The Neurology of Psychosis

Abstract

The neural basis of psychosis is yet to be fully elucidated. In this review the contribution of schizophrenia-like psychosis of epilepsy, delusional misidentification syndromes and psychotic phenomena, such as auditory and visual hallucinations, to our understanding of the neural basis of psychosis is examined. Schizophrenia-like psychosis of epilepsy is associated with seizures originating from the limbic structures. Reduced seizure frequency, left-sided electrical foci, and neurodevelopmental lesions manifesting as cortical dysgenesis are known to influence the likelihood of developing schizophrenia-like psychosis of epilepsy. The delusional misidentification syndromes are a group of rare psychiatric symptoms in which impairments of face recognition memory are present. These conditions appear also to be associated with organic lesions affecting limbic structures and also involving both the frontal and parietal lobes. There is evidence that right-sided lesions predominate in the aetiology of delusional misidentification syndromes. Thus, the common link between schizophrenia, schizophrenia-like psychosis of epilepsy and delusional misidentification syndromes appears to be involvement of limbic structures in their pathophysiology. Discrete psychotic phenomena such as visual and auditory hallucinations appear to arise from functional changes in the same cortical areas subserving the normal physiological functions of vision and audition but also involving limbic structures. In conclusion, the limbic structures appear to be central to the psychopathology of psychosis but with involvement of frontal and parietal structures. These inquiries are revealing as much about psychosis as they are about the nature of normal brain function.

The functional anatomy and connectivity of thought insertion and alien control of movement

“…In the case of alien control of movement, an executive control interpretation would entail that a lack of sensory suppression associated with increased cerebellar-parietal activations may underlie an altered sensory quality of unexpected movements, rather than the loss of the sense of their control and ownership per se. An executive control model is also relevant to understanding similarities and differences between thought insertion and auditory verbal hallucinations (AVH), which are both first rank symptoms of schizophrenia but which also occur in the general population (Linden et al, 2010;Oyebode, 2008;Van Os, Linscott, Myin-Germeys, Delespaul, & Krabbendam, 2009). Auditory verbal hallucinations occur when a patient reports hearing a voice or voices when no such sound is present, whereas during thought insertion the patient "believes that thoughts that are not his own have been inserted into his mind" (Mullins & Spence, 2003).…”

Delusional Misidentification Syndromes and Dementia

“…Neuropsychological, cognitive, and neuroanatomic findings converge and support the hypothesis that DSM symptoms are produced at least in part by a damaged or disfunctional brain, predominantly in the right hemisphere so that DSM appear as neuropsychiatric encompasses symptoms that lie in the gray zone between neurology and psychiatry. 26 Oyebode 69 described a common link between schizophrenia, schizophrenia-like psychosis of epilepsy, and DMS; it appears to be the involvement of limbic structures in their pathophysiology.…”

Acute Psychosis in Two Patients with Bartter Syndrome

“…Each associated receptor is expressed in multiple brain tissues, including the limbic, frontal, and parietal systems (Allen Institute for Brain Science 2014). Psychosis is a neuropsychological phenomena tied to these brain structures (Oyebode 2008), and abnormal neuronal ion transport (Seeman et al 2006). In our patients, chronic electrolyte disturbances may underlie shared pathophysiologic mechanisms between these conditions.…”