SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
The CT and angiographic appearances in multi-infarct dementia have been compared with those of primary neuronal degeneration. It was possible to make a CT or angiographic diagnosis of multi-infarct dementia in about 40% of patients diagnosed by the ischaemic scoring method of Hachinski et al.
Ten patients with severe dementia due to Alzheimer's disease (AD) or multi-infarct dementia (MID) or both, were treated with the precursor amino acids of the neurotransmitters serotonin and dopamine. The precursor amino acids (PAA) were given orally in a preparation that included tyrosine (4 gm daily) and 5-hydroxy-tryptophan (5-HTP) (800 mg daily), plus carbidopa (100 mg daily) as an aromatic amino-acid decarboxylase inhibitor. Diagnosis was established by an electroencephalogram, brain scan, computerized axial tomographic scan, and in one case by necropsy findings. Serial clinical evaluations and measurements of neuropsychologic function were performed. Levels of homovanillic acid (HVA) and 5-hydroxyindole-acetic acid (5-HIAA) were determined before and after administration of probenecid. Side effects of the PAA therapy were diarrhea, drowsiness, nausea, vomiting and agitation, all of which were controlled by reducing the dosage. One patient with MID and one with AD+MID showed clinical and psychologic improvement, but the others did not improve. Analysis of the cerebrospinal fluid for HVA and 5-HIAA before and after the probenecid test indicated some improvement in the metabolic turnover of these acid metabolites of serotonin and dopamine after administration of their precursor amino acids.
A prominent feature in dementia is intellectual deterioration. Review of the clinical literature indicates a lack of suitably quantitated studies of specific intellectual defects in dementia. The present study investigated the performance of patients with multi-infarct dementia (MID), dementia due to Alzheimer's disease (AD), and vertebrobasilar insufficiency (VBI) with dementia using the Wechsler Adult Intelligence Scale (WAIS). Forty-two patients ranging in age from 45 to 85 years (x 66) were included. Significant differences in cognitive and intellectual performance were found between patients with dementia due to VBI and MID versus neuronal atrophy of the Alzheimer's type. The group with AD performed significantly and consistently lower on all measures. There were no significant differences between the two cerebrovascular disease groups, even though the MID group performed consistently more poorly than the VBI group. A discriminant function analysis classified 74% of the patients correctly based on the individual WAIS scores. The diagnosis was more easily made when tasks measuring visual motor coordination and abstract reasoning were included in the analysis.
Fifty-two patients presenting with dementia were divided into a group in whom clinical features suggested an ischaemic basis (multi-infarct dementia) and a group in whom a primary degenerative process seemed more likely. Focal EEG changes and angiographic evidence of ischeamic areas and atheromatous disease of intracranial vessels were more common in the "ischaemic" than in the primary degenerative group. CBF was significantly reduced in the former but the regional pattern was equally distorted in the two groups. These findings strengthen the belief that the ischaemic score can identify those patients whose dementia is associated with vascular disease.
Multivariate data analysis statistical procedures were applied to identify regional cerebral blood flow (rCBF) patterns in patients with multi-infarct dementia (M.I.D.) and Alzheimer's disease (A.D.) when compared to a control group (C.). A fronto-temporal-parietal pattern was identified for the A.D. group. The M.I.D. group demonstrated a predominant temporal parietal pattern. A discriminant function analysis classified 96% of the A.D. and C. patients correctly. One hundred per cent hit rate was obtained in discriminating between M.I.D. and C. Discrimination of A.D. and M.I.D. obtained 82% diagnostic accuracy. When the three groups were compared the hit rate was 93%. Mean rCBF and mean relative weight of the gray matter (Wg) differences were found when each dementia group was compared with C.M.I.D. and A.D. did not differ in mean rCBF but significant differences were found for Wg, with M.I.D. having greater reduction. The performance on standardized psychological tests of two independent samples of A.D. and M.I.D. were compared. The Memory Quotient from the Wechsler Memory Scale was consistently more imparied for the A.D. group. No correlation between degree of psychological impairment and rCBF or Wg reduction was found.
A consistent feature in dementia is an overall intellectual deterioration. The present study investigated the intellectual performance of patients with Alzeheimer's disease (AD) and multi-infarct dementia (MID) using the Wechsler Adult Intelligence Scale (WAIS). For reliability and generality purposes two independent samples of patients were collected. Significant differences in Education Level (EDU) and Performance IQ (PIQ) were obtained for the first sample, with the AD group having a significantly higher EDU level. The MID group obtained a higher PIQ. No significant differences were found in the second sample, but EDU level approached significance with the AD group again having a higher EDU level. A discriminant function analysis classified 81% of the patients in the first sample and 100% diagnostic accuracy was obtained for the second sample using the 11 predictor variables. A maximum R2 stepwise regression was performed in order to detect the "best" model of variables discriminating between the diagnostic groups. For the first sample the "best" model was the two variable model, including EDU and Full Scale IQ, accounting for 40% of the variance. The simplest model for the second sample was the one variable model including EDU, accounting for 20% of the variance. Quantitative differences were found between the AD samples. Time since onset of the disease was offered as a possible influence in the quantitative differences in the AD samples. Sampling biases in the behavioral study of dementia are discussed. Successful replication was obtained.
Tinofedrine, a new derivative of l-norephedrine, was examined for cerebral vasodilator activity in man. Ten patients with reduced cerebral blood flow (CBF) and multi-infarct dementia were given the drug intravenously. Cerebral blood flow increased significantly by 28% from a mean of 43.3 to 55.5 ml/100 g/min.
A family is described in which for three subsequent generations numerous individuals were affected with a progressive neuropsychiatric disease with pyramidal, bulbar and cerebellar symptoms, relapsing course and gradually evolving severe dementia. Post-mortem studies performed on three siblings afflicted with the disease suggest that the remarkably uniform macroscopic picture of the cerebral changes consisting in multiple small cystic infarctions, particularly localized to the central grey and white matter and pons as well as the cortical and central brain atrophy, is caused by an occlusive disease of small intracerebral and leptomeningeal arteries and arterioles. Collected pertinent information concerning the affected family members shows that the illness begins in early adulthood (at 29--38 years of age), affects both sexes and generally lasts for 10--15 years. The only exception so far noticed was a second generation descendant of one of the siblings. This patient died about 5 months after clinical onset of the disease in massive cerebral haemorrhage and showed similar vascular changes as the older members of the family. The disease is considered to be genetically caused and transmitted as a dominant autosomal character. For this apparently new nosological entity the eponym "hereditary multi-infarct dementia" is suggested.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The incidence of both atherosclerosis and demential increases with age and therefore the terms "cerebral atherosclerosis" or "cerebro-vascular dementia" are commonly used for any mental deterioration in elderly persons. These names depend on the proposition of a gradual narrowing of cerebral arteries as an inevitable accompaniement of ageing which ends in dementia through a progressive reduction of cerebral blood flow. This apparently reasonnable hypothesis has now been shown to be wrong. ;t has been established that first, senile dementia is not due to cerebral atherosclerosis in spite of the frequent coexistence of degenerative and vascular lesions; and secondly, true cerebro vascular dementia results from the destruction of brain tissue following cerebral infarction; hence the proper term is "multi-infarct dementia". This neuronal destruction leads to decrease in cerebral metabolism and blood flow and to intellectual deterioration. The diagnostic criteria are therefore those of cerebral infarcts i.e: arterial hypertension and/or signs of atherosclerosis, sudden onset and/or stepwise progression, and focal neurological signs. If one follow those criteria, multi-infarct dementia accounts for only about 10% of all dementias; if one does not, the diagnosis will continue to be made to the exclusion of other potentially curable causes of dementias. Five clinico-pathological forms can be distinguished according to the size, number and site of the infarcts: lacunar state, large multiple infarcts, watershed infarction, single infarct and Binswanger's encephalopathy. This distinction is always arbitrary because the association of lacunes and large infarcts is very common in multi-infarct dementia. The almost invariable failure of all therapeutic measures once multi-infarct dementia has been established stresses the importance of prevention. This depends on prevention of cerebral infarcts, i.e. on the correction of risk factors amongst which arterial hypertension is by far, the most important. Some cases benefit also from carotid surgery, anticoagulants, and antiplatelet drugs but antihypertensive drugs are the most essential part. It is very likely that if all cases of arterial hypertension are properly treated, the incidence of multi-infarct dementia will decrease greatly.
As part of an interdisciplinary study of organic dementia, a psychologic test for assessing the degree of dementia--the Extended Scale for Dementia--was developed through the expansion and rescoring of the original Mattis Dementia Scale. Statistical analyses of the 23 test items resulted in a scoring scheme which includes the "weighting" of items for scoring purposes. The test was successfully administered to 90 subjects from 6 hospitals in the London (Ontario) region. With use of the Extended Scale, it was possible to discriminate between dementia and non-dementia groups of psychogeriatric inpatients and to correlate the findings closely with those of another measure of the degree of dementia, viz, the London Psychogeriatric Rating Scale (Ment.). Dementia patients who were retested after 6-month and 12-month intervals showed a significant decline in scores. No significant scoring differences were noted between males and females or between Alzheimer dementia and multi-infarct dementia.
Senile dementia of the Alzheimer type is becoming one of the most common of the malignant diseases as our society ages. Currently, research has identified several pathophysiological changes, including the bihelical filament and the loss of the enzyme choline acetyltransferase from the cortex. Although genetic factors play some role in this disease, the important environmental risk factors have not yet been identified and there is, at present, no specific treatment. The second most common cause of dementia, cerebrovascular disease, produces dementia only when there is destruction of brain tissue, as in individuals who have multiple strokes or who have hypertensive vascular disease leading to multiple lacunae. In both multi-infarct dementia and in the lacunar state, hypertension appears to play a greater role than it does in other forms of vascular disease. Many of the other causes of dementia, including normal pressure hydrocephalus, CNS infections or tumors, metabolic disorders produced by thiamine or vitamin B12 deficiency or thyroid dysfunction, are often reversible. Every patient, whatever the age, with a developing dementia deserves a thorough workup to identify these treatable disorders.
Acetyl- and butyryl-cholinesterase activities have been measured biochemically in normal brain tissue, in senile dementia of Alzheimer type and in mental disorders without Alzheimer-type abnormalities. Acetylcholinesterase was significantly reduced and butyrylcholinesterase significantly increased, compared with the normal, in the hippocampus and temporal cortex of the Alzheimer cases. No significant enzyme changes were seen in the other diseases investigated including multi-infarct dementia, schizophrenia and depression. There was no correlation between age and acetylcholinesterase activity, but a significant positive correlation between the butyrylcholinesterase activities with increasing age (60-90 years) was found in the hippocampus. The possible connection between cholinergic system pathology and these cholinesterase abnormalities in Alzheimer dementia is discussed.
The historical events in the evolution of Alzheimer's disease are reviewed, including the initial description by Alois Alzheimer and the subsequent controversy regarding the nosological specificity of this entity. The similarity of senile dementia and Alzheimer's disease is emphasized. The basis for the modern concept of Alzheimer's disease as premature or accelerated aging is included in the review. The pathological correlates of the major categories of adult dementia have been described. The traditional criteria of neurofibrillary tangles and senile plaques have been re-evaluated using the current insight into these changes afforded by electron microscopy and biochemistry. The significance of amyloid has been described because it occurs within the senile plaque and also as the essential component of congophilic angiopathy. The new information regarding neuronal cell counts and the loss of choline acetyltransferase has been evaluated in terms of an indication of a pathogenic mechanism of Alzheimer's disease. The current understanding of normal pressure hydrocephalus, Creutzfeldt-Jakob disease, and multi-infarct dementia has been described. Brain biopsy in dementia has been described as having diagnostic, research, pathogenic, and prognostic value. The precautions involving the performance and handling of the biopsy have been stressed, particularly because these procedures involve conditions of possible slow virus etiology. The polemic for Alzheimer's disease as aging or slow virus infection has been summarized. At this time a consideration seems justified that Alzheimer's disease is an age-related, slow virus disease due to a hitherto unknown immune defect. Aging as an etiological agent must be clarified before Alzheimer's disease, in any form, can be considered to be an inevitable consequence of longevity.
The regional cerebral metabolism-to-perfusion imbalance has been studied in the three main categories of cerebrovascular disorders in a chronic phase of the disease, using the non-invasive oxygen-15 inhalation technique. In patients presenting with a history of transient ischaemic attacks, regional defects in cerebral perfusion were greater than for the corresponding oxygen uptakes. Areas of relative ischaemia within which there was an enforced increase in the oxygen extraction ratio were highlighted. The reverse pattern was observed frequently in patients with brain infarcts arising from strokes, so indicating areas of relative luxury perfusion as is inferred from the reduction in the oxygen extraction ratio. In the multi-infarct dementia group of patients, there were parallel focal reductions in both flow and metabolism. The oxygen-15 inhalation technique is shown to be a unique tool in investigating cerebrovascular disorders because of its non-invasiveness and its ability to define regional metabolism-to-perfusion imbalance within the brain.
Cerebrospinal fluid gamma-aminobutyric acid (CSF GABA) was analyzed in 151 patients who underwent evaluation for central nervous system disease. CSF GABA was not detected in 19 of these patients, who had no evidence of neurologic disease and who served as controls. GABA was most frequently detected in patients with cerebrovascular disease, and was detected only in Parkinson's syndrome of atherosclerotic origin and dementia of multi-infarct type. CSF GABA was not detected in Alzheimer's disease or Huntington's disease. Patients with grand mal seizures exhibited CSF GABA elevation within 24 hours of the ictus. In patients with multiple sclerosis GABA detection was related to the presence or exacerbation of spinal cord lesions. Further study is necessary to evaluate the significance of elevated CSF GABA in central nervous system disease.
Twenty-four patients of comparable age, blood pressure, and degree of dementia were classified by an "Ischemic Score" based on clinical features into "multi-infarct" and "primary degenerative" dementia. Regional cerebral blood flow (CBF) was measured by the intracarotid xenon 133 method. Both groups showed a decreased proportion of rapidly clearing brain tissue (largely gray matter). Cerebral blood flow per 100 gm brain per minute was normal in the primary degenerative group but low in the multi-infarct group. This suggests the blood flow is adequate for metabolic needs of the brain in patients with primary degenerative dementia but inadequate for those with multi-infarct dementia. There was no correlation between degree of dementia and CBF in the primary degenerative group but an inverse relationship existed in the multi-infarct group. Reactivity of blood vessels to reduction of arterial carbon dioxide pressure was normal in both groups.