BACKGROUND: Addressing the need to uniformly classify arteriopathies among patients with arterial ischemic stroke (AIS) due to tubercular meningitis (TBM), we used the Childhood AIS Standardised Classification and Diagnostic Evaluation (CASCADE) criteria.
METHODS: This tri-centric prospective study included children aged 0.5-12 years with TBM and AIS. Magnetic resonance angiographies (MRAs) were done during admission and repeated 3 and 12 months after discharge. Arteriopathies were classified according to the primary CASCADE criteria. We used the modified Pediatric Alberta Stroke Programme Early Computed Tomography Score as an ordinal measure of infarct volume. The severity of arteriopathies was graded using the focal cerebral arteriopathy severity score (FCASS). The final outcomes were measured at the 12-month follow-up visit using the Pediatric Stroke Outcome Measure (PSOM).
RESULTS: Out of 55 patients, 64% had MRA-evidenced arteriopathies and 84% had multiple infarcts. The middle cerebral (46%) and internal carotid arteries (22%) were most commonly affected. The basal ganglia (70%) and the cerebral cortex (61%) were most commonly infarcted. CASCADE categories included 3b (40%), 1d (38%), 2b (16%), 2c (5%), progressive (32%), and stable (44%) arteriopathies. Younger age, hypertrophic pachymeningitis, cortical infarcts, recurrent strokes, progressive arteriopathies, EEG abnormalities, and mortality were significantly higher among patients with MRA-proven arteriopathies. Patients with progressive arteriopathies had a significantly higher prevalence of hypertrophic pachymeningitis, cortical infarcts, and recurrent strokes. FCASS correlated positively with outcomes measured by the Pediatric Stroke Outcome Measure and modified Pediatric Alberta Stroke Programme Early Computed Tomography Score.
CONCLUSIONS: The CASCADE classification clarified the arteriopathy patterns, enabling us to correlate them with the characteristics of the infarcts. FCASS is useful to grade the arteriopathy severity and progression in TBM.

Lemierre\'s syndrome is characterized by internal jugular vein thrombophlebitis and bacteremia, primarily from anaerobic organisms. The condition usually arises after a recent oropharyngeal infection. Young, healthy people with prolonged pharyngitis that progresses into septicemia, pneumonia, or lateral neck stiffness should be suspected of having Lemierre\'s syndrome. Identifying internal jugular vein thrombophlebitis and developing anaerobic bacterial growth on blood culture are frequently used to confirm the diagnosis. Treatment consists of long-term antibiotic treatment, sometimes in conjunction with anticoagulant medication. In this case report, we describe the unique case of a 29-year-old male with Mycobacterium tuberculosis with pulmonary tuberculosis, tubercular meningitis, tuberculosis-related acute ischemic stroke with septic thrombophlebitis. The patient presented with sudden onset altered sensorium for 4 hours. Magnetic resonance imaging of the brain was done, which suggested obstructive hydrocephalus with periventricular ooze. The patient was started on antibacillary treatment, antibiotics, anticoagulants, and systemic steroids. The patient was vitally stable when he was discharged. Therefore, it is crucial to consider the likelihood of such atypical tuberculosis presentations while providing a prompt and relevant diagnosis and recommending the right course of therapy.

Tuberculous meningitis (TBM) is a severe form of extrapulmonary tuberculosis (TB) characterized by the invasion of Mycobacterium tuberculosis into the meninges surrounding the brain and spinal cord. It triggers an intense inflammatory response, leading to neurological complications if not promptly and adequately managed. TBM often precipitates muscle weakness, neurological deficits, respiratory challenges, swallowing difficulties, joint contractures, and pain. Physiotherapy intervention is essential in treating these problems by personalized treatment strategies and treatment plans to enhance muscle strength, motor control, coordination, and overall mobility. This case report aims to highlight the significant role of physiotherapy in improving the quality of life (QOL) and functional abilities of patients with TBM. The current case report reviews the case of a 73-year-old male who presented with complaints of generalized weakness and difficulty in swallowing. The patient had a history of fever for the last six months. Magnetic resonance imaging (MRI) and high-resolution computed tomography (HRCT) diagnosed the case as TBM with miliary TB. Six weeks of targeted intensive rehabilitation program was designed according to the patient\'s impairments initiated from the intensive care unit (ICU) phase. The main goals of physiotherapy were to start early bed mobility, maintain joint integrity, improve postural strength and swallowing, and make the patient independent in transfer and activities of daily living (ADLs). After a six-week intensive physiotherapy (TIP-6) program, the patient exhibited significant improvements in muscle strength and independence in ADLs. This case highlights the critical role of physiotherapy in enhancing the QOL and functional abilities of patients with severe TB-related conditions.

Tuberculosis (TB) is a global health concern and central nervous system (CNS) TB leads to high mortality and morbidity. CNS TB can manifest as tubercular meningitis, tuberculoma, myelitis, and arachnoiditis. Neuro-ophthalmological involvement by TB can lead to permanent blindness, ocular nerve palsies and gaze restriction. Visual impairment is a dreaded complication of tubercular meningitis (TBM), which can result from visual pathway involvement at different levels with varying pathogenesis. Efferent pathway involvement includes cranial nerve palsies and disorders of gaze. The purpose of this review is to outline the various neuro-ophthalmological manifestations of TB along with a description of their unique pathogenesis and management. Optochiasmatic arachnoiditis and tuberculomas are the most common causes of vision loss followed by chronic papilloedema. Abducens nerve palsy is the most commonly seen ocular nerve palsy in TBM. Gaze palsies with deficits in saccades and pursuits can occur due to brainstem tuberculomas. Corticosteroids are the cornerstone in the management of paradoxical reactions, but other immunomodulators such as thalidomide and infliximab are being explored. Toxic optic neuropathy caused by ethambutol necessitates careful monitoring and immediate drug discontinuation. Cerebrospinal fluid diversion through ventriculo-peritoneal shunting may be required in patients with hydrocephalus in stage I and II of TBM to prevent visual impairment. Early diagnosis and prompt management are crucial to prevent permanent disability. Prevention strategies, public health initiatives, regular follow-up and timely intervention are essential in reducing the burden of CNS TB and its neuro-ophthalmological complications.

There is a complex link between tuberculous meningitis (TBM) and aphasia, in which a language impairment is caused by an injury to the cortical language centre. The parts of the brain that function for speech and language production are the Wernicke\'s, Broca\'s, and arcuate fasciculus regions. This case report mainly highlights the neurological consequences of TBM, and how it affects language and speech functioning. It outlines a comprehensive physiotherapy rehabilitation program that targets a range of issues for the patient, such as verbal output, weakness, motor deficits, articulation issues in speech, and coordination issues. Various treatment modalities can help correct weakness, improve balance and coordination, increase flexibility and range of motion (ROM), and make speech more fluent. The case report emphasizes the necessity of using an integrated approach that combines speech-language therapy (SLT), melodic intonation therapy (MIT), constraint-induced aphasia therapy (CIAT), medication treatments, and physical therapy to address the multifaceted impacts of TBM-induced aphasia on a patient\'s quality of life (QOL).

UNASSIGNED: The aim of the study was to evaluate cerebrospinal fluid (CSF) findings in tuberculous meningitis (TBM) and correlate it with severity, radiological features, and outcome of TBM.
UNASSIGNED: In a retrospective study, data from admitted TBM patients were analyzed, and findings of CSF examinations were recorded. The CSF was categorized as typical (protein 50-500 mg/dL, cells 50-500/mm3, and glucose 50% or lower of blood sugar); those above and below these values were categorized as increased or decreased, respectively. The CSF findings were correlated with stage of TBM, and 3-month outcome and radiological features. Paradoxical response was also noted.
UNASSIGNED: There were 111 patients with TBM (definite 34, highly probable 77). On admission, 20 patients were in Stage I, 63 in Stage II, and 28 in Stage III TBM. CSF cells were in typical range in 73, low in 27 and increased in 11 patients. Protein was in typical range in 92 patients decreased in 11 patients and increased in eight patients. Sugar was normal in 41 and reduced in 70 patients. CSF cells, glucose, and protein did not correlate with the severity of meningitis. Fifteen patients had normal initial magnetic resonance imaging (MRI). Tuberculomas were present in 53 patients, hydrocephalus in 43 patients, basal exudates in 43 patients, and infarction in 44 patients. Mixed findings were present in 65 patients. The MRI features did not correlate with CSF. Second CSF was available after a median duration of 26 (13-276) days in 50 patients. The CSF cells were decreased in 20 and increased in 30 patients, protein increased in 30 and sugars decreased in 16 patients. Paradoxical worsening occurred in 27 patients. Fifty-one patients recovered completely, 41 partially, 15 had poor, three patients were lost to follow-up, and one died. CSF parameters did not correlate with 3-month outcome or paradoxical worsening. CSF parameters do not differ significantly between baseline and 1 month CSF, but cells and lymphocytes changed significantly between 1st month and 3rd month CSF.
UNASSIGNED: Typical CSF findings were present in 66% and did not correlate severity of TBM, radiological features paradoxical worsening or 3-month outcome. CSF cell count decreased within 3 months of treatment.

UNASSIGNED: Tuberculous meningitis (TBM) is a severe form of tuberculosis affecting the meninges, primarily caused by Mycobacterium tuberculosis. Diagnosis of TBM poses numerous challenges due to its nonspecific clinical presentation and the limitations of diagnostic tests like GeneXpert.
UNASSIGNED: The authors report a case of a 22-year-old female from Eastern Nepal presenting with acute-onset fever, headache, vomiting, and neck pain. Cerebrospinal fluid (CSF) analysis showed lymphocytic pleocytosis, elevated protein, low glucose levels, and cobweb coagulum indicative of TBM. However, the GeneXpert test revealed negative results.
UNASSIGNED: In resource-limited settings like Nepal, where access to GeneXpert MTB/Rif is limited, CSF analysis and clinical algorithms play a crucial role in diagnosing TBM. Relying solely on GeneXpert results may lead to false negatives, so a high level of suspicion based on patient risk factors is essential. Prompt initiation of empirical antitubercular therapy is vital for a favorable outcome in TBM cases.
UNASSIGNED: Negative MTB PCR results from CSF can be misleading in diagnosis of tubercular meningitis. Therefore, comprehensive evaluations, including detailed patient history, physical examination, and CSF fluid analysis, are crucial in high tuberculous prevalence countries to ensure accurate and timely diagnosis.

Tubercular meningitis is a rare yet devastating type of extrapulmonary tuberculosis (TB) posing great diagnostic challenges due to the nonspecific clinical presentation of the patients. Here, we present a rare diagnosis of hypertrophic pachymeningitis due to Mycobacterium tuberculosis. A 36-year-old male presented with a history of headaches and giddiness for one month. Neurological examination revealed hypo-reflexive triceps and ankle reflexes. Routine blood tests and autoimmune workup were normal. Brain MRI with contrast revealed diffuse dural thickening, focal leptomeningeal enhancement in the right temporal sulci, and enhancement in both the frontal and parietal convexity and the falx cerebri and along the tentorium cerebelli. Cerebrospinal fluid (CSF) analysis revealed elevated proteins, suggestive of aseptic meningitis. Meningeal biopsy revealed a chronic ill-formed granulomatous inflammatory lesion with occasional acid-fast bacilli, consistent with tubercular pachymeningitis. The patient was administered intravenous (IV) methylprednisolone for five days, following which the symptoms subsided. He was advised tablet prednisolone on discharge, and immunomodulation with rituximab was recommended as outpatient treatment. Hypertrophic pachymeningitis is a rare diagnosis characterized by the inflammation and fibrosis of the dura matter due to a diverse etiology. Tubercular etiology must be considered when the routine laboratory tests are negative, and the diagnosis should be confirmed by meningeal biopsy. The treatment of the underlying cause and corticosteroids remain the mainstay management of hypertrophic pachymeningitis. Hence, mycobacterial tuberculosis should be considered as a possible differential diagnosis while evaluating hypertrophic pachymeningitis, especially when the routine laboratory tests and immunological workup are negative.

UNASSIGNED: Cortical venous thrombosis is a rare but severe complication of TBM that requires a high index of suspicion for early diagnosis. The treatment of CVT in TBM is based on anticoagulant therapy, which is known to improve the outcomes of the patients.
UNASSIGNED: The case report describes an 18-year-old male in India with symptoms of tubercular meningitis complicated by cortical venous thrombosis. Tubercular meningitis is a rare but severe form of meningitis caused by tuberculosis bacteria and is a significant public health concern in India. The patient presented to the emergency department with a history of fever, headache, and vomiting for the past month, with a positive Mycobacterium tuberculosis test. The patient was started on standard antitubercular therapy and was diagnosed with cortical venous thrombosis via an MRI scan. Treatment included antitubercular therapy, anticoagulation therapy, dexamethasone, and antiemetic drugs. The patient\'s symptoms improved over 2 weeks of therapy. The case highlights the importance of early detection, treatment, and prevention strategies, such as the National Tuberculosis elimination program, in controlling the spread of tuberculosis in India. It also emphasizes the importance of close monitoring for complications in patients with tubercular meningitis, such as cortical venous thrombosis, which can be life-threatening.

BACKGROUND: Tuberculous meningitis (TBM), complicated with cerebral venous thrombosis (CVT), has been sparsely reported and needs to be investigated further.
METHODS: Among those with tuberculous meningitis in Haihe Hospital, Tianjin University, 3 patients with venous sinus thrombosis were identified retrospectively. \"Tuberculous meningitis\" and \"cerebral venous thrombosis\" were used as keywords, and the retrieved literature was summarized and analyzed. Our data were combined with previously reported case data to describe this new condition.
RESULTS: Among 28 patients with a median onset age of 31 years for TBM, 17 were females. The manifestations were fever, headache, and seizure. Magnetic resonance imaging (MRI) venography showed that the most common site of venous sinus thrombosis involved superior sagittal sinus, left transverse sinus, left sigmoid sinus, cavernous sinus, and straight sinus. The abnormalities found on MRI include hydrocephalus, exudates, hemorrhage, meningeal enhancement, infarction, and tuberculoma. In the acute phase, all patients received standard anti-TB treatment, and 14/28 patients received anticoagulant treatment. The mortality rate of these patients was 17.9%, and 21/28 (75%) became functionally independent.
CONCLUSIONS: CVT is one of the rare complications of TMB and must be considered a differential diagnosis in patients with TBM who show poor clinical features and/or develop new neurological signs.