Biomedical subjects
Publications and source records attributed to C S Kase.
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.
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.
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.
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.
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.
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.
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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.
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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.
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.
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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.
Two patients developed intracerebral hemorrhage within hours from first-time ingestion of phenylpropanolamine-containing medications. One patient had marked hypertension, presented with three intracerebral hematomas, and developed a fourth hemorrhage 10 days later. Angiogram in one patient revealed "beading" of intracranial arteries, an abnormality also detected in a third patient who developed severe headache, vomiting, and acute hypertension following a single dose of phenylpropanolamine. These cases and others reported in the literature strongly suggest an association between phenylpropanolamine ingestion and hemorrhagic stroke. Direct questioning of use of this medication in cases of unexplained intracranial hemorrhage in previously healthy young individuals may reveal an unsuspected high frequency of this association.
Interobserver agreement is essential to the reliability of clinical data from cooperative studies and provides the foundation for applying research results to clinical practice. In the Stroke Data Bank, a large cooperative study of stroke, we sought to establish the reliability of a key aspect of stroke diagnosis: the mechanism of stroke. Seventeen patients were evaluated by six neurologists. Interobserver agreement was measured when diagnosis was based on patient history and neurologic examination only, as well as when it was based on results of a completed workup, including a computed tomographic scan. Initial clinical impressions, based solely on history and one neurologic examination, were fairly reliable in establishing the mechanism of stroke (ie, distinguishing among infarcts, subarachnoid hemorrhages, and parenchymatous hemorrhages). Classification into one of nine stroke subtypes was substantially reliable when diagnoses were based on a completed workup. Compared with previous findings for the same physicians and patients, the diagnosis of stroke type was generally more reliable than individual signs and symptoms. These results suggest that multicentered studies can rely on the independent diagnostic choices of several physicians when common definitions are employed and data from a completed workup are available. Furthermore, reliability may be less for individual measurements such as signs or symptoms than for more-complex judgments such as diagnoses.
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We searched the Stroke Data Bank and personal files to find patients with CT-documented infarcts in the territory of the inferior division of the right middle cerebral artery. The most common findings among the 10 patients were left hemianopia, left visual neglect, and constructional apraxia (4 of 5 tested). Five patients had an agitated confusional state that was characterized by hyperactivity, restlessness, and easy distractibility. Motor and sensory abnormalities were not severe or persistent. The most common cause was cardiogenic embolism.
Interobserver reliability in obtaining neurologic histories and examinations was investigated among neurologists collaborating in the Stroke Data Bank (SDB). Seventeen in-hospital stroke patients were examined by six neurologists experienced in stroke over the course of three days. Patients were examined twice a day for two successive days, with each patient seen by four different neurologists. Data were recorded on SDB forms, according to definitions and procedures established for the SDB. Percent agreement and kappa coefficients were calculated to assess the levels of agreement for each item. Important differences in levels of agreement were found among items on both neurologic history and examination. Agreement among neurologists was higher for neurologic examination than for history. Patterns of agreement for items with low prevalence or with numerous unknown ratings are discussed. Improvement in interobserver agreement due to data editing for intra-observer consistency was shown.