PubMed HealthSearch

Biomedical subjects

C S Kase

Publications and source records attributed to C S Kase.

At least 19 recordsLinked to original sources

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

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

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

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

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

Diagnosis and management of intracerebral hemorrhage in elderly patients.

An analysis of the risk factors and clinical presentation of intracerebral hemorrhage in the elderly is provided. Specific pathogenic mechanisms that apply to the elderly, such as cerebral amyloid angiopathy, are discussed in detail. General management of intracerebral hemorrhage is discussed, along with specific issues related to the surgical indications of the various types of intracerebral hemorrhage.

Aged

Intracranial hemorrhage after use of tissue plasminogen activator for coronary thrombolysis.

Tissue plasminogen activator (tPA), an approved coronary thrombolytic agent, can cause serious bleeding. We report the cases of six patients with intracranial hemorrhage after tPA treatment for acute myocardial infarction. None of the patients were hypertensive at admission, and only one was hypertensive during therapy. Intravenous tPA, 100 mg, was followed by continuous intravenous heparin infusion; intracranial hemorrhage occurred between 2 and 14 hours after tPA infusion ended and between 3 and 17 hours after heparin therapy was started. The partial thromboplastin time (PTT) was excessively prolonged (from 81 s to more than 150 s) in all patients at onset of intracranial hemorrhage. The intracerebral hematomas were predominantly of lobar location, and two patients had multiple simultaneous hemorrhages. Four patients died from massive intracranial hemorrhage; the mechanism for these hemorrhages was unclear. Factors possibly related to hemorrhage include a systemic fibrinolytic state or a platelet anti-aggregant effect produced by tPA and enhanced hemorrhagic tendency caused by the combined effects of tPA and heparin. Local vascular changes at the bleeding site remain as potential contributing factors for isolated intracranial hemorrhage.

Aged

Caudate infarcts.

Eighteen patients had caudate nucleus infarcts (10 left-sided; 8 right-sided). Infarcts extended into the anterior limb of the internal capsule in 9 patients, and also the anterior putamen in 5 patients. Thirteen patients had motor signs, most often a slight transient hemiparesis. Dysarthria was common (11 patients). Cognitive and behavioral abnormalities were frequent, and included abulia (10 patients), agitation and hyperactivity (7 patients), contralateral neglect (3 patients, all right caudate), and language abnormalities (2 patients, both left caudate). The majority of patients had risk factors for penetrating artery disease. Branch occlusion of Heubner's artery, or perforators from the proximal anterior or middle cerebral arteries were the posited mechanism of infarction.

Adult

Infarcts with a cardiac source of embolism in the NINCDS Stroke Data Bank: historical features.

To gain insight into the historical features relevant to the diagnosis of cardiac embolic strokes, we studied the 1,290 patients with cerebral infarcts in the NINCDS Stroke Data Bank. Based solely on the presence of cardiac sources of embolism, we divided the patients into groups of high (n = 250), medium (n = 166), and low (n = 874) risk of a cardiogenic mechanism for their stroke. There was a highly significant graded relationship between increasing risk of a cardiac source and a history, or presence of, systemic embolism, abrupt onset, and diminished level of consciousness at onset. These clinical features may be useful for assessing the likelihood of a cardiac embolic mechanism in patients with cerebral infarcts.

Cerebral Infarction

Intracerebral hemorrhage in stroke patients anticoagulated with heparin.

To characterize the clinical features of patients with acute cerebral infarction who sustained intracerebral hemorrhage related to heparin anticoagulation, we describe 10 patients and review reports of 16 cases. Cardiac-source embolism was identified in seven (70%) of the 10 patients and consisted of atrial fibrillation in six of the seven. The middle cerebral artery territory was affected in nine patients (90%), with moderate-sized or large infarcts by clinical and computed tomographic criteria. The interval between stroke onset and intracerebral hemorrhage was less than 72 hours in 80% of the patients. Intracerebral hemorrhage occurred less than or equal to 24 hours after the time heparin was started in 80% of the patients. The activated partial thromboplastin time closest to the time of intracerebral hemorrhage was greater than 2 x control in seven patients. Our findings in the 10 patients are similar to those of the 16 cases previously reported and suggest that heparin-related intracerebral hemorrhage occurs early after stroke onset, usually with moderate-sized or large infarcts, and with excessive anticoagulation in some patients.

Adult

Prevalence of silent stroke in patients presenting with initial stroke: the Framingham Study.

It is common to find computed tomography scan evidence of prior stroke without a history of such an event. The frequency, risk factors for, and relevance of silent strokes are unknown. The Framingham cohort of 5,184 men and women aged 30-62 years and free of stroke at entry to the study have been followed with periodic examinations since 1950. We studied the silent strokes found on computed tomography scan of all initial strokes that occurred between January 1, 1979, and July 31, 1987. During these 8 1/2 years, 164 initial strokes occurred; 124 had computed tomography scans performed. There were 13 (10%) with silent stroke, 71 had abnormalities related to their presenting acute stroke, and 40 had normal computed tomography scans. There were 15 silent lesions; eight were lacunar infarcts in the basal ganglia-internal capsule area, seven were small cortical infarcts. Glucose intolerance was the sole risk factor that occurred significantly more frequently (11 of 13) in the group with silent lesions (p less than 0.04) than in the group with computed tomography evidence of acute stroke. Silent stroke is not rare; it was present in at least 10% of acute initial stroke patients arising in a general population. The relation of these silent lesions to the development of "vascular" dementia and poststroke disability deserves further study.

Cerebral Infarction

Prediction of intracerebral hemorrhage survival.

The Pilot Stroke Data Bank obtained information on 94 patients with intracerebral hemorrhage. These data were used to identify factors predictive of 30-day outcome from among 85 demographic, historical, clinical, and laboratory variables generally available to clinicians on the day of admission. The 9 univariate factors statistically associated with outcome were Glasgow Coma Scale score, systolic blood pressure, pulse pressure, horizontal and vertical gaze palsies, severity of weakness, presence of brainstem-cerebellar deficits, interval stroke course, and parenchymal hemorrhage size. Beginning with these factors, a step-down variable selection procedure was used to derive a logistic regression model, containing only Glasgow Coma Scale score, pulse pressure, and hemorrhage size, that could be used to categorize correctly 92% of the patients as alive or dead at 30 days after onset.

Cerebral Hemorrhage

Ischemic stroke after cardiac pacemaker implantation in sick sinus syndrome.

The risk of embolic stroke during sick sinus syndrome before cardiac pacemaker insertion is substantial, but stroke after pacemaker insertion has not been well studied. We observed 10 sick sinus syndrome patients who developed an ischemic stroke 4 days to 112 months after pacemaker insertion. Nine patients represented 6% of the 156 ischemic stroke patients observed during a 30-month period. Eight had a ventricular-demand pacemaker, one had a dual-chamber pacemaker, and one had an atrial-inhibited pacemaker. Six patients were in atrial fibrillation at stroke onset, but none had atrial fibrillation when the pacemaker was inserted. Six patients were taking aspirin, and one was anticoagulated when stroke occurred. Stroke in sick sinus syndrome after pacemaker insertion is not rare, and pacing does not appear to be protective. Sick sinus syndrome patients who convert to atrial fibrillation or who have a ventricular-demand pacemaker might represent high-risk groups for stroke.

Aged

Silent stroke in the NINCDS Stroke Data Bank.

Previous brain infarctions seen on CT are common in the absence of history of stroke. Eleven percent of patients (135/1,203) without stroke history had ischemic lesions on their first CT, unrelated to the presenting stroke. Stroke Data Bank files were reviewed to determine whether the occurrence, location, and CT characteristics of those lesions are associated with their undetected status. Two distinct patterns were seen: (1) Small lesions of 1 cm or less were left hemisphere predominant and involved the deep structures of the brain; the majority of these were clinically silent. (2) Lesions greater than 1 cm occurred more frequently in the right hemisphere and were mostly superficial; these infarcts produced signs unrecognized by the patient or family. Risk factors for silent stroke were similar to those for stroke in general. Frequencies of in-hospital complications and 30-day fatality rates from the presenting stroke were not influenced by the existence of a prior silent stroke.

Adult

Interobserver reliability in the interpretation of computed tomographic scans of stroke patients.

Interobserver reliability in interpretation of computed tomographic images was studied by six senior neurologists who independently evaluated on a standardized Stroke Data Bank form the brain lesions of 17 patients. The results analyzed with kappa statistics yielded moderate to substantial agreement on most items of interest including the stroke pathology and anatomy. In general, the levels of agreement were as high as previously reported for the diagnosis of the mechanism of the stroke, and much higher than on many stroke history items and items of neurologic examination. Excellent agreement was obtained for the detection of infarcts and intracerebral hemorrhage, and substantial agreement was obtained on whether the computed tomographic images were normal or indicative of small deep infarcts, superficial and deep infarcts, and aneurysms. The level of agreement on anatomy of the lesions was best for the frontal, parietal, and temporal lobes, putamen, cerebellum, and subarachnoid space. Implications for clinical research and diagnosis are discussed.

Adult