Officially, diagnosing post-schizophrenia depression in a patient requires for the patient to be experiencing a depressive episode of either short or long term following the overcoming of schizophrenia. The patient must still demonstrate some schizophrenic symptoms but those symptoms must no longer be the focus of the illness. Typically, the depressive symptoms are not severe enough to be classified as a severe depressive episode. Formally, diagnosis entails the patient having had schizophrenia within the past year, a number of schizophrenic symptoms, and depression being present for two weeks or more. Mild schizophrenic signs may be withdrawing socially, agitation or hostility, and irregular sleep such as in the case of insomnia and hypersomnia. Causes
There is no clear cause to how certain patients with schizophrenia develop post-schizophrenic depression while others may surpass this stage. However, there are a few theories as to possible causes. Those with post-schizophrenic depression often experience social isolation due to their illness, which may increase depression levels. There is strong evidence of stigma-related isolation against those with mental illnesses in a variety of societies, especially those with schizophrenia as they are often viewed as dangerous and unpredictable. Because of this isolation and studies linking social isolation and depression, it is possible that patients under these stigmas eventually develop post-schizophrenic depression. Depression in patients with schizophrenia may also be caused by substance abuse, which is fairly common among those with schizophrenia, as depressants such as alcohol and cannabis can be relaxing.
Increases in white matter volume may be correlated to improvements of fine motor performance, auditory processing, as well as sensory information transfer between language areas of the brain. In contrast, cortical gray matter increases in early life, peaks in preadolescence, and declines through adulthood, with the exception of occipital lobe gray matter. For example, parietal lobe gray matter peaks at age 10 in girls and 12 in boys, while frontal lobe gray matter peaks at age 11 in girls and 12 in boys. Such changes might reflect overproduction of synapses in the preadolescent years; in subsequent years, there seems to be pruning dependent on environmental context, corresponding to increased synchronicity of neuron firing. A key caveat from these imaging studies, however, is that there exists significant variability in the timing and characteristics of neurological change in preadolescents. Neurological changes, particularly in the prefrontal cortex, appear to be highly dependent on environmental input. Toxins, hormones, and lifestyle factors including stress and nutrition impact neurological maturation, demonstrating the importance of early lifestyle health interventions in preadolescence with regards to neurological and psychological development.