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Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the period of February 1972 until February 1976, we documented six cases of influenza A-associated acute encephalopathy. The illnesses occurred during periods of influenza A activity in our community. The encephalopathy was invariably preceded by an upper respiratory tract infection, and, thereafter, patients soon became confused, vomited, and showed noticeable restlessness. Patients then followed either of two courses, some becoming comatose within 24 hours and others improving rapidly within three days or less. None of these patients exhibited the hepatic and biochemical abnormalities associated with Reye's syndrome. All patients survived but some had sequelae. The syndrome of influenza-associated acute encephalopathy deserves wider recognition.
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PMID:Influenza A virus associated with acute encephalopathy. 22 36

The phenomenon of "talking and deteriorating" after closed head injury exists in children. A variety of causes have been identified, few of which are operatively remedial. Four cases of children with head trauma are reported, in each of whom there was an interval during which the child verbalized to some degree. Rapid neurological decline then occurred approximately 30-50 h postinjury in each child, who subsequently died from their trauma. In all instances the children were injured in motor vehicle accidents or falls, had initial Glasgow Coma Scale ratings of 9 or better, and demonstrated irritability and restlessness just prior to their deterioration. In no circumstance was a space-occupying intracranial hematoma present. Post-mortem brain examinations in two of the children showed in common multiple cerebral contusions, brain edema with herniation phenomena and hypoxic-ischemic encephalopathy.
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PMID:The head-injured child who "talks and dies". A report of 4 cases. 235 10

A 43-year-old man exhibited agitation and nondirected aggression related to anoxic encephalopathy after a myocardial infarction. These symptoms abated upon treatment with amitriptyline, only to return upon its inadvertent discontinuation. The drug was well tolerated, in contrast to neuroleptics, which are frequently associated with serious side effects in this population. Although further experience is needed, amitriptyline may be an effective treatment option in agitation associated with anoxic encephalopathy.
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PMID:Amitriptyline treatment of agitation associated with anoxic encephalopathy. 236 2

The case of a patient developing hypomagnesemic encephalopathy and coma secondary to intensive treatment for severe cardiac failure, is reported. Following an early improvement of symptoms and signs of cardiac failure, a rapidly developing neurologic disorder appeared. This was characterized by insomnia, agitation, mental derangement and, finally, sopor and I-II degree coma. Serum magnesium concentration was 1.0 mEq/l. Magnesium sulfate iv infusion was followed by a immediate and complete recovery from the neurological disorder. Patients with cardiac failure undergoing prolonged intensive therapy are prone to develop hypomagnesemia. This electrolyte alteration may be responsible for symptoms and signs of central nervous system involvement (metabolic encephalopathy) that need to be differentiated from those of organic origin.
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PMID:[Hypomagnesemic coma in heart failure: description of a case]. 237 57

Six new cases of psychogenic water intoxication are discussed in the light of 150 observations published in the literature since 1935. 87% of all patients were schizophrenic, and 13% had other psychoses and a variety of functional and organic psychopathies. Psychogenic polydipsia is a prerequisite of psychogenic water intoxication. Water intake either overrides an intact osmoregulation (46% of all cases) or, allied to an inadequate urinary dilutional capacity (54%), leads to a transitory, sometimes repeated, and (in 8% of all cases) lethal water intoxication and hypoosmolality. - The consequence of hypoosmolality is metabolic encephalopathy, with agitation, convulsions and coma as its most common symptoms. Profuse diuresis, enuresis and urinary retention, gastric dilatation, watery vomiting and watery diarrhea are diagnostically helpful symptoms of polydipsia typically denied by the patients. Hypoosmolality/hyponatremia are the hallmarks of water intoxication. However, fewer than 50% of all patients present with the expected maximal urinary dilution. Inadequate ADH activity and increased sensitivity of the renal tubule to antidiuretic hormone are the pathogenetic factors in this inappropriate urinary dilution, while psychosis, psychotropic drugs, diuretics, nicotine and alcohol withdrawal are possible causes and cofactors of polydipsia and inadequate urinary dilution. New aspects of treatment are discussed.
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PMID:[Psychogenic water intoxication]. 264 58

Eighteen consecutive cases of encephalopathy occurring after ifosfamide/mesna chemotherapy were prospectively assessed. No relationship was found with tumour type or chemotherapy response. Onset was from 12 to 146 (mean 46) h after the start of the infusion and median duration was 3 days (range 1-12). In two patients recovery was incomplete. A confusional state and agitation were the major clinical features. Plasma potassium fell from a mean of 4.12 mmol/l before chemotherapy to 2.94 mmol/l at the onset of encephalopathy (P less than 0.001) with plasma potassium less than 3.0 mmol/l in 10 patients. Duration of hypokalaemia was not related to duration of encephalopathy. Median survival following encephalopathy was 25 days. The incidence of encephalopathy in 82 patients treated on two protocols was 11% and the sensitivity of a published nomogram was 18%. It is concluded that ifosfamide/mesna encephalopathy is a serious complication which may be irreversible and remains difficult to predict.
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PMID:Ifosfamide encephalopathy: a reappraisal. 280 53

Delayed neurological deterioration following anoxia is known to result from carbon monoxide exposure. However, it may also occur with anoxia of other types as well. The present report describes a case of delayed postanoxic encephalopathy with bilateral striatal lesions demonstrated by magnetic resonance imaging. A 27-year-old man exhibited anoxic anoxia caused by upper airway obstruction following general anesthesia for shoulder fracture surgery. Initially he was delirious and markedly excited for one day and became apparently normal for the following three days. Then he relapsed into delayed neurological deterioration with speech and gait disturbance, clumsiness of hand, pyramidal signs and metamorphopsia. Thereafter, he became bed-ridden and fell into semicomatose state with marked motor restlessness, involuntary movement of the tongue and decorticate posture. Twenty-five days later he had a second recovery period after hyperbaric oxygenation that lead to the sequelae with speech and motor disturbances and mild mental changes. I examined the present case as an expert witness in a civil suit eleven years after initial anoxia. The patient showed slight intellectual impairment and personality change. Impairment in figure-ground differentiation and disorders of spatial thought were also observed. Neurological examination revealed anisocoria, dysarthria with acquired stuttering, disturbances of fractionated movement of fingers, writer's cramp and Babinski's sign bilaterally. Postural dystonia of both hands and fingers, rigidity and spasticity of all extremities were also present. Magnetic resonance imaging (MRI) showed bilateral lesions of the corpus striatum, especially of the putamen. Some portion of the caudate nucleus was also involved. Cerebral cortices and white matter were slightly atrophic. From the above clinical course and neurological findings, we diagnosed the present case as delayed postanoxic encephalopathy. Ginsberg (1979) noted that in cases of anoxia not related to carbon monoxide, diffuse demyelinative changes of cerebral hemispheral white matter tended to be associated with relapsing clinical course, and gray matter injury was only seen in a few cases. MRI findings in the present case suggest that main site of the lesion to be in gray matter of the corpus striatum. In this respect, the present case is considered to be noteworthy.
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PMID:[A case of delayed postanoxic encephalopathy with bilateral lesions of the corpus striatum]. 281 6

A seventy-two-year-old man with hypertensive cerebral hemorrhage acutely developed severe headache, nausea, vomiting, agitation, and disorientation with abrupt rise in blood pressure on the sixth day after the onset. At that time, there were no remarkable changes in focal neurologic deficits, and repeated brain CT scans revealed a small hematoma located in the right basal ganglia without further enlargement or herniation. Blood chemistry and arterial gas analysis were within the normal ranges except for a slight rise in blood urea nitrogen. Similar episodes occurred three times within two days, and each time the cerebral symptoms disappeared in accordance with lowering of blood pressure by antihypertensive therapy. Complication of hypertensive encephalopathy was strongly suggested. The authors discuss the pathophysiology of this encephalopathy in relation to cerebral hemorrhage.
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PMID:Transient encephalopathy related to rapidly and markedly elevated blood pressure in acute stage of hypertensive cerebral hemorrhage--relationship to hypertensive encephalopathy--a case report. 317 64

A pilot-study to explore the efficacy of oral hydergine in seven cases of alcohol-related encephalopathy was undertaken. It showed significant improvement in symptoms of depression, plus some improvement in sleep disturbance and agitation, as measured by the Geriatric Profile (GP).
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PMID:Efficacy of oral hydergine (ergoloid mesylates) in alcohol related encephalopathy. 329 96

Twenty-five patients with various forms of dyskinesia were given tiapride for three months. Maximal dosage was 900 mg per day. A double-blind trial of tiapride versus placebo showed significantly better results in the group given tiapride. The forms of dyskinesia which responded best to tiapride were the following: iatrogenic dyskinesia, tics (Gilles de la Tourette syndrome), and chronic chorea (Huntington disease). Patients with complex dyskinesia resulting from neonatal encephalopathy or vascular disease were not improved. The protocol used in l-dopa-induced dyskinesia is described. Changes in dyskinesia and "on-off" effect following variations in tiapride and l-dopa dosage are detailed. An unequivocal, although minor, tiapride-induced parkinson syndrome was recorded in a few patients. No instances of tiapride-induced dyskinesia or akathisia were seen. The other side-effects were either psychic (depression, drowsiness, agitation) or endocrinologic (menstrual disorders, overeating, galactorrhea).
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PMID:[Clinical trial of tiapride in patients with dyskinesia (author's transl)]. 628 45


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