Elevation of monocyte chemoattractant protein-1 in patients experiencing neurocognitive decline following carotid endarterectomy.

BACKGROUND: Previous studies have demonstrated that elevated pre-operative monocyte count is an independent predictor of acute neurocognitive decline following carotid endarterectomy (CEA). Monocyte chemoattractant protein-1 (MCP-1), secreted by human endothelial and monocyte-like cells, is a potent mediator of inflammation and mononuclear cell trafficking. This study examines the relationship between peri-operative serum MCP-1 elevation and post-operative neurocognitive injury following CEA. METHODS: Fifty-two patients undergoing CEA and 67 lumbar laminectomy (LL) controls were administered a battery of five neuropsychological tests pre-operatively and on post-operative day 1 (POD 1). Change in individual test scores from baseline to POD 1 were converted into Z-score and used to develop a point system quantifying the degree of neurocognitive dysfunction relative to change within the LL group. Neurocognitive injury following CEA was defined as a score greater than 2 standard deviations above mean total deficit scores of LL controls. Serum MCP-1 levels were measured pre-operatively and on POD 1 by enzyme-linked immunosorbent assay. FINDINGS: Mean percent MCP-1 elevation was higher for the 13 injured CEA patients (147.7 +/- 32.4%) in our cohort compared to 39 age- and sex-matched uninjured CEA patients (76.0 +/- 16.5%). In unconditional multivariate logistic regression analysis, percent elevation in serum MCP-1 level was associated with neurocognitive injury one day after CEA (OR = 2.19, 95% CI = 1.13-4.26, P = 0.021, for a 100% elevation from pre-operative levels). CONCLUSIONS: Peri-operative elevations in serum MCP-1 levels correlate with acute neurocognitive dysfunction following CEA. These data implicate an inflammatory mechanism in the pathogenesis of Ischaemic neurocognitive decline.

Inactivation of monazomycin-induced voltage-dependent conductance in thin lipid membranes. I. Inactivation produced by long chain quaternary ammonium ions.

The voltage-dependent conductance induced in thin lipid membranes by monazomycin undergoes inactivation upon the introduction of quaternary ammonium ions (QA) having a long alkyl chain (e.g. dodecyltrimethylammonium [C12]) to the side containing monazomycin. That is, in response to a step of voltage the conductance rises to a peak and then falls to a much lower steady-state value. We demonstrate that the basis of this phenomenon is the ability of QA to pass through the stimulated membrane and bind to the opposite surface. As a consequence, the surface potential on that side becomes more positive, thus reducing the voltage across the membrane proper and turning off the monazomycin-induced conductance. Because the flux of QA through the membrane increases linearly with conductance, we believe that these ions pass through the monazomycin channels. QA permeability increases with alkyl chain length; remarkably, in spite of its much larger size, C12 is about 150 times more permeant than K+. It appears, therefore, that there is a hydrophobic region of the cahnnel that favors the alkyl chain; we propose that this region is formed by the hydrophobic faces of the monazomycin channels in lipid bilayers to QA inactivation of potassium channels in the squid giant azon, and suggest that there may be a common structural feature for the two channels. It is possible that some of the inactivation phenomena in excitable cells may arise from local field changes not measurable by the recording electrodes.

Bicuculline: a convulsant with synaptic and nonsynaptic actions.

The convulsant bicuculline (BICUC) had both synaptic and nonsynaptic actions on mouse spinal cord neurons in primary dissociated cell culture. BICUC antagonized postsynaptic responses to the inhibitory neurotransmitter GABA (a synaptic action) and produced direct membrane depolarization by blocking a membrane potassium conductance and directly prolonging calcium-dependent action potentials (nonsynaptic actions). In cultured spinal cord neurons, BICUC also produced paroxysmal depolarizing events (PDE), which might be equivalent to in vivo convulsant-induced bursting in spinal cord neurons or paroxysmal depolarizing shifts (PDS) in cortical neurons. Thus, the concentrations of BICUC producing both synaptic and nonsynaptic actions overlapped those producing paroxysmal activity. The results suggest that in addition to antagonism of GABA-mediated synaptic inhibition, direct nonsynaptic actions of BICUC may be required for some neurons to develop PDS.

Nitrous oxide: clinical and electrophysiologic investigation of neurologic complications.

Prolonged exposure to nitrous oxide produces a recognized neurologic syndrome. We report clinical and electrophysiologic studies of nervous system involvement in a 25-year-old student who abused nitrous oxide. He developed signs of a sensorimotor polyneuropathy and of myelopathy. Routine blood studies, CSF examination, and myelogram were normal. Clinical electrophysiologic studies were performed serially. Nerve conduction studies demonstrated reduced amplitude and slowed sensory potentials, and mildly prolonged late responses. Sensory evoked potentials revealed prolonged latency of scalp-evoked potentials from tibial nerve stimulation with normal median nerve values. The foveal visual evoked potential was delayed in the right eye, with normal visual acuity, funduscopic examination, and spatial contrast sensitivity. Repeat electrophysiologic studies demonstrated improvement. Nitrous oxide produces multifocal reversible dysfunction within the nervous system similar to that described in patients with vitamin B12 deficiency.

Intraoperative monitoring of motor evoked potentials: a review of 116 cases.

We reviewed the results of motor evoked potential (MEP) and somatosensory evoked potential (SEP) monitoring during 116 operations on the spine or spinal cord. We monitored MEPs by electrically stimulating the spinal cord and recording compound muscle action potentials from lower extremity muscles and monitored SEPs by stimulating posterior tibial or peroneal nerves and recording both cortical and subcortical evoked potentials. We maintained anesthesia with an N2O/O2/opioid technique supplemented with a halogenated inhalational agent and maintained partial neuromuscular blockade using a vecuronium infusion. Both MEPs and SEPs could be recorded in 99 cases (85%). Neither MEPs nor SEPs were recorded in eight patients, all of whom had preexisting severe myelopathies. Only SEPs could be recorded in two patients, and only MEPs were obtained in seven cases. Deterioration of evoked potentials occurred during nine operations (8%). In eight cases, both SEPs and MEPs deteriorated; in one case, only MEPs deteriorated. In four cases, the changes in the monitored signals led to major alterations in the surgery. We believe that optimal monitoring during spinal surgery requires recording both SEPs and MEPs. This provides independent verification of spinal cord integrity using two parallel but independent systems, and also allows detection of the occasional insults that selectively affect either motor or sensory systems.

Cerebral dysfunction after coronary artery bypass grafting done with mild or moderate hypothermia.

OBJECTIVE: Ninety-nine patients undergoing elective coronary artery bypass grafting were enrolled in a prospective, randomized study to evaluate the incidence of cerebral dysfunction after "mild" or "moderate" hypothermia during cardiopulmonary bypass. METHODS: Patients were evaluated before and after operation before hospital discharge and in some cases at follow-up at least 6 weeks later with a complete neurologic examination (85 patients) and a battery of standard neuropsychometric tests (86 patients). RESULTS: Postoperative changes detected by neurologic examination consisted of the appearance of new primitive reflexes in both groups. No statistically significant differences in incidence were found. The neuropsychometric performances of the two groups were statistically similar by either event-rate or group-rate analysis. CONCLUSIONS: There is no detectable difference in postoperative cerebral dysfunction in patients undergoing coronary artery bypass grafting who are supported by cardiopulmonary bypass with either mild or moderate hypothermia.

Implantable cardioverter-defibrillator. Evaluation of clinical neurologic outcome and electroencephalographic changes during implantation.

During placement of implantable cardioverter-defibrillators, ventricular arrhythmias are induced to test the function of the devices. Although cerebral hypoperfusion and ischemic electroencephalographic changes occur in patients while implantable cardioverter-defibrillators are being tested, no investigation has assessed neurologic outcome in these patients. Nine patients having either implantation or change of an implantable cardioverter-defibrillator underwent neurologic examination and neuropsychometric tests before and after the operation. After induction of general anesthesia and insertion of implantable cardioverter-defibrillator leads (when needed), ventricular fibrillation, ventricular flutter, or ventricular tachycardia, was induced by means of programmed electrical stimulation. Implantable cardioverter-defibrillator testing continued until satisfactory lead placement was confirmed. The intraoperative electroencephalographic recording was analyzed for evidence of ischemic change. In all, an electroencephalogram was recorded during 50 periods of circulatory arrest. Mean duration of the arrest periods was 13.6 seconds. By means of conventional visual inspection of the raw electroencephalogram, high-amplitude rhythmic delta or theta, voltage attenuation, or loss of fast frequency activity was observed in 30 of the arrests. By means of an automated technique of electroencephalographic interpretation based on power spectral analysis, electroencephalographic changes were correctly identified in 26 of the arrests. The incidence of these electroencephalographic changes was dependent on the arrest duration. The mean interval from arrest onset to electroencephalographic change was 7.5 seconds (standard deviation +/- 1.8 seconds). In patients with electroencephalographic changes during multiple arrests, no downward trend in this interval was detected in later arrests and no evidence of persistent ischemic change was observed in electroencephalograms recorded after the conclusion of implantable cardioverter-defibrillator testing. Postoperative neurologic and neuropsychometric testing was completed in eight patients, none of whom exhibited a new neurologic deficit, exacerbation of a preexisting neurologic condition, or significant deterioration in neuropsychometric performance. We conclude that the brief arrest of cerebral circulation induced during insertion of an implantable cardioverter-defibrillator is not associated with permanent neurologic injury.

Cerebral dysfunction after cardiac operations in elderly patients.

BACKGROUND: Cerebral injury remains a significant complication of cardiac operations. We determined the incidence of cerebral dysfunction in a population of elderly patients undergoing open chamber cardiac operations (group 1) as compared with a younger population (group 2) and an age-matched group of elderly patients undergoing major noncardiac operations (group 3). METHODS: Sixty-eight patients (55 for open chamber cardiac operations and 13 for noncardiac operations) were prospectively studied. Patients were evaluated preoperatively and postoperatively before hospital discharge using a complete neurologic examination and a battery of standard neuropsychometric tests, and at surgical follow-up with neuropsychometric tests only. RESULTS: Postoperative changes detected by neurologic examination consisted of the appearance of new primitive reflexes in all groups. No statistically significant differences in incidence were found. The neuropsychometric performance of group 1 patients was statistically different from that of patients in groups 2 and 3 only in the early follow-up period. CONCLUSIONS: Elderly patients having open chamber cardiac operations exhibit significantly more cerebral dysfunction in the early postoperative period than those undergoing major noncardiac operations and younger patients after open chamber procedures. These changes do not persist into the late follow-up period.

Electrophysiological study of mammalian neurons from ventral mesencephalon grown in primary dissociated cell culture.

Mammalian neurons from ventral mesencephalon were grown in primary dissociated cell culture. While dopaminergic neurons were found in culture and used as a marker for this area of the nervous system, our study did not segregate the neurons in terms of their dopaminergic nature. Indeed all of the results were probably from nondopaminergic neurons. Action potentials dependent on sodium and potassium could be elicited from neurons placed in a balanced salt solution. Following blockage of sodium current by tetrodotoxin, and reduction of potassium current by tetraethylammonium and 3-aminopyridine, long-duration action potentials could be elicited by intracellular stimulation. These action potentials were most probably calcium-dependent since they could not be elicited in bathing solution containing manganese, a calcium-conductance blocker.

Dopamine antagonists reduce spontaneous electrical activity in cultured mammalian neurons from ventral mesencephalon.

Mammalian neurons from ventral mesencephalon (VM) were grown in primary dissociated cell (PDC) culture. These neurons are predominantly non-dopaminergic. Many of these non-dopaminergic neurons have dopamine agonist and antagonist binding sites. Intracellular recordings were obtained from these neurons. When bathed in phosphate-buffered saline (PBS) solution they generated action potentials spontaneously. However, in the presence of haloperidol dissolved in PBS solution, the percentage of neurons which generated action potentials spontaneously was reduced in a dose-dependent manner (1-10 microM). This response was also obtained with (+) butaclamol (1 microM) but not with (-) butaclamol (1 microM). This neuroleptic inhibition of spontaneously generated action potentials was specific for neurons in PDC cultures of VM since neurons in PDC cultures of spinal cord did not demonstrate this phenomenon.

Barbiturate reduction of calcium-dependent action potentials: correlation with anesthetic action.

Calcium-dependent action potentials were recorded from mouse spinal cord neurons in primary dissociated cell culture following addition of the potassium channel blockers tetraethylammonium ion and 3-aminopyridine. The pharmacologically active barbiturates, pentobarbital and phenobarbital, but not the pharmacologically inactive barbiturate, barbituric acid, produced reversible, dose-dependent reduction of action potential duration at sedative-hypnotic and anesthetic concentrations. Pentobarbital reduced action potential duration at concentrations from 25 to 600 microM (50% reduction at 170 microM) while phenobarbital reduced action potential duration at concentrations from 100 to 5000 microM (50% reduction at 900 microM). The barbiturate concentrations which reduced calcium-dependent action potential duration in this study correlate with reduction of neurotransmitter release from other neuronal preparations and with reduction of calcium uptake by synaptosomes. The results suggest that barbiturates may produce anesthesia in part by reduction of presynaptic calcium entry and consequent reduction of neurotransmitter release in addition to postsynaptic increase of membrane chloride ion conductance. Barbiturate anticonvulsant actions are probably due to postsynaptic augmentation of GABA-mediated inhibition and depression of excitatory synaptic transmission. The major difference between anticonvulsant (phenobarbital) and anesthetic (pentobarbital) barbiturates was the dose-dependency of these actions. Phenobarbital produced postsynaptic modulation of neurotransmitter responses at low concentrations and decreased calcium-dependent action potential duration and increased chloride ion conductance at high concentrations. In contrast, pentobarbital produced all actions at low concentrations. Thus for phenobarbital there would be a large therapeutic index for anticonvulsant activity compared to anesthetic activity but for pentobarbital there would be a small therapeutic index.

Droperidol suppresses spontaneous electrical activity in neurons cultured from ventral midbrain. Implications for neuroleptanesthesia.

Droperidol is used in anesthesia as an antiemetic and as a component in neuroleptanalgesia. Its mechanism of action is thought to involve dopamine receptor blockade in the brain. The electrophysiological consequences associated with this action however, have not been elucidated. In this study we demonstrate a dose-dependent electrophysiological response to droperidol in central nervous system (CNS) neurons that express dopamine receptors that is absent in CNS neurons that do not express dopamine receptors. Primary dissociated cell (PDC) cultures were prepared from embryonal tissue dissected from ventral mesencephalon (VM) and spinal cord (SC). VM neurons were used to investigate the electrophysiological action of droperidol, a dopamine receptor antagonist, since these cultures contain neurons having dopamine receptors on their surface. SC neurons were used as a control as they do not express dopamine receptors. Some dopamine receptors are on dopaminergic neurons and therefore are called autoreceptors, while others are on nondopaminergic neurons, such as GABA producing (GABAergic) neurons. All neurons in both PDC cultures were spontaneously active. The percentage of neurons which spontaneously generated action potentials was reduced in a dose-dependent manner by droperidol (1 nM-10 microM) only in PDC cultures of VM. Exposure to droperidol had no effect on neurons from PDC cultures of SC which lack dopamine receptors. Our results suggest that droperidol modulates the electrophysiological properties of VM neurons with dopamine receptors possibly through facilitation of inhibitory interneurons. The reduced activity of VM neurons might contribute to the antiemetic and/or anesthetic activity of droperidol, since the concentrations of droperidol used in this study are at clinically relevant concentrations.

Membrane depolarization and prolongation of calcium-dependent action potentials of mouse neurons in cell culture by two convulsants: bicuculline and penicillin.

The convulsant compounds bicuculline (BICUC) and penicillin (PCN) are antagonists of GABA-mediated synaptic inhibition. In addition, we have shown that BICUC and PCN produced membrane depolarization of mouse spinal cord neurons in primary dissociated cell culture by blocking a potassium conductance, a non-synaptic direct effect. Both compounds also prolonged calcium-dependent action potentials of mouse dorsal root ganglion and spinal cord neurons in cell culture. Thus, BICUC and PCN had both synaptic and non-synaptic actions. The possibility that both synaptic and non-synaptic actions of BICUC and PCN are involved in their convulsant mechanism of action is discussed.

Characterization of dopamine receptors on neurons grown in primary dissociated cell culture from ventral mesencephalon of mouse.

Mammalian neurons from ventral mesencephalon were grown in primary dissociated cell culture. These cultures were examined for dopamine sensitive adenylate cyclase activity and specific ligand binding of [3H]spiroperidol and [3H]flupenthixol. No stimulation of adenylate cyclase activity by 10 microM dopamine was demonstrable in cell culture homogenates. [3H]Spiroperidol bound to cell culture homogenates with high affinity and was displaced by (+)-butaclamol but not by 5-hydroxytryptamine, suggesting that the [3H]spiroperidol was bound to dopamine receptors. While [3H]flupenthixol binding was also present, it could be displaced by spiroperidol indicating that the dopamine receptor was probably of the D2 subtype. Binding of spiroperidol was proportional to the amount of cell culture homogenate, and was saturable. Are these receptors autoreceptors? The toxin 1-methyl-4-phenylpyridine (MPP+) was used to destroy dopaminergic neurons; spiroperidol binding in these cultures was found to be increased, demonstrating that most of these D2 receptors are not autoreceptors.

Calcium-dependent action potentials in mouse spinal cord neurons in cell culture.

Following blockade of membrane potassium conductance with tetraethylammonium ions or 3-aminopyridine, long-duration action potentials were recorded from mouse spinal cord neurons in primary dissociated cell culture. The action potentials were calcium-dependent since they: (1) were not blocked by the sodium-channel blocker tetrodotoxin, (2) could be recorded in sodium-free, calcium-containing medium (3) could not be evoked in sodium-containing, calcium-free medium, (4) were blocked by calcium channel blockers manganese and cobalt and (5) had overshoot amplitudes that varied linearly with the log of the extracellular calcium concentration (slope of 27.5 mV/decade change in calcium concentration).

Serum S100B protein levels are correlated with subclinical neurocognitive declines after carotid endarterectomy.

OBJECTIVE: Carotid endarterectomy (CEA) is an effective means of stroke prevention among appropriately selected patients; however, neuropsychometric testing has revealed subtle cognitive injuries in the early postoperative period. The purpose of this study was to establish whether serum levels of two biochemical markers of cerebral injury were correlated with postoperative declines in neuropsychometric test performance after CEA. METHODS: Fifty-five consecutive patients underwent a battery of neuropsychometric tests 24 hours before and 24 hours after elective CEA. Two patients were excluded because of postoperative strokes. The pre- and postoperative serum levels of S100B protein and neuron-specific enolase for injured patients, defined as those who exhibited significant declines in neuropsychometric test performance (n = 12), were compared with the levels for uninjured patients (n = 41). RESULTS: There were no significant differences in the baseline S100B levels for the two groups. Injured patients exhibited significantly higher S100B levels, compared with uninjured patients, at 24, 48, and 72 hours after surgery (P < 0.05). There were no significant differences in neuron-specific enolase levels for injured and uninjured patients at any time point. CONCLUSION: These data suggest that subtle cerebral injuries after CEA, even in the absence of overt strokes, are associated with significant increases in serum S100B but not neuron-specific enolase levels. Analyses of earlier time points in future studies of subtle cognitive injuries and biochemical markers of cerebral injury after CEA may be revealing.

Safety and efficacy of fixed-dose heparin in carotid endarterectomy.

OBJECTIVE: Although fixed dosage of heparin is frequently used during vascular surgery, there are very few studies that document the appropriateness of this type of dosing. We have undertaken a prospective study to determine the physiological response to a fixed dose of heparin, using a conventional measure of anticoagulation, and have correlated this measure with complications. METHODS: We studied 140 consecutive patients undergoing elective carotid endarterectomy. Serial activated clotting times (ACT values) were obtained in duplicate before administration of heparin, 15 minutes after application of a carotid artery cross-clamp, and 1 hour after administration of 5000 U of heparin by intravenous bolus. Postoperatively, patients were assessed for new neurological deficits (transient ischemic attack and stroke) and neck hematomas. A battery of neuropsychometric tests was performed in 49 patients at baseline and on the day after carotid endarterectomy to identify subtle new neurological deficits. RESULTS: ACT values were found to be highly reproducible, with less than a 1.5% difference between duplicate baseline samples. Although all patients received 5000 U of heparin, the dose received per kilogram of body weight varied considerably (44-116 U/kg), as did ACT values at both 15 minutes (178-423 s) and 1 hour (173-390 s). Nevertheless, there was a significant correlation between heparin dose per kilogram and ACT values at 15 minutes (r = 0.45) and at 1 hour (r = 0.38) postinfusion, as well as ACT ratios (final ACT/initial ACT) at 15 minutes (r = 0.43) and at 1 hour (r = 0.34) after heparin bolus. Eight patients (5.7%) developed postoperative wound hematomas, one of which (0.7%) required reoperation. No patient had a stroke, but one patient had a transient ischemic attack, and 19 (39%) of 49 patients demonstrated significant early postoperative neuropsychometric deficits. Although the incidence of neck hematoma was not influenced by the heparin dose (P = 0.23), the ACT value at 15 minutes (P = 0.71) or 1 hour (P = 0.61), or the ACT ratio (P = 0.68), the only severe hematoma requiring reoperation occurred when the maximal ACT value was more than 400 seconds. Although performance on neuropsychometric tests did not appear to be statistically influenced by heparin dosing, the ACT value, or the degree of ACT elevation, there was a trend for deficits to be associated with lower heparin doses. CONCLUSION: Fixed heparin dosing achieves safe and efficacious anticoagulation in the great majority of patients having carotid endarterectomy, with 5000 U expected to result in 15-minute and 1-hour ACT values of 175 to 425 seconds and 170 to 390 seconds, respectively. Although weight-based heparin dosing may reduce the incidence of subtle complications (hematoma formation or decline on neuropsychometric tests) and may result in more predictable 15-minute and 1-hour ACT values (85 U/kg; 225-375 and 200-340 s, respectively), no statistically compelling clinical advantage could be demonstrated. Therefore, either weight-based or fixed dosing is acceptable, with both obviating the need for routine pre-clamp ACT confirmation, thereby saving operative time and expense.

Transcranial Doppler monitoring during carotid endarterectomy: a technical case report.

We report a case involving a patient undergoing carotid endarterectomy in whom transcranial doppler monitoring demonstrated impaired cerebral blood flow during the initial dissection of the carotid artery, during cross-clamping of the carotid artery, and after the shunt was kinked inadvertently. Only when the carotid artery was cross-clamped were these ischemic changes also seen by electroencephalography. During the other episodes, the electroencephalography tracings demonstrated no detectable changes. This case illustrates the importance of using multiple modalities to determine the adequacy of cerebral blood flow and neuronal integrity.

APOE-epsilon4 predisposes to cognitive dysfunction following uncomplicated carotid endarterectomy.

BACKGROUND: Between 9% and 23% of patients undergoing otherwise uncomplicated carotid endarterectomy (CEA) develop subtle cognitive decline 1 month postoperatively. The APOE-epsilon4 allele has been associated with worse outcome following stroke. OBJECTIVE: To investigate the ability of APOE-epsilon4 to predict post-CEA neurocognitive dysfunction. METHODS: Seventy-five patients with CEA undergoing elective CEA were prospectively recruited in this nested cohort study and demographic variables were recorded. Patients were evaluated before and 1 month after surgery with a standard battery of five neuropsychological tests. APOE genotyping was performed by restriction fragment length polymorphism analysis in all patients. Neuropsychological deficits were identified by comparing changes (before to 1 month post-operation) in individual performance on the test battery. Logistic regression was performed for APOE-epsilon4 and previously identified risk factors. RESULTS: Twelve of 75 (16%) CEA patients possessed the APOE-epsilon4 allele. Eight of 75 (11%) patients experienced neurocognitive dysfunction on postoperative day 30. One month post-CEA, APOE-epsilon4-positive patients were more likely to be cognitively injured (42%) than APOE-epsilon4-negative patients (5%) (p = 0.002). In multivariate analysis, the presence of the APOE-epsilon4 allele increased the risk of neurocognitive dysfunction at 1 month 62-fold (62.28, 3.15 to 1229, p = 0.007). Diabetes (51.42, 1.94 to 1363, p = 0.02), and obesity (24.43, 1.41 to 422.9, p = 0.03) also predisposed to injury. CONCLUSION: The APOE-epsilon4 allele is a robust independent predictor of neurocognitive decline 1 month following CEA.

Neurologic assessment and cardiac surgery.

Cerebral injury remains a significant complication of cardiac surgery. This complication is evaluated by clinical means that include a neurologic examination. In this report, the most important components of this type of evaluation are described. The neurologic complications of cardiac surgery can be determined by comparing structured preoperative and postoperative clinical evaluations. The neurologic examination must include a mental state examination, examination of cranial nerves, motor, sensory, and cerebellar systems, examination of gait and station, and deep tendon and primitive reflexes. The purpose of this report is to discuss the relevance of the neurologic examination in the assessment of cerebral injury after cardiac surgery, review the components of a structured neurologic examination, and explore the role of "quantitative" stroke scales as a research tool.