Launching November 2016, the Reference Module combines thousands of encyclopedic and comprehensive articles into one interdisciplinary resource that is continuously reviewed and updated, essential in the rapidly evolving fields of Neuroscience and Biobehavioral Psychology. The following is an exclusive preview excerpt taken from the forthcoming Reference Module in Neuroscience and Biobehavioral Psychology.

About 5% of patients with an infection of the central nervous system will experience a seizure. A seizure may be the presenting symptom, or only one manifestation, of the infection. Common infections of the central nervous system that may present with seizures include: herpes simplex, cytomegalovirus, arbovirus, human immunodeficiency virus, neurocysticercosis, malaria, toxoplasmosis, bacterial meningitis and brain abscess. The seizures may be due to direct invasion of brain tissue by the infecting organism, production of toxins by the organism or production of inflammatory mediators by the brain. Infectious processes in the brain can lead to breakdown of the blood–brain barrier and brain edema. Severe systemic infections can also be associated with seizures, even if the infection is not present in the central nervous system. In this instance the seizures are most likely due to hypoxia or other severe metabolic changes, such as hyponatremia, that are the result of the overwhelming infection. In all cases, treatment for the seizures associated with infection usually involves treatment of the underlying infection.

Bacterial infections in the central nervous system are less likely to cause seizures than viral infections. However, generalized convulsions may occur with bacterial meningitis. Compared to other bacteria, infections with Haemophilus influenzae are more commonly associated with seizures. The mechanism of the seizures is not known. As with other infectious processes, it has been postulated that the seizures are either a result of the primary infection or due to the inflammatory response to the bacterial infection. To date there is not much data for either possibility.

Encephalitis due to a viral infection of the brain can be associated with both focal and generalized seizures. Viral encephalitis is characterized by neuronal and glial degeneration, inflammatory infiltrate, edema, and tissue necrosis. Herpes simplex virus is the most common pathogen associated with seizures in cases of viral encephalitis. But, seizures occur in approximately 85% of children infected with Japanese encephalitis and up to 10% of adults with West Nile virus. Equine encephalitis, St. Louis encephalitis, cytomegalovirus and rabies have also been reported to cause seizures. Finally, it has been estimated that 2–5% of HIV-infected patients have seizures due to the primary infection of the brain by the virus.

The issues surrounding the relationship between herpes virus infections of the central nervous system and seizures is a bit more complicated. Infection with herpes virus, particularly herpesvirus 6B (HHV-6B) is quite common. Recently, it has been questioned whether the association between acute infection with HHV-6B and seizures in infants less that 1 month old is a causal relationship. It could be that the infection is causing the seizures, but it is also possible that infants susceptible to the infection are those most likely to have seizures. The evidence is not clear one way or the other. Herpesviruses can also result in a latent or persistent infection. This persistent infection has been implicated in febrile seizures and some forms of epilepsy – in the absence of symptomatic encephalitis.

HHV-6B has been found in resected tissue from a substantial proportion of patients with temporal lobe epilepsy. The virus is found in astrocytes in this tissue. The current hypothesis is that the presence of the virus is a result of an early infection and its continued presence somehow lowers the seizure threshold or likelihood of developing epilepsy. Herpes is easily reactivated, particularly

by other viral infections. It is possible that reactivation of the virus results in a series of consequences that result in a lowering of the seizure threshold. One hypothesis is that reactivation of HHV-6 alters gene expression in astrocytes, which in turn alters glutamate pathways. Thus the seizures could be due to an action of the reactivated virus or a secondary action initiated by the presence of the virus in the latent form. There is not enough data to state definitively one way or the other.

Other infections that involve the central nervous system have been reported to cause seizures. Neurocysticercosis, infection of the central nervous system with the cyst form of tapeworms, is the most common parasitic infection of the brain. In developing countries, up to 50% of adult-onset epilepsy is due to neurocysticercosis. Malaria is estimated to spread into the central nervous system in approximately one third of the cases and cerebral malaria can present with seizures. The incidence of acute seizures in neurosyphilis is 14–60%. Infectious diseases in which seizures have been reported, but are not typically the presenting feature, include: rubeola, schistosomiasis, trichinosis, paragonimiasis, echinococcosis, trypanosomiasis, typhus and amebiasis.

In summary, infections of the central nervous system are clearly associated with seizures, either during the acute infection or as a delayed response. The mechanism underlying these seizures are not understood and are most likely dependent on the infectious agent and time course of the infection. In addition, inflammatory processes in the brain have been implicated in a number of cases and could be the underlying cause of seizures in some, if not all, infections.

This exclusive preview  excerpt was taken from the forthcoming Reference Module in Neuroscience and Biobehavioral Psychology. Launching November 2016, the Reference Module combines thousands of encyclopedic and comprehensive articles into one interdisciplinary resource that is continuously reviewed and updated, essential in the rapidly evolving fields of Neuroscience and Biobehavioral Psychology. The article this excerpt was taken from is an updated article, the previous article was reviewed and deemed out of date and therefore was updated to be included in the new Reference Module. Articles within the Reference Module are on a review cycle to keep them up to date. Learn more here.