitivity BACTEC culture—sterile
Gastric aspirate—no AFB seen
Urine routine microscopy—RBCs+
Urine C/S—RBC—4.4, WBC—0.3, Yeast—61.20
Bacteria Rods—0.40, Bacteria Cocci—8.60, culture sterile
CSF analysis
Outside hospital—total cells two (all lymphocytes) protein 117 mg/dL sugar—18.2 mg/dL
At PGIMER—total counts (311/mm3) N/L (%) 83.3/16.7, protein (mg/dL)—298, and sugar (mg/dL)—30
CSF AFB negative
CSF GeneXpert MTB detected, rifampicin-sensitive
Fungal culture negative
India Ink and crypto LA negative
CSF toxoplasmosis PCR negative

CKNAC, N-acetyl-cysteine-(NAC)—activated creatine kinase (CK); BACTEC, Becton Dickinson and Company; PT, prothrombin time; INR, International normalized ratio; APTT, activated partial thromboplastin time

Figs 1A to G: (A) Axial FLAIR image shows evidence of mild communicating hydrocephalus (B) axial DW image shows bilateral basal ganglia acute infarcts (arrows); (C and D) axial FLAIR images show evidence of hyperintense exudates in the basal cisterns (black arrows) and cranial nerves (white arrow) with the presence of left uncal herniation (star). (E) MR angiography time of flight images show attenuated bilateral (right > left) MCA (white arrows) and bilateral PCA (black arrows) arteries; (F and G) axial postcontrast images show thick basal meningeal enhancement (black arrows). Multiple nodular and ring-enhancing lesions are also seen

Course and Management

A 22-year-old female presented with a fever for 1.5 months which was intermittent, associated with an evening rise of temperature and holocranial headache for 1 month with the blurring of vision. A history of loss of appetite and weight loss was present and she had altered mental status for 20 days with decreased responsiveness, irrelevant talks and involuntary abnormal body movements. Based on the MRI brain findings, a clinical diagnosis of neurocysticercosis (NCC) was considered, and she was managed outside with albendazole and steroids; however, there was no improvement and referred to the Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India. At the time of admission to PGIMER, she had a Glasgow Coma Scale of E4V2M5, with neck rigidity, anisocoria, and left eye ptosis. As the CSF picture suggested tubercular etiology with positive GeneXpert, ATT was started with dexamethasone. However, she developed ATT-induced hepatitis on day 7 of admission; thus, a modified ATT was initiated. Subsequent to this patient’s sensorium worsened and diffuse crepitations were noted on auscultation. A possibility of aspiration was kept, and she was intubated with mechanical ventilation. She again developed a fever on 22nd August 2022, for which a sepsis workup was sent. The antibiotics were upgraded to piperacillin/tazobactam. After a negative sepsis workup and discussion with the neurology team, the cause of the fever was attributed to being central/central nervous system fever. Following this, a methylprednisolone pulse was started as advised by the neurology team; however, there was no clinical improvement, and her sensorium progressively deteriorated. On 26th August 2022, at 7:10 am, the patient had a cardiac arrest and CPR was started as per advanced cardiovascular life support protocol, but the patient couldn’t be revived and was declared dead.

Final Clinical Diagnosis

  • Tubercular meningitis (TBM) with meningo-vasculitis with multiple infarcts and tuberculomas with left oculomotor nerve palsy.

  • Raised intracranial pressure.

  • ATT-induced hepatitis.

  • Pulmonary TB (centrilobular nodules).

Cause of Death

Raised intracranial pressure.


Dr Sanjay Jain (Chairperson): Thank you, Dr Ritin. Now the clinical protocol is open for discussion. This seems to be a straightforward open-and-shut case of TB involving the brain and lungs. In the brain, it involves all three compartments, that is, parenchyma, meninges, and vessels. With this, I open the case for discussion.

Dr Ashish Bhalla: On the face of it, there is nothing which would take us away from TB. However, there are a few odd points. The patient was pregnant, and she had a stillborn child at 7 months of gestation. Pregnancy itself is an immunocompromised state, which can aggravate TB. There are two things which are difficult to explain. In extensive TB, steroid treatment would have reduced the cerebral edema and improved the clinical symptoms, which did not happen with this patient, although she received 8 or 9 days of steroids in an outside hospital. The second point is persistent hypoglycorrhachia in the absence of bacterial sepsis. Neurosyphilis can cause hypoglycorrhachia; however, there are no other features to substantiate neurosyphilis. The third point, the patient showed temporal lobe involvement without infarction, which is odd.

Dr Nipun Verma: There was a sudden jump in glutamic-oxaloacetic transaminase/glutamic-pyruvic transaminase in 2 days. Whether viral markers were done? What were the ultrasound, sonogram, or ultrasonogram abdomen findings? What was the dose of ATT given? Since she was a young female, the dose could be adjusted to reduce the drug-induced liver injury.

Dr Sanjay Jain: Any takers for choriocarcinoma or other pregnancy-related malignancies?

Dr Karthik: The radiological images are typical of TB. Choriocarcinoma would have caused hemorrhagic lesions. The patient was treated for neurocysticercosis outside, and a dose of 30 mg steroid was given. However, the dose is too less to cause any significant improvement in such extensive brain lesions. As the patient presented with uncal herniation, we could have started ATT much earlier, considering the 1.5 months of fever.

Neurologist 1: This patient was amenable to a ventriculoperitoneal shunt, which could have improved the symptoms. The patient was possibly immunocompromised.

Dr Sanjay Jain: This brings up a very important question about dexamethasone. Why was dexamethasone not given upfront?

Neurologist 1: Dexamethasone had to be used to be given in this patient. Methylprednisolone was given, though.

Neurologist 2: There is no denying that this patient had TB. But the question is if this is a tubercular or nontubercular mycobacterium. That could explain no response to ATT. The lymphocyte count was always below 500, so this patient had very severe lymphopenia. The clusters of differentiation 4 (CD4) count is also likely to be very low; it cannot be normal.

Dr Manoj: It is a case of disseminated TB and at autopsy, we can expect the involvement of multiple organs.

Dr Sanjay Jain: What about the GeneXpert positivity? Is it TB or nontubercular mycobacterium?

Dr Pankaj: This is definite tubercular meningovasculitis and tuberculoma. There is no point in considering choriocarcinoma or NCC. The only question is temporal lobe involvement. In the absence of an infarct, this degree of temporal lobe edema is difficult to explain. Is there a dual pathology like Herpes simplex virus? Neurosyphilis can involve the temporal lobe, but it will not show such thick exudates. Secondly, the lack of response to ATT does not mean anything. In spite of full-fledged ATT, 25% of such patients die. Fungal etiology is unlikely because of the lack of hemorrhagic lesions.

Dr Ritin: Weight-based ATT was given to the patient. Viral markers were negative. CD subset was discussed with immunopathology, and it was said that it was within normal limits.

Dr Sanjay Jain: It appears that it’s a straightforward case of TB meningitis with its complications. Is there a dual pathology that only autopsy can tell us? Now I invite Dr Debajyoti to present the autopsy findings.

Autopsy Protocol

Good morning, everyone. I will be presenting the autopsy protocol of this patient.

Lungs—bilateral lungs weighed 674 gm. The pleura showed fibrinous tags (Fig. 2A). The cut surface of bilateral lungs showed numerous miliary nodules ranging in size from 2–3 mm, some of which were airway-centric (Fig. 2B). Microscopic examination showed multiple small epithelioid cell granulomas with central necrosis (Fig. 2C). There was vasculitis and an endobronchial pattern of spread (Fig. 2D). The ZN stain was strongly positive for acid-fast bacilli (Fig. 2E). Pulmonary thromboembolism was also noted (Fig. 2F).

Figs 2A to F: (A) Bilateral dull pleural surface with fibrinous tags (black arrow); (B) Cut surface of the lung shows multiple miliary nodules (arrow); (C) Multiple granulomas in the lung (arrow); (D) Branches of pulmonary artery show necrotizing vasculitis (arrow); (E) ZN stain highlights numerous acid-fast bacilli; (F) Branches of major pulmonary artery show fibrin thrombus (arrow)

Liver—it is around weighed 1,200 gm and bile stained. Microscopy showed multiacinar confluent hepatic necrosis, mostly in the centrizonal areas (Fig. 3A). There was reticulin collapse and condensation. Few granulomas were seen in the portal tracts (Fig. 3B).

Figs 3A to D: (A) Multiacinar confluent hepatic necrosis involving the centrizonal area; (B) Portal-based tiny granuloma in the liver (star); (C) White pulp of spleen shows tiny granulomas (arrow); (D) Renal parenchyma shows granuloma (star)

Spleen—the spleen was enlarged and weighed 250 gm. Microscopic examination showed red pulp congestion and a few tiny granulomas involving the white pulp (Fig. 3C).

Kidney—both kidneys weighed 290 gm and showed partial autolytic changes. The glomeruli were essentially normal. Medullary congestion was seen. A few tiny granulomas were seen in the cortex and medulla (Fig. 3D).

Brain—brain weighed 1,200 gm. A thick basal exudate was present, covering the base of the brain and the ventral part of the brainstem (Fig. 4A). The cranial nerves and the circle of Willis were embedded within the exudate. On slicing, bilateral basal ganglia and thalami (left > right) showed discoloration, softening, and granularity, indicating infarction in bilateral middle cerebral artery territory (Figs 4B and C). Large hemorrhagic infarct was also noted in the midbrain, dorsal pons, and vermis of the cerebellum (basilar artery territory) of size ranging from 1.0 cm in the brainstem to 2.5 cm in the cerebellum (Figs 4D and E). In addition, cortical infarcts were seen in anterior, middle, and posterior cerebral artery territories, indicating global hypoxia (Fig. 4F).

Figs 4A to F: (A) The base of the brain shows thick meningeal exudate involving the brainstem (black arrow). Left uncal herniation noted (red arrow); (B and C) Coronal slices of the brain show multiple bilateral infarcts in the middle cerebral artery territory (left > right); (D and E) Hemorrhagic infarcts in pons and cerebellum (arrow); (F) Subcortical white matter in the frontal lobe shows infarcts (black arrow) and a tuberculoma (red arrow)

A microscopic examination of basal ganglia and thalami showed infarcts of various duration. The cortical infarcts seem to be more recent. The meninges showed predominantly necrosis with degenerated macrophages and lymphocytes with border zone encephalitis (Fig. 5A). The large arteries showed proliferative changes, while the smaller ones showed infiltrative and necrotizing changes (Fig. 5B). The elastic stain highlighted the loss of elastic lamina (Fig. 5C). Pons showed acute infarcts along with hemorrhages (Fig. 5D). The smaller pontine arteries showed fibrinoid necrosis. Few tuberculomas were seen in the cortex and subcortical white matter (Fig. 5E). The ZN stain for acid-fast bacilli was strongly positive (Fig. 5F).

Figs 5A to F: (A) Thick meningeal exudate with border zone encephalitis; (B) Meningeal arteries show necrotizing vasculitis; (C) Elastin van Gieson stain highlights break of the internal elastic lamina; (D) Pontine tracts show acute infarcts and hemorrhages; (E) Subcortical white matter shows tuberculoma; (F) ZN stain highlights the acid-fast bacilli

Heart—the heart weighed 190 gm. Grossly and microscopically, it was unremarkable.

Esophagus, stomach, small and large intestine—grossly and microscopically unremarkable.

Final Autopsy Diagnosis (PM 30950)

The 22-year-old female with tuberculous meningitis:

  • Tuberculous meningitis with choroid plexitis and vasculitis with multiple hemorrhagic infarcts in bilateral middle cerebral, and basilar artery territory and multiple tuberculomas.

  • Global hypoxic changes—brain.

  • Miliary TB involves the lungs, liver, spleen, and kidneys.

  • Multiacinar confluent hepatic necrosis—consistent with antitubercular treatment induced.

  • Pulmonary thromboembolism.


Dr Sanjay Jain: Thank you, Dr Debajyoti. Now the clinical and autopsy protocol is open for discussion. It goes without saying if there is vasculitis because of an infection, we need to treat the infection. But ATT takes time to start acting. In such a situation, dexamethasone becomes a must. This patient received dexamethasone in an outside hospital considering NCC. However, there needs to be a delicate balance in the dose of steroids, as an excessive dose might flare-up the infection. Is there any role of surgical intervention in such conditions?

Dr Karthik: Presently, we are using high-dose pulse steroids. But in severe cases, where there is thick exudate and nerve entrapment, we start Thalidomide with a good response. There have been studies where intrathecal hyaluronidase is being used. For this patient, a ventriculoperitoneal shunt could have been done.

Dr Inder: There was endobronchial spread as well as hematogenous spread. What came first? The main manifestation was due to vasculitis secondary to TB, which in retrospect, can be assessed by thrombocytosis.

Dr Debajyoti: The dominant pathology in the lung, in this case, was endobronchial involvement with peribronchial spread.

Dr Karthik: The patient took alternative medication 2 months before presentation, which could have contributed to the dissemination of the disease. In our experience, the brunt of the immunological insult in TB is more commonly seen in young adult female patients of the reproductive age group. The reason could be a perinatal insult or social neglect and the reason is not well known.

Dr Ashish Bhalla: What was the lesion in the temporal lobe? Was it an infarct? And did the radiologist note the temporal infarct in antemortem MRI scan?

Dr Debajyoti: The temporal lobe lesion was a fresh ischemic infarct due to middle cerebral artery vascular compromise.

Radiologist: The temporal infarct was not apparent in the diffusion-weighted images when the MRI was done. Back then, it only showed basal ganglia infarct.


TB is an endemic disease in India, with a reported incidence of 210/1,00,000 individuals. Miliary TB accounts for 1–2% of all TB and is one of the leading causes of TB-related morbidity and mortality. TBM is the most common type of TB of the central nervous system and represents 1% of extrapulmonary TB, with an incidence of 1.5/1,00,000 individuals. Hydrocephalus is the most frequent complication and is more prominent in children. Cerebral infarction secondary to TBM is relatively less common and cerebral hemorrhage is even rarer, with a high-risk of morbidity and mortality.1 Dastur et al. have reported infarcts in 41% of such patients in an autopsy series of 100 patients.2 Chatterjee et al. from PGIMER published a much higher incidence (72.5%) of cerebral infarcts in their autopsy series.3 The spectrum of vascular pathology in TBM includes arteritis, arterial spasm, arterial thrombosis, and compression of larger arteries by a thick exudate. The arteritis mainly affects perforating branches of major arteries at the base of the brain resulting in basal ganglia infarction. Brainstem involvement is relatively uncommon in TB though MRI has a high sensitivity in detecting small brainstem infarcts in 40–46% of patients with TBM.5 It is speculated that arterial inflammation starts from a periarterial location with the direct effect of proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukins secreted by lymphocytes and macrophages. TNF-α demonstrated in CSF of TBM patients may induce vasculotoxicity, causing prothrombotic activity.4

Necrotizing lesions can cause the destruction of media and weakening of the vessel wall, making them susceptible to aneurysm formation and rupture, causing subarachnoid or parenchymal hemorrhage.6 We found fragmented internal elastic lamina of cerebral arteries in addition to intimal proliferation and endarteritis obliterans with fibrin platelet thrombus and vascular occlusion. As brainstem infarcts are difficult to visualize on macroscopic examination and multiple sections are required to identify them.

The index case highlights brainstem hemorrhage as an additional cause of mortality in TBM.

The use of high-dose steroids in such patients becomes extremely important. Timely intervention with steroids reduces the chances of disintegration of internal elastic lamina by suppressing the inflammatory process, which may prevent the aneurysm formation or rupture.


1. Wasay M, Farooq S, Khowaja ZA, et al. Cerebral infarction and tuberculoma in central nervous system tuberculosis: frequency and prognostic implications. J Neurol Neurosurg Psychiatry 2014;85(11):1260–1264. DOI: 10.1136/jnnp-2013-307178

2. Dastur DK, Lalitha VS, Udani PM, et al. The brain and meninges in tuberculous meningitis-gross pathology in 100 cases and pathogenesis. Neurol India 1970;18:86–100. PMID: 5459296.

3. Chatterjee D, Radotra BD, Vasishta RK, et al. Vascular complications of tuberculous meningitis: an autopsy study. Neurol India 2015;63(6):926–932. DOI: 10.4103/0028-3886.170086

4. Tureen J. Effect of recombinant tumor necrosis factor-alpha on cerebral oxygen uptake, cerebrospinal fluid lactate, and cerebral blood flow in the rabbit: role of nitric oxide. J Clin Invest 1995;95(3):1086–1091. DOI: 10.1172/JCI117755

5. van der Merwe DJ, Andronikou S, Van Toorn R, et al. Brainstem ischemic lesions on MRI in children with tuberculous meningitis: with diffusion weighted confirmation. Childs Nerv Syst 2009;25(8):949–954. DOI: 10.1007/s00381-009-0899-2

6. Shuangshoti S, Phisitbutr M. Fatal haemorrhage in tuberculosis of the brain. J Med Assoc Thai 1979;62(11):639–645. PMID: 512519.

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