Robert H. Rosenwasser

An early comparative analysis of the use of fibular allograft versus autologous iliac crest graft for interbody fusion after anterior cervical discectomy

During a 2-year period (1988-1989), 23 cases of anterior cervical discectomy were performed with cadaveric fibular allograft instead of autologous iliac crest graft. The mean age of the patients was 35 years. There were 10 men and 13 women. In most cases, a one-level fusion was performed at the C5-6 level. The Smith-Robinson technique was used for discectomy and fusion, for both one- and two-level fusions. Evidence of radiographic fusion was achieved in 92% of the cases. Twenty-five cases of anterior cervical discectomy in which autologous iliac crest graft was used (1987-1988) were examined retrospectively for comparison. The mean duration of hospital stay was less in the allograft group (5.4 days vs. 7.25 days). In addition, postoperative pain was less in the allograft group because the allograft group did not have pain from the donor site. In conclusion, the use of fibular allograft for interbody fusion after anterior cervical discectomy can be performed with acceptable rates of fusion and less postoperative pain, as compared to the use of autologous iliac crest graft.

Leukocyte involvement in cerebral infarct generation after ischemia and reperfusion

White blood cell involvement in the generation of cerebral infarcts was evaluated following ischemia and reperfusion injury in the rat. Control and leukopenic rats (induced by vinblastine, WBC counts < 1500/mm3) were compared in a global forebrain ischemic model after 1 h of ischemia and 1 h 15 min of reperfusion. Cerebral infarcts were defined on coronal brain sections using Triphenyl tetrazolium chloride (TTC) staining. Electroencephalographic activity (EEG) and somatosensory evoked potentials (SSEP) were also compared. Results indicate that the area infarcted in leukopenic rats was significantly less than infarcts generated in corresponding controls (21 +/- 16% vs. 70 +/- 16%). In addition, EEG was preserved in all leukopenic animals when compared to controls, both during ischemia and after reperfusion. The cortical peak component of the SSEP was also better preserved in the leukopenic animals both during ischemia and at 60 min of reperfusion. These results indicate white blood cell participation in the generation of cerebral damage in a model of global forebrain ischemia and reperfusion as indicated by TTC staining of cerebral infarcts.

Leukocyte involvement in cerebral ischemia and reperfusion injury

Leukocytes have been postulated to contribute to cerebral ischemia and reperfusion injury. The present study implies that leukocytes have a deleterious effect in the brain following ischemia. We compared the alteration of cortical electrical activity following transient, incomplete cerebral ischemia in control and leukopenic rats by monitoring somatosensory evoked potentials and electroencephalographic activity. There was complete cessation of electroencephalographic activity, and the cortical peak of the evoked potential was abolished during ischemia in the control animals. However, when the animals were rendered leukopenic, there was maintenance of electroencephalographic activity with reduced amplitude and preservation of the cortical peak of the evoked response during the ischemic period. This indicates that when the animals are made leukopenic, even under ischemic conditions, the neurophysiologic functioning is still maintained to a certain extent.

Complement Depletion Improves Neurological Function in Cerebral Ischemia

The contribution of the complement system to the exacerbation of cerebral ischemia/reperfusion injury was studied by comparing a group of rats with normal complement levels to another group that was complement depleted by cobra venom factor (CVF). The magnitude of reactive hyperemia was significantly greater in the complement depleted animals. There was also better preservation of somatosensory evoked potentials (SSEPs) in the complement depleted animals. These differences were not associated with changes in leukocyte infiltration as evidenced by myeloperoxidase and Leukotriene B4 activity. These data demonstrate that depleting the complement system can improve flow and outcome following cerebral ischemia with reperfusion.

Electroencephalographic activity and serum and cerebrospinal fluid pentobarbital levels in determining the therapeutic end point during barbiturate coma

Controversy exists regarding the optimal means for monitoring the patient receiving pentobarbital therapy during medical coma. Serum pentobarbital levels have been used traditionally to gauge cerebral penetration and efficacy of the drug. These peripheral levels have been assumed to reflect pentobarbital concentrations in the cerebrospinal fluid (CSF) and, therefore, the physiological effect on the central nervous system. To determine the relative accuracy of serum versus CSF pentobarbital levels, continuous electroencephalographic (EEG) monitoring in 10 consecutive patients was studied prospectively. Each patient received pentobarbital therapy for cerebral protection in the face of a traumatic injury. Simultaneous serum and CSF pentobarbital levels were obtained 1) before and after the initial barbiturate bolus, 2) every 12 hours during constant infusion therapy, and 3) before and after subsequent boluses necessary because of elevated intracranial pressure (ICP) (ICP greater than 15 mm Hg) or loss of burst suppression by continuous EEG monitoring (defined as greater than five bursts per minute). ICP and relevant clinical events were recorded hourly. Serum and CSF levels ranged from 33 to 74 mg/L and 4 to 54 mg/L, respectively. There was poor correlation between serum and CSF pentobarbital levels at any given time, although patients remained in burst suppression 73% of the time during their therapy. The EEG monitoring not only provided dynamic physiological monitoring, but it also permitted the lowest pentobarbital dose to maintain burst suppression for a specific patients metabolism, reducing the likelihood of toxicity. In conclusion, CSF pentobarbital levels are of no greater accuracy than serum pentobarbital levels in predicting physiological effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Facial reanimation after facial nerve injury.

Patients with facial paralysis are often seen in neurosurgical practice. Obtaining full facial symmetry and function after facial nerve damage presents the neurosurgeon with a difficult challenge. Various surgical techniques have been developed to deal with this problem. These include primary nerve repair, nerve to nerve anastomosis, nerve grafting, neurovascular pedicle grafts, regional muscle transposition, microvascular muscle transfers, and nerve transfers. Patient selection, timing of surgery, and details of surgical technique are discussed. The results of hypoglossal-facial anastomosis in 24 patients are described.

Penetrating Craniocerebral Trauma

The authors review the pathophysiology of penetrating and perforating cranial wounds. Radiologic evaluation includes computed tomography and angiography. Operative technique and perioperative critical care are discussed, with special emphasis on the control of the intracranial pressure. Other problems such as fluid and electrolyte disorders and nutrition are discussed in relation to neurosurgery.

Routine use of etomidate and temporary vessel occlusion during aneurysm surgery

This study included 72 cases of surgically treated aneurysms, Hunt and Hess Grades 1-4, operated on within 72 hours of the ictus. All had anterior circulation aneurysms, and exposure was standard pterional approach. Once dissection had progressed to the point that the site of the aneurysm was identified, the patient was placed in burst suppression (6-8 bursts/minute), using etomidate 0.5 mg/Kg, with a constant infusion of 12 mg/min to maintain burst suppression. Sugita temporary clips were applied to the feeding vessel(s), the C1 or C4 portion of the carotid artery, the A1 segment(s) of the anterior cerebral or M1 segment of MCA. For ACOM aneurysms. Heubner was not included in the clip, and for MCA aneurysm an attempt was made to apply the clip distal to the lenticulostriates. Mean arterial pressure was elevated by 10% with neosynephrine. Once the temporary clips were applied, dissection of the neck and final clipping was accomplished, followed by removal of the temporary clips. Clip placement was inspected to assess for complete obliteration of the lesion. In 40% of cases, two or more permanent clips were required for aneurysmal obliteration. Occlusion time ranged from 3 to 63 minutes. Reperfusion at 5 minute intervals was not performed, based on the hypothesis that reperfusional injury potentiates an ischaemic insult. No vessel injury occurred as a result of temporary clip placement, as assessed by direct visual inspection at the time of surgery and angiographic picture one week following surgery. No new neurologic deficit was encountered postoperatively in any patient in the distribution of the occluded vessel.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of intravenous lidoflazine on whole blood-induced basilar artery contraction. An in vivo study

Lidoflazine, a piperazine derivative of known selectivity for vascular smooth muscle, was evaluated as a possible agent for prophylaxis of cerebral vascular contraction induced by subarachnoid perfusion with whole blood. Previous studies from this laboratory have indicated its efficacy in preventing basilar artery contraction induced by serotonin. The animals treated with a subarachnoid perfusion of whole blood had a mean 30% reduction in vessel diameter over the control value. Groups that were treated with 0.5 mg/kg of lidoflazine and 1.0 mg/kg of lidoflazine and then perfused with whole blood in the subarachnoid space had reductions in control diameter of 2.8% and 6.8%, respectively. One group treated with 2.0 mg/kg of lidoflazine and then perfused with whole blood actually had an increase in diameter of 6.8% over the control value. Lidoflazine, when administered intravenously at a slow rate, will not adversely lower systemic blood pressure and can prevent the contraction of cerebral vessels when the stimulus for contraction is whole blood within the subarachnoid space.

Temporary Motor and Sensory Paralysis Associated with Intrathecal Administration Of Morphine

We are reporting a temporary, totally reversed motor and sensory paralysis subsequent to the intrathecal administration of 1.6 mg of morphine sulfate. This may represent an event which is not based on medication-induced myelopathy but on cardiovascular changes occurring as a result of pain relief.