The Secondary Schizophrenias

A New Perspective on Delusional States – Evidence for Claustrum Involvement

“…Insufficient inhibition of PFC pyramidal cells has been suggested as a pathway for excessive release of glutamate in the ventral tegmental area (VTA), leading to excess dopamine release in nucleus accumbens ( 88 ). Mesolimbic dopamine hyperactivity is implicated in delusions ( 89 – 91 ), as evidenced by the observation that phencyclidine and ketamine, both of which are known to cause delusions ( 92 ), affect glutamatergic neurotransmission in PV-IN of the PFC ( 93 , 94 ). The glutamate model is further supported by the nearly uniform co-occurrence of delusions with NHALE ( 95 ), an encephalitis characterized by the presence of anti-glutamate (NMDA) receptor antibodies in the blood and/or the cerebrospinal fluid, and in which delusions are present in 90% of diagnosed patients.…”

Chromosome 8p as a potential hub for developmental neuropsychiatric disorders: implications for schizophrenia, autism and cancer

“…68 Furthermore, the occurrence of schizophrenia-like symptoms and secondary affective symptoms has been shown in patients with epilepsy. 69 Even more interestingly, a family history of epilepsy is a significant risk factor for schizophrenia. 70 Aberrations in the short arm of chromosome 8 may also be a relatively common cause of corpus callosum malformations.…”

First Episode of Psychosis in a Middle-Aged Patient with a 14-Year History of Conversion Disorder

“…The patients' symptoms cannot be attributed to B 12 deficiency. Such deficiency has been reported to induce mental symptoms but psychosis is unusual [ 19 ], and in this case deficiency was rather slight (132 pg/mL). Another laboratory finding, revealed by the MRI scan of the brain, was the cerebral atrophy which was incompatible with patient's age.…”