Do You Know of Cases of Wernicke’s Aphasia Post Herpes Simplex Viral Encephalitis?

This editorial is a request for clinician researchers to report on speech recovery in cases of Wernicke’s Aphasia post Herpes Simplex Viral Encephalitis. The literature, while it contains detailed case histories of Wernicke’s cases post stroke, does not contain extensive material on speech recovery post encephalitis. A case report is now in progress, but there is little current and detailed literature in which to compare the clients progress. What is clear in the literature is the etiology of the disorder Herpes Simplex Virus Type 1 (HSV-1), along with HSV-2, are neurotropic members of the Herpesviridae family. HSV-1 most commonly causes cold sores but can also lead to genital herpes infections, while HSV-2 predominately causes genital herpes. Transmission occurs via mucosal surfaces including the oral and respiratory surfaces or through compromised skin, such as by sharing drinking vessels or utensils, kissing, and other high-risk skin-to-skin contact. HSV-1 is usually contracted during infancy or childhood through exposure to an infected adult. Transmission does not require an active infection or visible sores and can be spread through asymptomatic viral shedding [1,2]. There is a high seroprevalence in the general population, with an estimated 70~90% of asymptomatic individuals harboring the HSV-1 [3,4]. There is currently no cure for HSV but symptoms can be managed with antiviral medications [5]. Exactly how HSV-1 infiltrates the central nervous system to cause to HSE is greatly debated, with the olfactory bulb and trigeminal ganglia implicated in mice models [6]. The olfactory pathway is the most likely avenue of infection, as recurrent herpes labialis, which occurs in the trigeminal ganglia, rarely leads to HSE [7]. HSE normally affects the temporal lobe, which is responsible for retention of visual memory, language comprehension, processing of sensory input, and emotion. Therefore, symptoms of HSE include aphasia, confusion, and behavioral changes there can also be extratemporal involvement, including the frontal and parietal lobes, with an estimated 16% of patients with HSE having extratemporal infections [8]. This localization of infection is thought to be caused by the proximity of the temporal lobe to the olfactory bulb or trigeminal nerve [9] or preference of HSV for limbic cortices. Briefly, HSV-1 causes degeneration of cell nuclei and loss of plasma membranes, leading to multi-nucleated giant cells. This in turn causes inflammation, hemorrhaging, and eventual tissue necrosis and liquefaction [10].