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 type II.
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 characterised 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 haemorrhagic 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 oedema or necrosis 3
- enhancement usually presents in a gyriform pattern
Affected areas, however, have a similar appearance regarding signal characteristics:
- may show general oedema in the affected region
- if complicated by subacute haemorrhage there may be areas of hyperintense signal
- hyperintensity of affected white matter and cortex, predominantly due to oedema
- 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 haemorrhagic
- 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 (aciclovir 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