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

The author reports on 86 cases of protracted disorders - without significant changed consciousness - which he named dysthymia. The clinical manifestations were characterized by peculiar emotional disorders, polymorphous autonomic and vascular shifts. These states occurred in the majority of cases after some somatic diseases in conjunction with other physical or psychological stresses in individuals with anxiety traits and 'neurocirculatory asthenia'. The first phase of the disease was accompanied by anxiety, restlessness, autonomic and vascular paroxysms, anorexia, insomnia and disturbances of other physiological functions. Subsequently dysphoric mood, somatic concerns, pseudoneurotic and neurotic syndromes appeared. The outcome of the disorders was either with slow practical recovery or with a relatively stable personality change in the form of weakened volition, a reduction of energy, and a narrowing of the 'zone of comfort' due to the impairment of homeostatic functions. Often hypochondriasis could develop on the background of such features. Dysthymia is viewed as a special entity which must not be included either in the group of neuroses or in the group of typical organic brain syndromes, or in the group of endogenous psychoses.
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PMID:Dysthymia: an atypical protracted depression. A preliminary report. 105 93

Some studies suggest that abnormal behaviors are associated with increasing cognitive loss in Alzheimer's disease (AD). Other studies do not show this association. We examined the relation of cognitive loss, represented by Folstein Mini-Mental State Examination (MMSE) score, with abnormal behaviors in 680 patients with probable AD. Six behaviors were examined: agitation/anger, personality change, wandering, hallucinations/delusions, insomnia, and depression. All but depression were associated with declining MMSE score. The number of abnormal behaviors present in each patient was also related to declining MMSE score. Several other associations were also found: hallucinations/delusions were associated with age and race; agitation/anger was related to male gender; and wandering was associated with increased age. Although these data support the general notion that five of the six abnormal behaviors studied are more likely to occur with increasing cognitive loss, the correlations are small and it is suggested that other as yet unproven factors may play an as large or greater role than MMSE score in predicting such behaviors.
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PMID:Relation of cognitive status and abnormal behaviors in Alzheimer's disease. 220 14

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

Baclofen is widely used in the treatment of spasticity of spinal origin. It is relatively free of side effects or toxic actions on the nervous system or other organs. Agitation, personality change, and auditory and visual hallucinations have been described following its abrupt withdrawal. One patient with generalized seizures and one with complex partial seizures after baclofen withdrawal have been reported. This paper presents a patient who developed status epilepticus after baclofen withdrawal, and who sustained hypoxic cerebral injury. This observation further emphasizes the possibility of infrequent complications of baclofen therapy, and the advisability of gradual changes in baclofen dosage.
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PMID:Status epilepticus after baclofen withdrawal. 673 10

Dementia is a complex syndrome associated with cognitive impairment, personality change, and behavioral disturbance. Behavioral symptoms frequently present the greatest challenge for caregivers and are often the determining factor in institutional placement. Determining the need for pharmacologic treatment of an agitated patient requires considering the full range of biopsychosocial variables and ultimately involves assessing the risks and benefits of the medications selected for the patient. In this article, the phenomenology of agitation is reviewed along with the pharmacologic treatment of agitation in patients with dementia, including the use of benzodiazepines, neuroleptics, beta-adrenergic-blocking agents, serotonergic agents, carbamazepine, and lithium.
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PMID:Pharmacologic approach to management of agitation associated with dementia. 791 10

We present the clinical, molecular genetic and neuropathological findings of an 81-year-old man with concurrent Huntington's disease (HD) and familial amyotrophic lateral sclerosis (FALS). His mother had been diagnosed clinically as having ALS. There was no known family history of HD, but a maternal uncle had died in a chronic care psychiatric hospital. The diagnosis of HD in the patient was suspected at age 66, after 8 years of personality change, hallucinations, agitation, cognitive decline and choreoathetosis. No symptoms of motor neuron disease were noticed at that time, but progressive weakness developed later. Postmortem examination revealed cerebral atrophy, marked atrophy of basal ganglia (grade 3), and atrophy of brain stem and spinal cord. The neostriatum displayed massive neuronal loss and gliosis. The neocortex showed changes characteristic of Alzheimer's disease. Pathological lesions also included loss of neurons and gliosis in the anterior horns, Clarke's columns and the hypoglossal nuclei; degeneration of the lateral corticospinal tracts, dorsal spinocerebellar tracts and fasciculus gracilis; and rare Bunina bodies and ubiquitin-positive filamentous skeins in motor-neuron perikarya. Molecular analysis demonstrated chromosome 4p16.3 expansion of trinucleotide repeats characteristic of HD. Analysis of Cu,Zn superoxide dismutase gene and heavy neurofilament subunit gene failed to demonstrate mutations. The concurrence of HD and FALS in our patient and three previously reported cases did not appear to be associated with cosegregation in other family members.
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PMID:Coexistence of Huntington's disease and familial amyotrophic lateral sclerosis: case presentation. 889 Oct 76

Interferon-alpha (IFN-alpha) is of high interest in the adjuvant treatment of malignant melanoma. During long term treatment, psychiatric side effects play an important role and not infrequently lead to reduction or discontinuation of therapy. Most common are sleeping disturbance, agitation, weariness, sleepiness, irritability, social withdrawal and depression, which most often develop during the first three months of the therapy. Also more severe side effects may occur, like delirium, organic depression, psychotic episodes and organic personality change, which in some patients may even lead to suicidal thoughts or suicide attempts, which is illustrated in two case reports. Therapeutic intervention depend to the severity of side effects. Moderate depressive syndromes may successfully be treated by antidepressive drugs like serotonin reuptake inhibitors (SSRI), which may even allow continuation of IFN-alpha therapy. In patients with severe depression or organic personality changes with increased risk of suicide, immideate discontinuation of IFN-alpha therapy is mandatory and treatment in a psychiatric hospital must be considered.
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PMID:[Psychiatric side effects during adjuvant therapy with interferon-alphain patients with malignant melanoma. Clinical evaluation as well as diagnostic and therapeutic possibilities]. 1050 82

An autopsy case with clinically and molecular genetically diagnosed Huntington's disease (HD) accompanied with minimal non-specific neuropathological features was reported. When the patient was 45 years old, he had faulty memory, mood swing, personality change and agitation. Neurological and psychiatric examinations revealed choreoathetoid movements in limbs and trunk, generalized hyperreflexia and mental deterioration. However, cerebellar ataxia and muscle rigidity were not disclosed. Neuroimaging study did not show a definite atrophy of heads of caudate nuclei. Neuroacanthocytosis and Wilson's disease were ruled out by the peripheral blood examination and serum Cu and ceruloplasmin examination. At the age of 55 he died of pneumonia. Post-mortem examination revealed minimal non-specific neuropathological features for HD (Vonsattel's grade 0), that is, no visible fibrillary gliosis in the striatum, and few neuronal loss and only proliferation of astrocytes (astrocytosis) in the striatum. Molecular-genetic study the patient's brain tissues and his youngest son's blood was performed. These studies revealed 40 CAG repeats in the patient, 56 CAG repeats in his youngest son. These results suggest they may be HD. Vonsattel et al. [ 1998] insist that grade 0 comprises 1% of all HD brains, and grade 1 comprises 4% of all HD brains. But we could not find any reports in which the clinical and neuropathological features were described in detail on the cases with clinically and molecular genetically diagnosed HD without specific pathological findings. Therefore, we present in detail the clinical and neuropathological features of such case.
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PMID:An autopsy case with clinically and molecular genetically diagnosed Huntington's disease with only minimal non-specific neuropathological findings. 1074 90

The aim of this study was to determine the prevalence of psychiatric symptoms among nondemented individuals with memory changes and whether such symptoms predict progression of functional decline or diagnosis of Alzheimer disease (AD). A semi-structured interview was administered at baseline to controls (n = 32) and to nondemented subjects with memory changes (n = 112) and to each subject's collateral source. The interview assessed the impact of cognition on functional abilities in daily life and a variety of psychiatric symptoms, including symptoms of psychosis, depression, and personality change. Participants were followed annually for 3 years to determine who had progressive functional decline and who progressed to meet clinical criteria for AD. Those diagnosed with AD on follow-up had more symptoms of personality change, such as agitation and passivity, at baseline than those who did not progress to meet clinical criteria for AD. Mild depressive symptoms were also more common among individuals at baseline who subsequently 'converted' to AD. Symptoms of personality change were associated with a more rapid increase in functional difficulty over time, whereas depressive symptoms were not. Changes in personality are more common among subjects with memory changes who go on to develop AD. Particular types of personality change, such as agitation and passivity, are related to progression of functional difficulty over time. Depressive symptoms, although common in prodromal AD, are not associated with a more rapid functional decline.
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PMID:Psychiatric symptomatology and prodromal Alzheimer's disease. 1262 14

Hepatic encephalopathy represents a reversible decrease in neurological function caused by liver disease. Overall incidence of seizures in hepatic encephalopathy varies between 2% and 33%. Non-convulsive status epilepticus may be particularly common in these patients. Psychiatric disturbances manifest as agitation, personality change, delusions, etc. Aims of seizure management include treatment of basic disease, correction of precipitant factors, imaging of head, and choice of a pharmacologically safe agent. It is important to consider non-convulsive status epilepticus and rule it out by an EEG. Absolute data for safety profile of drugs in liver disease is still not clear, as changes of pharmacokinetics make choice of drugs difficult. Free drug concentrations may be higher, making plasma concentration monitoring essential in such circumstances. A single seizure may not require therapy. However when started, antiepileptic drugs are usually discontinued early. Drugs with sedative effects are best avoided because of a risk of precipitating coma. Phenytoin and gabapentin are relatively preferred drugs; however, monitoring of drug levels is desirable. Management of agitation includes physical restraint and medication. Benzodiazepines are best avoided. Haloperidol is a safer choice in the presence of liver disease. Overall management of neuropsychiatric state aims at management of underlying pathology, the resolution of which leads to improvement in the clinical symptomatology.
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PMID:Management of agitation and convulsions in hepatic encephalopathy. 1502 57


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