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


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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

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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

  • WBC Counts: 9500

  • HIV: -ve


MRI brain


  • 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


CT scan brain


  • 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


Repeat CT scan brain


  • 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


Case 2


  • 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 pressure40 cm

    • Proteins34

    • Sugar76(BSL 122)

    • Cells2 (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


  • Lateral sinus stenosis


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


Repeat MRI


  • Venous channels are becoming more important and controversial with association with more and more neurological diseases

    • IIH

    • MS


Case 3


  • 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

      • Sugar45 (BSL 109)

      • Cells30 (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


  • Dr Pallavi Bhargav


Case 4


  • 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


MR-angio


  • When seen

    • Comfortable

    • No deficit

  • Investigations

    • Metabolic lab: normal

    • Counts: normal

    • CSF

      • No xanthochromia

      • Protein83

      • Sugar98

      • 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


DSA


Repeat MR-angio


Thunderclap headache (TCH)

  • IHS 2 Diagnostic criteria:

    A. Severe head pain fulfilling criteria B and C

    B. Both of the following characteristics:

    • Sudden onset, reaching maximum intensity in <1 minute

    • Lasting from 1 hour to 10 days

      C. Does not recur regularly over subsequent weeks or months

      D. Not attributed to another disorder (in case of primary)

  • Notes:

    • Headache may recur within the first week after onset

    • In case of primary, normal CSF and normal brain imaging are required


    • Causes of secondary TCH:

      • SAH

      • Sentinel hemorrhage

      • Intracerebral haemorrhage

      • Venous sinus thrombosis

      • Arterial dissection (intra- and extracranial)

      • CNS angiitis

      • Reversible cerebral vasoconstriction syndromes

      • Pituitary apoplexy

      • Colloid cyst of the third ventricle

      • CSF hypotension

      • Acute sinusitis


    Comparison of MRAs (9/12 and 13/12)


    Comparison of MRAs (9/12 and 13/12)


    9/12/2010


    12/12/2010


    Reversible cerebral vasoconstriction syndrome (RCV)

    • Relatively newer name

    • Previous names

      • Benign angiopathy of the central nervous system

      • Migrainous angiitis

      • Post-partum angiopathy

      • Call-Fleming syndrome

        • Stroke 1988; 19: 1159-1170


    • Clinical features

      • Thunderclap headache

        • Tend to recur for few weeks

      • Focal deficits

        • Strokes

        • Bleeds

        • Posterior reversible leucoencephalopathy

      • Seizures

    • Predisposing factors in 60% patients

      • Pregnancy and puerperium

      • Exposure to drugs


    • Diagnosis

      • Angiography (CTA / MRA / DSA) demonstrated multifocal or segmental narrowing

        • Improvement in vasoconstricton in 12 weeks

      • No CT or CSF evidence of SAH

      • Normal or near normal CSF

      • Appropriate clinical history (thunderclap headache)


    • Differential diagnosis

      • Posterior reversible leucoencephalopathy syndrome

      • CNS vasculitis

    • Treatment

      • No large studies

      • Nimodepine or verapamil

      • Short course of steroids (mostly in earlier reports)

      • Intra-arterial therapy in severe cases


    • Underdiagnosed

      • 83 patients with TCH

        • Neurology 2006; 67: 2164-9

      • 56 patients had thunderclap headache of unknown etiology

      • When these patients underwent MRA, 39% were found to have reversible cerebral vasoconstriction

      • In cases of thunderclap headache, if CT and CSF are normal, a noninvasive angiography should be done


    • 67 patients with RCVS

      • Brain 2007; 130 (12): 3091-31

    • 21% of patients who ultimately demonstrated vasoconstriction initially had normal angiographic studies

    • In other words, there was a lag between the onset of symptoms and the presence of vasoconstriction

    • This suggests that cerebral vasoconstriction may begin in smaller distal vessels that extend beyond the resolution of MRA before involving larger proximal cerebral blood vessels


    Bath induced thunderclap headache

    • Cephalalgia 2008; 28: 524-530

  • 21 patients

  • Bathing was the initial trigger for thunderclap headaches in 9 (43%)

  • 15 (71%) had other non-bath-related attacks

  • 18 (86%) reported that the headache occurred immediately when water was sprayed over their body, with warm water (52%) as the most common

  • 13 (62%) had RCV on imaging

  • Nimodipine was effective in stopping further attacks in 84%


    • In case of thunderclap headache, if CT and CSF are normal, angio should be done in all to look for not only aneurysm but also for RCV


    Case 5


    • 65/M

    • Acute right hemiparesis

    • Clinically

      • Right hemianopia

      • Right hemiparesis

      • Right hypoaesthesia


    Hyperdense PCA sign

    • HPCA sign

      • Stroke 2006; 37: 399

    • Detected in >1/3 of all patients with PCA infarct, suiting incidence ofhyperdense MCA

    • This sign may notonly be helpful in the early diagnosis of PCA infarction butmight also act as a prognostic marker in acute PCA territoryischemic stroke


    Case 6


    • Young lady

    • H/O electric shock

    • Became unconsciousness

    • When came to casualty had cardiorespiratory arrest

      • Monitor showed asystole

    • Resuscitated

    • Shifted to ICU


    • On examination

      • On ventilator and intropic support

      • Unconscious (GCS 3/15)

      • Pupils 3 mm NRL

      • Doll eye movement absent

      • Corneal reflexes absent

    • Diagnosis:

      • Hypoxic brain injury secondary to cardio-respiratory arrest

    • Treatment?


    Therapeutic hypothermia

    • Decreases cerebral metabolic demand

    • Clinical trials and meta-analysis showed improved outcome with hypothermia

      • Resuscitation 2007; 73: 29-39

      • NEJM 2002; 346(22): 1756

    • 16-23% improved outcome

    • Cool up to 33°C (32-34°C) for 12-24 hours

    • To be started within min to hours after arrest


    • Problems

      • Technically difficult

      • Ideal induction technique

        • Internal vs. external

      • Target temperature

      • Duration

      • Re-warming rate

    • Complications

      • Shivering

      • Arrhythmias


    Hypothermia: technique

    • Dr. Sameer Jog


    Case 7


    Middle aged male

    Immunocompramised

    CD4+ count 55

    On ART

    Presented with 2 months H/O

    Asymmetric ataxia (R>L)

    Dysarthria

    No pyramidal signs/dementia/bladder involvement


    • CSF

      • Protein55

      • Sugar67

      • Cells4 (100% L)

    • Treatment

      • Continued on ART

      • Physiotherapy

    • Continued worsening

      • Bed ridden


    • Diagnosis?

      • PML


    • He underwent follow up MRI after 1 year

      • CD4+ count at this stage was 107


    Hot cross bun appearance

    • The sign is due to

      • Selective loss of myelinated transverse pontocerebellar fibers and neurons in pontine raphe

      • Preservation of pontine tegmentum and corticospinal tracts

    • Has been described in

      • MSA-c

      • Parkinsonism due to vasculitis

      • SCA 2

      • SCA 3

      • vCJD

    • Has not been descried in PML till date


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