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Edit Comment Close Premium member Presentation Transcript CNS Tuberculosis: CNS Tuberculosis Dr Rahul Chakor MD DM Lecturer – Dept of Neurology T N Medical College B Y L Nair Hospital MumbaiSyndromes: Syndromes Tuberculosis (TB) Meningitis Intracranial Tuberculomas, TB abscess Spinal meningitis Tuberculous Osteomyelitis of Spine with myelopathy (Potts disease)TB: TB Most important infectious disease M. tuberculosis – obligate aerobic organism Host susceptibility, bacterial virulence, immunosuppression Reactivation of earlier infection due to immunosuppression Primary infectionTB Meningitis: TB Meningitis Hematogenous spread of tubercle bacilli from lung or other organ Subpial, subependymal tubercles ( Rich focus ) Rupture into subarachnoid, ventricular space Meningial inflammationTB Meningitis (TBM): Spread during miliary TB Spread from parameningeal (vertebral column, middle ear) infection Rupture of Choroid plexus tuberculomas TB Meningitis (TBM)Pathology (TBM): Pathology (TBM) Gross Basal exudates - interpeduncular fossa (midbrain, pons), anterior brain stem, orbitofrontal, temporal lobes, optic chiasma Exudates and tubercles along the sylvian fissure Entrapment of the basilar artery, middle cerebral artery and branchesPathology (TBM): Pathology (TBM) Microscopy Serofibrinous exudates along the two layers of leptomeninges, Lymphocytes, plasma cells, caseous necrosis, dilated congested blood vessels Tuberculous granulomas – epithelioid cells, giant cells AFB along margin of caseous necrosis and blood vessels MeningesPathology (TBM): Pathology (TBM) Microscopy MCA, Basilar artery and branches - Congested, aneurysmal dilation, narrowed, thrombosed. Subintimal fibrosis and thickening, small vessel medial necrosis, inflammation, subintimal edema Reaction to surrounding inflammation Vascular obstruction, necrosis or obliteration leading to infarcts in MCA territory Blood vesselsPathology (TBM): Pathology (TBM) Hydrocephalus Acute - mechanical blockage of basal cisterns Chronic – fibrous obliteration of leptomeningeal space (communicating hydrocephalus) Narrowing of cerebral aqueduct by exudates around brainstem, subependymal exudates Trapped venricle – due to infarctTuberculoma: Tuberculoma Granulomas, tiny to massive size (5cm or >) multiple conglomerate or single Central caseous necrosis, surrounded by several discrete or confluent granulomas composed of epithelioid cells and Langhans type giant cells, few AFB and areas of necrosis along the periphery Surrounding hyperemia and edema, gliosis Heal with calcification and fibrosisTuberculosis Abscess: Tuberculosis Abscess Failure of immune reaction Pus filled within a capsule rich in TB bacilli. No granulomatous reaction Immune compromisedSpinal Meningitis and arachnoiditis: Spinal Meningitis and arachnoiditis Meningeal inflammation around the spinal cord With cranial meningitis, isolated Extension of cranial tuberculous exudates Thick exudates with matted and entrapped spinal nerve roots Radiculomyelopathy, spinal infarctionTB Meningitis: TB Meningitis Clinical Staging of Tuberculous Meningitis Stage I - Prodromal stage (early) Nonspecific symptoms and signs, No clouding of consciousness, No neurologic deficits, lasts 2wk Stage II - Meningeal irritation (intermediate) Lethargy, alteration in behavior, Minor neurologic deficits (cranial nerve palsies), lasts days to wks Stage III - Cerebral involvement (advanced) Abnormal movements, convulsions, stupor, coma, severe neurologic deficits (pareses), death in 6 to 12 wksTB Meningitis: Papilledema , retinal, choroidal tuberculoma or a small grayish-white nodule, pallor of the disc Cranial neuropathies (CN) – VI, III, IV, VII. Less commonly CN II, VIII, X, XI, and XII, Focal neurological deficits - Hemiplegia, aphasia, tetraparesis, choreoathetosis and hemiballismus, TB Meningitis Physical signsSlide 15: differential diagnosis in any patient presenting with fever and a change in sensorium. Infections Acute hemorrhagic leukoencephalopathy Behçet disease Chemical meningitis Chronic benign lymphocytic meningitis Neoplastic - Metastatic, lymphoma Systemic lupus erythematosus Vascular - Multiple emboli, subacute bacterial endocarditis, sinus thrombosis Vasculitis - Isolated CNS angiitis, systemic giant cell arteritis, Wegener granulomatosis, polyarteritis nodosa, noninfectious granulomatosis, lymphomatoid granulomatosis Vogt-Koyanagi-Harada syndromeDiagnosis: Diagnosis Routine Investigations – of limited utility CSF – "spider's web clot" very high level of protein in the CSF (ie, 1-8 g/L) Lymphocytic pleocytosis (500 μ L) proteins > 200mg/dl glucose <40mg/dl CSF - Atypical findings common CSF – ADA level, smear for AFB, culture for AFB CSF – TB DNA detected by PCRNeuroimaging: NeuroimagingNeuroimaging: NeuroimagingNeuroimaging: NeuroimagingNeuroimaging: NeuroimagingTreatment: Treatment (1) Multiple antimicrobial drugs are required (2) Drugs must adequately cross the blood- CSF barrier to achieve therapeutic concentrations in CSF (3) Drugs should be taken on a regular basis (4) Drugs should be taken for a sufficient duration to eradicate the CNS infection.Treatment: TreatmentAnti tuberculous drugs: Anti tuberculous drugs Ethionamide, Prothionamide Cycloserine Para amino salicylic acid (PAS) Aminoglycosides - Amikacin, Kanamycin, Capreomycin Thiacetazone Macrolides - Clarithromycin Fluoroquinolones - Ofloxacin, Levofloxacin, Gatifloxacin, Sparfloxacin, Moxifloxacin Rifapentine, Rifabutin Clofazimine Amoxycillin- Clavulinic acidSteroids in TB: Steroids in TB Prednisone (children, 4 mg/kg/day) or dexamethasone (adults, 12 to 16 mg/day, children, 8 mg/day) for 4 to 8 weeks and tapered graduallyCNS TB and paradoxical response: CNS TB and paradoxical response Develops after 2 weeks of treatment Clinical or radiological worsening of preexisting tuberculous lesions Development of new lesions Initial improvement with antituberculous therapy.Neurologic sequelae: Neurologic sequelae Hemiparesis, Aphasia Developmental delay, Dementia, Blindness, deafness, cranial nerve palsies Epilepsy Hypothalamic pituitary dysfunction.Slide 27: Thank You You do not have the permission to view this presentation. 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CNS Tuberculosis neurology1 Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 749 Category: Science & Tech.. License: All Rights Reserved Like it (2) Dislike it (0) Added: February 26, 2011 This Presentation is Public Favorites: 1 Presentation Description No description available. Comments Posting comment... By: clumstgirl (7 month(s) ago) good Saving..... Post Reply Close Saving..... Edit Comment Close By: pradeepgujar (15 month(s) ago) goood Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript CNS Tuberculosis: CNS Tuberculosis Dr Rahul Chakor MD DM Lecturer – Dept of Neurology T N Medical College B Y L Nair Hospital MumbaiSyndromes: Syndromes Tuberculosis (TB) Meningitis Intracranial Tuberculomas, TB abscess Spinal meningitis Tuberculous Osteomyelitis of Spine with myelopathy (Potts disease)TB: TB Most important infectious disease M. tuberculosis – obligate aerobic organism Host susceptibility, bacterial virulence, immunosuppression Reactivation of earlier infection due to immunosuppression Primary infectionTB Meningitis: TB Meningitis Hematogenous spread of tubercle bacilli from lung or other organ Subpial, subependymal tubercles ( Rich focus ) Rupture into subarachnoid, ventricular space Meningial inflammationTB Meningitis (TBM): Spread during miliary TB Spread from parameningeal (vertebral column, middle ear) infection Rupture of Choroid plexus tuberculomas TB Meningitis (TBM)Pathology (TBM): Pathology (TBM) Gross Basal exudates - interpeduncular fossa (midbrain, pons), anterior brain stem, orbitofrontal, temporal lobes, optic chiasma Exudates and tubercles along the sylvian fissure Entrapment of the basilar artery, middle cerebral artery and branchesPathology (TBM): Pathology (TBM) Microscopy Serofibrinous exudates along the two layers of leptomeninges, Lymphocytes, plasma cells, caseous necrosis, dilated congested blood vessels Tuberculous granulomas – epithelioid cells, giant cells AFB along margin of caseous necrosis and blood vessels MeningesPathology (TBM): Pathology (TBM) Microscopy MCA, Basilar artery and branches - Congested, aneurysmal dilation, narrowed, thrombosed. Subintimal fibrosis and thickening, small vessel medial necrosis, inflammation, subintimal edema Reaction to surrounding inflammation Vascular obstruction, necrosis or obliteration leading to infarcts in MCA territory Blood vesselsPathology (TBM): Pathology (TBM) Hydrocephalus Acute - mechanical blockage of basal cisterns Chronic – fibrous obliteration of leptomeningeal space (communicating hydrocephalus) Narrowing of cerebral aqueduct by exudates around brainstem, subependymal exudates Trapped venricle – due to infarctTuberculoma: Tuberculoma Granulomas, tiny to massive size (5cm or >) multiple conglomerate or single Central caseous necrosis, surrounded by several discrete or confluent granulomas composed of epithelioid cells and Langhans type giant cells, few AFB and areas of necrosis along the periphery Surrounding hyperemia and edema, gliosis Heal with calcification and fibrosisTuberculosis Abscess: Tuberculosis Abscess Failure of immune reaction Pus filled within a capsule rich in TB bacilli. No granulomatous reaction Immune compromisedSpinal Meningitis and arachnoiditis: Spinal Meningitis and arachnoiditis Meningeal inflammation around the spinal cord With cranial meningitis, isolated Extension of cranial tuberculous exudates Thick exudates with matted and entrapped spinal nerve roots Radiculomyelopathy, spinal infarctionTB Meningitis: TB Meningitis Clinical Staging of Tuberculous Meningitis Stage I - Prodromal stage (early) Nonspecific symptoms and signs, No clouding of consciousness, No neurologic deficits, lasts 2wk Stage II - Meningeal irritation (intermediate) Lethargy, alteration in behavior, Minor neurologic deficits (cranial nerve palsies), lasts days to wks Stage III - Cerebral involvement (advanced) Abnormal movements, convulsions, stupor, coma, severe neurologic deficits (pareses), death in 6 to 12 wksTB Meningitis: Papilledema , retinal, choroidal tuberculoma or a small grayish-white nodule, pallor of the disc Cranial neuropathies (CN) – VI, III, IV, VII. Less commonly CN II, VIII, X, XI, and XII, Focal neurological deficits - Hemiplegia, aphasia, tetraparesis, choreoathetosis and hemiballismus, TB Meningitis Physical signsSlide 15: differential diagnosis in any patient presenting with fever and a change in sensorium. Infections Acute hemorrhagic leukoencephalopathy Behçet disease Chemical meningitis Chronic benign lymphocytic meningitis Neoplastic - Metastatic, lymphoma Systemic lupus erythematosus Vascular - Multiple emboli, subacute bacterial endocarditis, sinus thrombosis Vasculitis - Isolated CNS angiitis, systemic giant cell arteritis, Wegener granulomatosis, polyarteritis nodosa, noninfectious granulomatosis, lymphomatoid granulomatosis Vogt-Koyanagi-Harada syndromeDiagnosis: Diagnosis Routine Investigations – of limited utility CSF – "spider's web clot" very high level of protein in the CSF (ie, 1-8 g/L) Lymphocytic pleocytosis (500 μ L) proteins > 200mg/dl glucose <40mg/dl CSF - Atypical findings common CSF – ADA level, smear for AFB, culture for AFB CSF – TB DNA detected by PCRNeuroimaging: NeuroimagingNeuroimaging: NeuroimagingNeuroimaging: NeuroimagingNeuroimaging: NeuroimagingTreatment: Treatment (1) Multiple antimicrobial drugs are required (2) Drugs must adequately cross the blood- CSF barrier to achieve therapeutic concentrations in CSF (3) Drugs should be taken on a regular basis (4) Drugs should be taken for a sufficient duration to eradicate the CNS infection.Treatment: TreatmentAnti tuberculous drugs: Anti tuberculous drugs Ethionamide, Prothionamide Cycloserine Para amino salicylic acid (PAS) Aminoglycosides - Amikacin, Kanamycin, Capreomycin Thiacetazone Macrolides - Clarithromycin Fluoroquinolones - Ofloxacin, Levofloxacin, Gatifloxacin, Sparfloxacin, Moxifloxacin Rifapentine, Rifabutin Clofazimine Amoxycillin- Clavulinic acidSteroids in TB: Steroids in TB Prednisone (children, 4 mg/kg/day) or dexamethasone (adults, 12 to 16 mg/day, children, 8 mg/day) for 4 to 8 weeks and tapered graduallyCNS TB and paradoxical response: CNS TB and paradoxical response Develops after 2 weeks of treatment Clinical or radiological worsening of preexisting tuberculous lesions Development of new lesions Initial improvement with antituberculous therapy.Neurologic sequelae: Neurologic sequelae Hemiparesis, Aphasia Developmental delay, Dementia, Blindness, deafness, cranial nerve palsies Epilepsy Hypothalamic pituitary dysfunction.Slide 27: Thank You