The biochemical processes involved in depression go beyond serotonin, norepinephrine, and dopamine. The N-methyl-D-aspartate (NMDA) receptor has a major role in the neurophysiology of depression. Ketamine, one of the prototypical NMDA antagonists, works rapidly in controlling depressive symptoms, including acutely suicidal behavior, by just a single injection. Ketamine may rapidly increase the glutamate levels and lead to structural neuronal changes. Increased neuronal dendritic growth may contribute to synaptogenesis and an increase in brain-derived neurotrophic factor (BDNF). Activation of the mechanistic target of rapamycin (mTOR), as well as increased levels of BDNF, may increase long-term potentiation and result in an improvement in the symptoms of depression. The mechanisms of ketamine’s proposed effect as an off-label treatment for resistant depression are outlined in this paper.
Schizophrenia is serious illness with high comorbidity of other psychiatric illnesses such as substance abuse disorders, depression and anxiety disorder. The dual diagnosis of schizophrenia and anorexia nervosa in an adolescent male is a rare occurrence and is understudied. The case presented is of a 12-year-old boy with complaints of auditory hallucinations, odd behaviors, paranoid delusions and suicidal attempt along with body image distortion, dread of fatness, food restriction and very low Body mass Index. This case report, describe the comorbidity of schizophrenia and anorexia nervosa by highlighting its assessment and treatment in light of available literature.
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