Epilepsy and schizophrenia: a neurochemical bridge

This paper reviews some of the evidence in the literature that suggests neurochemical processes by which the regulation of seizure threshold and the onset of schizophrenic-like symptoms are interrelated. For those patients who experience the alternation of seizures and acute psychoses the following working hypothesis is presented: The central dopaminergic synapse is described as a malfunctioning regulatory circuit. Insufficient feedback inhibition or lifting of the setpoint leads to an increased number of occupied receptors. This might cause schizophrenic-like symptoms. Insufficient release of feedback control or lowering of the setpoint leads to a decreased number of occupied receptors. This might increase seizure susceptibility. The neurochemical arguments in support of this hypothesis will be discussed in detail. The localization of the dopaminergic synapses involved in the development of schizophrenic-like symptoms is subject to speculation. The meso-limbic dopaminergic system has to be taken into consideration.