Citations

The effect of cerebral anoxia on leucine incorporation into proteins of various subcellular fractions from rabbit brain was studied by using a previously reported in vitro model. Although the decrease in leucine incorporation was observed earlier in nuclei and microsomes, other fractions also demonstrated a rapid decrease. These results were quite different from the pattern of leucine incorporation observed in a type of reversible suppression produced with diphenylhydantoin.

The three factors other than age that are the most important determinants of stroke occurrence are (1) transient cerebral ischemic attacks (TIAs), (2) hypertension, and (3) cardiac disease. In the Rochester population study, a stroke developed during the period of observation in 36% of the patients with TIAs. Fifty-one percent of all the strokes occurred during the first year after the TIA, and 21% occurred during the first month after the first attack. Hypertensive persons have an increased incidence of each of the major atherothrombotic diseases as compared to normotensive persons. During the full 25 years of study of the Rochester population, there was a decrease from the earliest to the latest five-year period of 32% for all strokes in women and 20% in men. This may reflect treatment of this population.

This study has attempted to identify all patients in the population of Rochester, Minnesota, who had stroke during the period 1955 through 1969, and to determine the course and survival of patients who have had stroke. Cerebral infarction from all causes, including embolic infarction, accounted for 79% of all strokes. Intracerebral hemorrhage accounted for 10% of the cases, and subarachnoid hemorrhage accounted for 6%. The average annual incidence rate for the 15 years of the study was 164 per 100,000 population per year. The rates for all strokes and for cerebral infarction were significantly higher for men than for women, except in the youngest age group. After the end of an earlier study, 1945 through 1954, the average annual incidence rate for all strokes decreased in each succeeding five-year interval and reached 141 during the period 1965 through 1969. The decrease in rates is apparent for all strokes and for cerebral infarction, and is more apparent for women than for men. The prevalence rate on January 1, 1960, and January 1, 1965, of about 700 per 100,000 population was higher than the rate for January 1, 1970, reflecting decreasing incidence rates. A study of the functioning capacity of survivors of stroke after six months indicates that only 4% required total care and nearly 30% were functioning normally. Fifty-four percent had some neurological deficit that may have been benefited by rehabilitative care. Aphasia was an important residual incapacity in 10%. The first-year recurrence rate of stroke was 10%, and the five-year recurrence rate was 20%. Among patients with stroke who died, 38% died of the initial stroke, 10% of a subsequent stroke, and 18% of heart disease. During the 25-year period, 1945 through 1969, there has been a trend toward gradually increasing survival for cerebral infarction in this community.

Background and Purpose —Hypercholesterolemia is associated with abnormal endothelium-dependent vasorelaxation due to decreased nitric oxide bioavailability. Our aim was to examine the effect of adenovirus-mediated gene transfer of endothelial nitric oxide synthase (eNOS) to the hypercholesterolemic rabbit carotid artery in vivo. In addition, we examined whether adenovirus-mediated gene transfer was associated with vascular dysfunction. Methods —Rabbits were fed a 1% cholesterol diet for 4 weeks followed by a 0.5% cholesterol diet for 6 weeks. Vascular reactivity was assessed in nontransduced carotid arteries from chow- and cholesterol-fed animals. In addition, carotid arteries were surgically isolated, and 2 separate doses of adenoviral vectors encoding eNOS or β-galactosidase (AdβGal) on the contralateral side were delivered to the lumen (1×10 10 and 5×10 10 pfu/mL). Results —Abnormal acetylcholine-mediated endothelium-dependent vasorelaxation was detected in the carotid artery from cholesterol-fed animals, whereas responses to calcium ionophore A23187 and diethylamine NONOate were normal. Vascular reactivity was similar in nontransduced and AdβGal-transduced hypercholesterolemic vessels. In vessels transduced with eNOS, transgene expression was demonstrated by immunostaining in both the endothelium and the adventitia and by Western blot analysis. High-dose but not low-dose eNOS gene transfer enhanced endothelium-dependent relaxation in vessels from cholesterol-fed rabbits. Conclusions —Adenovirus-mediated gene transfer of eNOS to carotid arteries of cholesterol-fed animals improves endothelium-dependent relaxation when an optimal viral titer is administered.

Background and Purpose —Intracerebral hemorrhage (ICH) is a highly morbid disease process. Perihematomal edema is reported to contribute to clinical deterioration and death. Recent experimental observations indicate that clotting of the intrahematomal blood is the essential prerequisite for hyperacute perihematomal edema formation rather than blood-brain barrier disruption. Methods —We compared a series of patients with spontaneous ICH (SICH) to a series of patients with thrombolysis-related ICH (TICH). All patients were imaged within 3 hours of clinical onset. We reviewed relevant neuroimaging features, emphasizing and quantifying perihematomal edema. We then analyzed clinical and radiological differences between the 2 ICH types and determined whether these factors were associated with perihematomal edema. Results —TICHs contained visible perihematomal edema less than half as often as SICHs (31% versus 69%, P <0.001) and had both lower absolute edema volumes (0 cc [25th, 75th percentiles: 0, 6] versus 6 cc [0, 13], P <0.0001) and relative edema volumes (0.16 [0.10, 0.33] versus 0.55 [0.40, 0.83], P <0.0001). Compared with SICHs, TICHs were 3 times larger in volume (median [25th, 75th percentiles] volume 69 cc [30, 106] versus 21 cc [8, 45], P <0.0001), 4 times more frequently lobar in location (62% versus 15%, P <0.001), 80 times more frequently contained blood-fluid level(s) (86% versus 1%, P <0.001), and were more frequently multifocal (22% versus 0%, P <0.001). Conclusions —The striking qualitative and quantitative lack of perihematomal edema observed in the thrombolysis-related ICHs compared with the SICHs provides the first substantial, although indirect, human evidence that intrahematomal blood clotting is a plausible pathogenetic factor in hyperacute perihematomal edema formation.

Background and Purpose —There are few population-based data available regarding nursing home use after stroke. This study clarifies the use of a nursing home after stroke, as well as its dependence on stroke severity, in a defined population. Methods —All first stroke events among residents of Rochester, Minn, during 1987–1989 were ascertained, subtyped, and assigned Rankin disability scores (RS) before the event, at maximal deficit, and at specified intervals after stroke. Persons were followed from the date of stroke event to death, emigration from Rochester, or December 31, 1994, in complete community-based medical records and Minnesota Case Mix Review Program data tapes to determine nursing home residency before stroke and at 90 days and 1 year after stroke, proportion of survival days in a nursing home, and cumulative risk of admission to a nursing home. Results —There were 251 cases of first cerebral infarction, 24 intracerebral hemorrhages, and 15 subarachnoid hemorrhages among residents of Rochester during 1987–1989. The maximal deficit RS was 1 or 2 for 62 (25%), RS 3 for 72 (29%), and RS 4 or 5 for 117 (47%) of the cerebral infarct patients. Among patients surviving to 90 days or 1 year after cerebral infarction, 25% were in nursing home at 90 days and 22% at 1 year, respectively. Within these maximal deficit RS categories, the percentages of follow-up time spent in a nursing home during the first post–cerebral infarction year are as follows: RS 1 to 2, 4%; RS 3, 10%; and RS 4 to 5, 54%. Multivariate logistic regression revealed that increasing age and RS 4 to 5 at maximal deficit were independent predictors ( P <0.0001) of nursing home residency at 90 days and 1 year after stroke, whereas stroke type was not an independent predictor. At 1 year after cerebral infarction, the Kaplan-Meier estimates of proportion of people with at least 1 nursing home admission were 11% for RS 1 to 2, 22% for RS 3, and 68% for RS 4 to 5. Conclusions —This study provides unique population-based data regarding the short- and long-term use of a nursing home after stroke and its dependence on stroke severity. More than 50% of people with a severe cerebral infarction are in a nursing home 90 days and 1 year after the stroke, and by 1 year, nearly 70% will have required some nursing home stay. Age and stroke severity are independent predictors of nursing home residency after stroke.

Amino acid incorporation into proteins of rabbit brain slices was studied during the recovery stage after various anoxic periods in an in vitro experimental model. There was a distinct difference between anoxic periods up to five minutes and those beyond ten minutes. In the former, inhibition of amino acid incorporation was of lesser degree and was reversible. On the other hand, more than 50% inhibition was observed following anoxic periods of 30 minutes and this inhibition was irreversible. Amino acid incorporation into proteins was more sensitive to anoxia than was amino acid transport into brain slices.

Smooth muscle strips from rabbit subarachnoid arteries did not respond to catecholamines in concentrations which caused strips from skin, mesentery, and kidney vessels to contract. The strips from subarachnoid arteries responded to serotonin, histamine, and angiotensin II but not to bradykinin, acetylcholine, methacholine, and adenosine phosphate compounds. Heart and lung vascular strips did not respond to catecholamines but responded to acetylcholine; cardiac strips responded to dilute methacholine. Lung strips often failed to respond to histamine in usual concentrations and did respond to bradykinin. The subarachnoid strips had a distinactive pattern of respone as compared to vascular tissue from other organs. Results of other isolated vessel studies are reviewed along with pertinent investigations of cerebral autoregulation, vasospasm, and autonomic nerves. The possible significance of these findings is discussed.

Rehabilitation offers means by which persons disabled after a stroke can be returned to patterns of daily living as close to normal as possible. Often simple and readily available restorative techniques suffice, but sophisticated methods and facilities may be needed in many cases. Certain complex problems require specialized attention by persons with detailed knowledge and specific training. Among these are rehabilitation of language and the management of incontinence, sensory loss, pain, spasticity, and psychosocial problems. High-quality rehabilitation is best delivered by a closely cooperating team, including the family physician, medical specialists, nurses, allied health professionals (physical therapist, occupational therapist, social worker, dietitian, rehabilitation counselor, speech therapist, psychologist), the patient's family, and also the patient. To accomplish these ends, hospitals, rehabilitation centers, extended care facilities, and nursing homes should give specific attention to the special needs of stroke patients. Careful discharge planning and follow-up are necessary in all cases. The home environment and the family attitudes may require considerable revision to meet the patient's individual needs. The family physician can offer many rehabilitation services in his office, and additional education in medical school and on a postgraduate level will belp him to reach his full potential in aiding both the acutely ill and the chronically disabled stroke patient.