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C S Kase

Publications and source records attributed to C S Kase.

At least 37 records · Page 2Linked to original sources
PubMed1996

Stroke severity in atrial fibrillation. The Framingham Study.

BACKGROUND AND PURPOSE: Stroke occurring with atrial fibrillation (AF) is more likely to be fatal or more severe than non-AF stroke based on clinical series, but data from prospective epidemiological studies are sparse and inconsistent. METHODS: Over 40-year follow-up of the original 5070 Framingham cohort, 501 initial ischemic strokes, including 103 with AF, were analyzed. Stroke severity was rated as none, mild, moderate, severe, or fatal. Since 1981, functional status indicated by the Barthel index has been evaluated acutely and at 3, 6, and 12 months. Severity and functional status of AF strokes were compared with non-AF strokes using chi 2 test and Student's t test. Thirty-day mortality was assessed by logistic regression analyses. RESULTS: AF was associated with increased stroke severity (P = .048). Thirty-day mortality was greater in AF strokes than in non-AF strokes (25% versus 14%). The multivariate-adjusted odds ratio for 30-day mortality for AF subjects was 1.84 (95% confidence interval, 1.04 to 3.27). Since 1981, follow-up was available for 150 initial ischemic strokes, including 30 with AF. Compared with the non-AF group, the AF group had poorer survival and more recurrences during 1 year of follow-up. The AF subjects had lower mean Barthel index scores acutely (29.6 versus 58.6, P < .001) and at 3 months (P = .005), 6 months (P = .003), and 12 months (P = .130) after stroke among survivors. CONCLUSIONS: Ischemic stroke associated with AF was nearly twice as likely to be fatal as non-AF stroke. Recurrence was more frequent, and functional deficits were more likely to be severe among survivors. Since stroke is usually the initial manifestation of embolism in AF, prevention is critical to reducing disability and mortality.

Adult↗
PubMed1996

Interobserver agreement in the classification of stroke in the physicians' health study.

BACKGROUND AND PURPOSE: The evaluation of cerebrovascular end points in prospective studies is often based exclusively on medical record examination and may be made by more than one observer over time. To address the issues of adequacy of medical record information and consistency in diagnosis over time, we evaluated interobserver agreement for the main items of the stroke classification system used in the Physicians' Health Study. This trial included 22,071 physicians randomly assigned in 1982 to receive either aspirin or placebo to assess the subsequent risk of cardiovascular events, including stroke. METHODS: Stroke subtype, stroke severity, and certainty of diagnosis were first classified from medical records from the years 1982 through 1988. The 216 stroke events reported in this period were independently reclassified in 1994 and compared with the initial classification using kappa statistics. RESULTS: Overall agreement in major stroke types (hemorrhagic, ischemic, undetermined stroke) as well as in hemorrhagic stroke subtypes was excellent (kappa = 0.81 and kappa = 0.95, respectively). A wide range of values for the ischemic stroke subtypes (kappa = 0.13 to kappa = 0.96) was obtained. Agreement was substantial in assessment of stroke severity (kappa = 0.71), and it was fair (kappa = 0.33) for certainty of diagnosis. CONCLUSIONS: Interobserver agreement is high for major stroke types as well as for categories of hemorrhagic stroke on the basis of review of medical records and results of imaging data. The classification of ischemic stroke subtypes, however, is subject to substantial interobserver disagreement. Periodic reclassification of random samples of end points might be considered in long-term prospective studies to assess potential misclassification of events by different observers.

Adult↗
PubMed1996

Apolipoprotein E epsilon 4 is associated with the presence and earlier onset of hemorrhage in cerebral amyloid angiopathy.

BACKGROUND AND PURPOSE: Cerebral amyloid angiopathy is an important cause of intracerebral hemorrhage in the elderly. The epsilon 4 allele of the apolipoprotein E gene, recently established as a genetic risk for Alzheimer's disease, has also been suggested as a possible risk factor for cerebral amyloid angiopathy. We sought to determine whether this allele is specifically associated with hemorrhages related to amyloid angiopathy and whether it correlates with the age at which first amyloid angiopathy-related hemorrhage occurs. METHODS: Forty-five consecutive patients presenting with lobar hemorrhage were prospectively classified according to clinical, radiological, and when available, pathological features and evaluated for apolipoprotein E genotype. They were compared with 1899 elderly patients from a population-based sample and with 18 consecutive patients with hemorrhages in deep regions typical of a hypertensive mechanism. RESULTS: Patients with multiple hemorrhages confined to the lobar territory demonstrated a greater than twofold overrepresentation (P < .001) in frequency of the apolipoprotein E epsilon 4 allele compared with the population-based sample. Apolipoprotein E genotypes of patients with hemorrhages in deep territories resembled the population sample. Among patients with strictly lobar hemorrhages, carriers of the epsilon 4 allele had their first hemorrhage more than 5 years earlier than noncarriers (mean age at first hemorrhage, 73.4 +/- 8.0 versus 78.9 +/- 7.4 years; P = .033). These effects were independent of the accompanying presence of Alzheimer's disease. CONCLUSIONS: The data support a specific role for apolipoprotein E epsilon 4 in accelerating the process that leads to amyloid angiopathy-related hemorrhage.

Age Factors↗
PubMed1995

Temporal patterns of stroke onset. The Framingham Study.

BACKGROUND AND PURPOSE: Several studies have shown stroke onset to vary by season, day of the week, and time of day. These temporal patterns, which may provide insights into pathogenesis, were found mainly in clinical series, which can be subject to selection bias. To obtain a less distorted picture of stroke onset, we examined the month and season, day of the week, time, and place stroke occurred in a community-based cohort. METHODS: Over a 40-year period of surveillance of the Framingham Study cohort of 5070 people aged 30 to 62 years and free of stroke and cardiovascular disease at entry, 637 completed initial strokes occurred. Month, season, day of the week, time of day, and place of occurrence of stroke were ascertained systematically and related prospectively to stroke incidence, subtype, and gender. RESULTS: Winter was the peak season for cerebral embolic strokes. Significantly more stroke events occurred on Mondays than any other day, particularly for working men. For intracerebral hemorrhages, a third happened on Mondays in both genders. The time of day when strokes most frequently occurred was between 8 AM and noon. This pattern was true for all stroke subtypes. This pattern persisted when individuals whose onset occurred while sleeping or on awakening were excluded. Stroke in general occurred more at home, with hemorrhagic strokes occurring outside the home and cerebral embolisms in the hospital more than other subtypes. CONCLUSIONS: Temporal patterns of stroke onset were observed for season, day of the week, time of day, and place in a community-based population. These findings suggest that there are periods of increased risk of stroke that may be amenable to preventive strategies.

Adult↗
PubMed1995

Intracerebral haemorrhage.

Intracerebral haemorrhage accounts for 15% of strokes. Its mechanisms include hypertension, cerebral amyloid angiopathy, rupture of vascular malformations, bleeding into primary or metastatic brain tumours, coagulopathies (due to the use of anticoagulants and thrombolytic agents), sympathomimetic drug effect (amphetamines, phenylpropanolamine, and cocaine), and vasculitis. The clinical presentation reflects both the general effects of increased intracranial pressure, and the neurological deficits that result from the specific location of the haemorrhage. Its diagnosis is based on computerized tomography, which identifies haemorrhage as a high-attenuation mass within the brain substance, and magnetic resonance imaging, which in addition estimates the age of the haemorrhage by identifying sequential patterns of transformation of the haemoglobin molecule within the haematoma. The mortality in intracerebral haemorrhage is dependent on the size and location of the haematoma. A reliable clinical parameter for the prediction of outcome is the Glasgow Coma Scale score at presentation. The management of intracerebral haemorrhage involves: (a) the prevention and treatment of increased intracranial pressure; and (b) the choice between surgical and nonsurgical treatment, a clinical decision that is still controversial as a result of the paucity of controlled clinical data comparing both treatment modalities.

Cerebral Hemorrhage↗
PubMed1995

Clinical stroke syndromes: clinical-anatomical correlations.

The vascular territories of the major cerebral arteries supplying the cerebral cortex, subcortical structures, cerebellum, and brainstem in humans are relatively uniform. Because of their anatomical distribution, and the specialized neurologic functions located within these territories, infraction due to arterial occlusion gives rise to distinct clinical syndromes. Thus, the physical findings on neurologic examination permit a reliable topographic diagnosis. With extensive infraction involving all or major portions of a particular vascular territory, the resultant clinical syndromes tend to be severe, reflecting the large area of involvement. More typically, however, infarcts do not involve a vascular territory in its entirety but are limited to the distribution of secondary branches by various mechanisms of arterial occlusion. Depending on their location, these smaller infarcts produce syndromes that may vary in severity and manifestations. Our understanding of the clinical approach of clinicoanatomical correlations in these forms of cerebral infarction has been facilitated by the widespread use of brain CT and MRI scans, that have virtually replaced the classical approach of clinicopathological correlations in autopsy material. In this review we have divided the manifestations of occlusive cerebrovascular disease according to the vascular territories affected. The distinct clinical syndromes which thus arise and their common mechanisms are described. Correlation is made with the typical CT and MRI images.

Cerebrovascular Circulation↗
PubMed1994

Precursors of extracranial carotid atherosclerosis in the Framingham Study.

To investigate cardiovascular risk factors and carotid atherosclerosis, we related previously measured risk factors to carotid atherosclerosis as determined by duplex ultrasonography in the Framingham Study cohort. Risk factors measured prospectively on 1,116 cohort members, ages 66 to 93, were related to the severity of carotid atherosclerosis measured by carotid ultrasonography performed during biennial examination no. 20 (1988 to 1990). The degree of carotid atherosclerosis was expressed as a percent carotid stenosis and, for statistical analysis, subjects were divided into four groups according to percent carotid stenosis. The prevalence of significant carotid stenosis in the general population was low--7% in women and 9% in men. A multivariate logistic regression model showed that age, cigarette smoking, systolic blood pressure, and cholesterol were independently related to carotid atherosclerosis. Alcohol consumption was also significant in men, but not in women. In addition, our results indicate that both current and former smoking in both sexes was related to the degree of carotid atherosclerosis.

Aged↗
PubMed1993

Very small (border zone) cerebellar infarcts. Distribution, causes, mechanisms and clinical features.

Computerized tomography (CT) and magnetic resonance imaging (MRI) allow accurate anatomical localization of large thromboembolic cerebellar infarcts in the territories of the cerebellar arteries and their branches. In addition, MRI and CT show very small cerebellar infarcts as discrete foci of signal change that are not easily localizable within well-defined arterial territories. They could be border zone infarcts. Their anatomy, mechanism and clinical features have not been studied. By reviewing our CT and MRI files over a 2-year period, we found 47 patients with very small cerebellar infarcts; 23 patients had angiography. Infarcts were cortical (32 patients), deep (10 patients) and both (five patients). Most lesions corresponded to border zone cerebellar infarcts. The mechanisms of infarction were (i) global hypoperfusion due to cardiac arrest (two patients); (ii) small or end (pial) artery disease due to intracranial atheroma or hypercoagulable states (nine patients); (iii) focal cerebellar hypoperfusion due to large artery (vertebral or basilar) occlusive disease (16 patients) or brain embolism (11 patients) resulting in infarcts in the watershed areas (27 patients total); (iv) unknown mechanism (nine patients, 19%). Large artery occlusive disease was more frequently observed in deep than in cortical infarcts (9 out of 15 versus 11 out of 37; P < 0.0001). The most frequent symptoms were dizziness, lightheadedness, unsteadiness with axial lateropulsion, dysarthria and limb clumsiness. These symptoms were either transient or recurrent, at times related to positional changes of the head or trunk. Position-related symptoms often persisted for weeks or months after the ischaemic event, and occurred mainly in patients with combined carotid and vertebrobasilar occlusive disease. Physical findings were either absent or included wide-based gait, lateropulsion, mild ipsilateral dysmetria, dysarthria or dysdiadochokinesia. We conclude that very small cerebellar infarcts are often found on CT and MRI. Their border zone distribution and frequent posturally related symptoms most often result from large or pial artery disease rather than from systemic hypotension.

Adult↗
PubMed1993

Infarct topography and hemiparesis profiles with cerebral convexity infarction: the Stroke Data Bank.

For the 183 of 1276 patients in the NINDS Stroke Data Bank with convexity infarction in the middle cerebral artery territory, the size of the infarct did not differ between the two sides but the location of the main site of the infarct differed: on the left side, it was centred in the inferior parietal region, and was mid-frontal on the right. There was a good correlation between infarct size and weakness severity whether estimated by overall motor function on one side, arm, or hand alone. There was a poor correlation, however, for lesion location (lower third, middle third or upper third on either side of the Rolandic fissure) and any of the specific syndromes of focal weakness, no two cases sharing the same lesion for the same syndrome and several cases sharing the same lesion with a different syndrome. The findings indicated a difference in weakness syndromes between the two hemispheres and great individual variation of the acute syndrome caused by a given site of focal infarction along the Rolandic convexity. These variations may explain some of the difficulties showing effects of a given therapeutic agent in studies of acute ischaemic stroke. Large sample sizes will be required for the reliable assessment of any treatment using currently popular clinical stroke scales.

Brain Mapping↗
PubMed1993

Cerebellar infarction. Clinical and anatomic observations in 66 cases.

BACKGROUND AND PURPOSE: Cerebellar infarction displays different clinical features, depending on the vascular territory involved. We studied patients with infarcts in the territories of the posterior inferior cerebellar artery or the superior cerebellar artery to compare their clinical presentation, course, and prognosis. METHODS: We retrospectively analyzed the clinical features, laboratory data, and imaging studies of 66 patients with cerebellar infarction collected consecutively at five institutions. All the cerebellar infarcts were documented on computed tomographic scan or magnetic resonance imaging. RESULTS: Two distinct profiles emerged, depending on the vascular territory involved. In 36 patients with posterior inferior cerebellar artery territory infarcts, a triad of vertigo, headache, and gait imbalance predominated at stroke onset. Computed tomography showed severe cerebellar mass effect in 11 cases (30%), with associated hydrocephalus in seven. In these seven patients (19%), postinfarct swelling led to brain stem compression that resulted in four deaths. In 30 patients with superior cerebellar artery infarcts, gait disturbance predominated at onset; vertigo and headache were significantly less common. The clinical course was usually benign. Computed tomography showed marked cerebellar mass effect, hydrocephalus, and brain stem compression in only two instances (7%). Presumed cerebral embolism was the predominant stroke mechanism in patients with superior cerebellar artery distribution infarcts, whereas in those with posterior inferior cerebellar artery distribution infarcts, the stroke mechanism was equally divided between cardiogenic embolism and posterior circulation arterial disease. CONCLUSIONS: Cerebellar infarcts in the posterior inferior cerebellar artery and superior cerebellar artery distribution have distinct differences in clinical presentation, course, and prognosis. These differences should help in the selection of appropriate monitoring and treatment strategies.

Adolescent↗
PubMed1992

Intracranial hemorrhage after coronary thrombolysis with tissue plasminogen activator.

PURPOSE AND METHODS: We analyzed the clinical, laboratory, and radiologic data in nine patients who sustained an intracranial hemorrhage (ICH) after receiving intravenous recombinant tissue plasminogen activator (rt-PA) and heparin for treatment of acute myocardial infarction (MI). Our purpose was to delineate the clinical and radiologic features of the ICHs, as well as to determine their potential risk factors and mechanisms. RESULTS: Among 1,700 patients with an acute MI treated with an investigational two-chain rt-PA, duteplase (Burroughs Wellcome Co., Research Triangle Park, NC), nine (0.53%) developed symptomatic ICH. Neurologic symptoms occurred between 7 and 96 hours after onset of rt-PA therapy. All patients received heparin concomitantly for prevention of coronary reocclusion. The activated partial thromboplastin times (aPTTs) in five of eight (63%) patients at onset of ICH were excessively prolonged (greater than two times control); hypofibrinogenemia occurred in only one of five (20%) patients tested; and thrombocytopenia was present in only one of the nine (11%) patients. Fibrin degradation products (FDPs) were elevated in all five patients tested. Minor hemorrhage (not requiring transfusion) outside the central nervous system occurred in five of the nine patients with ICH. The ICHs were often of lobar location and of moderate to large size. They occurred at multiple sites in three patients, and were fatal in four instances (44%). CONCLUSIONS: The incidence of ICH in this series was low, and consistent with figures reported from studies with alteplase in patients with acute MI. The mechanisms of these hemorrhages remain unclear; while hypofibrinogenemia was not a uniform finding, excessive prolongation of the aPTT and elevated FDPs may have contributed to the occurrence of ICH in some patients. Still unidentified local cerebrovascular factors may play an additional role in causing ICH. In order to further clarify the mechanisms of ICH in the setting of thrombolytic therapy, prospective data collection on probable risk factors for ICH in patients with acute MI treated with rt-PA will be required.

Aged↗
PubMed1992

Secular trends in stroke incidence and mortality. The Framingham Study.

BACKGROUND: The reduction in US stroke mortality has been attributed to declining stroke incidence. However, evidence is accumulating of a trend in declining stroke severity. METHODS: We examined secular trends in stroke incidence, prevalence, and fatality in Framingham Study subjects aged 55-64 years in three successive decades beginning in 1953, 1963, and 1973. RESULTS: No significant decline in overall stroke and transient ischemic attack incidence or prevalence occurred. In women, but not men, incidence of completed ischemic stroke declined significantly. Stroke severity, however, decreased significantly over time. Stroke with severe neurological deficit decreased in later decades, with a fall in rates of severe stroke cases in which patients were unconscious on admission to the hospital. There was no substantial change in the case mix of infarcts and hemorrhages and no decline in hemorrhage to account for the decline in severity. The proportion of isolated transient ischemic attacks increased significantly over the 30 years studied, yielding an apparent and significant decline in case-fatality rates in men only. CONCLUSIONS: Secular trends in stroke incidence and fatality did not follow a clear or definite pattern of decline. While a significant decline in stroke severity occurred over three decades, incidence of infarction fell only in women. The decline in total case fatality rates occurred only in men and resulted largely from an increased incidence of isolated transient ischemic attacks. The severity of completed stroke was significantly lower in the later decades under study.

Adult↗
PubMed1991

Intracerebral hemorrhage: external validation and extension of a model for prediction of 30-day survival.

We report validation of a previously reported logistic regression model for predicting 30-day survival after supratentorial intracerebral hemorrhage using independent, prospectively collected data. The original model, using initial Glasgow Coma Scale score, hemorrhage size, and pulse pressure, accounted for mortality or survival at 30 days in 92% of patients in the Pilot Stroke Data Bank with a sensitivity of 0.84 and a specificity of 0.96. For external validation, the model was used to predict 30-day status for each patient in the Main Phase Stroke Data Bank for whom complete risk factor information was available. Overall, 90% of patients' outcomes were correctly predicted with a sensitivity of 0.85 and a specificity of 0.92. Two factors not collected in the Pilot Stroke Data Bank, hyperglycemia and intraventricular hemorrhage extension, were assessed to determine if they provided additional predictive information on 30-day mortality. Intraventricular hemorrhage extension contributed significant predictive information in a logistic regression, whereas hyperglycemia did not. The resulting four-factor model with an interaction term (intraventricular hemorrhage extension and Glasgow Coma Scale score) correctly classified the survival status of 94% of patients at 30 days. A more general outcome, death or failure to achieve a "good" Activities of Daily Living Score by one year, was analyzed with respect to the same four factors. The resulting model correctly classified 95% of the patients in the cohort.

Blood Glucose↗
PubMed1991

Epidemiology of multi-infarct dementia.

Multi-infarct dementia (MID), thought to result from the cumulative effect of repeated episodes of cerebral infarction, represents a sizable proportion of the dementia cases in the population. The frequency of MID as the cause of dementia is commonly quoted as 12-20%, but a more conservative figure on the order of 10% is suggested from prospective epidemiologic studies. Its prevalence increases steadily with advancing age, and a male predominance has been noted. Geographical variations in prevalence of MID may reflect true geographic/ethnic differences or lack of uniformity in the use of diagnostic criteria. Risk factors possibly associated with dementia after stroke include advancing age, previous cerebral or myocardial infarction, an atherothrombotic stroke mechanism, and cerebral atrophy as detected by imaging studies. In order to clarify the role of cerebrovascular disease as a cause of dementia, future epidemiologic studies should define the entity in precise terms, and place emphasis on clearly establishing the temporal relationship between stroke and dementia; new onset of dementia should be correlated with the clinical and anatomic features of the stroke.

Age Factors↗
PubMed1991

Clinical-computed tomographic correlations of lacunar infarction in the Stroke Data Bank.

Lacunar stroke was diagnosed in 337 (26%) of the 1,273 patients with cerebral infarction among the 1,805 total in the Stroke Data Bank. We analyzed the 316 patients with classic lacunar syndromes. Among these, 181 (57%) had pure motor hemiparesis, 63 (20%) sensorimotor syndrome, 33 (10%) ataxic hemiparesis, 21 (7%) pure sensory syndrome, and 18 (6%) dysarthria-clumsy hand syndrome. No striking differences were found among the risk factors for the lacunar subtypes, but differences were found between lacunar stroke as a group and other types of infarcts. Compared to 113 patients with large-vessel atherosclerotic infarction, those with lacunar stroke had fewer previous transient ischemic attacks and strokes. Compared to 246 with cardioembolic infarction, patients with lacunar stroke more frequently had hypertension and diabetes and less frequently had cardiac disease. We found a lesion in 35% of the lacunar stroke patients' computed tomograms, with most lesions located in the internal capsule and corona radiata. The mean infarct volume was greater in patients with pure motor hemiparesis or sensorimotor syndrome than in those with the other lacunar stroke subtypes. In patients with pure motor hemiparesis and infarcts in the posterior limb of the internal capsule, there was a correlation between lesion volume and hemiparesis severity except for the few whose infarct involved the lowest portion of the internal capsule; in these patients severe deficits occurred regardless of lesion volume. Taken together, the computed tomographic correlations with the syndromes of hemiparesis showed only slight support for the classical view of a homunculus in the internal capsule.

Aged↗