Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Curative electroconvulsive therapy (ECT) remains a very useful treatment, still irreplaceable for some specific rare cases, as long as other brain stimulation methods, such as transcranial magnetic stimulation, remain experimental. ECT must be preceded by a rigorous evaluation of its therapeutic index, based on its advantages and risks compared with other potential treatments, in view of the patient's medical and psychiatric history. The principal indication is very severe depressive illness. In view of its efficacy and speed of action, ECT may be a first-line treatment for life-threatening depression and a second line treatment for patients with major depressive disorder who do not respond or respond incompletely to antidepressant drugs. ECT can be given to patients with catatonia, including as first-line treatment for some. ECT remains an important treatment option for depression in the elderly, especially those with depression and reversible dementia. Other indications classically considered, although for fewer patients and never as first-line treatment, are difficult-to-treat patients whose acute mania, mixed mania, schizo-affective state or schizophrenia has failed to respond to an adequate dose of psychotropic drugs and can be considered drug-refractory. It has also been used in Parkinson's psychosis and drug-resistant epilepsy. Preventive or maintenance ECT is appropriate for a few depressed patients who respond to it and it alone. It is the only effective option for these severely and recurrently depressed, medication-resistant patients. Some technical issues remain very empirical: seizure threshold determination, number of sessions, and concomitant pharmacotherapy. The practice of ECT must comply with very strict rules: information to and consent by the patient or family, performance at a hospital center by a team including a psychiatrist, anesthetist, and trained nurses.
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PMID:[Indications for electroconvulsive therapy]. 1838 9

We encountered 2 patients with a psychiatric disorder (depression in one and catatonia in one) accompanied by motor inhibition that was complicated by pulmonary embolism (PE). In both cases, the psychiatric disorder was safely resolved with electroconvulsive therapy (ECT) during anticoagulant therapy. The 2 cases direct our attention to at least 3 important points regarding safe administration of ECT shortly after the occurrence of PE, that is, careful evaluation of cardiac function and residual deep vein thrombosis before the start of an ECT course, adjustment of anticoagulants, and prevention of recurrent deep vein thrombosis and PE by methods in addition to anticoagulant therapy (fluid infusion, use of support hose, and timely ECT).
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PMID:Safety of electroconvulsive therapy in psychiatric patients shortly after the occurrence of pulmonary embolism. 1861 65

Patients with severe psychiatric and somatic disorders may require admission to a combined psychiatric-somatic care unit. These units provide specialised psychiatric and somatic care as well as palliative care. This is illustrated by two case reports. A 51-year-old man with a malignant brain tumour was admitted to our psychiatric-somatic care unit after threatening his wife and children. He was aggressive and confused. Seizures were suspected and palliative care was needed. Within a few weeks his condition deteriorated. He died 1 day after terminal sedation had been initiated. A 78-year-old woman was admitted to receive daily electroconvulsive treatment (ECT) for depression with catatonia. The ECT had to be interrupted repeatedly due to comorbid infections and complications. She died 3 days after palliative care was initiated.
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PMID:[Palliative care in a psychiatric-somatic care unit]. 1880 28

We report the successful use of electroconvulsive therapy in a 19-year-old man with autism and mild mental retardation who developed severe depression with repeated suicide attempts, multiple symptoms of catatonia, and life-threatening repetitive self-injurious behaviors. After 3 years of failed psychotropic and behavioral interventions in inpatient settings, the patient demonstrated excellent remission of symptoms with bilateral electroconvulsive therapy.
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PMID:Electroconvulsive therapy in a man with autism experiencing severe depression, catatonia, and self-injury. 1948 40

Catatonia is a motor dysregulation syndrome described by Karl Kahlbaum in 1874. He understood catatonia as a disease of its own. Others quickly recognized it among diverse disorders, but Emil Kraepelin made it a linchpin of his concept of dementia praecox. Eugen Bleuler endorsed this singular association. During the 20th century, catatonia has been considered a type of schizophrenia. In the 1970s, American authors identified catatonia in patients with mania and depression, as a toxic response, and in general medical and neurologic illnesses. It was only occasionally found in patients with schizophrenia. When looked for, catatonia is found in 10% or more of acute psychiatric admissions. It is readily diagnosable, verifiable by a lorazepam challenge test, and rapidly treatable. Even in its most lethal forms, it responds to high doses of lorazepam or to electroconvulsive therapy. These treatments are not accepted for patients with schizophrenia. Prompt recognition and treatment saves lives. It is time to place catatonia into its own home in the psychiatric classification.
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PMID:Catatonia is not schizophrenia: Kraepelin's error and the need to recognize catatonia as an independent syndrome in medical nomenclature. 1996 91

Catatonia is the psychiatric syndrome of disturbed motor functions amid disturbances in mood and thought first described in 1874. It was quickly found in 10% to 38% of psychiatric populations. After it was tied to schizophrenia as a type in the psychiatric classification, its recognition became increasingly limited and by the 1980s questions were asked as to where the catatonics had gone. The decline is largely owing to the change in venue for psychiatric practice from asylum to office, the rejection of physical examination, and the dependence on item rating scales for diagnosis. In the 1970s, broad surveys again showed that catatonia was as common as before among patients with mania and depression, and as a toxic response to neuroleptic drugs. The latter recognition, that the neuroleptic malignant syndrome is the same syndrome as malignant catatonia, and is effectively treated as such, sparked a renewed interest. Clinicians developed rating scales to identify the catatonia syndrome and applied the immediate relief afforded by a barbiturate or a benzodiazepine as a diagnostic test, the lorazepam test. Effective treatments were described as high doses of benzodiazepines and electroconvulsive therapy (ECT). Surveys using catatonia rating scales showed catatonia to have many faces. Catatonia is presently limited to a type of schizophrenia in the psychiatric classification. Its recognition as a disorder of its own, such as delirium and dementia, should now be recognized. This experience reinforced the utility of the medical model for diagnosis. An application for melancholia is described.
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PMID:Catatonia: a syndrome appears, disappears, and is rediscovered. 1966 Jan 65

Multiple sclerosis can create a variety of somatic, cognitive, and behavioral symptoms. Here we report a patient with early psychiatric symptoms including depression, dementia, and catatonia, who was eventually diagnosed as having primary progressive multiple sclerosis.
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PMID:Early psychiatric manifestation in a patient with primary progressive multiple sclerosis. 1987 55

The incidence of pressure ulcers in patients with psychiatric illness, especially with catatonia might be more than what is reported in the literature. We report a case of catatonia secondary to severe depression presenting with multiple pressure ulcers. Single case report - description and management. An 18 yrs old boy reported with a continuous course illness characterized by features of catatonia secondary to severe depression with multiple pressure ulcers over sacrum and heels. Ulcers were effectively managed by a multidisciplinary team of physiatrist, psychiatrist, and rehabilitation nurses. Immobility, reduced nocturnal movements, increased skin fragility, and poor nutrition contribute to the development of the pressure ulcer in bed-bound psychiatric patients. Efforts should be directed toward the prevention of pressure ulcers in these patients to reduce additional morbidity.
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PMID:Catatonia and multiple pressure ulcers: A rare complication in psychiatric setting. 1988 Oct 50

In this review, the symptoms contributing to the opioid-induced 'catatonia' are presented in detail, and efforts are made to relate these symptoms to opioid-induced alterations in neurotransmitter metabolism in several parts of brain, in particular in the basal ganglia. One important symptom is the muscular rigidity, which is, at least to a great part, mediated by opioid receptors in the striatum. This effect is probably not due to an action on opioid receptors located on endings of nigro-striatal dopaminergic neurones (localization I in Fig. 2), but on receptors located on neurones, the cell bodies of which are within the striatum (localization II) or much less likely on receptors on endings of glutamergic, cortico-striatal neurones (localization IV). Another characteristic symptom, the akinesia, can be induced by injections into the nucleus accumbens, which do not lead to any significant muscular rigidity. Accordingly, opioid-induced muscular rigidity and akinesia can be dissociated topographically, and it is shown by this observation that the opioid-induced 'catatonia' is due to an interference of at least two different signs. 'Catalepsy', on the other hand, is probably the consequence of a very pronounced akinesia, and spontaneously occurring rigidity does not seem to contribute to it. In addition, opioids can induce-after low doses immediately, after high doses subsequently to the depressory phase-signs of behavioural stimulation (locomotor stimulation, some stereotypic behaviour), which seem to be antagonistic to the 'catatonia' from the functional standpoint. Several types of behavioural stimulation seem to exist, with different localizations. An activation of nigro-striatal and mesolimbic dopaminergic neurones seems to be of particular relevance in the behavioural stimulation, which is due to actions of opioids on receptors located within the substantia nigra (on endings of afferent neurones, localization III in Fig. 2) and/or within the ventral tegmentum. Part of this dopaminergic activation might be, in addition, due to actions on opioid receptors located on dopaminergic nerve endings within the striatum (localization I) or the nucleus accumbens. A hypothesis for the biphasic action of opioids (first behavioural depression, then activation is presented, involving a lower sensitivity (eg affinity) of those receptors mediating 'catatonia'. Finally, it is discussed that a detailed study of opioid action on basal ganglia might perhaps give relevant information about some pathophysiological mechanisms in schizophrenic diseases, in Parkinson's disease and in psychic dependence on opioids.
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PMID:Neurochemical aspects of the opioid-induced 'catatonia'. 2048 69

Pernicious anaemia can present with psychiatric symptoms before haematological or neurological manifestations appear. We describe a young woman who presented with insidious onset catatonia without evidence of psychosis or depression. Blood count and mean cell volume were normal and neurological findings were equivocal. Low B(12) levels and intrinsic factor antibodies were found only by chance when they were included in a battery of further investigations. B(12) replacement was followed by prompt improvement. This case provides an argument for wider screening for B(12) deficiency in certain individuals with psychiatric disorders.
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PMID:Pernicious anaemia presenting as catatonia without signs of anaemia or macrocytosis. 2080 71


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