Search

Eight of 90 patients with ischemic neurologic events were found to have persistent, isolated high-level IgM anticardiolipin antibodies. Strokes were multiple in four patients. Six patients were under 50 years of age at the time of the first stroke.

The combined evaluation of the motor response to stimulation and the oculovestibular (OV) reflex gives useful indicants to the outcome of medical coma. We examined 48 patients during the first 12 h and at 24 h after the onset of medical coma. We excluded patients who had ingested drugs or who had hypothermia. Motor responses to a noxious stimulus were scored on a 6 'best' and 1 'worst' scale, and the presence or absence of oculovestibular responses to icewater irrigations was recorded. Subjects were divided by outcome at three months into three groups: death or persistent vegetative state, severe disability, and moderate disability or good recovery. On the basis of the present series it was often possible to distinguish among the outcomes at or before 24 h. The patient's age and the presence or absence of pupillary responses, spontaneous eye movements and oculocephalic responses were not predictive of outcome, nor were the respiratory pattern, blood gases, blood pressure, heart rate and temperature. A minimal motor score and an absence of oculovestibular responses at 12 h always were assoicated with death. With higher motor scores, the absence of oculovestibular responses at either 12 or 24 h implied an outcome no better than severe disability. The results of the present study imply that early bedside assessments can yield accurate predictive information in medical coma.

Sudden cardiac death is an important clinical problem that accounts for 750,000 deaths in the United States each year. There are 200,000 cardiac resuscitations each year, of which only 70,000 are successful. Survival depends upon early cardiopulmonary resuscitation and defibrillation. The brain's ability to tolerate no more than a few minutes of circulatory arrest is the major factor limiting the success of cardiopulmonary resusci tation. Cardiac arrest results in a spectrum of clinical disorders depending on the severity of cerebral anoxia. Neurological sequelae in survivors range from transient states of confusion and amnesia to prolonged uncon sciousness in a coma or in the vegetative state. Sequen tial neurological examinations alone or in conjunction with evoked potentials, electroencephalogram, com puted tomography, and positron emission tomography can indicate the degree of central nervous system dam age and the likely outcome. The clinical management of patients in coma following cardiac arrest involves resto ration of cardiopulmonary and metabolic homeostasis. No effective delayed therapy yet exists that can reverse anoxic damage, but several promising therapeutic agents are under laboratory and clinical investigation.

The effects of polyunsaturated fatty acids on brain edema formation have been studied in rats. Intracerebral injection of polyunsaturated fatty acids (PUFAs), including linolenic acid (18:3) and arachidonic acid (20:4), caused significant increases in cerebral water and sodium content concomitant with decreases in potassium content and Na+- and K+- dependent adenosine triphosphatase activity. There was gross and microscopic evidence of edema. Saturated fatty acids and monounsaturated fatty acid were not effective in inducing brain edema. The [125I]-bovine serum albumin spaces increased twofold and threefold at 24 hours with 18:3 and 20:4, respectively, indicating vasogenic edema with increased permeability of brain endothelial cells. Staining of the brain was observed five minutes after injection of Evans blue dye followed by arachidonic acid perfusion. A major decrease in brain potassium content was evidence of concurrent cellular (cytotoxic) edema as well. The induction of brain edema by arachidonic acid was dose dependent and maximal between 24 and 48 hours after perfusion. Dexamethasone (10 mg/kg) was effective in ameliorating the brain edema, whereas a cyclooxygenase inhibitor, indomethacin (10 mg/kg), was not. These data indicate that arachidonic acid and other PUFAs have the ability to induce vasogenic and cellular brain edema and further support the hypothesis that the degradation of phospholipids and accumulation of PUFAs, particularly arachidonic acid, initiate the development of brain edema in various disease states.

A comprehensive analysis of cerebral hemodynamics and metabolism was carried out in 14 patients with pseudotumor cerebri. Tracer techniques were employed to measure cerebral blood flow (CBF) and vascular reactivity to acute changes in arterial carbon dioxide tension and blood pressure, cerebral blood volume (CBV), and the cerebral metabolic rate for oxygen and glucose. There was a small reduction (p less than 0.01) in CBF (44 +/- 7 ml/100 gm/min; normal, 54 +/- 9) with normal vascular reactivity; an increase (p less than 0.005) in CBV (4.8 +/- 0.8 ml/100 gm; normal, 3.6 +/- 0.5), and normal cerebral metabolism. We conclude that an abnormality of the cerebral microvasculature is responsible for an elevation in CBV, but the intracranial hypertension can be explained only by tissue swelling due to an increase in water content. The relationship between the vascular abnormality and the tissue swelling remains to be defined.

There is substantial evidence to support the concept that most transient ischemic attacks (TIAs) are caused by microemboli that originate in areas of atherosclerosis in the blood vessels of the neck. TIA's are important risk factors in the development of stroke. The most common clinical features of TIAs caused by carotid insufficiency are hemianesthesia and hemiparesis; other symptoms in these cases include headache, dysphasia, and visual field distrubance. By far the most common clinical manifestation of vertebrobasilar insufficiency is vertigo.

Stroke is the most common neurologic disorder of adults and one of the three leading causes of death in North America. Results of a study suggest that inexpensive and easily obtained clinical variables can be used to predict which patients with stroke will do well and which will not. This capability is invaluable to physicians, patients with stroke and their families, and future investigators

A twenty-five year old woman suffered the acute onset of dysequilibrium followed by headache, nausea, vomiting, vertigo, and slurred speech while swimming. Brain imaging revealed a right cerebellar infarct. Intravenous digital subtraction angiography showed a hypoplastic right vertebral artery and focal narrowing of the dominant left vertebral at the level of the C1-C2 junction. The patient was treated with aspirin and dipyridamole and immobilized for two weeks. She achieved almost complete recovery. Repeat angiography showed resolution of the left vertebral artery defect. Other cases of posterior circulation infarction associated with head turning during sports and ordinary activities are reviewed.

Blood flow has been measured locally in the hypothalamus of anaesthetized rabbits by measuring the clearance of small volumes (5-20 mul.) of a mock cerebrospinal fluid solution containing 133Xe. The effect of varying the [K+] or [HCO-3] of the 133Xe-containing solution on local hypothalamic blood flow has been investigated. 2. There was an increase in local hypothalamic blood flow if the 133Xe-containing solution was HCO3--free; raising the [HCO--3,] of the solution to 40 mM caused a fall in local blood flow. 3. There was an increase in local hypothalamic blood flow when 133Xe was injectedin a mock cerebrospinal fluid containing 10 or 20 mM-[K+]. There was no significant change in blood flow if a K+-free or a 40 mM [K+] solution was used. 4. The decrease in hypothalamic blood flow caused by injecting a 40 mM-[HCO3] solution could be reversed by the addition of 20 mM [K+] to the solution. There was no further increase in blood flow if 20 mM-[K+] was added to a HCO3--free solution. 5. It is concluded that local blood flow in the hypothalamus changes as a result of variation in local [K+] as well as local [HCO-3]. The changes in blood flow in the brain which accompany neuronal activity could be mediated by variation in local [K+].

The clinical features of TIAs in the anterior and posterior cerebral circulations are fairly uniform and usually easily recognized. The pathogenesis of TIAs is varied, complex, and incompletely understood. The importance of TIAs rests on the fact that they may serve as dramatic warnings of an impending stroke. Depending on the type and cause of a TIA, medical therapy, alone or in combination with surgical intervention, can postpone or sometimes prevent permanent neurologic deficit. It is the task of the clinician first to determine which among many mechanisms—vascular, cardiac hematologic, or circulatory—is responsible for transient neurologic symptoms in an individual patient, and then to supply appropriate therapy as prophylaxis against a stroke.

Neurological signs and outcome are compared in the first 310 patients from a continuing prospective study of coma not caused by trauma or drugs. Sixteen percent of the patients achieved an independent existence within a month; severe disability or the vegetative state developed in 25% of patients comatose for six hours and in 79% of those still in coma after a week. The chance of regaining an independent existence was greater in patients who, by one day, obeyed commands or moved the limbs appropriately in response to noxious stimuli or who had attained any of the following: orienting eye movements, normal responses to oclulocephalic or ocluovestibular stimulation, or normal muscle tone. Conversely, the chance of regaining an independent existence fell in patients who, after one day, had either extensor responses of the limbs or failed to move them in response to noxious stimuli or who lacked eye opening, pupillary reactions, corneal responses, or any eye movement in response to oculovestibular or oculocephalic stimulation. Beyond these general guidelines, numbers of patients with particular signs are presently too small for confident prediction of outcome.

This paper presents a simple method of maintaining good donor organ oxygenation during a prolonged test of apnea used to determine brain death prior to cadaver transplantation. Apneic diffusion oxygenation can maintain arterial pO2 above 200 torr for periods exceeding 15 minutes, thereby allowing a more definitive determination of brain death without concomitant tissue hypoxia and possible damage to donor organs.

When the supply of substrate to the brain is threatened, homeostatic mechanisms induce cerebral vasodilatation to compensate for the insufficiency. When a region of the brain is rendered completely ischemic, local infarction occurs. The size of the infarct depends partly on the availability of collateral circulation and the adequacy of the homeostatic mechanisms controlling blood flow in stillpatent vessels. Several approaches to acute-phase treatment of stroke derive from clinical and experimental studies of cerebral blood flow and metabolism. We must conclude that both surgical and nonsurgical therapeutic measures have been of limited value in the treatment of cerebral infarction and that the basic therapy for completed stroke remains good medical management of complications and attentive nursing care.

Udgivelsesdato: 1975-Jul The Kety-Schmidt washout technique has been modified to measure whole-brain blood flow and metabolism in the rat. During nitrous oxide anesthesia, 14 rats exhaled (133)Xe, and continuous and simultaneous arterial and cerebral venous samples were drawn from a femoral artery and the transverse sinus of the brain. Extracerebral contamination of the venous sample was minimal, and equilibration of (133)Xe in brain tissue and blood was obtained after 10-24 min of inhalation. Cerebral blood flow was calculated from the total activity of the mechanically integrated arterial and venous samples according to the principle of Scheinberg and Stead. At a mean Paco2 of 40 mmHg, CBF averaged 98 +/- 6 (SEM) ml/100 g-min and CMRO2 averaged 5.4 +/- 0.7 (SEM) ml/100 g-min. CBF changed 2.4% with each millimeter Hg change of Paco2 while CMRO2 changed only insignificantly. The values obtained for CBF are higher than reported for man and large laboratory animals bur reflect the proportionately greater amount of gray matter in the rat brain.

Udgivelsesdato: 1977-Jul The cerebral blood flow and, in some rats, the cerebral rate of oxygen consumption were measured in three groups of male rats. Fractionation of radioisotope-labeled microspheres was used to measure regional cerebral blood flow in four parts of the rat brain. The arterial and cerebral venous concentrations of radioactive xenon during desaturation were used to measure the blood flow and oxygen consumption of cortex when venous blood was collected from the superior sagittal sinus, or of whole brain when the transverse sinus was sampled. The regional cerebral flow measured with microspheres had a large standard error reflecting the technical difficulty of this method. The cerebral blood flow measured with xenon was higher when venous blood was sampled from the superior sagittal sinus than when sampled from the transverse sinus, but cerebral oxygen consumption rates were similar. The difference reflects the greater trauma involved in the superior sagittal approach and possible extracerebral contamination present in the transverse sinus approach.

Cerebral blood flow was measured in four subjects with chronic idiopathic autonomic insufficiency using 85 Kr inhalation, cerebral A-V samples for scintillation counting, and O 2 content determination. Blood pressure was varied by up or down tilting and L-norepinephrine infusion. In three patients with typical Shy-Drager syndrome and preganglionic denervation, CBF regulation to pressure and Pa CO CO 2 change was intact. In a fourth patient with postganglionic denervation, CBF autoregulation was absent to changes in blood pressure but was preserved normally to increases or decreases in Pa CO CO 2 CBF and CMRO 2 , at rest were normal (52.6 cc and 3.1 cc). Hyperventilation to Pa CO CO 2 34.3 mm failed to restore autoregulation to increased blood pressure. The results imply a functional role for postganglionic autonomic fibers in CBF autoregulation.

Outcome from coma caused by cerebral hypoxia-ischemia (eg, cardiac arrest) was compared with serial neurological findings in 210 patients. Thirteen percent of patients regained independent function at some point during the first postarrest year. Computer application of new multivariate techniques to the prospectively observed findings generated easily utilized rules that classified patients by likely outcome. At the time of initial examination, 52 patients (one fourth of the total population) had absent pupillary light reflexes, and none of these patients ever regained independent daily function. By contrast, the initial presence of pupillary light reflexes, the development of spontaneous eye movements that were roving conjugate or better, and the findings of extensor, flexor, or withdrawal responses to pain identified a smaller group of 27 patients, 11 (41%) of whom regained independence in their daily lives. By 24 hours after onset, 93 poor-outcome patients were identified by motor responses that were absent, extensor, or flexor and by spontaneous eye movements that were neither orienting nor roving conjugate; only one regained independent function. This contrasts with recovery in 19 (63%) of 30 patients who at that time showed improvement in their eye-opening responses and obeyed commands or had motor responses that were withdrawal or localizing. Similarly simple rules distinguished between good- and poor-prognosis patients on postarrest days 3, 7, and 14.

We conducted serial neurologic examinations on 500 patients in nontraumatic coma to identify factors predicting recovery. Overall, 81 patients (16%) led an independent life at some point within the first year; the remainder either died without recovery from coma (61%), never improved beyond the vegetative state (12%), or regained consciousness but remained dependent on others for daily activities (11%). Functional recovery did not depend on age but was to some degree related to the cause of coma (subarachnoid hemorrhage and other cerebrovascular disease having the worst recovery; hypoxia-ischemia, intermediate; and hepatic and miscellaneous causes, best) and especially to early clinical signs of brain dysfunction. Even within hours of the onset of coma, only one of 120 patients lacking two of corneal, pupillary, and oculovestibular responses ever regained independent function. The study identifies clinical features of comatose patients that appear within the first week and that are important for predicting recovery and designing future therapeutic trials.

Seven cases of upward transtentorial herniation occurred. In each patient, coma with reactive, miotic pupils, asymmetrical or absent caloric responses, and decerebrate posture indicated brain-stem compression. In this setting, the development of unequal, then midposition, fixed pupils signaled midbrain failure from upward herniation. Vertebral angiography showed upward displacement of the superior cerebellar arteries. Results of autopsy confirmed the existence of grooving of the vermis by the tentorial margins and, in one case, of anterior displacement and distortion of the midbrain. In five of 45 reported cases of upward herniation, the conditions were diagnosed antemortem. Instances of cerebellar hematoma and tumor predominated. In at least seven patients, performance of ventriculography may have precipitated herniation. Clinical details were provided in only nine patients and did not separate upward herniation from brain-stem compression. Cerebellar ischemic infarct found in one of our patients is a rarely reported cause of upward herniation.

This book, the 12th in the Physical Medicine Library series, is a collection of essays dealing with stroke from the physical medicine and rehabilitation viewpoint. Sixteen authors from the fields of physical medicine, neurology, neuropathology, nursing, and social work have contributed 18 chapters and an appendix on stroke. The basic points of the epidemiology, pathology, diagnosis, and acute care of strokes are reviewed in several chapters before the more chronic aspects of stroke care and rehabilitation are discussed. The avowed purpose of this volume is to provide a textbook and reference source on stroke for the resident in rehabilitation medicine; in my opinion, it falls short of its goal. The essays vary in their merit; several are balanced, well-referenced reviews of a topic. Others are personal and anecdotal with few, and in one case no, references. The editor appears to have exercised little control over content, eg, the chapter dealing

This collection of essays provides an excellent overview of the topic of cerebral ischemia and a thorough review of the relevant literature. As may be inferred from its subtitles, the book is divided into three sections. The first deals with the applied anatomy and physiology of the cerebral circulation and serves to clarify subsequent discussion of the natural history and treatment of stroke. This section is followed by a superb chapter by Drs A. J. McCall and P. J. H. Fletcher summarizing current concepts of the pathogenesis of stroke. Succinct chapters on epidemiology and risk factors are included. The third section includes a short chapter (9 pages) on medical treatment that, unfortunately, does not discuss the role of antiplatelet agents in the treatment of transient ischemic attacks and does not mention the diagnostic value of the computerized tomographic scan. The chapter on surgical treatment is long (39 pages), anecdotal, and

The use of oral contraceptives has been associated with a variety of disorders including pulmonary embolism, depression, stroke, chorea, hypertension, migraine, pseudotumor cerebri, optic neuritis, and seizures. Cerebral arterial occlusive disease, especially of the vertebral and basilar arteries, has been documented in otherwise healthy young women using the Pill. Considerable controversy surrounds the issue of a causal relationship between the Pill and several neurologic conditions, chiefly stroke. In this brief monograph, Dr Bicker-staff traces the development of this controversy and reviews the published evidence, mainly case reports and retrospective clinical surveys, for and against a causal relationship. A large part of the book is devoted to the problem of cerebral arterial occlusive disease, but the relationship of the use of the Pill to the development of chorea and the exacerbation of migraine and epilepsy is considered. The author indicates where the relationship is certain, where it is merely possible, and

To determine the duration of respiratory arrest needed to attain a PaCO2 level high enough to provide maximal stimulation of respiration, we evaluated changes in PaCO2, PaO2 and apH during periods of apnea lasting as long as 10 minutes in 10 apparently brain-dead subjects. Before apnea, mean PaCO2 was 33 mm Hg. In seven subjects who did not breathe for 10 minutes, the mean rate of rise of PaCO2 was 3.2 mm Hg per minute. PaCO2 at 4 minutes was 50 mm Hg and at 10 minutes was 67 mm Hg. Three subjects breathed, two after less than 2 minutes of apnea, when PaCO2 was 47 and 54 mm Hg, and one after 4.5 minutes, when PaCO2 was 47 mm Hg. These data indicate: (1) that the threshold for respiratory stimulation may approach a PaCO2 of 60 mm Hg in patients with brain damage; (2) that the rate of increase in PaCO2 is such that, even in a normocapnic subject after 3 minutes of apnea, the PaCO2 may not be sufficiently high to stimulate respiration; and (3) if a patient is hypocapnic prior to the onset of apnea, PaCO2 may not reach 60 mm Hg even after 15 minutes. To confirm absolute apnea, then, blood gas monitoring is necessary for verification of normocapnia prior to the beginning of apnea. In the absence of blood gas determinations, no fixed period of apnea, sufficient in all cases to establish absolute apnea, can be ascertained.