HSVE IIH ICL Pallavi to talk TCH DSA PCA sign Hypothermia Jog to talk PML
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Transcript of 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 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 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
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 Dural venous fistulas Venous sinus compression
In many patients with IIH, neuroimaging shows narrowing of the transverse sinuses
Controversy Whether this abnormality is cause or consequence of
increased intracranial pressure?
Cause: Stenoses → Obstruction to venous outflow → ↑ intracranial
venous pressure proximal to the stenosis → reduction in CSF absorption via the arachnoid granulations → ↑ CSF pressure
In this setting, a pressure gradient across the stenosis can
be measured Reconstruction of the venous lumen with endovascular
stents would be effective in lowering elevated CSF pressure
Controversy Whether this abnormality is cause or
consequence of increased intracranial pressure?
Consequence: ↑ intracranial CSF pressure → secondary narrowing
of sinus lumen by compression It can be reversed by lumbar 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 etiology of IIH
is underestimated Patients with IIH in whom a venous sinus stenosis is
demonstrated by MRV should be evaluated with direct retrograde cerebral venography and manometry
In patients with venous sinus stenosis who do not respond to medical treatment, endovascular stent
placement 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 by MR
venography, persist in patients with idiopathic intracranial hypertension after normalization of CSF pressure, suggesting the lack of a direct relationship between the caliber of sinus and 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 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
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 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
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 of hyperdense MCA This sign may not only be helpful in the early
diagnosis of PCA infarction but might also act as a prognostic marker in acute PCA territory
ischemic 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 Protein 55 Sugar 67 Cells 4 (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