Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Advanced chronic hepatic disease was observed in 5 dogs that had received anticonvulsant drug therapy for 2 to 3 years. Clinical signs included anorexia, weakness, and restlessness, and 2 dogs also had ascites. There were remarkable increases in the serum activities of alanine aminotransferase, alkaline phosphatase, and gamma-glutamyl transferase. The total serum bile acid concentration was high in 3 of 4 dogs that were tested. Sulfobromophthalein excretion was delayed in all dogs. Histologic examination of liver specimens from 4 of the dogs demonstrated macronodular or micronodular cirrhosis.
 ...
PMID:Hepatic cirrhosis associated with long-term anticonvulsant drug therapy in dogs. 711 8

The withdrawal of heterocyclic antidepressants and antipsychotic agents can produce nausea, emesis, anorexia, diarrhoea, rhinorrhoea, diaphoresis, myalgias, paraesthesias, anxiety, agitation, restlessness and insomnia. The withdrawal of monoamine oxidase (MAO) inhibitors may result in severe anxiety, agitation, pressured speech, sleeplessness or drowsiness, hallucinations, cognitive impairment, delirium, suicidality and delusions of persecution. The withdrawal of antipsychotic agents may give rise to symptoms preceding the onset of psychosis. These potential harbingers of relapse include anxiety, agitation, restlessness and insomnia. The withdrawal phenomena reviewed are usually prevented by gradually reducing the total daily dosage of the pertinent drug. Antimuscarinic agents often alleviate the distress produced by the withdrawal of tricyclic antidepressants and antipsychotic agents. MAO inhibitor withdrawal syndromes may constitute medical emergencies. The prevention of the evolution of a MAO inhibitor withdrawal-precipitated syndrome is a high priority.
 ...
PMID:Withdrawal phenomena associated with antidepressant and antipsychotic agents. 791 78

Similar clinical and biological features in lethal catatonia (LC) and neuroleptic malignant syndrome (NMS) suggest a relationship between both affections and common physiopathologic mechanisms. Pharmacological effects of several drugs--dopaminergic agonists, benzodiazepines, carbamazepine--suggest an impairment of several systems of neurotransmitters. We report the case of a young woman with infantile psychosis who developed catatonic syndrome worsened by neuroleptic treatment, arising the problem of the chronology of both affections. The evolution with treatment may partially explain the physiopathology. A 18-year old woman with an history of infantile psychosis, experienced insomnia, anorexia, paradoxical agitation developed after affective traumatism (mother's hospitalization). Chlorazepate (150 mg) remained inefficient and hospitalization was necessary. The patient was dumb, prostate in bed. She presented negativism, rigidity of the four limbs, catalepsia and hyperpyrexia (38.5 degrees C). Hepatic transaminases were increased (SGOT: 71 UI/l; N < 30). After cumulated dose of levomepromazine (100 mg) profuse sudation, thermic and cardiovascular instability, alteration of consciousness, major rigidity of limbs appeared. (Blood) hepatic transaminases and muscular enzymes increased. Bacteriological samples, cerebrospinal fluid analysis, CT-scan and EEG were normal. Within 48 hours after rehydratation and bromocriptine (30 mg per day) alteration of consciousness and autonomic disorders decreased but hyperpyrexia (38 degrees C) persisted. Biological parameters were normalized 10 days later. Negativism and psychomotor inertia remained. Lorazepam (3 mg per day) failed to be clinically beneficial. On carbamazepine (600 mg per day) she started speaking and moving spontaneously. Catalepsia disappeared but rigidity and anorexia persisted. Electroconvulsivotherapy (ECT) was necessary. After 2 shocks she started standing up, walking, taking food and speaking fluently.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Acute catatonia and neuroleptic malignant syndrome. A case of infantile psychosis]. 791 82

Ornithine transcarbamylase deficiency (OTCD) is caused by an alteration of urea synthesis, linked with partial modification of the X-chromosome, whose clinical manifestations are: lethargy, nausea, vomiting and cerebral edema. While in newborn males OTCD presents with hyperammoniemia leading to cerebral palsy with profound neurological impairment and eventually death, in women who are healthy carriers, it is possible to detect the disorder only through specific tests, since heterozygote women are rarely symptomatic. We describe the case of a young woman admitted to the hospital after an episode of mental confusion with vomiting and psychomotor restlessness, which had previously occurred several times during the premenstruum and lasted a few hours. A 2 day history of stupor made admission mandatory. Tests carried out during the hospital stay showed marked hyperammoniemia and unconjugated hyperbilirubinemia, marked cerebral edema documented by a CT scan. Liver biopsy and CSF test were normal. Screening of plasma and urinary aminoacids, level of orotic acid in the urine and OTC activity in the liver, confirmed the diagnosis of OTCD. The possibility of early diagnosis and therapy of a disease which otherwise leads to death, emphasizes the importance of precise evaluation of a possible organic cause of anorexia and behaviour disorders in young women.
 ...
PMID:Hyperammoniemic coma in an adolescent girl: an unusual case of ornithine transcarbamylase deficiency. 828 23

Primary adrenal insufficiency (PAI) is a relatively rare but serious condition that can lead to signs and symptoms ranging from mild generalized weakness and fatigue to fulminant shock and death. We present the case of a previously healthy 31-year-old man who developed PAI while undergoing rehabilitation after a severe traumatic brain injury (TBI). The patient suffered a TBI with comminuted skull fractures, bifrontal confusions, and bilateral epidural hematomas in a jet-ski accident. Acute hospitalization was prolonged by several medical complications, and the patient was admitted for subacute rehabilitation 1 month after his injury with cognitive deficits, persistent agitation, confusion, generalized weakness, and poor endurance for therapy. His weakness, fatigue, and orthostasis did not improve with attempts at gradual remobilization. The patient also had persistent anorexia, nausea, and hyponatremia despite various treatment regimens. Endocrinology workup showed normal anterior pituitary function but an abnormal response to adrenocorticotropic hormone (ACTH) stimulation, leading to the diagnosis of PAI. The patient was treated with prednisone and fludrocortisone, which resulted in improvement in clinical symptoms followed by rapid gains in all functional areas. No previous descriptions of PAI following head injury were found in the medical literature. It is important for physiatrists to be aware of this entity because symptoms of adrenal insufficiency can be similar to those commonly seen with TBI alone. PAI may also be confused with other endocrine disorders more frequently seen after TBI such as the syndrome of inappropriate antidiuretic hormone secretion. Recognition and appropriate management of adrenal insufficiency can lead to significant clinical and functional gains.
 ...
PMID:Primary adrenal insufficiency following traumatic brain injury: a case report and review of the literature. 908 56

Nefazodone hydrochloride is a phenylpiperazine antidepressant with a mechanism of action that is distinct from those of other currently available drugs. It potently and selectively blocks postsynaptic serotonin (5-hydroxytryptamine; 5-HT) 5-HT2A receptors and moderately inhibits serotonin and noradrenaline (norepinephrine) reuptake. In short term clinical trials of 6 or 8 weeks' duration, nefazodone produced clinical improvements that were significantly greater than those with placebo and similar to those achieved with imipramine, and the selective serotonin reuptake inhibitors (SSRIs) fluoxetine, paroxetine and sertraline. The optimum therapeutic dosage of nefazodone appears to be between 300 and 600 mg/day. Limited long term data suggest that nefazodone is effective in preventing relapse of depression in patients treated for up to 1 year. Analyses of pooled clinical trial results indicate that nefazodone and imipramine produces similar and significant improvements on anxiety- and agitation-related rating scales compared with placebo in patients with major depression. Short term tolerability data indicate that nefazodone has a lower incidence of adverse anticholinergic, antihistaminergic and adrenergic effects than imipramine. Compared with SSRIs, nefazodone causes fewer activating symptoms, adverse gastrointestinal effects (nausea, diarrhoea, anorexia) and adverse effects on sexual function, but is associated with more dizziness, dry mouth, constipation, visual disturbances and confusion. Available data also suggest that nefazodone is not associated with abnormal weight gain, seizures, priapism or significant sleep disruption, and appears to be relatively safe in overdosage. Nefazodone inhibits the cytochrome P450 3A4 isoenzyme and thus has the potential to interact with a number of drugs. Further long term and comparative studies will provide a more accurate assessment of the relative place of nefazodone in the management of major depression. Nonetheless, available data suggest that nefazodone is a worthwhile treatment alternative to tricyclic antidepressants and SSRIs in patients with major depression.
 ...
PMID:Nefazodone. A review of its pharmacology and clinical efficacy in the management of major depression. 921 Oct 88

Prader-Willi syndrome is caused by a deletion of 15q11-13 or maternal disomy of chromosome 15. A female patient with Prader-Willi syndrome, who was 19 years of age at the first onset of her recurrent brief episodes, is described. The episodes showed a near-monthly rhythm and were followed by a spontaneous remission in 7-18 days. The symptoms during the episodes were anorexia, insomnia, guilt feelings, ideas of being doomed, ostracized and persecuted, and stupor alternating with agitation.
 ...
PMID:Recurrent brief depression in Prader-Willi syndrome: a case report. 926 38

Dexamethasone was administered orally for 7.5 or 9.5 days to 80 pregnant bitches to terminate unwanted pregnancy at an outpatient clinic. Treatment was initiated at day 30-35 (n = 74) or day 45-50 (n = 6) of confirmed pregnancy using one of two dosages. In 62 bitches, dexamethasone was administered twice a day for 7.5 days increasing from 0.1 to 0.2 mg kg-1 over the first 2 days of administration and decreasing from 0.16 to 0.02 mg kg-1 over the last five administrations. The 18 remaining bitches were given dexamethasone twice a day for 9.5 days, at a dosage of 0.2 mg kg-1 for 7 days and then decreasing from 0.16 to 0.02 mg kg-1 over the last five administrations. Pregnancy was terminated without complication in 75 of the 80 bitches, and uterine contents were absorbed or aborted or both. Pregnancy was not terminated in five bitches treated for 7.5 days beginning at day 30-35 of gestation. In four of them parturition occurred at the normal time; in one, pregnancy was terminated by a second treatment. Pregnancy termination occurred at 7-15 days after the start of treatment. During ultrasonographic imaging of 13 bitches treated with dexamethasone, fetal deaths occurred between 5 and 13 days after the start of treatment. The side effects reported by the owners included polydipsia and polyuria, which were observed in all of the bitches and which disappeared when the treatment was discontinued. Some bitches also experienced vaginal discharge, restlessness, anorexia or emesis. At the first or second cycle after treatment, 20 bitches were mated and had normal pregnancies and normal litters. The results suggest that oral treatment with dexamethasone can be used to terminate pregnancy in bitches, but that in some cases the withdrawal of treatment after 8 days can result in retention of live pups and require a further treatment or the use of another abortifacient.
 ...
PMID:Clinical use of dexamethasone for termination of unwanted pregnancy in dogs. 940 90

Myoporum laetum was collected in the municipalities of Rio Grande and Capao do Leao in winter and in Santa Vitoria in summer, autumn, winter and spring, in the state of Rio Grande do Sul, Brazil, and in the Department of Rocha, Uruguay, in winter and spring. The fresh green plant was fed to 17 sheep. All sheep developed clinical signs, except 1 that consumed only 4 g/kg bw daily during 10 d. Five of the 9 sheep dosed with 40 g/kg died. Four sheep dosed with plants from Uruguay at 40 g/kg, 6 sheep dosed with 20 g/kg, and 1 sheep dosed with 2 daily doses of 8 g/kg survived. Clinical signs were anorexia, restlessness, ruminal stasis, jaundice and dry feces with mucus or blood. All surviving sheep had photodermatitis in the face, ears, eyes and lips. Histologic lesions were characterized by periportal liver necrosis. Serum levels of AST, GGT and bilirubin were increased. M laetum from Uruguay was less toxic, suggesting a variation in toxicity among plants from different regions.
 ...
PMID:Experimental intoxication by Myoporum laetum in sheep. 961 Apr 88

The authors prospectively assessed symptoms induced by the interruption of antidepressants in 16 patients (11 women and 5 men), aged from 33 to 85 years (mean = 52.4 +/- 16.4), treated with antidepressants since at least two weeks. All patients were free of alcohol abuse or dependence disorder and of other dependence to psychoactive substances. None of them presented medical illness. Diagnosis were made by separate evaluations by two authors and confirmed with a semistructered assessment instrument: the Schedule for Affective Disorders and Schizophrenia (Lifetime Version). All patients were submitted to a brutal discontinuation of their antidepressant agent. Patients were assessed twice, before the interruption of the antidepressant, and 72 hours later. Effects of antidepressant interruption were assessed by several means. Modification of anxiety and depression were evaluated using the Montgomery Asberg Depression Rating Scale (MADRS) and the Hamilton Anxiety Scale. Symptoms of withdrawal were assessed with Cassano and al.'s scale SESSH including an evaluation of anxiety, agitation, irritability, anergy, difficulty on concentrating, depersonalization, sleep and appetite disorders, muscle pains, nausea, tremor, sweating, altered taste, hyperosmia, paresthesias, photophobia, motor incoordination, dizziness, hyperacousia pain, delirium. Fourteen of the 16 patients (87.5%) presented modifications of their somatic or psychic state 3 days after the interruption of the antidepressant treatment. Most frequent symptoms were: increase in anxiety (31%), increase in irritability (25%), sleep disorders (19%), decrease of anergia and fatigue (19%). Mean scores of anxiety and depression were not significantly modified by the withdrawal. Following TCAs interruption (7 patients) most frequent symptoms were sleep disorders; increase in anxiety, nausea. Among patients withdrawn from SSRIs (6 patients), most frequent symptoms were increase in anxiety, increase in irritability, headache. Patients also presented a decrease of nausea, and of anorexia.
 ...
PMID:[Prospective evaluation of antidepressant discontinuation]. 969 14


<< Previous 1 2 3 4 5 6 7 8 9 Next >>