Encephalitis

Question 1

HSV lives where in the body

Answer 1

DRG

Question 2

HSV 1 or 2 more common

Answer 2

Some 90% of HSV encephalitis cases in adults are caused by HSV-1

Question 3

HSV transmission

Answer 3

HSV-1 is usually transmitted during childhood via nonsexual contact with an infected host, whereas HSV-2 is typically transmitted via sexual contact (although HSV-1 can be transmitted sexually as well).

HSV-2 can also cause recurrent meningitis without encephalitis in adults.

Question 4

Pathologic hallmarks of HSV infection

Answer 4

Necrotizing hemorrhagic encephalitis of orbitofrontal and temporal lobes with spread to the cingulate and insular cortices with unilateral or bilateral involvement. Eintranuclear inclusion bodies in neurons (Cowdry type A) is characteristic. In the immunocompromised, HSV can affect the brain more diffusely.

Question 5

EEG HSV

Answer 5

Acute-slowing or spike/slow wave complexes in area involved (~ 65% of patients)

Question 6

MRI HSV

Answer 6

T2 hyperintense and T1 hypointense lesions are located typically in the anterior temporal lobe, the limbic structures, the insular cortex, and the frontal lobe

Question 7

CSF of HSV caveats

Answer 7

~5% have initially NORMAL CSF. HSV PCR is best test. False neg early in disease! (esp first 2d). Unclear how long after acyclovir started that senstivity drops (may be many days).

Question 8

Predictors of poor outcome w/ HSV

Answer 8

Age > 30
Initial GCS < 6
> 4 days of symptoms prior to starting acyclovir

Question 9

VZV reactivation can infrequently cause…

Answer 9

Affects more central structures: meningitis, intracranial arterial vasculopathy, encephalitis, cerebellitis, radiculitis, and/or myelitis

Question 10

VZV vasculopathy?

Answer 10

Can affect large arteries (large-sized ischemic or hemorrhagic infarctions) & small arteries (foci of ischemic infarctions with variable degrees of necrosis and demyelination). Anterior and posterior circulation can be affected.

Question 11

Labs to send for VZV

Answer 11

VZV PCR and VZV IgG should. Sensitivity of VZV PCR can be as low as 30%, particularly with prolonged syndrome. VZV IgG up to 90% sens!

Question 12

MRI VZV

Answer 12

Almost always abnormal. Highly variable lesion pattern: large infarcts to small punctate lesions in both gray and white matter.
ESPECIALLY lesions at the gray/white matter junction

Question 13

VZV sequelae?

Answer 13

• Pure cerebellitis, particularly in the young, following primary infection. Case report of adult cerebellitis from VZV without rash.
• Myelopathy (either w or wo rash)
• VASCULAR: aneurysm, dissection, spinal cord infarction, intracerebral hemorrhage, and even peripheral arterial disease

Question 14

VZV RX

Answer 14

IV duration varies. But after the initial intravenous treatment, for those at high risk with immunosuppression and persistent symptoms, oral valacyclovir 1,000 mg three times daily for 1 to 2 months may be added

Question 15

CMV location in body

Answer 15

Replicate in salivary glands, kidneys, peripheral blood leukocytes. Chronic infection can result in persistent viral shedding.

Question 16

CMV encephalitis associated exam findings

Answer 16

may have additional or prominent cerebellar signs and even Wernicke-Korsakoff syndrome; this latter entity is more commonly associated with CMV radiculitis, so radicular pain and weakness may provide a clue

Question 17

CMV time course

Answer 17

INDOLENT, may accumulate over several weeks. +/- Fever

Question 18

CMV treatmnet

Answer 18

ganciclovir 5 mg/kg and/or foscarnet 90 mg/kg BID x 14-21d as induction followed by maintenance daily dosing until immune reconstitution is achieved or indefinitely if ongoing immunosuppression is required

Question 19

HHV6 transmission

Answer 19

Transmitted by oral secretions from adults to infants or less commonly by transplanted organs. HSCT in adult!

Question 20

You have a PCR positive for HHV but pt is fine…

Answer 20

Given the high frequency of asymptomatic HHV-6 PCR positivity, caution should be used before implicating a causal role of HHV-6 for encephalitis based on a positive PCR alone

Question 21

HHV6 clinical manifestations

Answer 21

limbic encephalitis marked by confusion, headache, anterograde amnesia, and decreased level of arousal. Fever often absent. Temporal lobe seizures frequently complicate the course of disease.

Question 22

HHV MRI

Answer 22

Early in disease course, (esp wk 1), brain MRI can be within normal limits and then evolve to show these lesions: bilateral hyperintense T2 lesions in the limbic structures, including insular and mesial temporal regions

Question 23

HHV6 rx

Answer 23

ganciclovir or foscarnet alone or in combination; if contraindicated cidofovir 2nd line. Mortality is high.

Question 24

West Nile virus infection

Answer 24

Majority asymptomatic. About one in five develops fever or a syndrome of fever, arthralgia, and rash (also known as West Nile fever.

Question 25

West Nile Encephalitis

Answer 25

Clinically, neuroinvasive disease is very variable in severity and can take the form of encephalitis (58 to 62%), meningitis (15 to 40%), and/or flaccid paralysis from anterior horn myelitis (about 18%).

Early encephalitis typically manifests as behavioral or personality changes. As with other flavivirus encephalitides, extrapyramidal symptoms can occur, including parkinsonism, coarse tremor, and myoclonus. Cranial nerves and bulbar abnormalities can be seen as well. Patients who go on to develop acute flaccid paralysis often complain initially of difficulty with walking or imbalance. The limb weakness can be asymmetrical in onset.

Question 26

WNV diagnosis

Answer 26

WNV-specific IgM antibody or RNA in the CSF or by a fourfold antibody titer increase from peripheral blood between the acute and the convalescent phase in the correct clinical setting. Sensitivity ~90%.