Neonatal herpes simplex encephalitis
Neonatal herpes simplex encephalitis is caused by vertical transmission of infection during passage from birth canal with diffuse cerebral involvement within the first month after birth; in contrast to adult herpes simplex encephalitis, it is commonly related to HSV-2.
The incidence of neonatal HSV infection at all is usually low and it varies by country. About 80% of cases are due to HSV-2.
There are three types of clinical manifestations related to this infection 2:
- skin lesions without any visceral or central nervous system (CNS) involvement, also known as skin, eye and mouth disease
- CNS disease (with or without skin lesions, but without involvement of visceral organs); usually this presentation has non-specific signs including decreased level of consciousness, seizures, lethargy and fever
- disseminated form characterized as a sepsis with multi-organ failure
Newborn babies are initially asymptomatic for one or two weeks.
The diagnosis is confirmed by detection of HSV DNA in the cerebrospinal fluid.
It is important to appreciate that the radiographic appearance of neonatal HSV encephalitis is different from its more common adult counterpart. Changes are typically diffuse which can be difficult to identify due to normal immature myelin (see normal myelination) and more commonly involving the cerebral cortex, the deep white matter, and thalamus 4. The medial temporal and inferior frontal lobes may be spared and hemorrhagic change is uncommon but can develop later and is best seen on gradient echo/susceptibility sequences 1.
As a sequel, areas of leukomalacia, diffuse multicystic encephalomalacia, and parenchymal punctate or gyral calcifications may be seen 3.
- may be negative in the early course of the disease
- in advanced stages may present with extensive areas of parenchymal hypoattenuation, predominantly in the white matter, as a result of edema or necrosis 3
- enhancement usually presents in a gyriform pattern
Affected areas, however, have a similar appearance regarding signal characteristics:
- may show general edema in the affected region
- if complicated by subacute hemorrhage there may be areas of hyperintense signal
- hyperintensity of affected white matter and cortex, predominantly due to edema
- as previously discussed, the incomplete white matter myelination in the neonate's brain and its high water content may mask subtle signal changes
- GE/SWI: may demonstrate blooming if hemorrhagic
- T1 C+ (Gd): enhancement usually presents in a gyriform pattern
Treatment and prognosis
Neonatal herpes simplex encephalitis is highly lethal (in about 50% of cases) and can cause permanent disability if left untreated 2.
Treatment is with intravenous antivirals (acyclovir is usually the drug of choice).
Sequelae are mostly seen in neurodevelopment, including deafness, vision loss, cerebral palsy, and seizure.
- 1. Leonard JR, Moran CJ, Cross DT et-al. MR imaging of herpes simplex type 1 encephalitis in infants and young children: a separate pattern of findings. AJR Am J Roentgenol. 2000;174 (6): 1651-5. AJR Am J Roentgenol (full text) - Pubmed citation
- 2. Wolfert SI, de Jong EP, Vossen AC et-al. Diagnostic and therapeutic management for suspected neonatal herpes simplex virus infection. J. Clin. Virol. 2011;51 (1): 8-11. doi:10.1016/j.jcv.2011.02.008 - Pubmed citation
- 3. Vossough A, Zimmerman RA, Bilaniuk LT et-al. Imaging findings of neonatal herpes simplex virus type 2 encephalitis. Neuroradiology. 2008;50 (4): 355-66. doi:10.1007/s00234-007-0349-3 - Pubmed citation
- 4. Maller VV, Bathla G, Moritani T, Helton KJ. Imaging in viral infections of the central nervous system: can images speak for an acutely ill brain?. Emergency radiology. 24 (3): 287-300. doi:10.1007/s10140-016-1463-5 - Pubmed
Related Radiopaedia articles
Infections of the central nervous system
- classification by etiology
- Eastern equine encephalitis
- enterovirus rhombencephalitis
- flavivirus encephalitis
herpes virus family
- herpes simplex virus 1 (HSV-1) encephalitis
- herpes simplex virus 2 (HSV-2) encephalitis
- varicella zoster virus (VZV) encephalitis
- Epstein-Barr virus (EBV) encephalitis
- cytomegalovirus (CMV) encephalitis
- human herpesvirus 6 (HHV-6) encephalitis
- HIV CNS manifestations
- HTLV-1-associated myelopathy
- JC virus
- measles encephalitis
- Nipah virus (NiV) encephalitis
- rabies encephalitis
- CNS listeriosis (Listeria monocytogenes)
- CNS nocardiosis (Nocardia spp)
- CNS tuberculosis (Mycobacterium tuberculosis)
- Lyme disease (Borrelia burgdorferi)
- neurobrucellosis (Brucella sp.)
- neurosyphilis (Treponema pallidum)
- Rocky Mountain spotted fever (Rickettsia rickettsii)
- cerebral amoebiasis
- cerebral malaria (Plasmodium falciparum)
- cerebral sparganosis (Spirometra mansonoides)
- neurocysticercosis (Taenia solium)
- neurohydatidosis (Echinococcus spp)
- neurotoxoplasmosis (Toxoplasma gondii)
- Creutzfeldt-Jakob disease (sporadic, variant, familial, and iatrogenic)
- fatal familial insomnia
- Gerstmann-Straussler-Scheinker disease
- variably protease sensitive prionopathy
- others or those with possible infectious etiologies
- classification by location
- classification by etiology