Some patients with TLE have greater preoccupation with existential aspects of religion.3,10,34 Other epilepsies and OCD Frontal lobe epilepsy (FLE) is another likely candidate

as a fellow traveler with OCD, possibly because of the executive and behavioral functions subserved by this part of the brain. From a neurobiological perspective, dysfunction in this region affects part of the frontal-cingulate-thalamic-limbic circuit, and hence might favor the functional dysregulation of this circuit, thus inducing elements of OCD.16,18,28 Another candidate is limbic epilepsy, Inhibitors,research,lifescience,medical with its unusual automatisms which may simulate the ritualistic behavior of OCS. Patients may display repetitive Inhibitors,research,lifescience,medical movements and types of automatic behavior. Other rarer conditions may buy Rigosertib possess both epilepsy and rituals or at least repetitive behaviors as clinical expressions of a particular disease. Examples include the handwringing seen with Rett Syndrome, and other behavioral features noted with Angelman syndrome and autism spectrum disorder. Neurobiology of the association between epilepsy and OCD There has been an increasing effort to formulate

a neurobiological underpinning to OCD. Various theories have been advanced, Inhibitors,research,lifescience,medical and have been supported by the findings of OCD triggered by a number of neurological conditions. These include head trauma, brain tumors, cerebral infarction, and seizures. Modell and colleagues suggest that there are two principal loops or circuits underlying control of the behaviors involved

Inhibitors,research,lifescience,medical in OCD.34 They are comprised of a thalamo-orbitofrontal connection mediated by glutamate, and a collateral loop that includes striatal-orbitofrontal-thalamic interconnections mediated additionally by serotonin, dopamine, and gammaaminobutyric acid (GAB A). The Inhibitors,research,lifescience,medical latter loop controls the activity in the thalamo-orbitofrontal circuit. Normally, orbitofrontal cortex activates the caudate and then the pallidum so as to inhibit the medial thalamic nucleus that then feeds into the frontal cortex. In this manner, medial thalamic inputs would regulate hyperactivity of the orbitofrontal thalamic relays. Dysfunction of these circuits might produce OCD, with increased activity inducing obsessive not characteristics and compulsive traits.34 However, complicating this paradigm is the paradoxical clinical resolution in some cases of established OCD by the new appearance of one of strokes, tumors, or by deep brain stimulation.35,36 Nonetheless, such serendipitous associations have spawned a neurobiological underpinning for OCD that includes the malfunctioning of various brain circuits. Abnormally functioning circuits include the thalamus, basal ganglia, anterior cingulate gyrus, and the orbito-frontal cortex.37,38 It has been postulated that there is an abnormality in the circuit linking frontal regions to the basal ganglia.