HERPES INFECTION of - medkorat.in.th virus in neulrology2.pdf · since 1960 medicine korat pawut mekawichai department of medicine maharaj nakhonratchasima hospital herpes infection

Since 1960

โรงพยาบาลมหาราชนครราชสมีา

Medicine Medicine Medicine Medicine Medicine Medicine Medicine Medicine KoratKoratKoratKoratKoratKoratKoratKorat

PAWUT MEKAWICHAI

DEPARTMENT of MEDICINE

MAHARAJ NAKHONRATCHASIMA HOSPITAL

HERPES INFECTION of

THE NERVOUS SYSTEM

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CONTENT

HERPES SIMPLEX VIRUS2

HERPES VERICELLA-ZOSTER3

NATURE of HERPES VIRUS1

Zoster and post herpetic neuralgiaZoster and post herpetic neuralgia

Herpes simplex encephalitis

Vericella

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NATURE OF HERPES VIRUS


FAMILY of HERPESVIRUS

� Herpes simplex virus type 1 (HSV-1)

� Herpes simplex virus type 2 (HSV-2)

� Varicella-Zoster virus VZV

� Cytomegalovirus (CMV)

� Ebstein-Barr virus (EBV)

� Human herpes virus type 6 (HHV-6)




HERPES VIRUS

�primary infection at epithelial surfaces

�state of latency at sensory ganglia after primary infection

�back down from ganglia to cutaneous surface

� HSV-1

- oral, eye

- latent at trigerminal ganglia

� HSV-2 genital

- genital

- latent at sacral ganglia


COMMON HERPES VIRAL INFECTION of

HSV-1

ENCEPHALITIS

MENINGITIS

MYELITIS

MENINGITIS

ENCEPHALITIS

MYELITIS

HSV-2 HVZ

MYELITIS

ENCEPHALITIS

MENINGITIS

ADEM

NERVOUS SYSTEM


HERPES SIMPLEX ENCEPHALITIS


� HSV-1 transmitted by respiratory or salivary

secretion

� spread from olfactory fiber (nose) to orbitofrontal

cortex and temporal lobe

HERPES SIMPLEX

ENCEPHALITIS (HSE)


HERPES SIMPLEX

�most common sporadic, fatal encephalitis

�reduce mortality 70% (untreated)

to 20% (treated)

�morbidity up to 70% of survivors

�HSV-1 > HSV-2 in adult

�HSV-2 in congenital/acquire neonatal

ENCEPHALITIS (HSE)


CLINICAL

CSF

BRAIN IMAGING

DIAGNOSISDIAGNOSIS

HERPES SIMPLEX

ENCEPHALITIS (HSE)


� increase pressure

� lymphocytic pleocytosis (10-1000 per mm3)

�RBC or xanthochromia may be present but

not sensitive and non specific

�moderately elevated protein

�normal glucose

CSF FINDING

HSE


�virus culture positive < 5%

�sensitivity and specificity > 95%

�false negative in first 24 hours of illness

Polymerase chain reaction (PCR)

for HSV DNA

HSE


�CT and MRI has been useful

�CT hypodensity at temporal region but 40% of

HSE normal CT

�MRI abnormal hypersignal intensity at T2W in

temporal region

�MRI is more sensitive than CT

BRAIN IMAGING

HSE

CT brian MRI brain


� abnormal in early course

� diffuse slow and focal abnormalities

in temporal region

� periodic lateralizing epileptiform discharge (PLED)

ELECTROENCEPHALOGRAM (EEG)

HSE


�mortality 70%

�most survivors severe neurological deficit

before effective antiviral treatment

after effective antiviral treatment-acyclovir

�6-months mortality 20%

�25-30% morbidity

�50% normal life

HSE

PROGONOSIS


�memory impairment

�personality, behavioral and psychiatric disorder

�anosmia

�epilepsy

�speech disorder

COMPLICATION

HSE


�delay in diagnosis and treatment

�coma before treatment

�CT abnormalities

COMPLICATION-factor

HSE


�empiric therapy with acyclovir immediately

�acyclovir 10 mg/kg q 8 hr 14-21 days or

until negative PCR (about 72 hours)

�monitor renal function and hydration

(crystal induce nephropathy)

TREATMENT

HSE


Acyclovir 10mg/kg q 8 hr

�reduce mortality from 70 to 20%

� 30% treated with acyclovir recover with mild or

no neurological impairment

�Foscarnet in acyclovir resistance strain

TREATMENT

HSE


HSV-2

�most common agent in neonatal

meningoencephalitis

�HSV-2 myelopathy rare, immunocompromise

� treated empirically with intravenous acyclovir

20 mg/kg q 8 hr 14-21 days

�risk of infection

duration of rupture membrane

severity of maternal infection

maternal immune status


CONCLUSION

�proven efficacy both experimental

and clinical trial

�administration is well-tolerate

�for adult with fever and altered

consciousness should be empirically treated

ACYCLOVIR

HSE


HERPES VERICELLA-ZOSTER


VERICELLA-ZOSTER VIRUS

�primary infection of HZV, latent at sensory ganglia

�chicken pox

�encephalitis, meningitis, myelitis in

immunocompromise host (treated by acyclovir)

�encephalitis in healthy patient (rarely)

�self-limited cerebellar ataxia

VERICELLA


�primary infection is chicken pox

�latency in sensory (dorsal root) ganglia

�secondary at age > 50 years (zoster)

�trunk 60%, head 20%, arm 15%, leg 15%


งูสวดั คอืความทรงจาํในวยัเดก็ที�ควรถูกลมืไปแล้ว แต่กลบัมาใหม่ในวยัชรา

HERPES ZOSTER


HERPES ZOSTER

� reactivation of varicella-zoster virus

� incidence increases with advancing age

� doubling in each decade past the age of 50

� uncommon in persons less than 15 years



HERPES ZOSTER

HERPES ZOSTER

COMPLICATION

CORNEAL CORNEAL

ULCERULCER

SKIN SKIN

INFECTIONINFECTIONVERTIGOVERTIGO

FACIAL WEAKNESSFACIAL WEAKNESS

ENCEPHALITISENCEPHALITIS

MYELITISMYELITIS

POST POST

HERPETIC HERPETIC

NEURALGIANEURALGIA


GOAL 1GOAL 1 GOAL 2GOAL 2 GOAL 3GOAL 3

treatment

of

infection

treatment

of

acute pain

prevention

of

PHN

GOAL for TREATMENT

HERPES ZOSTER


� about 20 % of zoster develop PHN

� the most established risk factor is age;

patients > 50 years, 15 times risk

� other possible risk factors

ophthalmic zoster

prodromal pain before lesions appear

immunocompromised state

POST HERPETIC NEURALGIA (PHN)

HERPES ZOSTER


POST HERPETIC NEURALGIA (PHN)

HERPES ZOSTER



� decrease the duration of rash and severity of pain

� benefits shown within 72 hours after onset of rash

� may be beneficial as long as new lesions are actively

� unlikely helpful after lesions have crusted

� effectiveness in preventing PHN is controversial.

ANTIVIRAL AGENT

HERPES ZOSTER

Triamquinolone Placebo > 2 Mo Yes Yes Yes

16 mg tid taper 21 d at 3 yr

Prednisolone Carbamazepine > 2 Mo Yes Yes40mg/d taper 28 d at 1 yr

Prednisolone Placebo > 6 Wk Yes No No

45 mg/d taper 21 d at 4 mo

Prednisolone Placebo Zoster Yes No No40 mg/d taper 21 d associated at 26 wk

Prednisolone Acyclovir Zoster Yes Yes No

60 mg/d taper 21 d or placebo associated at 6 mo

ACTIVE

TREATMENT

COMPARATIVE

TREATMENT

PAIN

DEFINITION

EFFICACY

REDUCED

EARLY

PAIN

REDUCED

PAIN

1 MO

REDUCED

PAIN

LAST VISIT


� Commonly used, trials shown variable results

� Prednisone with acyclovir shown reduce the pain

� If prednisone is not contraindicated, adjunctive

treatment with antiviral agent for reducing pain

� for concern about immunosuppression

may used only > 50 years

� no study about steroid with valacyclovir, famciclovir

CORTICOSTEROID

HERPES ZOSTER


TREATMENT

�Severity depend on location and immune status

�Acyclovir 800 mg 5 times/d 7-10d

�Famciclovir ( 500 mg 3 times/d 10-14d)

Decrease pain at onset, viral spreading/complication

Increase healing

NOT reduce post herpetic neuralgia (PHN)

HERPES ZOSTER


CONCLUSION

�Severity depend on location and immune status

�Acyclovir 800 mg 5 times/d 7-10d

�Famciclovir ( 500 mg 3 times/d 10-14d)

Decrease pain at onset, viral spreading/complication

Increase healing

NOT reduce post herpetic neuralgia (PHN)

HERPES ZOSTER

ACYCLOVIR

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HERPES INFECTION of - medkorat.in.th virus in neulrology2.pdf · since 1960 medicine korat pawut mekawichai department of medicine maharaj nakhonratchasima hospital herpes infection