Recent evidence favors the view of catatonia as an autonomous syndrome, frequently associated with mood disorders, but also observed in neurological, neurodevelop-mental, physical and toxic conditions. From our system...Recent evidence favors the view of catatonia as an autonomous syndrome, frequently associated with mood disorders, but also observed in neurological, neurodevelop-mental, physical and toxic conditions. From our systematic literature review, electroconvulsive therapy(ECT) results effective in all forms of catatonia, even after pharmacotherapy with benzodiazepines has failed. Response rate ranges from 80% to 100% and results superior to those of any other therapy in psychiatry. ECT should be considered first-line treatment in patients with malignant catatonia, neuroleptic malignant syndrome, delirious mania or severe catatonic excitement, and in general in all catatonic patients that are refractory or partially responsive to benzodiazepines. Early intervention with ECT is encouraged to avoid undue deterioration of the patient's medical condition. Little is known about the long-term treatment outcomes following administration of ECT for catatonia. The presence of a concomitant chronic neurologic disease or extrapyramidal deficit seems to be related to ECT non-response. On the contrary, the presence of acute, severe and psychotic mood disorder is associated with good response. Severe psychotic features in responders may be related with a prominent GABAergic mediated deficit in orbitofrontal cortex, whereas non-responders may be characterized by a prevalent dopaminergic mediated extrapyramidal deficit. These observations are consistent with the hypothesis that ECT is more effective in "top-down" variant of catatonia, in which the psychomotor syndrome may be sustained by a dysregulation of the orbitofrontal cortex, than in "bottom-up" variant, in which an extrapyramidal dysregulation may be prevalent. Future research should focus on ECT response in different subtype of catatonia and on efficacy of maintenance ECT in long-term prevention of recurrent catatonia. Further research on mechanism of action of ECT in catatonia may also contribute to the development of other brain stimulation techniques.展开更多
Recent research on autoimmune disorders suggests additional links between systemic and central nervous system(CNS)pathophysiology,among which the identification of antibody-induced limbic encephalitis provided the str...Recent research on autoimmune disorders suggests additional links between systemic and central nervous system(CNS)pathophysiology,among which the identification of antibody-induced limbic encephalitis provided the strongest evidence for the potential involvement of autoimmunity in the pathogenesis of severe mood and psychotic symptoms.In these illnesses,psychiatric symptoms predominate in the initial phase of the disorder in up to 70%of the cases,and they often lead patients to early psychiatric evaluation.For this reason,it is very important to increase the limited knowledge among psychiatrists about these autoimmune neuropsychiatric diseases,which can mimic psychiatric syndromes,in particular,those typically presented in severe mood disorders and schizophrenia.On the other hand,similarities in clinical presentation suggest that neuroinflammation and systemic immune dysregulation may play a role in the pathophysiology of severe mood and psychotic disorders.A complex interaction between periphery and immune cells of the CNS may result in cellular damage through mechanisms involving excitotoxicity,oxidative stress,and mitochondrial dysfunction.These pathways are possibly shared between comorbid medical disorders and severe mood and psychotic disorders and may reflect common underlying vulnerability.展开更多
文摘Recent evidence favors the view of catatonia as an autonomous syndrome, frequently associated with mood disorders, but also observed in neurological, neurodevelop-mental, physical and toxic conditions. From our systematic literature review, electroconvulsive therapy(ECT) results effective in all forms of catatonia, even after pharmacotherapy with benzodiazepines has failed. Response rate ranges from 80% to 100% and results superior to those of any other therapy in psychiatry. ECT should be considered first-line treatment in patients with malignant catatonia, neuroleptic malignant syndrome, delirious mania or severe catatonic excitement, and in general in all catatonic patients that are refractory or partially responsive to benzodiazepines. Early intervention with ECT is encouraged to avoid undue deterioration of the patient's medical condition. Little is known about the long-term treatment outcomes following administration of ECT for catatonia. The presence of a concomitant chronic neurologic disease or extrapyramidal deficit seems to be related to ECT non-response. On the contrary, the presence of acute, severe and psychotic mood disorder is associated with good response. Severe psychotic features in responders may be related with a prominent GABAergic mediated deficit in orbitofrontal cortex, whereas non-responders may be characterized by a prevalent dopaminergic mediated extrapyramidal deficit. These observations are consistent with the hypothesis that ECT is more effective in "top-down" variant of catatonia, in which the psychomotor syndrome may be sustained by a dysregulation of the orbitofrontal cortex, than in "bottom-up" variant, in which an extrapyramidal dysregulation may be prevalent. Future research should focus on ECT response in different subtype of catatonia and on efficacy of maintenance ECT in long-term prevention of recurrent catatonia. Further research on mechanism of action of ECT in catatonia may also contribute to the development of other brain stimulation techniques.
文摘Recent research on autoimmune disorders suggests additional links between systemic and central nervous system(CNS)pathophysiology,among which the identification of antibody-induced limbic encephalitis provided the strongest evidence for the potential involvement of autoimmunity in the pathogenesis of severe mood and psychotic symptoms.In these illnesses,psychiatric symptoms predominate in the initial phase of the disorder in up to 70%of the cases,and they often lead patients to early psychiatric evaluation.For this reason,it is very important to increase the limited knowledge among psychiatrists about these autoimmune neuropsychiatric diseases,which can mimic psychiatric syndromes,in particular,those typically presented in severe mood disorders and schizophrenia.On the other hand,similarities in clinical presentation suggest that neuroinflammation and systemic immune dysregulation may play a role in the pathophysiology of severe mood and psychotic disorders.A complex interaction between periphery and immune cells of the CNS may result in cellular damage through mechanisms involving excitotoxicity,oxidative stress,and mitochondrial dysfunction.These pathways are possibly shared between comorbid medical disorders and severe mood and psychotic disorders and may reflect common underlying vulnerability.
