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Biomedical subjects

V Hachinski

Publications and source records attributed to V Hachinski.

141 records · Page 8Linked to original sources
PubMed1978

Cerebrospinal fluid homovanillic acid in cerebral infarction.

Cerebrospinal fluid (CSF) homovanillic acid (HVA) concentration was measured in 39 consecutive cases of hemispheric infarction, 7 cases of brainstem infarction, and in 16 controls. The CSF-HVA level was 38 +/- 15 ng/ml (mean +/- S.D.) in the control patients, 15 +/- 6 ng/ml in patients with brainstem infarcts, and 49 +/- 41 ng/ml in those with hemispheric infarcts. The CSF-HVA levels were decreased in brainstem infarct cases (p less than 0.001) and greatly scattered in patients with hemispheric infarcts (range 4--207 ng/ml) when compared to controls. The decrease of levels of CSF-HVA in brainstem infarct cases may reflect interference with the dopaminergic pathways. CSF-HVA values in hemispheric infarction could not be related to the acuteness, location, nor severity of the lesion. The broad range of CSF-HVA values may be due to the interaction of multiple, as yet unknown factors. These findings suggest that dopamine metabolism is altered in many cases with acute brain infarction.

Adolescent↗
PubMed1977

Symptomatic intracranial steal.

The phenomenon of shunting of blood in association with various intracranial lesions is well known; however, usually clinical symptoms are attributable to the lesion and not to the redistribution of regional cerebral blood flow (rCBF). We report three patients investigated by angiography and rCBF studies in whom symptoms appeared to be due to a hemodynamic steal within one cerebral hemisphere, between hemispheres, and from the brain into a tumor, respectively.

Adult↗
PubMedDate not supplied

Clinical and pathologic features of two groups of patients with dementia with Lewy bodies: effect of coexisting Alzheimer-type lesion load.

The objectives of this study were to examine the clinical and pathologic features of two subgroups of patients with dementia with Lewy bodies (DLB) differing in Alzheimer disease (AD)-type pathology load and to identify clinical variables useful in the differential diagnosis from AD. The records of 64 consecutive demented patients were reviewed. Pathologic diagnoses were independently established [35 AD cases, 11 cases of pure dementia with Lewy bodies (pDLB), and 18 cases of combined AD plus Lewy bodies (AD+LB)], and several neurodegenerative lesions were quantified. Clinical and pathologic data were compared between groups with univariate and multivariate analyses. Compared with the other groups, pDLB cases had more frequent acute-subacute onset of dementia [45% vs. AD (3%) and AD+LB (16%)], early parkinsonism [45% vs. AD (0%) and AD+LB (0%)], early [27% vs. AD (0%) and AD+LB (0%)] and late [73% vs. AD (11%) and AD+LB (16%)] hallucinations, fluctuating course [46% vs. AD (9%) and AD+LB (22%)], delusions [45% vs. AD (11%) and AD+LB (6%)], spontaneous parkinsonism [63% vs. AD (8%) and AD+LB (16%)], less frequent ideomotor apraxia and loss of insight, earlier urinary incontinence [3.2 +/- 1.4 years after onset vs. AD (6.3 years) and AD+LB (5.8 years)], shorter duration of dementia [7.7 +/- 2.4 years vs. AD (9.6 years) and AD+LB (11 years)], milder atrophy in computed tomography scans, greater brain weight, more transcortical spongiosis, wider cortex and subcortex, and less amyloid angiopathy. All pDLB cases but no AD cases had abnormal CA2 neurites. The clinical features of AD+LB patients were similar to those of AD patients other than more frequent acute-subacute onset and fluctuating evolution. Discriminant analyses selected four clinical variables differentiating pDLB from the other two groups as a whole: acute-subacute onset, early parkinsonism, early hallucinations, and early onset of urinary incontinence. Two or more of these features identified pDLB with a sensitivity of 81.8% and a specificity of 95.9%. Differentiation between the three groups (pDLB, AD+LB, and AD) or between both groups with LB (DLB) from AD could be only attained in 70% of cases. We conclude that early symptomatology is the main clue for the diagnosis of pDLB. We identified by discriminant analysis a set of clinical diagnostic criteria similar to those proposed by the Consortium on Dementia With Lewy Bodies. Accuracy was excellent for the diagnosis of pDLB but only mediocre for separating AD+LB as well as the entire DLB group from AD.

Age of Onset↗
PubMedDate not supplied

Vascular dementia: a radical redefinition.

'Vascular dementia' may be the leading cause of cognitive impairment in the world, yet there is little agreement as to what this concept encompasses or how it is defined. A critical review reaches the conclusion that the concept of 'vascular dementia' has become obsolete. 'Vascular' is too generic, and fails to identify specific etiologies which may be subject to current and future preventive measures. 'Dementia' identifies patients too late to do much about their problem. An alternate approach is suggested. Identify patients across the whole spectrum of vascular cognitive impairment, from high risk with no deficit ('brain-at-risk stage') to full-blown dementia. Describe the cognitive impairment in terms of standardized neuropsychological measures, and relate the dementia to the specific vascular cause, so that the appropriate preventive measures can be implemented.

Cognition Disorders↗
PubMedDate not supplied

Brain stem dysfunction in transient global amnesia.

A patient with transient global amnesia also had transient bilateral gaze nystagmus which was detected both by conventional bedside examination and upon electronystagmographic recording. The nystagmus was absent one week later indicating recovery of the temporary brain stem deficit. The recording of objective evidence of brain stem dysfunction in the form of gaze nystagmus in a patient who had transient global amnesia, suggests that both were due to a transient ischemic attack involving the cerebral blood supply in the vertebrobasilar distribution.

Aged↗
PubMedDate not supplied

Decreased incidence and mortality of stroke.

Dr. Whisnant argues persuasively that control of hypertension has played a major role in the decline of stroke. He offers a cohesive and logical overview on this decline and does so with data from his own vast experience and with the advantages of the Mayo Clinic system which includes a centralized population-based diagnostic index, neurological expertise and a high autopsy rate. However, neither Dr. Whisnant's arguments nor the Mayo Clinic data justify the conclusion that "treatment of hypertension is the only significant contributor to the decline of stroke."

Cerebrovascular Disorders↗
PubMedDate not supplied

A secondary prevention, randomized trial of suloctidil in patients with a recent history of thromboembolic stroke.

Four hundred and thirty-eight patients who had suffered a thromboembolic stroke not less than two weeks or more than four months previously, were entered into a placebo-controlled randomized clinical trial to determine whether suloctidil (200 mg t.i.d.) would influence the subsequent recurrence of stroke, the occurrence of myocardial infarction, or cardiovascular death. The two treatment groups were comparable at baseline with respect to important prognostic variables and there was good adherence to the study protocol during an average follow-up of 20 months. Significantly more patients complained of side-effects in the suloctidil group and more hepatotoxicity was also reported in the suloctidil group. Four cases of clinical hepatitis were suspected to be due to suloctidil, each of which was reversible on termination of study treatment; relative increases in SGOT and SGPT at three months in the suloctidil group were found to be mild and transient. The primary analysis of efficacy was based on the incidence of the first event of stroke, myocardial infarction or cardiovascular death, but excluding events that occurred more than 28 days after complete withdrawal from study medication for whatever reason. Thus, the primary analysis included 38 events in the suloctidil group and 47 in the placebo group (p = 0.17) representing a risk reduction of 24%. If total mortality is substituted for cardiovascular death, the corresponding figures are 47 in the suloctidil group and 58 in the placebo group (p = 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebrovascular Disorders↗
PubMedDate not supplied

Ergotamine and cerebral blood flow.

We measured the cerebral blood flow (CBF) of 16 patients by the xenon-133 intracarotid method before and after the intramuscular injection of ergotamine tartrate. The regional and hemispheric CBF was unaltered, even in 3 migraneurs in who ergotamine relieved the headache. Ergotamine tartrate in therapeutic doses has no effect on the cerebral circulation.

Adult↗
PubMedDate not supplied

Conceptual background to vascular cognitive impairment.

The current criteria for vascular dementia use a paradigm that first diagnoses dementia on the basis of Alzheimer-type criteria and then superimposes upon this vascular events and risk factors to convert a diagnosis of Alzheimer disease to one of vascular dementia. There are two fundamental flaws with this approach. First, the neuropsychological features of Alzheimer disease are not the same as those for vascular dementia and so use of the current criteria will fail to diagnose many cases, particularly those in whom memory loss is not prominent. Second, progression of vascular dementia should be modifiable by adjustment of risk factors and, possibly, by the use of neuroprotective agents. Given this, it is absurd to wait until patients are frankly demented. It is far more appropriate to detect patients at risk of developing cognitive loss as soon as possible. This could be in the earliest symptomatic stage (vascular cognitive impairment) or even prior to this (brain-at-risk) stage. New criteria, based on evidence rather than on supposition, that focus on early disease are urgently needed.

Alzheimer Disease↗
PubMedDate not supplied

Role of white matter lesions in cognitive impairment of vascular origin.

White matter changes are detected with high frequency by neuroimaging techniques in aged subjects with cerebrovascular risk factors or diseases and in cognitively impaired patients. Their direct role in causing cognitive deterioration has not been established, although their frequency is higher in demented subjects than in normal controls, and they are associated with specific cognitive deficits, particularly those related to impairment of frontal lobe functions. The aim of this paper is to critically review the existing knowledge about the role of white matter lesions in cognitive impairment of vascular origin. After reviewing the scarce evidence and the numerous clues suggesting a possible role of white matter lesions in causing mental decline, proposals are advanced about elements that could be a basis for revised criteria for vascular dementia for clinical trials. Finally, some items requiring future joint investigations in the fields of age-related white matter lesions are identified.

Cerebrovascular Disorders↗
PubMedDate not supplied

Subtypes of vascular dementia.

The challenge of describing subgroups is particularly important in vascular dementia, which, in contrast to more stereotypic processes affecting cognitive function, is better thought of as several syndromes rather than as a disease. Many current diagnostic descriptions lack a strong empiric basis. Some of the categories now in use suffer from a priori assumptions about causality and pattern associations, which themselves have not been validated. The so-called mixed dementia syndrome may have been underrepresented in our estimation of dementia subtypes, in comparison with so-called pure vascular causes. Within the vascular syndrome, whether seen in isolation or in combination with other causes of dementia, the relative contributions of white matter changes as compared with multiple cortical strokes needs to be clarified. It remains a matter of controversy as to whether prolonged or chronic intermittent cerebral ischemia is a statistically important part of the dementia. The variable relation between clinical presentation and neuroimaging localization has important consequences for understanding the pathophysiology of cognitive impairment arising from vascular causes. Recent data also suggest that we should focus away from both the Alzheimer disease model of dementia and the multi-infarct model of vascular dementia. There are important opportunities available to clinicians from many disciplines to collaborate in precise clinical descriptions of large numbers of patients to advance our understanding of the spectrum of vascular cognitive impairment.

Brain Diseases↗
PubMedDate not supplied

[Dementia and stroke: the importance of coexisting brain pathologies].

AIM: In this paper we present evidence to support the idea that vascular and degenerative pathological processes interact synergically in the genesis of post stroke dementia. METHOD: Characteristics of vascular lesions have been identified that are linked to the development of a clinical picture of dementia. Yet, the characteristics of the brain in which infarction or brain haemorrhage occur are equally important. Recent (clinical, epidemiological and neuropathological) studies highlight the high frequency with which neurodegenerative and vascular processes coexist in the same brain, and the fact that both processes share environmental and genetic risk factors. The diagnostic criteria currently in use consider the existence of a vascular pathology as being an exclusion criterion for the diagnosis of an Alzheimer type dementia, and thus rule out the possibility of studying the interaction between the two processes. Instead of restrictive criteria, pragmatic instruments must be used to classify the possible aetiology in these patients. CONCLUSIONS: It is important to study the coexistence of vascular and degenerative pathologies in the brains of patients with a post stroke deterioration. Proving the existence of a synergic relation between the two processes would open up the possibility of performing an operation to prevent and treat the dementia displayed by these patients.

Dementia↗
PubMedDate not supplied

Magnetic resonance imaging of small medullary infarctions.

Small infarctions of the medulla produce typical neurologic deficits and can be clinically recognized fairly reliably. High-field magnetic resonance imaging with a 1.5 T prototype scanner successfully demonstrated very tiny medulla infarctions in three of five patients. These lesions were imaged readily by a fairly rapid (approximately 1-2 min scan time) partial-saturation technique and confirmed on multiple spin-echo images. In addition, in two cases vertebral occlusion ipsilateral to the infarction was suggested by high signal on T2 weighted spin-echo images.

Aged↗