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V Hachinski

Publications and source records attributed to V Hachinski.

At least 55 records · Page 3Linked to original sources
PubMed1998

Canadian guidelines for intravenous thrombolytic treatment in acute stroke. A consensus statement of the Canadian Stroke Consortium.

BACKGROUND: The thromobolytic drug, tissue plasminogen activator (tPA) has been approved in the United States for the treatment of acute ischemic stroke amid controversy and concern about the balance of risk and benefit. The Canadian Stroke Consortium (CSC), a national network of neurologists who collaborate on joint projects in stroke medicine, including clinical trials and consensus statements, has developed guidelines for the use of tPA in Canada. METHODS AND RESULTS: The CSC Board of Directors wrote a preliminary report based on existing publications, including randomized drug trials and the report of a special committee struck by the Stroke Council of the American Heart Association. This draft was circulated to the CSC membership-at-large for suggestions or amendments, to produce this final draft. CONCLUSIONS: The present guidelines have been devised to represent a Canadian viewpoint of management. The Health Protection Branch of the Ministry of Health of Canada has not yet produced an evaluation. Further modification of these guidelines may be necessary when more data from clinical trials and experience with the drug become available.

Acute Disease↗
PubMed1998

Subcortical vascular dementia: survey of treatment patterns and research considerations.

BACKGROUND: Since few studies have examined the effectiveness of therapies for subcortical vascular dementia, treatment guidelines are not available. Current patterns in the treatment of such dementias have not been studied. OBJECTIVE: To determine the practice patterns of Canadian specialists for the treatment of subcortical vascular dementia, and to survey their opinions regarding issues which are important in the design of a randomized controlled trial (RCT) in this field. DESIGN: National survey of all specialists certified in Neurology or Geriatric Medicine. RESULTS: Of responding physicians (78%) prescribed antithrombotic therapy for patients with vascular dementia. Most begin treatment with aspirin 325 mg daily (64%). The next three most common initial treatments were; no pharmacotherapy (12%), aspirin 650 mg daily (11%), and aspirin 1300 mg daily (11%). If the dementia continued to progress despite initial therapy, the treatment options were more varied. Most specialists (69%) believed that an RCT to assess the efficacy of aspirin in vascular dementia is warranted. The majority (69%) also felt that serial neuroimaging would be required for participants in such a trial, with magnetic resonance imaging being cited most frequently (41%). The majority of specialists considered three years as the minimum duration for such a trial. CONCLUSIONS: Specialist physician practice patterns vary significantly for the treatment of patients with subcortical vascular dementia. Most physicians believe that an RCT testing the efficacy of aspirin in this condition is required. However, before such a trial can be conducted, many methodological difficulties need to be addressed.

Aspirin↗
PubMed1998

Fallacies in the pathological confirmation of the diagnosis of Alzheimer's disease.

OBJECTIVE: Necropsy confirmed clinical diagnostic accuracy for Alzheimer's disease is claimed to exceed 90%. This figure contains two fallacies; it includes cases in which Alzheimer's disease exists with other diseases affecting cognition and the studies that report these figures excluded cases without necropsy (verification bias). The effect of these errors is estimated. METHODS: Data were taken from the University of Western Ontario Dementia Study, a registry of dementia cases with clinical and psychometric follow up to necropsy based in a university memory disorders clinic with secondary and tertiary referrals. Data were available on 307 patients; 200 (65%) had clinically diagnosed Alzheimer's disease, 12 (4%) vascular dementia, 47 (15%) mixed dementia, and 48 (16%) had other diagnoses. One hundred and ninety two of 307 cases (63%) died and 122 of 192 fatalities (64%) had necropsies. The pathological material was interpreted in two ways, allowing and disallowing coexistent disease in making a diagnosis of Alzheimer's disease. In cases without necropsy, progressive cognitive loss was used as a marker for degenerative dementia. The outcome measures of interest were the positive predictive value of a clinical diagnosis of Alzheimer's disease allowing and disallowing coexistent diseases and with and without correction for cases that were not necropsied. RESULTS: The clinical diagnoses differed significantly between the population who died and those who did not. In cases without necropsy, 22% had no dementia on follow up, concentrated in early cases and men, showing considerable scope for verification bias. The positive predictive value of a diagnosis of Alzheimer's disease was 81% including coexistent diseases, falling to 44% when limited to pure cases. Combined, these factors reduce the positive predictive value to 38% for pure Alzheimer's disease. CONCLUSIONS: Correction for dual pathology and verification bias halves the positive predictive value of the clinical diagnosis of Alzheimer's disease. Data derived from necropsy studies cannot be extrapolated to the whole population. This has important implications including uncertainty about diagnosis and prognosis and a dilution effect in therapeutic trials in Alzheimer's disease.

Alzheimer Disease↗
PubMed1998

Factors affecting the age of onset and rate of progression of Alzheimer's disease.

OBJECTIVES: To assess the role of cerebrovascular disease, sex, education, occupation, year of birth, leukoaraiosis, congophilic angiopathy, family history, and other demographic factors on the reported age of onset and rate of progression of Alzheimer's disease. METHODS: Analysis of data from the University of Western Ontario Dementia Study, a prospective longitudinal study of dementia patients with clinical and 6 monthly psychometric follow up to postmortem based in a university memory disorders clinic with secondary and tertiary referrals. There were 172 patients with dementia. The main outcome measures were the reported age of onset of cognitive decline as described by the family (available in 168) and rate of progression as measured during the linear phase of the extended scale for dementia, which could be calculated in 66. The cases subdivided into 49 cases of definite Alzheimer's disease without infarcts, 25 cases of otherwise definite Alzheimer's disease with infarcts, 79 cases of probable Alzheimer's disease without infarcts, and 19 such cases with infarcts. RESULTS: The age of onset was not influenced by the rate of progression, the presence of cerebral infarcts, or congophilic angiopathy. Educational level, occupational level, sex, family history, year of birth, reported age of onset, severity at entry, an ischaemic score, and the presence of leukoariosis, affected neither age of onset nor the rate of progression. An earlier year of birth had a major effect and higher education had a minor effect on earlier age of onset. The earlier the year of birth, the lower the educational level and the greater the accrual of cerebral infarcts. CONCLUSIONS: Contrary to series without pathological verification, age of onset in this study was not affected by occupation. Education had a modest effect on earlier reported onset, probably reflecting earlier recognition. As birth year has a strong effect on educational level and the occurrence of cerebral infarcts, this must be taken into account when analysing for risk factors for Alzheimer's disease.

Adult↗
PubMed1997

The effect of different diagnostic criteria on the prevalence of dementia.

BACKGROUND: There are several widely used sets of criteria for the diagnosis of dementia, but little is known about their degree of agreement and their effects on estimates of the prevalence of dementia. METHODS: We examined 1879 men and women 65 years of age or older who were enrolled in the Canadian Study of Health and Aging and calculated the proportion given a diagnosis of dementia according to six commonly used classification systems: the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM), third edition (DSM-III), the third edition, revised of the DSM (DSM-III-R), the fourth edition of the DSM (DSM-IV), the World Health Organization's International Classification of Diseases (ICD), 9th revision (ICD-9) and 10th revision (ICD-10), and the Cambridge Examination for Mental Disorders of the Elderly (CAMDEX). The degree of concordance among classification schemes and the importance of various factors in determining diagnostic agreement or disagreement were examined. RESULTS: The proportion of subjects with dementia varied from 3.1 percent when we used the criteria of the ICD-10 to 29.1 percent when the DSM-III criteria were used. The six classification systems identified different groups of subjects as having dementia; only 20 subjects were given a diagnosis of dementia according to all six systems. The classifications based on the various systems differed little according to the patients' age, sex, educational level, or status with respect to institutionalization. The factors that most often caused disagreement in diagnosis between DSM-III and ICD-10 were long-term memory, executive function, social activities, and duration of symptoms. CONCLUSIONS: The commonly used criteria for diagnosis can differ by a factor of 10 in the number of subjects classified as having dementia. Such disagreement has serious implications for research and treatment, as well as for the right of many older persons to drive, make a will, and handle financial affairs.

Aged↗
PubMed1997

Cerebrovascular pathology in Alzheimer's disease: cause, effect or epiphenomenon?

Cerebrovascular pathology abounds in Alzheimer's disease. Changes in the endothelium, disruption of the blood-brain barrier and amyloid deposition in the cerebral blood vessels are almost universal in advanced cases. Do these changes represent the cause, the effect, or the consequences of a common pathogenesis of Alzheimer's disease? This volume addresses some of these issues by presenting new knowledge gained from a diversity of fields. Recognition of the mechanisms involved will open new possibilities for therapeutic trials.

Aged↗
PubMed1997

Serum protein leakage in Alzheimer's disease revisited.

Leakage of serum proteins into the brain parenchyma has been repeatedly used as evidence of blood-brain barrier (BBB) damage in experimental and human studies. However, there is no consensus in the literature concerning this phenomenon in Alzheimer's disease (AD). We have examined this question by comparing frontal lobe sections in seven groups of patients: Multi-infarct dementia (n = 6), AD with (n = 10) and without (n = 10) infarcts, age-matched controls with (n = 10) and without (n = 10) infarcts, controls with neurodegenerative diseases other than AD, and young controls (n = 10). An additional series compared prospectively followed patients with a diagnosis of either multi-infarct dementia (n = 5) or AD (n = 4). Albumin was detected in white-matter astrocytes in all cases, without significant variation in intensity. In addition, diverse combinations of neurons, astrocytes, and (in AD patients) senile plaques were present in the cerebral cortex in an inconsistent manner. Semiquantitative analysis showed no statistically significant differences among groups. Anti-IgG labeled astrocytes in infarcts only. Complement C3c component was detected in rare amyloid plaques in a minority (15%) of AD cases. Selective labeling of AD-specific lesions in a patchy manner was observed for serum amyloid P. We conclude that there is no immunohistochemical evidence of alteration of the BBB in Alzheimer's disease with or without vascular factors or in old age. Serum amyloid P binds avidly to AD lesions, but our findings are consistent with leakage through the BBB during the agonal or immediate postmortem period. Finally, no specific pattern of abnormality in the BBB was detected in multi-infarct dementia.

Alzheimer Disease↗
PubMed1997

Presence and treatment of vascular risk factors in patients with vascular cognitive impairment.

OBJECTIVE: To document the presence and treatment of selected vascular risk factors in patients with vascular cognitive impairment and elements affecting undertreatment of vascular risk factors. DESIGN: Secondary analysis of the Canadian Study of Health and Aging database, which is a national, representative, cross-sectional study of the epidemiologic distribution of dementia in elderly people in Canada. SETTING: Survey. PATIENTS: Institutionalized and community-dwelling elderly people. MAIN OUTCOME MEASURES: Vascular risk factors, dementia diagnosed by standard methods, and medication use. RESULTS: Treatable vascular risk factors occurred significantly more often in patients with vascular cognitive impairment (with and without dementia) than in patients with probable Alzheimer disease or normal cognitive function. For example, 76% of patients with vascular dementia and 57% of those with vascular cognitive impairment without dementia had a history of stroke, compared with only 5% of those with probable Alzheimer disease and 7% of those with no cognitive loss. (For hypertension, the comparable figures are 55%, 48%, 24%, and 38%, respectively.) Potential undertreatment of vascular risk factors had little effect on mean control of vascular risk factors. For example, the mean (+/- SD) systolic blood pressure in those being treated was 144 +/- 26 mm Hg, compared with 142 +/- 25 mm Hg in those not receiving pharmacological treatment. In each group (treated vs untreated), the proportion of patients with a systolic blood pressure higher than 160 mm Hg was 20% and 16%, respectively. Potential undertreatment occurred most often in those with severe dementia and those living in nursing homes. CONCLUSIONS: Vascular risk factors occurred more commonly in patients with vascular cognitive impairment compared with other patients, including those with other forms of dementia. When present, such risk factors were often treated pharmacologically, except in patients with severe dementia and those in long-term care institutions. Undertreatment does not, in general, result in worsened risk factor control.

Aged↗
PubMed1997

Cerebral hemispheric lateralization in cardiac autonomic control.

OBJECTIVE: To identify cerebral hemispheric lateralization in cardiac autonomic control. PATIENTS: Eight patients undergoing an intracarotid amobarbital sodium test as a presurgical evaluation of temporal lobe epilepsy. DESIGN: Power spectral analysis of heart rate variability before and after intracarotid amobarbital injection. SETTING: University hospital and research center. MAIN OUTCOME MEASURE: The changes in the ratio of low-frequency (LF) (sympathetic) to high-frequency (HF) (parasympathetic) power (LF/HF ratio), a measure of sympathovagal balance, after hemispheric inactivation. RESULTS: The LF/HF ratio changed as follows: right preinactivation = 3.81 +/- 0.96, postinactivation = 3.40 +/- 1.23; left preinactivation = 2.74 +/- 0.49, postinactivation = 4.34 +/- 0.59 (mean +/- SEM). The test of interaction between laterality and inactivation using a 2-way repeated-measures analysis of variance was statistically significant (P = .001). The increased ratio on the left side (1.61 +/- 0.70) was statistically significant (P = .03), but the decrease on the right side (-0.40 +/- 0.46) was not (P < or = .70). CONCLUSIONS: These findings suggest that there is a cerebral lateralization in cardiac autonomic control and that the right cerebral hemisphere predominantly modulates sympathetic activity. This study may help identify subgroups of patients with intracranial disease at high risk of cardiac complications.

Adolescent↗
PubMed1997

Managed care and the survival of neurology referral centers. A commitment to centers of excellence.

Since the collapse of federal health system reform legislation in 1994, there has been a growing concern with the quality of care provided within managed care systems. Just as physicians practicing under a traditional fee-for-service payment base have financial incentives to do as much as possible for each patient (doing well by doing good), physicians working for managed care plans are sometimes given perverse incentives to do as little as possible. A major quality-related concern among patients and payers (often referred to jointly and ambiguously as consumers of care) is the much larger role assigned to primary care physicians in managed care plans than is usually the case with traditional indemnity insurance.

Aged↗
PubMed1997

Tissue plasminogen activator in a vertebral artery dissection.

BACKGROUND: Spontaneous dissection of the vertebral artery is uncommon. METHOD: Case study. RESULTS: We report a 49-year-old woman who presented with the rapidly progressing basilar artery syndrome who was given an intravenous dose of tissue plasminogen activator seven hours after the onset of first symptoms. Thirty minutes after the injection, a dramatic recovery of the patient's consciousness and neurological signs was noted. CONCLUSION: To our knowledge, this is the first reported case of intravenous tissue plasminogen activator use in acute vertebral artery dissection.

Arterial Occlusive Diseases↗
PubMed1997

Cardiovascular consequence of experimental stroke.

Clinically, it has been observed that stroke causes a number of cardiovascular disturbances that are detrimental to prognosis and may cause death. We have developed an experimental model of stroke, a middle cerebral artery occlusion in the rat, that can mimic the acute cardiovascular responses observed clinically. This model has clearly demonstrated that the insular cortex is necessary to produced the autonomic changes and that these changes are exacerbated by right-sided infarcts and increasing age. In addition, we have demonstrated that there are neurochemical changes associated with our stroke model that may mediate the cardiovascular complications. In particular, an increase in dynorphin in the central nucleus of the amygdala occurs with a peak at 3 to 5 days after the stroke and is directly due to damage in the insular cortex. Finally, we have shown that there is a similar time course in the exaggerated cardiovascular responses to stress following middle cerebral artery occlusion. Direct injection of dynorphin into the central nucleus of the amygdala can enhance the cardiovascular response obtained by stimulation of the acoustic stress pathway. These observations have direct relevance to clinical stroke.

Animals↗