Stroke in patients with isolated IgM anticardiolipin antibody.

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.

Vertebral artery injury and cerebellar stroke while swimming: case report.

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.

Predicting outcome from hypoxic-ischemic coma.

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.

Induction of brain edema following intracerebral injection of arachidonic acid.

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.

Clinical predictors of outcome in ischemic stroke.

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.

Prognosis in nontraumatic coma.

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.

Neurologic outcome after emergency room thoracotomy for trauma.

The charts of 168 patients undergoing resuscitative thoracotomy for trauma in the emergency room at the San Francisco General Hospital from 1972 through 1978 were reviewed to assess factors affecting neurologic recovery after cardiac arrest. Forty-nine patients survived resuscitation and definitive operation, but 8 of them died in the first 24 hours postoperatively. Four patients in this group made some neurologic recovery (two good recoveries, two severe disabilities) but died later (12 to 44 days postoperatively) of septic complications. Thirteen nonsurvivors made no neurologic recovery before death. There were 33 long-term survivors (19.6 percent), 10 of whom were agonal or had no vital signs when first admitted to the emergency room. A persistent vegetative state developed in two patients who later died of sepsis (10 days and 14 months postoperatively). The remaining 32 patients all made good neurologic recovery that was apparent within 12 hours postoperatively. Transient amnesia was present during recovery in three patients. Wakefulness was the best prognostic sign of full neurologic recovery. In conclusion, emergency room thoracotomy can save a substantial number of moribund trauma patients who can be expected to sustain full neurologic recovery if they awaken within 12 hours.

Upward transtentorial herniation: seven cases and a literature review.

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.

Cerebral hemodynamics and metabolism in pseudotumor cerebri.

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.

Duration of apnea needed to confirm brain death.

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.

Brain death, apneic diffusion oxygenation, and organ transplantation.

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.