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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
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 • WBC Counts: 9500 • HIV: -ve
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
3rd day • No fever • Single SG seizure • More drowsy (GCS 7/15) • Left hemiparesis • At night • Right pupil dilated • Intubated
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
7th day • Unconscious (GCS 4/15) • On ventilator • Right III nerve palsy • Left pupil also became dilated • Dense left hemiparesis
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
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?
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
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
21/F • Headache • Bilateral • Throbbing • Increasing severity • Occasional vomiting
On examination • Conscious/oriented • Bilateral papilloedema • No other deficit • No neck stiffness
Routine lab: normal • CSF • Opening pressure 40 cm • Proteins 34 • Sugar 76 (BSL 122) • Cells 2 (100% Lympho)
Management • Drained 30 cc CSF • Low salt diet • Acetazolamide 1000 mg/d • Weight loss 3 kg • Improved gradually • At present • No symptoms • No papilloedema
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
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
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
The role of lateral sinus stenosis remains to be evaluated • There are studies in favor of both hypotheses
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
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
Venous channels are becoming more important and controversial with association with more and more neurological diseases • IIH • MS
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
On examination: • Conscious; oriented • Fundi: normal • Neck stiffness • No other deficit • CT scan brain: • Normal
Investigations: • CSF: • Proteins 176 • Sugar 45 (BSL 109) • Cells 30 (100% L) • Hemogram • HIV: -ve • Metabolic lab: normal
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
His headache gradually reduced • Required CSF drainage twice • HIV was repeated by ELISA: -ve • CD4+ count: 68 • DNA quantative PCR for HIV: -ve
Improved subsequently • Discharged on • Fluconazole • TMP/SMX • AKT
Repeat CD4+ count after 2 months: 212 • Now presented with • Fever • Weight loss • Lymphadenopathy
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
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
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
Next day again had similar headache while taking hot water bath • Lasted for 1 hour • Readmitted • No deficit • MR-angio was done
When seen • Comfortable • No deficit • Investigations • Metabolic lab: normal • Counts: normal • CSF • No xanthochromia • Protein 83 • Sugar 98 • Cells 15 (100% L)
What is the diagnosis? • Thunderclap headache • To be investigated for cause • Any further investigations? • DSA • Treatment options? • Received indomethacin on SOS basis