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)

Extrapyramidal symptoms cause much misery, often go undiagnosed, and can interfere with treatment and rehabilitation. Akinesia is a behavioral state of diminished motoric and psychic spontaneity that is difficult to distinguish from the negative symptoms of schizophrenia. The most useful clinical correlates of akinesia are a subjective sense of sedation and excessive sleeping. Akinesia interferes with social adjustment and may manifest as "postpsychotic depression." The subjective restlessness of akathisia is usually accompanied by telltale foot movements: rocking from foot to foot while standing or walking on the spot. Akathisia is strongly associated with depression and dysphoric responses to neuroleptics and has even been linked to suicidal and homicidal behavior in extreme cases.
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PMID:Behavioral toxicity of antipsychotic drugs. 288 52

A complete, unselected series of 68 patients who were seen during their first episode of an undoubtedly schizophrenic illness, and followed up one year later (for 56 patients) is described clinically. Depressive symptoms were common at onset, and 22% of patients could have been considered cases of depression from these symptoms alone. At follow-up, depressive symptoms had reduced in prevalence and only 7% of subjects were depressed cases. Only two cases of depression at follow-up had not been cases at onset. These changes could not be attributed to the use of antidepressants or ECT. Depressive syndromes could be distinguished from akinesia and the negative syndromes. The findings indicate that depression cannot be attributed solely to the administration of neuroleptics.
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PMID:Depressive syndromes in the year following onset of a first schizophrenic illness*. 290 85

The novel antidepressant moclobemide is a reversible inhibitor of monoamine oxidase (MAO), preferentially of type A. Moclomide was active in three animal models considered predictive for antidepressant activity: 1) it prevented dose-dependently akinesia and blepharospasm induced in mice and rats by Ro 4-1284, a short-acting amine releasing agent. Prevention of akinesia by moclobemide also depended upon the dose of Ro 4-1284. For comparison also, effects of cimoxatone, harmaline, tranylcypromine and clorgyline are presented: 2) in cats, it selectively and dose-dependently suppressed rapid eye movement sleep without disturbing the sleep-wakefulness cycle; and 3) in the behavioral despair test in mice, it decreased the immobility score to a similar degree as amitriptyline or imipramine. In addition, moclobemide potentiated 5-hydroxytryptophan-induced stereotypies in rats with a potency similar to cimoxatone and with a duration of action of less than 24 hr. Moclobemide had almost no effect on the spontaneous behavior in mice, rats, cats and monkeys. Only in higher doses, marginal sedation and slight impairment in motor performance were seen. Moclobemide did not prevent pilcarpine-induced salivation in mice, demonstrating the absence of anticholinergic activity. Blood pressure and heart rate of freely moving, spontaneously hypertensive rats were only slightly decreased for less than 3 hr. Moclobemide moderately potentiated the pressor effect of p.o. tyramine in rats. In conclusion, the reversible MAO inhibitor moclobemide is active in animal models sensitive to all major drugs used in the treatment of depression. In contrast to imipramine-like antidepressants, it lacks anticholinergic activity and it differs from classic MAO inhibitors by potentiating only weakly the pressor effect of p.o. tyramine.
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PMID:Pharmacological profile of moclobemide, a short-acting and reversible inhibitor of monoamine oxidase type A. 291 84

An examination was made of the effect of REM sleep deprivation (REMSD) on some forms of altered motor activity, such as akinesia and catalepsy, induced by intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) administration of morphine in adult, male Wistar rats. Administration of morphine (25 mg/kg i.p.) induced an akinetic-cataleptic syndrome and decreased spontaneous vertical motor activity (SVMA) in animals allowed undisturbed sleep. REMSD decreased the morphine-induced akinesia and catalepsy that are known to be mediated by an inhibitory mu-opiate system. The locomotor depressant action of morphine was converted to excitation (manifested as increased SVMA and hopping behavior) by REMSD. Similarly, decreased motor activity following i.c.v. administration of morphine (25 micrograms) was replaced by excitation in the form of jumping behavior after REMSD. Naltrexone (1 mg/kg i.p.) blocked the akinetic and cataleptic effects, but not the excitatory effects, of morphine. It is suggested that REMSD is associated with a functional insufficiency of an inhibitory mu-opiate system, thus unmasking the excitatory morphine effects. The proposed insufficiency of an endogenous opioid system might explain an increase in neuronal excitation during REMSD and the therapeutic effect of REM deficiency in some types of depression.
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PMID:REM sleep deprivation antagonizes morphine-induced akinesia and catalepsy. 302 Jun 74

Alfentanil, a short-acting and powerful analgesic, when injected peripherally to rats (0.5 mg/kg) produced a catatonic state characterized by a rigid akinesia. The present study was designed to explore the neuroanatomical location of the opiate receptors mediating the alfentanil induced catatonia. The catatonic effect of alfentanil was measured using a bar test and depression of locomotor activity in rats tested in photocell cages during an active nocturnal phase of their cycle. Methylnaloxonium HCl (MN), a quaternary derivative of naloxone which does not readily cross the blood-brain barrier, injected into the lateral ventricle significantly reduced the catatonia at doses of 0.125-2.0 micrograms as measured in both the locomotor and bar test. MN perfusion of similar doses directly into the nucleus raphe pontis, but not in the caudate nucleus significantly antagonized the catatonia. These data complement results on alfentanil-induced muscular rigidity (Blasco et al., see companion paper) where EMG indices of rigidity in rats were reversed by microinjections of low doses of MN (0.125 and 0.5 microgram) in the nucleus raphe pontis, but not the caudate nucleus even at a high dose (4.0 micrograms). Together these results suggest that the region of the nucleus raphe pontis is an important neural substrate for opiate-induced muscular rigidity, and that the catatonic state produced by opiates depends on more diffuse opiate receptor activation of which one important component may be the nucleus raphe pontis.
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PMID:'Catatonia' produced by alfentanil is reversed by methylnaloxonium microinjections into the brain. 302 82

To quantify the clinical benefit of an additional deprenyl administration in L-dopa pretreated patients we have performed a study of 30 patients suffering from advanced parkinsonism. During the first phase of the study over three months under controlled conditions deprenyl showed in a cross-over design a similar therapeutic potential as the control-substance methixene, but it was markedly better tolerated. The therapeutic effect persisted over a follow-up observation period of 1 year with only a slight tendency to deterioration. There was no marked positive influence on fluctuations, only end-of-dose akinesia improved slightly. The substance was well tolerated by the patients, the frequency of side effects was less than under methixene. In contrast to the good clinical improvement there was only a slight reduction in depression score. Thus the therapeutic effect seems not only to be mediated by a nonspecific antidepressant effect. The most remarkable advantage of deprenyl compared to other substances in adjuvant therapy of advanced parkinsonism is probably the reduction of serious side effects.
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PMID:Therapeutic efficacy of R-(-)-deprenyl as adjuvant therapy in advanced parkinsonism. 312

Increasingly longer balloon inflation times during coronary angioplasty can create significant left ventricular ischemia, amelioration of which was attempted in this study using nitroglycerin. Hemodynamic variables were assessed during inflation of an angioplasty balloon in the proximal left anterior descending coronary artery of 10 patients. Regional wall motion was assessed by left ventriculography during a separate balloon inflation. Nitroglycerin (200 micrograms) was then administered intravenously, and hemodynamic and ventriculographic assessments during balloon inflations were repeated. Balloon inflation resulted in a marked increase in left ventricular end-diastolic pressure (from 9.2 +/- 2.1 to 19.4 +/- 2.9 mm Hg) and time constant of left ventricular relaxation (from 44.2 +/- 6.2 to 62.3 +/- 11.3 ms) and a decrease in distal coronary artery perfusion pressure (from 54 +/- 9 to 33.1 +/- 4 mm Hg). Time to onset of angina was 29 +/- 3 seconds and time to ST segment depression of 1 mm or greater was 30 +/- 3 seconds. Regional wall motion analysis 30 seconds after onset of balloon inflation revealed marked hypokinesia and akinesia in the anteroapical segments with graduated depression of inferior wall motion, greatest at the apex. After the administration of nitroglycerin, balloon inflation resulted in a smaller increase in end-diastolic pressure (from 5.0 +/- 2.7 to 8.3 +/- 2.6 mm Hg) and time constant (from 47.9 +/- 4.7 to 54.4 +/- 9.2 ms; both p less than 0.01 versus standard balloon inflation). Distal coronary artery pressure remained similar to standard balloon inflation (32 +/- 3 mm Hg) despite lower mean arterial pressure (89 +/- 5 mm Hg, p less than or equal to 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amelioration by nitroglycerin of left ventricular ischemia induced by percutaneous transluminal coronary angioplasty: assessment by hemodynamic variables and left ventriculography. 316 Jul 55

Apathy, mood depression and extrapyramidal signs consisting of akinesia, amimia, gait apraxia, slight rigidity and tremor were induced in 10 patients by long-term treatment with flunarizine for trivial complaints. These symptoms suggest a mild antidopaminergic activity of flunarizine. Long-term administration of flunarizine should be avoided particularly in the elderly and in patients with extrapyramidal disorders.
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PMID:Extrapyramidal syndrome and depression induced by flunarizine. 341 89

Mean-age of onset of Parkinson's disease is 56 years. The older the patient is the more rapid is on average the progression of disability. In the early phase the motor symptoms respond well to therapy. Later, variations of response to therapy and side-effects of therapy occur (wearing-off, end-of-dose akinesia, end-of-dose dystonia, dopaminergic abnormal involuntary movements, pharmacogenic psychoses etc.). Due to the modern pharmacologic treatment of Parkinson's disease with dopaminergic substances disabling stages of the disease occur mean 3 to 5 years later than before levodopa-substitution was initiated. The incidence of depression, distinct cognitive deficits (impairment of memory, visuospatial deficits) and dementia increases in the course of the disease. The tremulous form of Parkinson's disease generally leads to less motor impairment than the rigid-akinetic form. Parkinson's disease of early onset (onset before the age of 40), may be regarded as a subtype of Parkinson's disease. Benign and malignant types of Parkinson's disease may be distinguished, as well as overlaps with multisystem atrophies.
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PMID:Nosography of Parkinson's disease. 346 66

The development over the last 60 years of the concept of bradyphrenia, a syndrome including slowing of cognitive processing in parkinsonism, is described. Psychic akinesia and subcortical dementia are seen as more recent synonyms for this syndrome. Its relations to akinesia and the psychomotor retardation of depression are considered in a historical context, as are its implications for the relation of neurological and psychiatric disorder.
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PMID:Bradyphrenia in parkinsonism: a historical review. 352 69


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