Exacerbation or unmasking of focal neurologic deficits by sedatives.

BACKGROUND: Transient focal neurologic deficits have been observed in patients emerging from brain tumor or carotid surgery, and a pharmacologic effect of anesthetic agents has been proposed as the cause of such neurologic dysfunction. Therefore, the effect of sedation with midazolam or fentanyl on motor neurologic function was studied prospectively and preoperatively in patients with carotid disease or mass lesions of the brain. METHODS: Fifty-four unpremedicated adult patients with carotid disease or a brain tumor were given small intravenous doses of either 2.8 +/- 1.3 mg midazolam or 170 +/- 60 micrograms fentanyl in the preoperative period. A thorough motor examination was performed at baseline and after sedation by an individual who was unaware of the details of the patient's disease or symptoms. A mental status examination also was performed to control for the effects of inattentiveness or lack of cooperation during the neurologic examination. RESULTS: Patients were sedated mildly but were fully cooperative. Focal motor deterioration occurred after sedation in 30% of patients, and the incidence was similar in patients in the fentanyl and midazolam groups. Among patients with a focal motor abnormality on baseline examination or a resolved prior motor deficit, 73% had exacerbation or unmasking of these signs by sedation, whereas no patient without a prior history of motor dysfunction had a sedative-induced change. Sedative-induced changes in neurologic function ranged from unilateral mild weakness to complete plegia, but appeared to be transient in nature. CONCLUSIONS: Sedation with midazolam or fentanyl can transiently exacerbate or unmask focal motor deficits in patients with prior motor dysfunction.

Myocardial perfusion following acute subarachnoid hemorrhage in patients with an abnormal electrocardiogram.

To test the hypothesis that acute subarachnoid hemorrhage is associated with abnormal myocardial perfusion, we assessed myocardial blood flow with thallium scintigraphy in 19 patients with a confirmed subarachnoid hemorrhage and an abnormal electrocardiogram. A thallium scan was performed at the bedside of each patient 3 +/- 2 days (mean +/- SD) after subarachnoid hemorrhage and subsequently was analyzed both qualitatively and quantitatively. Patients averaged 58 +/- 13 yr of age and 68% had one or more cardiac risk factors. The neurologic condition of patients on the day of the scan was II (median; range I-V) on the standard 5-point scale of Botterell. Abnormalities on a standard 12-lead electrocardiogram obtained on the same day as the scan consisted of repolarization changes in most patients; 10 had T wave inversions and 8 had nonspecific ST segment changes. Thirty-two percent (n = 6) of patients had an abnormal thallium scan. There were, however, no features of the clinical history, electrocardiogram pattern, or neurologic condition that were associated with a positive scan. For instance, 2 of 4 patients with diffuse deeply inverted T waves had a normal thallium scan, whereas the scan was abnormal in 2 of 8 patients with minor nonspecific electrocardiographic abnormalities. The thallium scan was also positive in neurologically intact (grade I) as well as severely injured (grade V) patients. Thus, abnormal myocardial perfusion and possibly myocardial ischemia occur frequently following subarachnoid hemorrhage, but no specific electrocardiographic characteristic identifies patients with a perfusion abnormality.

Excessive atlanto-occipital flexion as a cause of complete airway obstruction following anterior cervical spine fusion.

This report describes complete airway obstruction following anterior cervical fusion caused by extreme, fixed flexion of the neck in a halo device. The causes and treatment of such an airway complication are reviewed.

Subarachnoid clonidine reduces spinal cord blood flow and glucose utilization in conscious rats.

The authors investigated the spinal blood flow and metabolic effects of subarachnoid clonidine in conscious rats prepared with chronically implanted subarachnoid catheters. For the blood flow experiments, rats received saline (n = 7) or clonidine 20 nmol (7 micrograms; n = 6), 100 nmol (27 micrograms; n = 5), or 400 nmol (107 micrograms; n = 7) intrathecally. Another group of rats received clonidine 400 nmol intravenously (n = 4). Spinal glucose utilization was measured in rats that received either saline (n = 5) or clonidine 100 nmol (n = 5) intrathecally. Spinal cord blood flow (SCBF) and glucose utilization were measured in five gray and three white matter areas of lumbar spinal cord 15 min after drug administration with the autoradiographic iodo-[14C]-antipyrine and 2-[14C]-deoxyglucose methods, respectively. Physiologic differences between the groups were minor. Rats in the blood flow experiments that received clonidine 100 nmol had a slightly lower arterial PO2 level (70 +/- 1 vs. 82 +/- 3 mmHg; P less than 0.05), whereas those in the glucose utilization group were mildly hypocarbic (PCO2 27 +/- 1 vs. 32 +/- 2 mmHg; P less than 0.01) relative to control animals. Only animals that received 400 nmol clonidine intrathecally had significant analgesia, as assessed by the tail-flick test. One control animal for the metabolism experiments was technically unsatisfactory and was excluded from data analysis. Subarachnoid clonidine reduced both SCBF and glucose utilization. In spinal gray matter, the largest decreases in flow (32-44%; P less than 0.01) occurred with 20 nmol clonidine, whereas flow decreased least (12-27%) with the 400-nmol dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertension does not cause spontaneous hemorrhage of intracranial arteriovenous malformations.

The authors measured blood pressure changes non-invasively in 56 conscious, unpremedicated patients with cerebral arteriovenous malformations (AVMs) during preparation for proton beam therapy. The procedure requires six injections of local anesthetic and application of a stereotactic frame by fixation into the outer table of the skull, and has been used during the past 20 yr to treat over 1,000 patients with cerebral AVMs. No effort was made to control blood pressure. Blood pressure increased during administration of the local anesthetic and application of the frame. Maximum systolic and mean arterial pressures averaged 160 +/- 17 and 118 +/- 7 mmHg (mean +/- SD), respectively. This represented an average increase of 44 mmHg (38%) in systolic pressure and 32 mmHg (37%) in mean blood pressure at some point during the procedure (P less than 0.01 compared with pretreatment control pressures). Systolic pressure increased more than 60 mmHg in 21% of patients. Nevertheless, none of these 56 patients nor any of the more than 1,000 patients treated in similar fashion suffered a clinically evident AVM hemorrhage during the procedure. Since the treatment protocol has not changed materially during the past 20 yr, the authors assume that most patients treated in this fashion developed a similar degree of hypertension and conclude from this large clinical experience that moderate arterial hypertension does not precipitate spontaneous hemorrhage of intracranial AVMs.

Effect of profound hypermagnesemia on spinal cord glucose utilization in rats.

The purpose of our study was to investigate the effect of hypermagnesemia on spinal metabolic rate. The 2-[14C]deoxyglucose technique was used to measure regional glucose utilization in the lumbar spinal cord of paralyzed, mechanically ventilated rats receiving 70% nitrous oxide and an intravenous infusion of either saline (n = 5) or magnesium sulfate (n = 5). Plasma magnesium concentrations were 6.75 +/- 0.5 and 0.9 +/- 0.5 mM (p less than 0.01) in hypermagnesemic and control rats, respectively. Hypermagnesemic rats were hypotensive (88 +/- 1 vs. 130 +/- 4 mm Hg, p less than 0.01) but blood pressure remained within the autoregulatory range. Glucose utilization was reduced 26-45% in spinal gray matter and 53-63% in spinal white matter during hypermagnesemia. We conclude that magnesium is a potent spinal metabolic depressant and that this action, which is unusually prominent in spinal white matter, is a plausible explanation for the recently reported beneficial effect of magnesium therapy during spinal cord ischemia.