Seventeen-Year-Old Female With History of Depression Presented With Mania and Enuresis.

A 17-year-old girl with a history of depression was referred by her psychologist to the emergency department (ED) because of concerning behavioral changes for the past 2 weeks. She was engaging in erratic behaviors, including excessive baking, handling broken glass, mixing chemicals, and swimming alone while clothed. She denied any intention to harm herself or others. She was feeling energized in the morning despite only sleeping a few hours at night. She also urinated on herself the day before her ED visit. Her examination and preliminary testing findings in the ED were largely normal. Her initial presentation was concerning for a psychiatric etiology, such as new-onset bipolar disorder given previous history of depression and recent impulsive symptoms suggestive of mania. As her clinical course evolved and urinary incontinence continued, her definitive diagnosis was made by an interdisciplinary team that included child psychiatry and pediatric neurology.

Pathology of layer V pyramidal neurons in the prefrontal cortex of patients with schizophrenia.

OBJECTIVE: Morphological indications of abnormal circuitry have been detected in the prefrontal neuropil of patients with schizophrenia. The authors tested the hypothesis that schizophrenia is associated with smaller dendritic field size in layer V pyramidal neurons in the prefrontal cortex. METHOD: Tissue from area 10 with a mean postmortem interval of 5.7 hours was obtained from 15 subjects with chronic schizophrenia and 18 normal comparison subjects. After Golgi impregnation, basilar dendritic field size was estimated for layer V pyramidal neurons by ring intersection analysis. RESULTS: The schizophrenia subjects had 40% fewer total ring intersections per neuron than comparison subjects. Smaller basilar dendritic field size was evident in proximal and distal branches. CONCLUSIONS: These results indicate that abnormal dendritic outgrowth or maintenance contributes to reduced neuropil and prefrontal connectivity in schizophrenia. Short postmortem intervals and resulting high tissue quality suggest that these dystrophic changes reflect schizophrenia pathology rather than postmortem artifact.

Experience effects on brain development: possible contributions to psychopathology.

Researchers and clinicians are increasingly recognizing that psychological and psychiatric disorders are often developmentally progressive, and that diagnosis often represents a point along that progression that is defined largely by our abilities to detect symptoms. As a result, strategies that guide our searches for the root causes and etiologies of these disorders are beginning to change. This review describes interactions between genetics and experience that influence the development of psychopathologies. Following a discussion of normal brain development that highlights how specific cellular processes may be targeted by genetic or environmental factors, we focus on four disorders whose origins range from genetic (fragile X syndrome) to environmental (fetal alcohol syndrome) or a mixture of both factors (depression and schizophrenia). C.H. Waddington's canalization model (slightly modified) is used as a tool to conceptualize the interactive influences of genetics and experience in the development of these psychopathologies. Although this model was originally proposed to describe the 'canalizing' role of genetics in promoting normative development, it serves here to help visualize, for example, the effects of adverse (stressful) experience in the kindling model of depression, and the multiple etiologies that may underlie the development of schizophrenia. Waddington's model is also useful in understanding the canalizing influence of experience-based therapeutic approaches, which also likely bring about 'organic' changes in the brain. Finally, in light of increased evidence for the role of experience in the development and treatment of psychopathologies, we suggest that future strategies for identifying the underlying causes of these disorders be based less on the mechanisms of action of effective pharmacological treatments, and more on increased knowledge of the brain's cellular mechanisms of plastic change.