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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Secondary mania is increasingly recognized clinically, and consists of acute exhibition of manic symptoms without past or family history of affective disorder. It has been reported with toxic and metabolic disturbances, primary and metastatic brain tumors, epilepsy, and cerebrovascular events. A multifactorial etiology has been suggested. We report two men, 52 and 56 years old, who developed grandiosity, sleeplessness, irritable mood, hyperactivity, and paranoid and religious delusions, with attempted violence in one case. Both had no premorbid psychiatric history and were healthy except for hypertension. One patient had a normal neurologic examination, and the other had mild left hemiparesis and hyperreflexia. EEGs, brainstem auditory-evoked responses, and median nerve somatosensory-evoked potentials were normal. Magnetic resonance studies demonstrated infarction of the ventral pons (on the right in the patient with left-sided signs and on the left in the patient with normal neurologic examination). The two patients responded to lithium carbonate and neuroleptics and have not had further psychiatric symptoms in 18 months of follow-up. These cases emphasize the relationship of late-onset mania with predisposing brain disease, and they suggest that brainstem disturbances can influence mood, sleep, libido, and thought.
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PMID:Secondary mania after ventral pontine infarction. 213 93

Overdose of pentazocine (Talwin), an agonist/antagonist opioid analgesic, is relatively uncommon. Fifty-seven cases occurring over ten years are reported. Twenty-three patients (40%) had ingested only pentazocine and did not have the classic opioid toxidrome of CNS and respiratory depression with miosis. Most patients were awake, and no patient had a respiratory rate below 12/minute. Other findings included: grand mal seizures, hypertension, hypotonia, dysphoria, hallucinations, delusions, and agitation. Eleven of 23 patients received IV naloxone (0.4-2.4 mg), but only two showed improvement. Thirty-four patients (60%) had coingested pentazocine with one to five additional substances. Patients who had ingested pentazocine with alcohol, a sedative/hypnotic drug, or an antihistamine, showed increased toxicity, including apnea, deep coma, and recurrent seizures. One patient developed opioid pulmonary edema. One patient died. Three of five patients with coma and inadequate respirations responded to IV naloxone in doses of 0.4 to 1.2 mg.
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PMID:Pentazocine (Talwin) intoxication: report of 57 cases. 235 1

An autopsy case of a 65-year-old female with dentatorubropallidoluysian atrophy (DRPLA) is reported. Her mother had gait disturbance and died at the age of 63. Her mother's brother developed psychotic symptoms. A daughter of her older sister was observed to have involuntary movement when she admitted to a mental hospital due to post-delivery psychotic state. Her younger brother has developed gait disturbance from about 56-year-old. Her older son has suffered from schizophrenia for long years. Since 58-year-old, she developed cerebellar ataxic gait and three years later, choreic involuntary movement developed in her extremities and face and progressively became prominent. Since 63-year-old, abnormal behavior brought about by the visual hallucination was occasionally observed. At the age of 63, she admitted to a mental hospital because of persistent persecutive delusion for her husband and was clinically diagnosed as Huntington's chorea for her remarkable choreic movement and psychotic state with dementia. Hypertension was also noticed. At the age of 65, she died of acute pneumonia. The duration of her illness was about 6 years. Histopathological findings of the CNS: the brain weighed 1,014 g. Brainstem and spinal cord were noticed to be relatively small in size. The cerebral cortex was well preserved. The cerebral white matter was diffusely demyelinated in the central semiovale where arteriosclerotic change of the small vessels was remarkable. Significant pathological changes consisted of marked symmetrical atrophy of the following two systems, i. e., dentatofugal pallidoluysian systems.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of dentatorubropallidoluysian atrophy (DRPLA) clinically diagnosed as Huntington's chorea]. 293 81

Phencyclidine (PCP), a widely abused drug currently, has multiple pharmacological actions, including psychotomimetic [1], anesthetic [2], sympathomimetic [2], anticholinergic [3-7], and dopaminergic [8-10]. Similarly, PCP intoxication in man can present with diverse symptoms: schizophrenia-like delusions and hallucinations; mania; violence, dyskinetic, catatonic, or stereotyped movements; hypertension; and coma [11, 12]. There is general agreement that the treatment of PCP intoxication includes support of vital functions and acidification of the urine [13]. However, there is no known specific antidote for PCP toxicity. Although diazepam [13], haloperidol [14, 15], and chlorpromazine [16] have been reported to improve the agitation and psychotic symptoms caused by PCP, the therapeutic efficacy of these agents has rarely been documented with objective clinical measures. Recently we found that intramuscular physostigmine and haloperidol [17, 18] improved several symptoms of acute PCP intoxication as measured by the Brief Psychiatric Rating Scale (BPRS) [19].
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PMID:Phencyclidine intoxication: assessment of possible antidotes. 713 17

A 39-year old woman presented with hallucinatory paranoid state, particularly with erotomania, around September, 1988 (at the age of 39), and was hospitalized in a mental hospital for 9 days from May 1, 1989, to receive major tranquilizer therapy. At admission, the leukocyte count was 10,400/mm3 showing a mild leukocytosis, and there was temporary adynamia in the upper extremities. Thereafter, mild leukocytosis persisted intermittently. On May 12, 1989, the patient visited the Department of Neuropsychiatry, Kansai Medical University, and clinical examinations revealed mental symptoms including insomnia and erotomania, delusion of reference and auditory hallucination without persecutory taint. She showed clear consciousness and well understanding. Characteristically, her expression and behavior were smooth and emotional communication was available. There were neither alterations in her basic mood, nor flaccid association of idea. No abnormalities were seen in the hair and skin, and buffalo hump was not observed. Blood examination revealed a leukocyte count of 10,700/mm3, suggesting a mild leukocytosis. According to the patient, the menses have been regular. Although major tranquilizer therapy has been maintained, she gradually developed emotional instability, and tended to show fatigue and regressive changes in her personality. She was hospitalized in a mental hospital from October 25, 1989 to July 24, 1991. Since 1990, when she was in the hospital, she gradually developed obesity, hypertension, acne, and diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of Cushing's disease: hallucinatory paranoid state preceding physical symptoms]. 793 10

Despite increased interest in dementia and the concomitant creation of dementia assessment centers, there has been a paucity of reports examining racial differences in the social and clinical presentation of dementia. Such information can enhance knowledge about dementia and assist in the planning of diagnostic centers located in areas with large minority populations. This study reviewed the charts of patients evaluated at a dementia assessment center in New York City. The sample comprised 102 white and 68 black patients. There were no racial differences in types of dementia nor reported length of illness. However, bivariate analysis revealed many significant differences between the groups in social, medical, and psychiatric variables. Most notably, a stepwise discriminant analysis identified seven variables--Medicaid recipient, gender, age, sleep disturbances, delusions of stealing, hypertension, and concentration--as correctly being able to classify 75% of cases. Racial differences in cognitive and behavioral symptoms may reflect the interaction of dementia with physical health, premorbid history, environment, or some basic difference in disease course.
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PMID:Racial differences in clinical and social variables among patients evaluated in a dementia assessment center. 849 91

"Diffuse neurofibrillary tangles with calcification (DNTC)" is a slowly progressive form of presenile dementia characterized by localized temporal atrophy, pronounced calcareous deposits and numerous neurofibrillary tangles (NFTs) without senile plaques. We report a 70-year-old woman with DNTC, multiple infarctions and hyaline arteriosclerosis. This case was clinically characterized by persistent delusional ideas and personality changes. Intellectual deterioration was mild, and no focal manifestations were noted. Neuropathologically, numerous NFTs were seen distributed primarily in the hippocampal region, and massive calcareous deposits were observed in the cerebrum, basal ganglia and cerebellum. There were no senile plaques. Although the findings in this case were compatible with a diagnosis of DNTC, certain additional findings were also noted. The first was the presence of multiple infarctions in the basal ganglia and hyaline arteriosclerosis. Although these lesions may have been induced by hypertension, our review of previous reports of DNTC revealed a high incidence of arteriosclerosis. The second was the absence of lobar atrophy, which may have been due to the cerebral edema caused by the subdural hemorrhage or related to the relatively short duration of the illness. The dilatation of the temporal horn of the lateral ventricle and prominent NFTs in the hippocampal region indicate the initial occurrence of the disease in this region.
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PMID:[An autopsy case of "diffuse neurofibrillary tangles with calcification", multiple infarctions and hyaline arteriosclerosis]. 867 23

We report a 76-year-old man who developed blurred vision and dementia. He was apparently well until April 4, 1990 (70-year-old at that time) when he had a sudden onset of bilateral loss of vision. Corrected vision was 0.1 (right) and 0.09 (left). He was admitted to the ophthalmology service of our hospital on April 9, 1990, and neurological consultation was asked on April 11. Neurologic examination revealed alert and oriented man without dementia. Higher cerebral functions were intact. He had bilateral large visual field defects with loss of vision; he was only able to count the digit number with his right eye and to recognize hand movement with his left eye. Otherwise neurologic examination was unremarkable. General physical examination was also unremarkable; he had no hypertension. Cranial CT scan was normal on April 11; lumber spinal fluid contained 1 cell/microliter, 63 mg/dl of sugar, and 97 mg/dl of protein; myelin basic protein was detected, however, oligoclonal bands were absent. He was treated with methylprednisolone pulse therapy and oral steroid, however, no improvement was noted in his vision. He started to show gaze paresis to left, ideomotor apraxia, agnosia of the body, and dementia. Cranial CT scan on June 11 revealed a low density area in the deep left parietal white matter facing the trigonal area of the lateral ventricle. He was discharged on July 2, 1990. Hasegawa dementia scale was 2/32.5 upon discharge. In the subsequent course, he showed improvement in his mental capacity and Hasegawa dementia scale was 22.5/32.5 in 1991, however, no improvement was noted in his vision. In 1994, he started to show mental decline in that he became disoriented, and showed delusional ideation of self persecution and depersonalization with occasional confusional state. He also showed unsteady gait. Cranial MRI on February 13, 1996 revealed a T2-high signal intensity lesion on each side of the parietal deep white matter more on the left and another T2-high signal intensity lesion in the left pons as well as in the right thalamus. He complained of right hypochondrial pain and was admitted to another hospital on April 22, 1996. He was markedly confused and demented. He continued to show bilateral loss of vision, but no motor palsy was noted. Cranial CT scan on April 23, 1996 revealed diffuse cortical atrophy and ventricular dilatation in addition to the low density areas in both parietal deep white matter. He developed jaundice in the middle of May. Abdominal CT scan revealed multiple low-to iso-density areas in the liver and marked iso-to high-density swelling of the right kidney. The patient expired on June 9th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had had a carcinomatous limbic encephalitis with optic neuropathy and a choleduct carcinoma. Other opinions entertained included acute disseminated encephalomyelitis with optic neuritis, and granulomatous angiitis of the central nervous system. Some participants thought the primary site of the carcinoma was the right kidney with metastasis to the liver. Post mortem examination revealed a mixed type carcinoma in the right kidney with liver metastases. Neuropathologic examination revealed an incomplete softening in the optic chiasm and the left optic nerve, and in the left parieto-occipital areas. (The right hemisphere was frozen for future biochemical assay.) One of the adjacent cortical arteries had an organized thrombus. Other arteries and arterioles also showed sclerotic changes. Some of the leptomeningeal arteries were positive for Congored staining as well as for beta-amyloid immunostaining. Many senile plaques were seen diffusely in the cerebral cortex and neurofibrillary tangles were seen in the CA1 area and the parahippocampal gylus. No cellular infiltrations or demyelinated foci were seen. The neuropathologic features were consistent with circulatory disturbance based on the amyloid angiopa
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PMID:[A 76-year-old man with loss of vision and dementia]. 928 74

Delusions associated with cerebrovascular diseases have been sporadically reported. Although both psychiatrists and neurologists attempted to link delusions with anatomical locations of the brain lesion, comorbid psychiatric and neurological disorders make the interpretation of delusions difficult. The purpose of the present paper is to report the clinical features and magnetic resonance imaging (MRI) characteristics in patients with delusional disorder due to diffuse cerebrovascular diseases, and to redefine the concept of 'vascular delusion'. The clinical features and MRI findings were reviewed retrospectively in a series of seven patients with 'delusional disorder due to cerebrovascular disease' as defined in Diagnostic and Statistical Manual of Mental Disorders (DSMIV). The average age of onset is 64. No patient had a prior personal or family history of major psychiatric illness. The illness is presented as acute, subacute or stepwise course. Hypertension was present in all patients. Two had diabetes mellitus, and one had atrial fibrillation. Three had clinical evidence of previous cerebrovascular attacks, only one showed minor neurological deficits. Three had diffuse cortical slow wave in electroencephalogram. No patient had significant cognitive impairment but had multiple cortical and subcortical cerebrovascular lesions in MRI, with white-matter lesions (WML) in bilateral frontal areas. Delusional disorder due to diffuse cerebrovascular change is characterized by late-onset, stepwise course, and comorbid medical and neurological diseases. The results of vascular changes in the present study did not establish a cause-effect relationship and should be considered as multifactorial in pathogenesis. The findings suggested the hypothesis of neural circuit theory. Further studies in larger numbers of patients and newer neuroimaging techniques are needed to expand the knowledge learned from these findings.
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PMID:Magnetic resonance imaging findings in patients with delusional disorder due to diffuse cerebrovascular disease: a report of seven cases. 1128 90

A 59-year-old male who had suffered from hypertension for 21 years was admitted because of manic and delusional symptoms. He was treated with 12 mg/day of haloperidol for psychotic symptoms and 8 mg/day of nilvadipine for hypertension. Due to insufficient effect of haloperidol on the patient's manic symptoms, carbamazepine was added to these medications. Abnormally high blood pressure was observed during carbamazepine coadministration, and it returned gradually to normal range after its discontinuation. Retrospective analyses revealed that the plasma concentrations of nilvadipine were undetectable during carbamazepine treatment. The clinical course and laboratory findings suggest that carbamazepine decreased the plasma concentration and hence the antihypertensive effect of nilvadipine probably via CYP3A induction. This interaction between nilvadipine and carbamazepine should be kept in mind when these drugs are administered concomitantly.
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PMID:Carbamazepine decreases antihypertensive effect of nilvadipine. 1180 19


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