Spinal cord blood flow and evoked potential responses after treatment with nimodipine or methylprednisolone in spinal cord-injured rats

This study examined the effect of nimodipine or methylprednisolone on spinal cord blood flow (SCBF) and electrophysiological function after spinal cord injury in rats. Three groups of male rats (n = 10 per group) were injured by compression of the cord at T1 for 1 minute with a 52-g clip. The hydrogen clearance technique was used to measure SCBF at the T1 segment. Motor and somatosensory evoked potentials were recorded. SCBF and evoked potentials were measured before injury and again at approximately 1 and 2.5 hours after injury. The methylprednisolone group received a bolus of methylprednisolone (30 mg/kg) at 5 minutes after injury and then at 15 minutes after injury, the group received an infusion of methylprednisolone at 5.4 mg/kg per hour. The nimodipine group received placebo at 5 minutes and then received an infusion of nimodipine at 0.02 mg/kg per hour at 15 minutes. The placebo group received placebo at both times. Physiological parameters were closely monitored and maintained within the normal range. Albumin was administered after injury to maintain mean arterial blood pressure at or above 80 mm Hg. The infusions were continued for approximately 3 hours after spinal cord injury. SCBF was not significantly different between the experimental groups at either 1 or 2.5 hours postinjury (P = 0.16 and 0.71, respectively), and evoked potential responses did not return in any rat at any time after injury. Thus, this experiment failed to demonstrate an improvement in SCBF or electrophysiological function with either drug.(ABSTRACT TRUNCATED AT 250 WORDS)     

A new method for estimating spinal cord function. Refractory period of conductive spinal cord evoked potentials

STUDY DESIGN: This study was designed to examine the possibility of a new spinal cord monitoring method using measurement of the refractory period to monitor spinal cord function. OBJECTIVES: To determine whether measuring the refractory period and the recovery rate of conductive spinal cord evoked potential is a useful method for estimating spinal cord function. BACKGROUND: Measuring the refractory period and constructing the recovery curve have been used to investigate peripheral nerve function. Spinal cord evoked potential elicited by the single stimulus usually is used to evaluate spinal cord function, and it has been said that 50% attenuation of the amplitude is the critical alarm level. METHODS: In anesthetized cats, amplitude, area, and latency were measured on a personal computer from subtracted data collected with a paired-stimulation technique. The authors constructed recovery curves of ascending and descending conductive spinal cord evoked potentials and measured the refractory period during spinal cord compression. RESULTS: When the amplitude of the ascending spinal cord evoked potential began to decrease during spinal cord compression, the amplitude of the response elicited by the second stimulus with interstimulus intervals of 0.8 msec and 1.0 msec decreased more significantly. When the amplitude of the ascending spinal cord evoked potential decreased to 50% of the precompression amplitude, the mean value of the absolute refractory periods of the ascending and descending spinal cord evoked potentials became prolonged from 0.40 +/- 0.007 msec to 0.53 +/- 0.014 msec, and the mean values of their amplitude and area recovery rates decreased from 75% +/- 1% to 35% +/- 2% (interstimulus interval, 0.8 msec) and from 81% +/- 1% to 46% +/- 2% (insterstimulus interval, 1.0 msec). CONCLUSIONS: The change of the responses elicited by the paired stimuli is more sensitive than those elicited by the single stimulus in the spinal cord evoked potentials. The absolute refractory periods and the recovery rate during 50% attenuation of the precompression amplitude is the critical alarm level in spinal cord monitoring.     

Effects of distraction on physiologic integrity of the spinal cord, spinal cord blood flow, and clinical status

The authors determined the effects of distraction of the spine on physiologic integrity of the spinal cord using neurogenic motor evoked potentials (NMEPs), somatosensory evoked potentials (SEPs), spinal cord blood flow measurements, and clinical status in nine hogs. Spinal cord blood flow was measured after each level of distraction using the hydrogen washout technique. The results indicated that blood flow of at least 65% of baseline was required to maintain physiologic integrity of the spinal cord, and that a decrease of blood flow to 12% of baseline was associated with paraplegia. Neurogenic motor evoked potentials always correlated with the animal's postsurgical clinical status, whereas the SEP was falsely negative in one animal.     

Anesthesia for surgery of degenerative and abnormal cervical spine

A feature common to all congenital or inflammatory abnormalities of the cervical spine is an actual or potential reduction in the lumen of the spinal canal. The spinal cord and nerve roots are at risk. During intubation, and positioning the patient on the table, all untoward movements of the cervical spine may lead to spinal cord compression. Abnormalities of the cervical spine carry the risk of a difficult intubation. If there is much debate as to what constitutes optimum management of the airway, there is no evidence that any one method is the best. Recognizing the possible instability and intubating with care, are probably much more important in preserving neurological function than any particular mode of intubation. During maintenance of anaesthesia, the main goal is to preserve adequate spinal cord perfusion in order to prevent further damage. Spinal cord blood flow seems to be regulated by the same factors as cerebral blood flow. Hypercapnia increases cord blood flow while hypocapnia decreases it. Therefore, normocapnia or mild hypocapnia is recommended. Induced hypotension is frequently used to decrease blood loss. However, in patients with a marginally perfused spinal cord, the reduction in blood flow may cause ischaemia of the spinal cord and may therefore be relatively contraindicated. In addition to standard intraoperative monitoring, spinal cord monitoring is almost mandatory. Monitoring somatosensory evoked potentials is used routinely. However, the major limitation is that this technique only monitors dorsal column function; theoretically, motor paralysis can occur despite a lack of change in recorded signals. Neurogenic motor evoked potentials may now be used to monitor anterior spinal cord integrity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of spinal cord ischemia on evoked potential recovery and postischemic regional spinal cord blood flow

The effects of spinal cord ischemia on spinal cord blood flow (SCBF) and somatosensory (SSEP) and motor (MEP) evoked potentials were investigated in a rabbit model of reversible spinal cord ischemia. Spinal cord ischemia was produced by balloon occlusion of the infrarenal aorta for 30, 60, and 90 min. SCBF, SSEPs, and MEPs were measured before, during, and 1 h after aortic occlusion. Aortic occlusion produced absolute ischemia of the caudal cord followed by hyperemia upon reperfusion. SSEP's and MEP's were obliterated during ischemia but demonstrated gradual albeit incomplete recovery following reperfusion with amplitude recovery inversely proportional to the duration of ischemia. Later peaks were more severely affected by a given period of ischemia than were early waves. In general, SSEP's were more resistant to ischemia than were MEP's although the differences were not significant.     

Pulmonary complications in AIDS: CT appearances

We investigated 33 cervical spinal cord injury patients (25 males and eight females) without bony injury. Patients whose neurologic recovery had reached a plateau and who had evidence on imaging of persistent spinal cord compression were considered candidates for surgical decompression. When imaging did not show spinal cord compression or patients were maintaining a good neurologic recovery from the early days after injury, we pursued conservative treatment. Age at injury varied from 20 to 76 years (mean, 55.6). Average follow-up was 31 months. Twelve patients were treated conservatively (Group 1). Groups 2 and 3 had surgery. Group 2 (14 cases) had multi-level compression of spinal cord due to pre-existing cervical spine conditions such as ossification of posterior longitudinal ligament, cervical canal stenosis, and cervical spondylosis. Group 3 (7 cases) patients existed single-level compression of spinal cord by cervical disc herniations or spondylosis. We evaluated clinical results according to the Frankel classification, the American Spinal Injury Association (ASIA) scales and Japanese Orthopaedic Association (JOA) scores. Overall improvement of JOA and ASIA scores after treatment was 56.3 +/- 35.5% and 67.1 +/- 38.0%, respectively. Patients in Group 1 showed very good recovery after conservative treatment, with improvement of JOA and ASIA scores being 70.4 +/- 40.2% and 77.4 +/- 34.2%, respectively. The average interval between injury and operation was 4.3 +/- 4.4 months. The improvement of the surgically treated patients (Groups 2 and 3) in JOA and ASIA score was 48.2 +/- 30.7% and 61.2 +/- 39.6% respectively. We obtained good neurological recovery after operation, with significantly more improvement in Group 3 than in Group 2. No significant neurologic recovery had occurred preoperatively in these groups. In such patients operative intervention is essential for neurologic recovery.     

Subacute combined degeneration: clinical, electrophysiological, and magnetic resonance imaging findings

OBJECTIVE: Vitamin B12 deficiency is a systemic disease that often affects the nervous system. One of the most prevalent manifestations is subacute combined degeneration (SCD) of the spinal cord. To access the clinical, electrophysiological, and structural abnormalities associated with SCD, a study was conducted in nine patients. METHODS: Clinical, electrophysiological (electroneurography, somatosensory and motor evoked potentials), and MRI evaluations were performed in patients before and after treatment. RESULTS: The most prominent clinical and electrophysiological findings in all patients were dysfunctions of the posterior column. Corresponding hyperintense lesions in the posterior column of the spinal cord were found in two patients by T2 weighted MRI. Damage to the central motor pathway was identified in four patients. Demyelinating neuropathy was present in one patient and axonal neuropathy in four. All patients showed improvement of their symptoms after treatment with cobalamin. Abnormalities of the spinal cord on MRI disappeared early in recovery. Motor evoked potentials and median somatosensory evoked potentials typically normalised after treatment, whereas tibial somatosensory evoked potentials remained abnormal in most patients. CONCLUSIONS: Clinical, electrophysiological, and MRI findings associated with SCD in vitamin B12 deficiency are diverse. Thus vitamin B12 deficiency should be considered in the differential diagnosis of all spinal cord, peripheral nerve, and neuropsychiatric disorders.     

Two-level spinal stenosis in minipigs. Hemodynamic effects of exercise

STUDY DESIGN: Twenty-two G?ttingen minipigs were trained to run on a treadmill. Two-level lumbar spinal stenosis was created in 12 pigs, 10 were unoperated control subjects. Blood flow of the spinal cord and nerve roots was determined with microspheres at rest, during exercise, and after exercise. OBJECTIVES: To study the effect of lumbar spinal stenosis and exercise on blood flow of spinal neural tissue. SUMMARY OF BACKGROUND DATA: Neurogenic claudication, the key symptom of lumbar spinal stenosis, may be caused by vascular impairment or mechanical distress of neural tissue during exercise. Experimental compression of the cauda equina causes reversible nerve root edema, stasis, blood flow decrease, and compromised neural function. The vascular pathophysiology of spinal stenosis during exercise has not been studied previously. METHODS: Pigs were trained daily for 3 months. Two-level 25% lumbar spinal stenosis was introduced by placement of stenosing bands around the dural sac. Neurologic function was monitored before surgery by evoked potentials and after surgery by the Tarlov score. Regional blood flow in lumbosacral neural tissue was measured 3 days after chronic catheterization using microspheres at rest, during exercise at 3 km/h for 15 minutes, and at rest 30 minutes after exercise. RESULTS: Blood flow of grey and white matter increased during exercise in both groups, with no differences between groups. slight hyperemia prevailed after exercise in white matter of the stenotic area but not in grey matter. Nerve root blood flow was largely unchanged in control subjects during exercise but was reduced in spinal stenosis at rest, further depressed during exercise, and normalized after exercise. Dural blood flow was elevated throughout. CONCLUSION: The study suggests that exercise-induced impairment of spinal nerve root blood flow plays a role in the pathophysiology of neurogenic claudication.     

Effects of various degrees of compression and active decompression on haemodynamics, end-tidal CO2, and ventilation during cardiopulmonary resuscitation of pigs

The effects of various degrees of compression and active decompression during cardiopulmonary resuscitation were tested in a randomized cross-over-design during ventricular fibrillation in eight pigs using an automatic hydraulic chest compression device. Compared with 4/0 (compression/decompression in cm), mean carotid arterial blood flow rose by 60% with 5/0, by 90% with 4/2 and 4/3, and 105% with 5/2. Two cm active decompression increased mean brain and myocardial blood flow by 53% and 37%, respectively, as compared with 4/0. Increasing standard compression from 4 to 5 cm caused no further increase in brain or heart tissue blood flow whether or not combined with active decompression. Tissue blood flow remained unchanged or decreased when active decompression (4/3) caused that 50% of the pigs were lifted from the table due to the force required. Myocardial blood flow was reduced with 5/0 vs. 4/0 despite no reduction in end decompression coronary perfusion pressure ((aortic-right atrial pressure) (CPP), (7 +/- 8 mmHg with 4/0, 14 +/- 11 mmHg with 5/0)(NS)). End decompression CPP increased by 186% with 4/2 vs. 4/0, by 200% with 4/3, and by 300% with 5/2. Endo-tracheal partial pressure of CO2 was significantly increased during the compression phase of active decompression CPR compared with standard CPR. Active decompression CPR generated an significantly increased ventilation compared with standard CPR. Conclusion: Carotid and tissue blood flow, ventilation, and CPP increase with 2 cm of active decompression. An attempt to further increase the level of active decompression or increasing the compression depth from 4 to 5 cm did not improve organ blood flow.     

Treatment of spinal fractures with paraplegia

Of 206 patients with vertebral fractures in the thoraco-lumbar spine with spinal cord injuries, an antero-lateral decompression with stabilization of the injured segment of the vertebral column was undertaken in 56 cases. In all these cases there was a compression of the spinal cord from the front. 8 patients made a complete recovery, 31 a good recovery, and 6 were improved. In 8 patients no improvement was noted. 2 patients developed pressure sores later and 1 patient died one year after the operation of uraemia. 22 patients out of 55 got a normal function of the bladder and 25 patients out of 54 a normal function of the anal sphincter. 16 patients out of 17 made a complete or good recovery after removal of a displaced rotated vertebral bony fragment from the spinal canal, and 7 patients out of 9 with wedge shaped fractures. In our clinic today, in cases of vertebral fractures with neural involvement, reduction and internal fixation with Harrington rods and fusion of the injured segment is undertaken as soon as possible, also during the night. If narrowing of the neural canal and compression of the spinal cord are verified, a decompression operation with interbody fusion is undertaken during the next days.     

Role of the premotor cortex in recovery from middle cerebral artery infarction

OBJECTIVE: To study the mechanisms underlying recovery from middle cerebral artery infarction in 7 patients with an average age of 53 years who showed marked recovery of hand function after acute severe hemiparesis caused by their first-ever stroke. INTERVENTIONS: Assessment of motor functions, transcranial magnetic stimulation, somatosensory evoked potentials, magnetic resonance imaging, and positron emission tomographic measurements of regional cerebral blood flow during finger movement activity. RESULTS: The infarctions involved the cerebral convexity along the central sulcus from the Sylvian fissure up to the hand area but spared the caudate nucleus, thalamus, middle and posterior portions of the internal capsule, and the dorsal part of the precentral gyrus in each patient. After recovery (and increase in motor function score of 57%, P<.001), the motor evoked potentials in the hand and leg muscles contralateral to the infarctions were normal, whereas the somatosensory evoked potentials from the contralateral median nerve were reduced. During fractionated finger movements of the recovered hand, regional cerebral blood flow increases occurred bilaterally in the dorsolateral and medial premotor areas but not in the sensorimotor cortex of either hemisphere. CONCLUSIONS: Motor recovery after cortical infarction in the middle cerebral artery territory appears to rely on activation of premotor cortical areas of both cerebral hemispheres. Thereby, short-term output from motor cortex is likely to be initiated.     

Effect of intrathecal nimodipine on spinal cord blood flow and evoked potentials in the normal or injured cord

A method was developed for administering intrathecal pharmacotherapy in a rat model of spinal cord injury. The effects of intrathecal administration of nimodipine on spinal cord blood flow (SCBF) and evoked potentials (EPs) were measured in the normal and injured spinal cord. It had previously been shown that systemic nimodipine caused severe hypotension after spinal cord injury. After baseline SCBF and EPs, 15 uninjured rats were blindly allocated to one of three groups: one placebo group (n = 5); and two groups with intrathecal nimodipine, 0.05 mg/kg (n = 5), or 0.2 mg/kg (n = 5). Ten other rats received a 35 g acute clip compression injury of the spinal cord for 1 minute and, were allocated to one of two groups: placebo (n = 5); and intrathecal nimodipine 0.05 mg/kg (n = 5) given 60 min after injury. In the uninjured groups, neither 0.05 nor 0.2 mg/kg of nimodipine increased SCBF during, or 30 min after, intrathecal infusion. However, the mean arterial blood pressure (MABP) decreased significantly to 69.73.1% after the infusion of 0.2 mg/kg nimodipine and did not recover by 98 min. In all three groups of uninjured rats, the amplitude of the cerebellar EP was decreased 30 min after infusion. After spinal cord injury, there were significant decreases in MABP, SCBF and EP amplitude in both placebo and treatment groups, but there was no therapeutic benefit from nimodipine. Thus, intrathecal infusion of nimodipine did not prevent the hypotension encountered with systemic administration and exerted no beneficial effect on SCBF or EPs after acute spinal cord injury.     

Cervical arachnoid cysts after craniocervical decompression for Chiari II malformations: report of three cases

OBJECTIVE AND IMPORTANCE: We describe three cases in which ventrally situated cervical arachnoid cysts led to spinal cord or cervicomedullary compression after repeat craniocervical decompression for Chiari II malformations. CLINICAL PRESENTATION: All three patients underwent craniocervical decompression when their Chiari malformations became symptomatic. The first patient developed chronic vertiginous spells and headache and was treated with repeated craniocervical decompression procedures during several years. Seven months after undergoing her third decompression procedure, she developed severe dizzy spells, which were determined to be of brain stem origin. The second patient had a small, asymptomatic arachnoid cyst anterior to the brain stem discovered at age 6 years. After undergoing repeat craniocervical decompression for headaches 8 years after undergoing his first procedure, the patient developed severe neck pain and acute quadraparesis. A third patient underwent repeat craniocervical decompression at age 14 years for cranial nerve dysfunction. Postoperatively, he acutely developed paresis of extraocular movements and incoordination of the upper extremities. All three patients were found to have anteriorly situated arachnoid cysts compressing the brain stem and/or cervical spinal cord. INTERVENTION AND TECHNIQUE: Fenestration of the arachnoid cyst or drainage with cystoperitoneal shunting adequately treated acute brain stem or cervical spinal cord compression. All three patients had achieved satisfactory relief from their acute symptoms of neural compression at their follow-up examinations. CONCLUSION: An association between spinal arachnoid cysts and neural tube defects has previously been reported. However, the development of previously undetected spinal arachnoid cysts after craniocervical decompression was unexpected. We hypothesize that extensive craniocervical decompression may alter the cerebrospinal fluid pressure dynamics in such a way that the anterior subarachnoid space, previously compressed, may dilate. Occasionally, because of perimedullary arachnoiditis, the cerebrospinal fluid may become loculated and act as a mass. Direct fenestration or shunting may successfully treat this problem, and less extensive craniocervical decompression may avoid it.     

Delayed postoperative paraparesis in scoliosis surgery. A case report

STUDY DESIGN: A case report is presented of an unusual complication of scoliosis surgery that, to the authors' knowledge, has never been reported in the literature. OBJECTIVE: Neurologic complications can occur after an uneventful posterior spinal instrumentation and fusion for scoliosis. Careful observation during the post-operative period is crucial for early detection of impending neurologic deficit. SUMMARY OF BACKGROUND DATA: Nerve compression of the cauda equina has been reported as a complication of different types of surgery in the lumbar spine, but an ascending paraparesis has never been described as a complication of scoliosis surgery. METHODS: A 12-year-old boy with a right thoracic scoliosis measuring 68 degrees and a 72 degrees left lumbar curve underwent Cotrel-Dubousset instrumentation and fusion from T5 to L4. Spinal cord monitoring with somatosensory evoked potentials and motor action potential were recorded and stable through out the entire procedure. Thirty hours later, a rapidly progressive ascending para-paresis developed that required urgent decompression. RESULTS: This patient underwent urgent decompression and removal of the Cotrel-Dubousset instrumentation. After surgery, the clinical picture improved gradually, and at 2-month follow-up he had regained normal strength in his lower limbs except for a grade 4 left extensor hallucis longus. By 4 months postdecompression, he had made a total recovery. CONCLUSIONS: Although clinical examination may be difficult to perform in patients who are unconscious, on large doses of narcotic drugs, or mentally retarded, careful observation during the postoperative period and awareness of this complication can allow early detection of impending reversible neurologic deficit and provision of appropriate treatment.     

Spinal cord compression secondary to epidural extramedullary hematopoiesis in thalassemia: a clinical case and review of literature

INTRODUCTION: Extramedullary hematopoiesis generally occurs in a variety of hematological disorders where the normal functioning of the blood forming organs is disturbed. It is a common manifestation in thalassemia where it occurs as a compensatory phenomenon in order to combat long standing anemia. Spinal cord compression as a consequence of extramedullary hematopoiesis in the intraspinal epidural space is an extremely rare complication, though this complication has been reported more commonly in thalassemia. CLINICAL CASE: A case of spinal cord compression due to extramedullary hematopoiesis in a patient with thalassemia is reported. The patient was successfully treated with radiation therapy and blood transfusions and he made a complete clinical recovery. Development. The literature is reviewed and the efficacy of several treatments such as surgery, radiotherapy and blood transfusion therapy is discussed. Until recently surgical decompression followed by radiation therapy remained the recommended treatment. Hematopoietic tissue is particularly sensitive to the ionizing radiation and low-dose radiotherapy is enough to relieve the spinal cord compression. Blood transfusion therapy may be diagnostically and therapeutically useful in the management of this entity. CONCLUSIONS: A prompt recognition of the syndrome and early treatment with radiotherapy and blood transfusion therapy is recommended to prevent irreversible damage to the spinal cord. Surgery may be only considered in the event of progressive neurological deficit despite of radiotherapy or blood transfusion therapy.     

Differential expression of heat shock proteins in normal and failing human hearts

OBJECTIVE: To predict spinal cord ischemia after endovascular stent graft repair of descending thoracic aortic aneurysms, temporary interruption of the intercostal arteries (including the aneurysm) was performed by placement of a novel retrievable stent graft (Retriever) in the aorta under evoked spinal cord potential monitoring. METHODS: From February 1995 to October 1997, endovascular stent graft repair of descending thoracic aortic aneurysms was performed in 49 patients after informed consent was obtained. In 16 patients with aneurysms located in the middle and distal segment of the descending aorta, the Retriever was placed temporarily before stent graft deployment. The Retriever consisted of two units of self-expanding zigzag stents connected in tandem with stainless steel struts. Each strut was collected in a bundle fixed to a pushing rod, and the stent framework was lined with an expanded polytetrafluoroethylene sheet. The Retriever was delivered beyond the aneurysm through a sheath and was retracted into the sheath 20 minutes later. A stent graft for permanent use was deployed in patients whose predeployment test results with the Retriever were favorable. Evoked spinal cord potential was monitored throughout placement of the Retriever and stent grafting until the next day. RESULTS: The Retriever was placed in 17 aneurysms in 16 patients. There were no changes in amplitude or latency of evoked spinal cord potential records obtained before or during Retriever placement. After withdrawal of the Retriever, all aneurysms were excluded from circulation immediately after permanent stent grafting. There were no changes in evoked spinal cord potential, nor were neurologic deficits seen after stent graft deployment in any patient. CONCLUSIONS: These results suggest that predeployment testing with the Retriever under evoked spinal cord potential monitoring is promising as a predictor of spinal cord ischemia in candidates for stent graft repair of thoracic aortic aneurysms.     

Inhibition of neutrophil adhesion does not prevent ischemic spinal cord injury

Paraplegia may occur after transient aortic occlusion as a consequence of primary ischemia to the spinal cord or injury during the reperfusion period. In animal models of ischemia/reperfusion there is evidence that reperfusion injury may be modulated partially by neutrophils. The efficacy of the neutrophil adherence blocking murine monoclonal antibody (MAb 60.3) was assessed in spinal cord ischemia/reperfusion in rabbits. Spinal cord ischemia was accomplished by balloon catheter occlusion of the infrarenal aorta. Neurologic assessment was graded as normal, partial neurologic deficit, or complete paralysis. Electrophysiologic monitoring with somatosensory evoked potentials was used to determine the optimal length of time of occlusion. Animals were treated randomly with 2 mg/kg of intravenous Mab 60.3 (n = 8) or saline solution (n = 9) with the investigator unaware of treatment. Mean occlusion times were no different between groups (control, 32.7 +/- 3.6 minutes versus MAb, 32.4 +/- 6.0 minutes). Five (55%) saline-treated and four (50%) MAb 60.3-treated animals became paraplegic. Animals with initial paraparesis all progressed to flaccid paraplegia within 24 hours. We conclude that spinal cord injury after transient aortic occlusion is independent of the CD11/CD18 glycoprotein complex of the neutrophil. Injury in this setting may occur during ischemia and thus may not be dependent on neutrophils or reperfusion.     

Spontaneous cervical extradural hematoma in a pregnant woman

Spontaneous spinal extradural hematomas are rare entities, especially during pregnancy. The authors report a case of a 26 years old women who developed as Brown-Sequard syndrome during pregnancy. The patient underwent first a caesarean and thereafter a prompt spinal surgical decompression. Complete sensory-motor recovery occurred after 48 hours. Differential diagnosis of cord compression, etiology of bleeding, conditions of recovery after surgery are discussed.     

Schizorchis arfaai sp. n. (Cestoda: Anoplocephalidae) from the wood-mouse, Apodemus sylvaticus, in Caspian area of Iran

An artificial, slowly expanding mass which compressed the spinal cord produced histological, electrophysiological, and neurological changes. A comparison was made of the effects of laminectomy in the cat with dorsally and ventrally placed masses. Laminectomy reversed declining cord function and produced prompt recovery of somatosensory evoked potentials in cats with dorsally placed masses. In contrast, a worsening of these functions occurred following laminectomy in animals with ventrally placed masses. In all cases, evoked potential changes were consistent with neurological status and were predictive of the outcome of surgery.     

Renal ACE immunohistochemical localization in NIDDM patients with nephropathy

PURPOSE: A new protective method against the spinal cord ischemia that occurs during aortic clamping was investigated in dogs. Oxygenated blood containing prostaglandin E1 (PGE1) was administered at the clamped aortic segment, and the effect was evaluated by measurement of the sensory evoked spinal potential (SESP). METHODS: In 30 dogs, a thoracotomy was made with dissection of the thoracic aorta. After intravenous heparin (100 units/kg) was administered, the proximal and distal descending thoracic aortas were cross-clamped for 60 minutes. Group A (n=10) received oxygenated blood at the rate of 1.0 ml/kg/min. Groups B (n=10) and C (n=10) received oxygenated blood at the same rate, with PGE1 at the dosage of 25 and 50 ng/kg/min, respectively. The infusion was continuously administered throughout the entire period of ischemia. SESP was measured with epidural electrodes before clamping, 10 and 60 minutes after clamping, and 10 and 60 minutes after declamping. Neurologic outcome was assessed at 24 hours after the operation and graded according to the method of Tarlov. RESULTS: There was no significant hemodynamic change in any group. At 60 minutes after damping and at 10 and 60 minutes after declamping, the amplitude of SESP was lower than that at preclamping in groups A and B (p < 0.05). At 60 minutes after damping and at 10 and 60 minutes after declamping, the SESP was more markedly decreased in group A compared with groups B and C. Regarding postoperative neurologic outcome, the dogs with SESP amplitude of more than 50% of the preclamping control value at 60 minutes after clamping showed neither paralysis nor paraplegia. Seven of nine dogs with less than 50% SESP amplitude showed neurogenic deficit. In a comparison of groups A, B, and C, the Tarlov score for group A dogs was significantly lower than that for group C dogs (p < 0.05). CONCLUSION: In this model, PGE1 administration at the rate of 50 ng/kg/min showed sufficient spinal cord protection against ischemia without a decrease in the blood pressure. Further studies are needed to determine the dose that will provide the maximal protective effect and to determine the maximum duration of ischemia against which PGE1 shows protective effects.