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Neurologic Recovery (neurologic + recovery)
Orthostatic Headaches in the Syndrome of the Trephined: Resolution Following CranioplastyHEADACHE, Issue 7 2010
Bahram Mokri MD
Objective., To draw attention to the syndrome of the trephined as a potential cause for orthostatic headaches without cerebrospinal fluid (CSF) leak. Background., Orthostatic headaches typically result from CSF leaks but sometimes may occur in conditions without any evidence of CSF leakage. Methods., A 37-year-old right-handed woman became comatose after a motor vehicle accident with cerebral contusions and massive left cerebral edema. A large frontoparietal craniectomy was carried out. In 5 months, she made good neurologic recovery. Freeze-preserved bone flap was placed back. In several weeks she was functionally near normal. Two years later, she began to complain of orthostatic headache and gradually additional manifestations appeared including progressive gait unsteadiness, imprecise speech, cognitive difficulties, and an increasing left hemiparesis along with progressive sinking of the skull defect and shift of the midline and ventricular distortion. She underwent removal of resorptive sinking bone flap and construction of an acrylic cranioplasty. Results., At 6-month follow-up, there was complete resolution of the orthostatic headaches, remarkable neurologic improvement along with resolution of midline shift and ventricular distortion. Conclusion., The syndrome of the trephined is yet another cause of orthostatic headaches without CSF leak. [source]
Application of a Cardiac Arrest Score in Patients with Sudden Death and ST Segment Elevation for Triage to Angiography and InterventionJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2002
PETER A. MCCULLOUGH M.D.
The aim of this study was to test a previously validated, prognostic, cardiac arrest score in patients with ST segment elevation acute myocardial infarction (AMI) who suffereda witnessed cardiac arrest and survived to emergency department admission. A consecutive series constructed retrospectively from a sudden death database (n= 22) of patients with ST segment elevation AMI resuscitated from cardiac arrest underwent angiography and angioplasty of the culprit vessel within 24 hours of presentation. A cardiac arrest score was assigned to each case by explicit criteria present on evaluation. Primary outcomes were survival to hospital discharge and the degree of neurological recovery during the hospitalization. All patients underwent successful coronary angioplasty and 77% received adjunctive intraaortic balloon counterpulsation. The overall rate of survival to discharge was 41%. For cardiac arrest scores of 0, 1, 2, and 3, respectively, the rates of neurologic recovery were 0 (0%) of 4 (95% CI 0,53%), 3 (50%) of 6 (95% CI 15,85%), 2 (67%) of 3 (95% CI 13,98%), and 9 (100%) of 9 (95% CI 72,100%), and the rates of survival to discharge were 0(0%) of 4, (95% CI 0,53%), 2 (33%) of 6 (95% CI 6,74%), 2 (67%) of 3 (95% CI 13,98%), and 9 (100%) of 9 (95% CI 72,100%), P<0.01 for both outcomes over ascending scores. These results suggest appropriate patients for primary angioplasty after cardiac arrest are those with ST segment elevation AMI and an emergency department cardiac arrest score of ,2, thus predicting a11 (92%) of 12 (95% CI 65,100%) chance of survival to discharge. [source]
Comparison of the Effects of Hypothermia at 33°C or 35°C after Cardiac Arrest in RatsACADEMIC EMERGENCY MEDICINE, Issue 4 2007
Eric S. Logue BS
Abstract Objectives: Hypothermia of 32°C,34°C induced after resuscitation from cardiac arrest improves neurologic recovery, but the optimal depth of cooling is unknown. Using a rat model, the authors tested the hypothesis that cooling to 35°C between hours 1 and 24 after resuscitation would improve neurologic outcome as much as cooling to 33°C. Methods: Halothane-anesthetized rats (n= 38) underwent 8 minutes of asphyxial cardiac arrest and resuscitation. Cranial temperature was maintained at 37°C before, during, and after arrest. Between one and 24 hours after resuscitation, cranial temperature was maintained at 33°C, 35°C, or 37°C using computer-controlled cooling fans and heating lamps. Neurologic scores were measured daily, and rats were killed at 14 days for histologic analysis. Neurons per high-powered field were counted in the CA1 region of the anterior hippocampus using neuronal nuclear antigen staining. Results: After 14 days, 12 of 12 rats (100%) cooled to 33°C, 11 of 12 rats (92%) cooled to 35°C, and ten of 14 rats (71%) cooled to 37°C survived, with hazard of death greater in the rats cooled to 37°C than in the combined hypothermia groups. Neurologic scores were worse in the rats cooled to 37°C than in the hypothermia groups on days 1, 2, and 3. Numbers of surviving neurons were similar between the groups cooled to 33°C and 35°C and were higher than in the group cooled to 37°C. Conclusions: These data illustrate that hypothermia of 35°C or 33°C over the first day of recovery improves neurologic scores and neuronal survival after cardiac arrest in rats. The benefit of induced hypothermia of 35°C appears to be similar to the benefit of 33°C. [source]
Induced hypothermia following out-of-hospital cardiac arrest; initial experience in a community hospitalCLINICAL CARDIOLOGY, Issue 12 2006
Brook D. Scott M.D.
Abstract Background Successful resuscitation from sudden cardiac death is frequently accompanied by severe and often fatal neurologic injury. Induced hypothermia (IH) may attenuate the neurologic damage observed in patients after cardiac arrest. Hypothesis This study examined a population of nonselected patients presenting to a community hospital following successful resuscitation of sudden cardiac death. We sought to determine whether a program of induced hypothermia would improve the clinical outcome of these critically ill patients. Methods We initiated a protocol of IH at the Oklahoma Heart Hospital in August of 2003. Study patients were consecutive adults admitted following successful resuscitation of out-of-hospital cardiac arrest. Moderate hypothermia was induced by surface cooling and maintained for 24 to 36 h in the Intensive Care Unit with passive rewarming over 8 h. Results Forty-nine patients who were resuscitated and had the return of spontaneous circulation completed the hypothermia protocol. The cause of cardiac arrest was acute myocardial infarction in 24 patients and cardiac arrhythmias in 19 patients. Nineteen patients (39%) survived and were discharged. Sixteen of the patients discharged had no or minimal residual neurologic dysfunction and 3 patients had clinically significant residual neurologic injury. Conclusion A program of induced hypothermia based in a community hospital is feasible, practical, and requires limited additional financial and nursing resources. Survival and neurologic recovery compare favorably with clinical trial outcomes. Copyright © 2006 Wiley Periodicals, Inc. Wiley Periodicals, Inc. [source]