Atypical cause of stroke in an 18 years old female (original) (raw)
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Tuberculous Meningitis, Vasculitis, andPericarditis presented by deep coma
Pakistan Journal of Medical Sciences, 2018
A 32 years old male patient presented to the emergency room with complete loss of consciousness since three hours. This was after two weeks of night fever, sweating and considerable loss of weight with selftreatment by antipyretic drugs. In the last two days, the patient develops confusion and altered behavior. Clinical examination revealed high-grade fever and coma. CXR revealed mild cardiomegaly. Treatment started with intravenous fluids, antipyretics, and antibiotics. On the next day, Echocardiography revealed mild Mitral regurgitation (MR), mild pericardial effusion with thickening of the pericardial membrane that suggested pericarditis. ESR was significantly elevated (57 mm/hour). After three days of treatment without improvement, Tuberculosis (TB) proposed and laboratory investigations implemented. Brain MRI T1 weighted images with Gadolinium injection revealed basal meningeal enhancement with multiple tiny cerebral granulomas.FLAIR-weighted images revealed multiple small high signal intensity foci in bilateral temporal lobes and the basal ganglia strongly suggesting vasculitis and ischemic lesions. CSF sample and culture was done, and anti-tuberculous drugs started with IV fluids, corticosteroids, and other supportive drugs.The results of CSF culture confirmed the diagnosis of Tuberculous meningitis. After two months of continuous anti-tuberculous treatment, the patient seemed to regain consciousness. The patient continued Rifampicin tab 700 mg, Isoniazid tab 350 mg, Ethambutol tab 400 mg, Pyridoxine tab 80 mg, Aspirin tab 100 mg and other supportive drugs for six months. The patient regained full health without any mental or motor disabilities.
Tuberculous Meningitis Presenting with Stroke in an Immunocompetent Adolescent: A Case Report
East Africa Science
Background: Tuberculous meningitis (TBM) is a severe infection of the central nervous system that has high mortality. The disease predominantly affects young children and those who are immuncompromised. Strokes have been reported in about one-third of children with tuberculous meningitis and are associated with poor clinical outcomes. Case report: A previously healthy 14-year-old girl living in Dar es Salam, Tanzania presented with one month history of weight loss associated with weakness, loss of appetite, apathy; without respiratory symptoms. Anti-TB therapy was started, based on radiological findings of the chest which showed multiple patchy centrilobular nodules with linear branching pattern bilaterally, mediastinum lymph node enlargement with punctate calcification. She then became aphasic and developed right-sided hemiparesis. Brain imaging showed infarction, hydrocephalus and meningeal enhancement. Diagnosis of tuberculous meningitis (TBM) with left sided ischaemic stroke was...
Tuberculous meningitis: many questions, too few answers
The Lancet Neurology, 2005
Tuberculous meningitis (TM) is difficult to diagnose and treat; clinical features are non-specific, conventional bacteriology is widely regarded as insensitive, and assessment of newer diagnostic methods is not complete. Treatment includes four drugs, which were developed more than 30 years ago, and prevents death or disability in less than half of patients. Mycobacterium tuberculosis resistant to these drugs threatens a return to the prechemotherapeutic era in which all patients with TM died. Research findings suggest that adjunctive treatment with corticosteroids improve survival but probably do not prevent severe disability, although how or why is not known. There are many important unanswered questions about the pathophysiology, diagnosis, and treatment of TM. Here we review the available evidence to answer some of these questions, particularly those on the diagnosis and treatment of TM. Panel 1: TM in clinical practice Associated with TM Recent exposure to tuberculosis (especially in children) Evidence of tuberculosis elsewhere (especially miliary tuberculosis on chest radiograph) HIV infection Diagnosis Acute Meticulous microscopy (and then culture) of у5 ml of CSF After treatment commencement PCR of CSF Treatment First 2 months Four drugs: isoniazid, rifampicin, pyrazinamide and either streptomycin, or ethambutol Next 7-10 months Isoniazid and rifampicin Patients without HIV Give dexamethasone, regardless of patient's age or disease severity Panel 2: TM symptoms on presentation 4-9
Pearls & Oy-sters: CSF analysis and the therapeutic paradox in tuberculous meningitis
Neurology, 2014
Pearls & Oy-sters: CSF analysis and the therapeutic paradox in tuberculous meningitis PEARLS 1. The diagnosis of tuberculous meningitis (TM) is often based on clinical findings due to the difficulty of isolating acid-fast bacilli (AFB) in the CSF. 2. After initiation of treatment for TM, the CSF profile may switch from a lymphocytic to a neutrophilic predominance, known as the therapeutic paradox.
Journal of Clinical Neuroscience, 2007
Cerebral infarction as a complication of tubercular (TB) meningitis is not uncommon, but an adequate comparison of patients with and without stroke has not been carried out. This study was performed to evaluate the clinical characteristics of cerebral infarction secondary to TB meningitis, and to investigate predictive factors for cerebral infarction in patients with TB meningitis. Patients with TB meningitis were recruited over a period of 56 months. They were divided into two groups, those with and those without stroke. Demographic features and clinical, laboratory, and neuroradiological findings were compared between the two groups. We classified strokes into subtypes using neuroimaging findings. Of the 38 patients who were diagnosed with TB meningitis, eight also experienced cerebral infarction. The percentage of cerebrospinal fluid leukocytes that were neutrophils was significantly higher in patients with stroke (68%) than in patients without stroke (31%; p = 0.0001). Upon initial CT imaging, meningeal enhancement was found in 11 patients, and of these patients, six experienced stroke. There were no significant differences between the groups with respect to other clinical and laboratory features, including demographic features, time between meningitis onset and treatment initiation, peripheral white blood cell count, and cerebrospinal fluid findings. Five of the eight patients who developed stroke had lacunar infarcts. One of the three patients with territorial nonlacunar infarction died due to herniation. When treating patients with TB meningitis, the possibility of cerebral infarction should be considered when patients develop focal neurological signs, meningeal enhancement on a CT scan, and sustained polymorphic cerebrospinal fluid pleocytosis.
Journal of Nepal Medical Association
Tubercular meningitis is a devastating presentation of extra pulmonary tuberculosis, with fatality in each case without treatment. A 39 years male, a regular consumer of alcohol and a known case of major depressive disorder, presented with the alleged history of using an electric heater in a closed room, and presented to emergency with unconsciousness and cardiac arrest. As his neurological status didn’t improve over 72 hrs, a magnetic resonance imaging brain was done which was non-conclusive. Electroencephalogram revealed diffuse right fronto-parietal seizure activity ceasing with midazolam injection, hence levetiracetam was started. Lumbar puncture revealed increased adenosine deaminase and nil white blood cells. Repeat lumbar puncture showed lymphocytic–predominant pleocytosis, elevated protein and low glucose. The patient was started on anti-tubercular therapy and an injection of dexamethasone was added. Repeat electroencephalogram didn’t show any seizure-like activity. It is im...