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HSVE IIH ICL Pallavi to talk TCH DSA PCA sign Hypothermia Jog to talk PML

HSVE IIH ICL Pallavi to talk TCH DSA PCA sign Hypothermia Jog to talk PML. Case 1. 42/F History since 3 days Fever Headache Confusion No seizures, rash On examination Drowsy, confused (GCS 10/15) Fundi normal No other deficit No neck stiffness. Metabolic lab: WNL

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HSVE IIH ICL Pallavi to talk TCH DSA PCA sign Hypothermia Jog to talk PML

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  1. HSVE IIH ICL Pallavi to talk TCH DSA PCA sign Hypothermia Jog to talk PML

  2. Case 1

  3. 42/F • History since 3 days • Fever • Headache • Confusion • No seizures, rash • On examination • Drowsy, confused (GCS 10/15) • Fundi normal • No other deficit • No neck stiffness

  4. Metabolic lab: WNL • WBC Counts: 9500 • HIV: -ve

  5. MRI brain

  6. CSF: • Proteins 110 • Sugar 65 (BSL 135) • Cells 26 (95% lympho) • HSV PCR sent • Started on I/V acyclovir 600 mg 8 hourly • Neurostatus same on day 2

  7. 3rd day • No fever • Single SG seizure • More drowsy (GCS 7/15) • Left hemiparesis • At night • Right pupil dilated • Intubated

  8. CT scan brain

  9. In view of large area of damage with mass effect • Underwent decompression craniotomy • Biopsy take from temporal lobe showed F/O encephalitis • Next 3 days (Day 4-6) • No significant change • On ventilator • Drowsy (GCS 5-6/15) • Developed right III nerve palsy • Occasional focal and SG seizures

  10. 7th day • Unconscious (GCS 4/15) • On ventilator • Right III nerve palsy • Left pupil also became dilated • Dense left hemiparesis

  11. Repeat CT scan brain

  12. Further course • Continued on I/V acyclovir for 3 weeks • Gradually improved • Weaned off ventilator • Became alert • Left hemiparesis improved • No seizures • Present condition • Oriented; independent • Right ptosis is persistent; though eye movements and pupillary size are normal

  13. Discussion • Decompression craniotomy in HSVE • Useful option in cases with mass effect and poor response to acyclovir and anti-oedema measurs • Some reports suggest that in addition partial resection of temporal lobe is of benefit additional reduction of infectious material can be achieved • Child’s Nerv Syst 1999; 15: 84–86 • Malignant HSVE?

  14. Surprisingly few cases of decompression have been described in literature • 2 cases • Surg. Neurol. 2002; 57 (1): 20 • Review of literature: • Total 13 cases of infectious encephalitis requiring decompression • 6 had HSVE • J Neurosurg. 2008; 108 (1): 174

  15. What is new in HSV encephalitis? • Long Term Treatment of Herpes Simplex Encephalitis With Valacyclovir • Ongoing trial • The purpose of the study is to determine if treatment with oral valacyclovir 2 gm TDS for 90 days is both effective and safe after completing i/v acyclovir treatment and if it can increase survival with or without mild impairment of the brain and mental functions

  16. Case 2

  17. 21/F • Headache • Bilateral • Throbbing • Increasing severity • Occasional vomiting

  18. On examination • Conscious/oriented • Bilateral papilloedema • No other deficit • No neck stiffness

  19. Routine lab: normal • CSF • Opening pressure 40 cm • Proteins 34 • Sugar 76 (BSL 122) • Cells 2 (100% Lympho)

  20. Management • Drained 30 cc CSF • Low salt diet • Acetazolamide 1000 mg/d • Weight loss 3 kg • Improved gradually • At present • No symptoms • No papilloedema

  21. Lateral sinus stenosis

  22. IIH and lateral sinus stenosis • By definition IIH is idiopathic • Venous disorders can cause rise in intracranial pressure and present with syndrome like IIH • Venous sinus thrombosis • Duralvenous fistulas • Venous sinus compression • In many patients with IIH,neuroimaging shows narrowing of the transverse sinuses

  23. Controversy • Whetherthis abnormality is cause or consequence of increasedintracranial pressure? • Cause: • Stenoses→ Obstruction to venous outflow → ↑ intracranial venous pressure proximalto the stenosis → reduction in CSF absorption via the arachnoid granulations → ↑ CSF pressure • In this setting, a pressure gradient across the stenosis canbe measured • Reconstruction of the venous lumen with endovascularstents would be effective in lowering elevated CSF pressure

  24. Controversy • Whetherthis abnormality is cause or consequence of increasedintracranial pressure? • Consequence: • ↑ intracranial CSF pressure → secondary narrowingof sinus lumen by compression • It can be reversed bylumbar puncture or shunt surgery procedures

  25. The role of lateral sinus stenosis remains to be evaluated • There are studies in favor of both hypotheses

  26. Cause • Endovascular treatment of idiopathic intracranial hypertension • Neurology 2008; 70: 641-647 • Conclusion: • Importance of venous sinus disease in etiologyof IIH is underestimated • Patients with IIH in whom avenous sinus stenosis is demonstrated by MRV should be evaluated with direct retrograde cerebral venographyand manometry • In patients with venous sinus stenosis who do not respond to medical treatment, endovascular stentplacement seems to be an interesting option

  27. Consequence • Transverse sinus stenoses persist after normalization of the CSF pressure in IIH • Neurology 2005; 65: 1090-1093 • Conclusion: • Transverse sinus stenoses, as revealed byMR venography, persist in patients with idiopathic intracranialhypertension after normalization of CSF pressure, suggestingthe lack of a direct relationship between the caliber of sinusand CSF pressure

  28. Repeat MRI

  29. Venous channels are becoming more important and controversial with association with more and more neurological diseases • IIH • MS

  30. Case 3

  31. Middle aged male • H/O pleural effusion 6 months ago • Treated with AKT • On INH and Rifa at present • No respiratory symptoms • CXR: normal • Presented with 14 days history of • Headache • Vomiting

  32. On examination: • Conscious; oriented • Fundi: normal • Neck stiffness • No other deficit • CT scan brain: • Normal

  33. Investigations: • CSF: • Proteins 176 • Sugar 45 (BSL 109) • Cells 30 (100% L) • Hemogram • HIV: -ve • Metabolic lab: normal

  34. Started on 4 drugs AKT with steroids after CSF report • Other CSF reports were pending • Next day • CSF India ink +ve • CSF PCR for TB -ve • Started on i/v amphotericine B

  35. His headache gradually reduced • Required CSF drainage twice • HIV was repeated by ELISA: -ve • CD4+ count: 68 • DNA quantative PCR for HIV: -ve

  36. Improved subsequently • Discharged on • Fluconazole • TMP/SMX • AKT

  37. Repeat CD4+ count after 2 months: 212 • Now presented with • Fever • Weight loss • Lymphadenopathy

  38. Idiopathic CD4 lymphocytopenia (ICL) • CD4+T cells <300 or a CD4+ cell count <20% of total T cell on two occasions • No evidence of infection on HIV testing • Absence of any defined immunodeficiency or therapy associated with depressed levels of CD4+ T cells

  39. Dr Pallavi Bhargav

  40. Case 4

  41. 40 years old male • Presented with sudden onset severe headache • Started while taking hot water bath • Over vertex and occipital region • Associated with nausea • No loss of consciousness • No past H/O similar headache, trauma, fever • C/O DM on OHAs

  42. Came to hospital in 1 hour • Headache was already subsiding then • No neurological deficit • No neck stiffness • Admitted • Received NSAID • Non-contrast CT scan brain: normal • No headache in next 36 hours • Discharged

  43. Next day again had similar headache while taking hot water bath • Lasted for 1 hour • Readmitted • No deficit • MR-angio was done

  44. MR-angio

  45. When seen • Comfortable • No deficit • Investigations • Metabolic lab: normal • Counts: normal • CSF • No xanthochromia • Protein 83 • Sugar 98 • Cells 15 (100% L)

  46. What is the diagnosis? • Thunderclap headache • To be investigated for cause • Any further investigations? • DSA • Treatment options? • Received indomethacin on SOS basis

  47. DSA

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