Search

A case of spontaneous regression of a large herniated disc at the lumbar level is presented. The disc regression correlated with clinical improvement and was documented on serial MRI studies. Although the phenomenon of spontaneous disappearance of decrease in size of herniated disc fragments is well known, the exact mechanism underlying this process remains unclear. This report discusses three possible explanations for disc regression: retraction into the intervertebral space, dehydration/shrinkage, and resorption due to inflammatory reaction.

✓ The authors present the rare case of a myxoma, a benign soft-tissue tumor of mesenchymal origin noted for occurring in the left atrium of the heart, which was found in the lumbar paraspinal muscles of an 80-year-old woman. This patient experienced low-back pain for over 20 years and had noted its increasing severity with the development of an L-5 radiculopathy over a 3-month period. Magnetic resonance imaging of the lumbar spine revealed a large paraspinal mass that invaded the L-5 vertebral body and the left foramen of L5—S1. A computerized tomography—guided biopsy sampling procedure was performed, and examination of the specimen revealed an intramuscular myxoma. The patient underwent resection of the tumor and nerve root decompression. The diagnosis of intramuscular myxoma was confirmed, and the patient experienced complete resolution of her presenting symptoms. This patient represents the third reported case (the first in the English-language literature) of an intramuscular (paraspinal) myxoma presenting with lumbar nerve root compression.

BACKGROUND Pain secondary to unresectable pancreatic cancer is frequently severe and extremely difficult to control with traditional methods of analgesia. This retrospective study reports the analgesic effects of intrathecal morphine sulfate by implanted infusion pumps in nine patients with unresectable adenocarcinoma of the pancreas. METHODS Nine patients were implanted over a 2-year period. Preoperative morphine IV equivalents were a mean of 81.51 mg/day, with a range of 20–140 mg/day. Patients were hospitalized for a trial dose of 1–2 mg of intrathecal Duramorph, 1 mg/ml, via lumbar puncture to assess whether adequate pain relief could be achieved and whether there would be drug-related side effects. RESULTS All patients who received a trial dose experienced excellent pain relief, and subsequently underwent implantation of a lumbar subarachnoid catheter and infusion pump during the same hospitalization. The mean number of days from diagnosis to pump implant was 119, with a range of 3–587 days. The mean maximum daily dose was 21.28 mg, with a range of 3–73.10 mg. No patient experienced respiratory depression or excess sedation which prevented achievement of pain control. Minor supplemental narcotic use was documented in three of the nine patients. Assessment of pain control was made by the level of activity and the analog pain scale, with 0 being no pain and 10 being the worst pain imaginable. All of the patients experienced good to excellent relief of pain. The mean duration of intrathecal morphine sulfate use until death was 137.3 days, with a range of 52–354 days. CONCLUSIONS This series of nine patients indicates that long-term administration of intrathecal morphine via implanted infusion pump in patients with pancreatic cancer is both efficacious and safe. All patients and their families reported an improved quality of life with an increased level of activity.

✓ Fine structural alterations in the microvasculature, primarily of the gray matter, occur as one aspect of experimental spinal cord contusion. A force of 300 gm-cm, shown by the authors to produce a transitory paraplegia, was applied to the T-10 level of exposed primate spinal cord. At 5 min post-contusion, the muscular venules of the central gray matter were distended with erythrocytes. Erythrocytes were seen within the perivascular spaces of the post-capillary venules and muscular venules at 15 and 30 min post-contusion, and there was hemorrhage into the gray matter at 1 hour post-contusion. The appearance of erythrocytes within the perivenular spaces was apparently due to small ruptures in the walls of the muscular venules, which were first demonstrated by electron microscopy 15 min after contusion. Alterations in capillary and post-capillary venule endothelium of both gray and white matter were present at 4 hours post-contusion and consisted of vacuolation and endothelial swelling. In conclusion, following experimental contusion of the spinal cord sufficient to cause a transitory paraplegia, the principal changes were early perivascular and parenchymal hemorrhages followed by later evidence of ischemic endothelial injury in the microvasculature.

With subaxial cervical spine fractures, it has not been established which injuries can be adequately stabilized by external orthoses and which will require surgical stabilization. After review of 64 consecutive patients with C3-C7 spinal injuries, fracture characteristics on admission roentgenograms were identified that accurately predict the success or failure of nonoperative management. These include evidence of severe ligamentous injury (SLI) and severe vertebral body injury (SVBI). The presence of SLI, SVBI, or both SLI and SVBI correlated strongly with nonoperative stabilization failure (p < 0.001, p = 0.002, and p = 0.004, respectively). Injuries without SLI or SVBI were all successfully stabilized by cervical orthoses. Additionally, characterizing injuries by evidence of SLI and SVBI directs the approach for surgical stabilization.

Experimental and clinical studies suggest that the calcium channel blocker nimodipine may reduce cerebral ischemic injury. Using rapid acquisition phosphorus-31 nuclear magnetic resonance (31P NMR) spectroscopy, we examined the effect of nimodipine on cerebral energy metabolism during severe ischemia in gerbils. High-energy phosphates and intracellular pH were characterized at baseline and at 2-min intervals following bilateral common carotid artery (CCA) ligation. Serial forebrain spectroscopy was continued until phosphocreatine (PCr) and adenosine triphosphate (ATP) resonances disappeared. Controls (n = 10) were compared to gerbils receiving intraperitoneal nimodipine 30 min prior to carotid ligation, at the following doses: 0.5 mg/kg (n = 8), 1.0 mg/kg (n = 10), 2.0 mg/kg (n = 8), or 4.0 mg/kg (n = 4). In the control group, PCr and ATP peaks were undetectable after a mean of 5.4 +/- 0.47 min following CCA ligation. Compared with controls, the mean time for depletion of high-energy phosphates following carotid ligation was prolonged at nimodipine doses of 0.5 mg/kg and 1.0 mg/kg, but the differences did not reach statistical significance. In the 2.0 mg/kg group, however, ATP was preserved until 9.8 +/- 1.0 min following the onset of ischemia, significantly longer than the control group (p = 0.005, Mann-Whitney test). Nimodipine had no effect on the time course or severity of intracellular acidosis. In this model of severe ischemia, relatively high doses of nimodipine slowed the depletion of high-energy phosphates without altering intracellular acidosis. This suggests that nimodipine may provide cerebral protection by directly altering ischemic cellular metabolism.

✓ Severe head injury results in suppression of cellular immunity associated with defectivein vitrofunctioning of effector lymphocytes, such as helper T cells and cytotoxic T cells. It is not known whether this suppression in effector lymphocyte function is due to intrinsic lymphocyte dysfunction, to suppressor peripheral blood mononuclear cells (PBMC's) such as suppressor lymphocytes or suppressor monocytes, or to serum factors capable of inhibiting effector lymphocyte function. The purpose of this study was to determine whether a subpopulation of PBMC's and/or serum factors) are responsible for this observed suppression in cell-mediated immunity.Cell-mediated immune activity was determined measuringin vitrolymphokine-activated killer (LAK) cytotoxicity following incubation of PBMC's from 15 head-injured patients with those from 15 heterologous normal subjects. The PBMC's were separated into lymphocyte-enriched and monocyte-enriched subpopulations by plastic adherence techniques, and the effect of each population on LAK cytotoxicity was determined. Additionally, the effect on cytotoxicity of serum from the head-injured patients was determined in a dose-response fashion.There was significant depression in LAK cytotoxicity when: 1) PBMC's from normal subjects were incubated with PBMC's from head-injured patients (p < 0.001); 2) lymphocytes (PBMC's depleted of monocytes) from head-injured patients were incubated with PBMC's from normal subjects (p < 0.001); and 3) PBMC's from normal subjects were incubated with serum from head-injured patients (p < 0.001). No suppression in cellular immunity was noted when lymphocytes from normal subjects were incubated with monocytes from head-injured patients.The results indicate that lymphocytes rather than monocytes actively inhibit cellular immunity following severe head injury. The detection of immmunosuppressive serum factors suggests a mechanism by which lymphocytes might be modulated by severe head injury.

The optimal surgical approach for spinal canal reconstruction of thoracolumbar fractures is controversial, and the relationship between spinal canal reconstruction and neurological recovery remains unclear. To address these issues, 22 consecutive cases of thoracolumbar fracture with accompanying neurological deficit were reviewed. Neurological status was graded at the time of admission, postoperatively, and at a mean of 15 months postinjury. By using preoperative and postoperative radiographs and computed tomographic scans, the degree of spinal canal compromise was quantified in the sagittal, coronal, and axial planes. All fractures were stabilized by posterior instrumentation and fusion, and in 10 injuries, retropulsed vertebral body fragments were further reduced by posterolateral decompression. Spinal canal dimensions, neurological function, and operative approach were compared by using nonparametric statistical analysis. The greater the initial spinal canal compromise, the more severe the neurological deficit (P = 0.04). With injuries involving L1 and above, this relationship increased (P = 0.003). The extent of spinal canal reconstruction failed to correlate with neurological recovery. Compared with spinal instrumentation alone, transpedicular decompression showed no benefit in terms of postoperative canal dimensions or neurological outcome. On the basis of this experience, transpedicular decompression offers no advantage over spinal instrumentation alone. The relationship between initial spinal canal encroachment and neurological deficit demonstrates that the degrees of bony and neurological injury directly reflect the kinetic energy transferred at the time of impact. The lack of correlation between the extent of spinal canal reconstruction and neurological recovery suggests that ongoing neural compression/distortion contributes little to the overall neurological injury.

✓ The 1-year follow-up data of a multicenter randomized controlled trial of methylprednisolone (30 mg/kg bolus and 5.4 mg/kg/hr for 23 hours) or naloxone (5.4 mg/kg bolus and 4.0 mg/kg/hr for 23 hours) treatment for acute spinal cord injury are reported and compared with placebo results. In patients treated with methylprednisolone within 8 hours of injury, increased recovery of neurological function was seen at 6 weeks and at 6 months and continued to be observed 1 year after injury. For motor function, this difference was statistically significant (p = 0.030), and was found in patients with total sensory and motor loss in the emergency room (p = 0.019) and in those with some preservation of motor and sensory function (p = 0.024). Naloxone-treated patients did not show significantly greater recovery. Patients treated after 8 hours of injury recovered less motor function if receiving methylprednisolone (p = 0.08) or naloxone (p = 0.10) as compared with those given placebo. Complication and mortality rates were similar in either group of treated patients as compared with the placebo group. The authors conclude that treatment with the study dose of methylprednisolone is indicated for acute spinal cord trauma, but only if it can be started within 8 hours of injury.

✓ Infection is a major complication of severe head injury, occurring in 50% to 75% of patients who survive to hospitalization. Previous investigations of immune activity following head injury have demonstrated suppression of helper T-cell activation. In this study, the in vitro production of interferon-gamma (INF-γ), interleukin-1 (IL-1), and interleukin-2 (IL-2) was determined in 25 head-injured patients following incubation of peripheral blood lymphocytes (PBL's) with the lymphocyte mitogen phytohemagglutinin (PHA). In order to elucidate the functional status of cellular cytotoxicity, lymphokine-activated killer (LAK) cell cytotoxicity assays were performed both prior to and following incubation of PBL's with IL-2 in five patients with severe head injury. The production of INF-γ and IL-2 by PHA-stimulated PBL's was maximally depressed within 24 hours of injury (p < 0.001 for INF-γ, p = 0.035 for IL-2) and partially normalized within 21 days of injury. There was no change in the production of IL-1. When comparing the in vitro LAK cell cytotoxicity of PBL's from head-injured patients and normal subjects, there was a significant depression in LAK cell cytotoxicity both prior to (p = 0.010) and following (p < 0.001) incubation of PBL's with IL-2. The results of this study indicate that IL-2 and INF-γ production, normally required for inducing cell-mediated immunity, is suppressed following severe head injury. The failure of IL-2 to enhance LAK cell cytotoxicity suggests that factors other than decreased IL-2 production, such as inhibitory soluble mediators or suppressor lymphocytes, may be responsible for the reduction in cellular immune activity following severe head injury. These findings may have significant implications in designing clinical studies aimed at reducing the incidence of infection following severe head injury.

Studies in animals indicate that methylprednisolone and naloxone are both potentially beneficial in acute spinal-cord injury, but whether any treatment is clinically effective remains uncertain. We evaluated the efficacy and safety of methylprednisolone and naloxone in a multicenter randomized, double-blind, placebo-controlled trial in patients with acute spinal-cord injury, 95 percent of whom were treated within 14 hours of injury. Methylprednisolone was given to 162 patients as a bolus of 30 mg per kilogram of body weight, followed by infusion at 5.4 mg per kilogram per hour for 23 hours. Naloxone was given to 154 patients as a bolus of 5.4 mg per kilogram, followed by infusion at 4.0 mg per kilogram per hour for 23 hours. Placebos were given to 171 patients by bolus and infusion. Motor and sensory functions were assessed by systematic neurological examination on admission and six weeks and six months after injury. After six months the patients who were treated with methylprednisolone within eight hours of their injury had significant improvement as compared with those given placebo in motor function (neurologic change scores of 16.0 and 11.2, respectively; P = 0.03) and sensation to pinprick (change scores of 11.4 and 6.6; P = 0.02) and touch (change scores, 8.9 and 4.3; P = 0.03). Benefit from methylprednisolone was seen in patients whose injuries were initially evaluated as neurologically complete, as well as in those believed to have incomplete lesions. The patients treated with naloxone, or with methylprednisolone more than eight hours after their injury, did not differ in their neurologic outcomes from those given placebo. Mortality and major morbidity were similar in all three groups. We conclude that in patients with acute spinal-cord injury, treatment with methylprednisolone in the dose used in this study improves neurologic recovery when the medication is given in the first eight hours. We also conclude that treatment with naloxone in the dose used in this study does not improve neurologic recovery after acute spinal-cord injury.

Infection is a major cause of morbidity following multiple traumatic and head injury. Although immunosuppression has been demonstrated after multiple traumatic injury, the effects of head injury on immune function have not been thoroughly investigated. In a prospective study of 10 severely head-injured patients, in vitro and in vivo parameters of cellular immune activity were assessed. In vitro measurements of lymphocyte surface antigen expression following mitogen stimulation were made serially over a 3-week period in 10 patients with severe head injury. The control group consisted of 20 healthy subjects. Phenotyping of peripheral blood lymphocytes (PBLs) was performed following incubation with and without mitogens. Phenotypes were determined by flow cytometry using monoclonal antibodies (MABs) to T lymphocyte subsets and the alpha subunit of interleukin 2 (IL-2) receptors. In vivo cellular immune function was determined by measuring patient responses to delayed-type hypersensitivity (DTH) skin testing within 24 h of injury. When head-injured patients were compared to controls, PBLs incubated in the presence of phytohemagglutinin (PHA) demonstrated a decrease in cells marking as T cells (p = 0.005), helper-inducer T cells (p = 0.001), and in the number of IL-2 receptor-bearing cells (p = 0.001). The functional ability of these lymphocyte subpopulations to proliferate in the presence of PHA was significantly suppressed within 24 h of injury and normalized within 3 weeks of injury. DTH skin testing to Candida, mumps, trichophyton, and PPD antigens was performed within 24 h of injury and resulted in anergic responses in all 10 patients when measured at 24, 48, and 72 h following administration. The overall infection rate was 60%, with the majority of infections occurring within the first 4 days following injury. The results of this study indicate that severe head injury results in suppression of cellular immune function with a corresponding high rate of infection. The possible significance of the decrease in the percentage of helper-inducer T cells and in the number of cells bearing IL-2 receptors following mitogen stimulation is discussed.

Objective Metastasis from lung cancer to the conus medullaris has never been reported in the English literature, although three cases have appeared in the French and Japanese literature. Our case report is unique because the patient presented with a lumbar radiculopathy, an atypical presentation that was found to be caused by metastasis from lung cancer to the conus medullaris. A critical review of the pertinent literature related to metastatic neoplasms to the conus medullaris is also presented. Clinical presentation We report the case of a 54-year-old man who presented with an L5 radiculopathy and was initially found to have a small disc herniation at L4-L5 on magnetic resonance imaging scans, which was ruled out as the case of his initial symptoms. In 3 weeks, the symptoms progressed with the development of urinary incontinence and right leg weakness. A magnetic resonance imaging scan of the lumbar spine showed a tumor at the conus medullaris. Intervention The patient underwent a laminectomy with removal of the tumor. Pathological examination of the tumor showed infiltrating differentiated adenocarcinoma. A 2.5 cm lung mass in the right middle lobe with surrounding adenopathy was found on a computed tomographic scan of the chest. The patient died 4 months later from systemic involvement and progression of his lung disease. Conclusion This case report illustrates the rare presentation of a lumbar radiculopathy caused by a metastatic tumor to the conus medullaris. This was the first presentation for the diagnosis of lung cancer in this patient.

✓ In 1961 Dr. Robert White, fresh from the Mayo Clinic, established the Brain Research Laboratory (BRL) at the Cleveland Metropolitan General Hospital, Cleveland, Ohio, under the auspices of Case Western Reserve University. During a span of 15 years, he and his colleagues contributed significantly to our knowledge and understanding of the central nervous system in deep hypothermic conditions, thus demonstrating the protective effects of cerebral and spinal cord cooling in patients with injuries as well as the ability of the brain to survive extended periods of total circulatory arrest at extremely low temperatures. It was there that isolated brain preparation and transplantation were first accomplished. These and other unique, surgically constructed brain models opened new fields of exploration in neurochemical, neurophysiological, rheological, immunological, and cognitive features of the brain in normothermic and various hypothermic states. During the laboratory's most productive years (1961–1976), there were 10 surgeons actively involved in scientific investigations who later became chairmen or chiefs of Departments or Divisions of Neurosurgery and another four who became professors of neurosurgery or other surgical specialties.

The main objective of this project is to produce an accurate parametric model of a human cervical vertebra and the intervertebral disc. This model is based on a well defined set of parameters that reflect the differences between the different vertebrae, allowing for the reconstruction of cervical segments of the spine by a simple control of these parameters.Copyright © 2002 by ASME

Disc degeneration leads to various spinal disorders like Spondylylosis, Stenosis and Osteophyte formation and Osteoporosis leads to Compression fracture of the vertebral body. Biomechanical investigation of stress changes in the lumbar spine caused by disc degeneration has been done using mathematical models and cadavaric studies (1). Osteoporosis has also been studied in a similar manner (2). However, very little is known of the combined effects of osteoporosis and disc degeneration in the lumbar spine and how it may affect the treatment planning. This paper presents our findings on the combined effect using detailed finite element model of L4-L5 segments.Copyright © 2002 by ASME

Induction of hypothermia in patients with brain injury was shown to improve outcomes in small clinical studies, but the results were not definitive. To study this issue, we conducted a multicenter trial comparing the effects of hypothermia with those of normothermia in patients with acute brain injury.The study subjects were 392 patients 16 to 65 years of age with coma after sustaining closed head injuries who were randomly assigned to be treated with hypothermia (body temperature, 33 degrees C), which was initiated within 6 hours after injury and maintained for 48 hours by means of surface cooling, or normothermia. All patients otherwise received standard treatment. The primary outcome measure was functional status six months after the injury.The mean age of the patients and the type and severity of injury in the two treatment groups were similar. The mean (+/-SD) time from injury to randomization was 4.3+/-1.1 hours in the hypothermia group and 4.1+/-1.2 hours in the normothermia group, and the mean time from injury to the achievement of the target temperature of 33 degrees C in the hypothermia group was 8.4+/-3.0 hours. The outcome was poor (defined as severe disability, a vegetative state, or death) in 57 percent of the patients in both groups. Mortality was 28 percent in the hypothermia group and 27 percent in the normothermia group (P=0.79). The patients in the hypothermia group had more hospital days with complications than the patients in the normothermia group. Fewer patients in the hypothermia group had high intracranial pressure than in the normothermia group.Treatment with hypothermia, with the body temperature reaching 33 degrees C within eight hours after injury, is not effective in improving outcomes in patients with severe brain injury.

Studies in animals indicate that methylprednisolone and naloxone are both potentially beneficial in acute spinal-cord injury, but whether any treatment is clinically effective remains uncertain. We evaluated the efficacy and safety of methylprednisolone and naloxone in a multicenter randomized, double-blind, placebo-controlled trial in patients with acute spinal-cord injury, 95 percent of whom were treated within 14 hours of injury. Methylprednisolone was given to 162 patients as a bolus of 30 mg per kilogram of body weight, followed by infusion at 5.4 mg per kilogram per hour for 23 hours. Naloxone was given to 154 patients as a bolus of 5.4 mg per kilogram, followed by infusion at 4.0 mg per kilogram per hour for 23 hours. Placebos were given to 171 patients by bolus and infusion. Motor and sensory functions were assessed by systematic neurologic examination on admission and six weeks and six months after injury. After six months the patients who were treated with methylprednisolone within eigh...

Study design Sixty-five consecutive cases of acute cervical spinal cord injuries were reviewed retrospectively for respiratory complications. Objectives The objectives were to identify factors that may contribute to respiratory dysfunction and to evaluate therapeutic measures designed to reduce respiratory complications. Summary of background data Respiratory complications continue to be a major cause of morbidity and mortality after cervical spinal cord injury with a reported incidence from 36 to 83%. Methods Multiple factors were evaluated which could potentially influence the incidence or severity of respiratory complications. These included age, pre-existing cardiac or pulmonary disease, accompanying major injuries, and the severity of the spinal cord injury. The effects of various therapeutic measures were also assessed including the benefit of rotating beds, early fracture stabilization and patient mobilization. Results Respiratory complications occurred in 62% of these patients and were transient in nature, variable in severity and duration, strongly associated with the severity of spinal cord injury, and only marginally affected by therapeutic interventions. Conclusions The characteristics of respiratory dysfunction following cervical spinal cord injury correspond to those of spinal shock.

Infection is a common and serious complication of severe head injury. Immunocompetence in 25 severely head injured patients was investigated by measuring: (1) delayed-type hypersensitivity (DTH) skin test responses to common antigens; (2) phytohaemagglutinin (PHA) stimulated peripheral blood lymphocyte (PBL): blastogenesis, phenotype expression, and lymphokine production; (3) lymphokine-activated killer (LAK) cytotoxicity, antibody dependent cellular cytotoxicity (ADCC) and natural killer (NK) cytotoxicity; and (4) immunoglobulin and complement levels. The incidence of anergy to DTH skin testing was 100%. There was a decrease in PHA stimulated: PBL blastogenesis (p = 0.002), T-cell expression (p = 0.018), helper T-cell expression (p less than 0.001), interleukin-2 receptor expression (p less than 0.001), interleukin-2 production (p = 0.035) and gamma-interferon production (p less than 0.001). LAK cytotoxicity was depressed following incubation with IL-2 (p less than 0.001). There was no significant decrease in immunoglobulin levels and all acute phase reactants tested increased. The results of this study indicate that the cellular arm of immune response, including lymphocyte activation and cytokine production, is suppressed following severe head injury. The lack of enhancement in LAK cytotoxicity following incubation of PBLs with interleukin-2 suggests that factors other than decreased interleukin-2 production, such as the inherent lymphocyte dysfunction, other soluble mediators or suppressor cells, may be responsible for the reduction in cellular immunity observed following severe head injury.

Infection is a major cause of morbidity following severe head injury. Although investigations have demonstrated central nervous system modulation of immune function, the effects of severe head injury on immune activity have not been well documented. This study prospectively investigated cellular immune function in 20 patients with isolated severe head injury. In vivo cellular immune status was determined by responses to delayed-type hypersensitivity (DTH) skin tests. In vitro studies included the effect of the lymphocyte mitogen, phytohaemagglutinin (PHA), on peripheral blood lymphocyte (PBL) phenotype expression and PBL blastogenesis. DTH skin testing demonstrated anergy to all antigens used during the first two weeks following head injury. Analysis of PBLs incubated with PHA demonstrated a decrease in the percent of PBL blastogenesis (p = 0.002), the percentage of cells marking as T-cells (p = 0.018), helper T-cells (p less than 0.001) and those expressing interleukin-2 receptors (p less than 0.001). There was a significant increase in the percentage of cells that marked as monocytes (p = 0.030), whereas there was no significant change in the percentage of B-cells, suppressor/cytotoxic T-cells, natural killer cells or in cells expressing the HLA-DR antigen. The infection rate was 55% with most occurring within 5 days of injury. The results of this study suggest that isolated severe head injury causes suppression of cellular immunity. The decrease in PHA stimulated PBL blastogenesis, helper T-cell phenotypic and interleukin-2 receptor expression, suggests suppression in early helper T-cell activation may be responsible for the high incidence of infection following severe head injury. The possible significance of increased monocyte phenotypic expression is discussed. Language: en

A retrospective study of patient outcome, based on admission computed tomography, was carried out in 75 consecutive patients with head injury. Computed tomography data collected included the type and extent of intracranial hemorrhage, the extent of midline shift, and the ratio of midline shift compared with the extent of intracranial hemorrhage. Midline shift was considered to be out of proportion to intracranial hemorrhage when the midline shift of the septum pellucidum exceeded the extent of the hemorrhage as measured radially from the inner table of the skull. When computed tomography data were analyzed by logistic regression, significant predictive factors for poor outcome were intracranial hemorrhage (34%), intracranial hemorrhage with midline shift (61%), and midline shift out of proportion to the extent of intracranial hemorrhage (88%). When patient outcome and mortality rates are considered, our study indicates that midline shift out of proportion to the extent of intracranial hemorrhage is a highly useful predictor of poor patient outcome following head injury.

Less than 10% of the 250 reported cases of traumatic intracranial aneurysms have involved the posterior circulation. Traumatic aneurysms of the superior cerebellar artery are extremely rare, with only three cases previously reported. This is the first report of a traumatic superior cerebellar artery aneurysm in which the diagnosis was suggested by computed tomographic scan. The potential for a good outcome suggests the value of early angiography when the history and diagnostic imaging studies suggest the possibility of a traumatic aneurysm.

✓ Computer analysis of digital subtraction angiography (DSA) was utilized to quantify the effectiveness of tissue-type plasminogen activator (TPA) in a rabbit cerebroembolic stroke model. Fourteen animals underwent cannulation of the facial artery and a preembolus angiogram. Autologous blood clots were then injected, and occlusion of the internal carotid artery at the circle of Willis was documented with repeat angiogram. The experimental group received a 1-mg/kg intravenous infusion of TPA via a femoral catheter for 90 minutes. A control group received an equivalent volume of saline. Follow-up angiograms were performed every 15 minutes. The TPA-treated animals showed progressive improvement in flow through previously occluded vessels. Time-density curves of the contrast material over the middle cerebral artery trunk and brain parenchyma were generated. The best integrated curves for the two groups were compared at 30 minutes after occlusion and 90 minutes after treatment. Animals were then observed for 24 hours and their neurological status was documented. Premortem infusion of either Evans blue dye or neutral red dye was performed and the integrity of the blood-brain barrier and tissue perfusion were assessed by video planometry. Significant improvements were noted by DSA, and Evans blue and neutral red dye studies in animals treated with TPA.

Acute craniocerebral trauma remains a difficult management problem. Optimal conditions for recovery require stabilization of vital signs, removal of a mass lesion when present, and control of intracranial pressure. While computerized tomography (CT) has helped achieve these objectives, there remain patients who may develop a second extracerebral hematoma not evident on their initial preoperative scan. This report concerns our experience with patients who developed such delayed post-traumatic extracerebral hematomas shortly after evacuation of hematomas at other sites. Between 1 January 1979 and 1 October 1980, 47 patients underwent emergency evacuation of a traumatic extracerebral hematoma (38 acute subdural and 18 acute epidural hematomas) at the Yale New Haven Hospital. Within 24 hours, four patients developed, in addition, a total of six delayed extracerebral hematomas (10%) which also required evacuation. In all of these patients a skull fracture was present at the site of the delayed hematomas. This experience suggests: 1) Exploration of the extracerebral space beneath a skull fracture should be considered following evacuation of a hematoma at another site. 2) Repeat CT is indicated if anticipated improvement does not occur after evacuation of a hematoma. 3) Decompression of the intracranial contents by removal of a hematoma may promote the development of another delayed hematoma.

✓ To evaluate the effect on neurological outcome of spinal cord compression persisting after a closed injury, the authors reviewed 44 of 62 consecutively managed cases of cervical spinal cord and spine injuries at C3–7, inclusive. Decompression within 48 hours of injury was confirmed by myelography or open reduction. Neurological status, graded numerically on a spinal trauma scale at admission and at follow-up review (an average of 1 year ± 2 months after admission), and percent recovery of neurological deficit were compared to canal narrowing (22 severe, ≥ 30%; versus 22 moderate, 11% to 29%; or mild, ≤ 10%) and to delay before treatment (30 within 8 hours of injury versus 14 treated 9 to 48 hours after injury). Severe narrowing was equated with compression. Status at admission and at follow-up review was positively correlated. Patients with admission scores of less than 2 recovered a mean of 15% of their deficit, while those with scores more than 2 recovered a mean of 77%. Admission status correlated significantly with spinal canal narrowing but not with vertebral body displacement. Time of treatment had no significant effect upon admission status and percent recovery. No significant difference in the percent of recovery was noted, whether decompression was early (up to 8 hours) or late (9 to 48 hours) after injury. Surgery did not significantly alter the percent of recovery. The findings indicate that the initial injury to the cervical spinal cord and spine remains the primary determinant of neurological outcome. Severe canal narrowing with cord compression thereafter appears to have comparatively little effect. The conclusion that decompression is without effect is not possible without comparison with a group of patients whose spinal canals remained narrowed at follow-up review.

The thioflavine S technique for delineating blood flow patterns in central nervous system tissue has been reviewed. Electron microscopic studies of the microvasculature of the feline spinal cord after intravascular administration of the thioflavine S demonstrated no fine structural alterations in arterioles, capillaries, or venules. It is suggested that the thioflavine S technique could be used in conjunction with electron microscopic studies to enhance correlation of microvascular structure with function.

The effect of continuous infusion of lidocaine on acute spinal cord trauma in cats was studied. Intravenous and subarachnoid administration of lidocaine did not alter generation and conduction of the spinal evoked responses (SERs) in intact animals. The cortical somatosensory evoked responses and SERs were abolished after weight drop injuries of 120 and 400 g-cm. No return of the evoked responses occurred within 4 hours after trauma in either the lidocaine- or the saline-treated groups. Loss of SERs and appearance of an evoked injury potential were sensitive determinants of spinal cord injury. We concluded that lidocaine treatment did not facilitate the return of spinal cord function in this model of acute spinal cord injury.

✓ A multi-center double-blind randomized clinical trial was conducted by the National Acute Spinal Cord Injury Study Group to examine the efficacy of high-dose methylprednisolone (1000-mg bolus and 1000 mg daily thereafter for 10 days) compared with that of a standard dose (100-mg bolus and 100 mg daily for 10 days). No significant difference was observed in neurological recovery of motor function, pinprick response, or touch sensation 1 year after injury between the two treatment groups, after adjustment for other potentially confounding factors. Analyses that specifically took into account the patients' total steroid dose and relative weight confirmed the lack of a steroid treatment effect. The case fatality rate was 10.7% during the 1st year after injury, and this was not associated with the steroid treatment protocol or the patient's gender. Deaths did occur significantly more frequently among patients who were completely (15.3%) and partially (8.6%) plegic than among those who were paretic (2.5%, p = 0.0005), and among patients aged 50 years or older (38.6%, p = 0.0001).

The effect of nimodipine on acute spinal cord trauma was studied in cats. Spinal evoked responses (SERs) were abolished after weight drop injury of 100 g-cm. All control animals showed spontaneous recovery of spinal cord function as measured by SERs. Treatment with a moderate intravenous dose of nimodipine resulted in a 32% drop in systemic blood pressure and delay in or failure of spinal cord recovery. We concluded that in this model, nimodipine treatment had deleterious effect on the spinal cord recovery due to the significant associated hypotension. It is likely that marked hypotension in the case of traumatic loss of autoregulation overrides the expected nimodipine-related increase in spinal cord blood flow with resultant additional ischemic damage.

Indications for surgery in the patient with a spinal cord injury may be either neurosurgical or orthopedic or a combination of the two. Neurologic and radiologic evaluations are described and types of treatment discussed.

In an attempt to overcome the possible radioresistance of glioblastoma multiforme related to the large shoulder on the in vitro survival curves and to sensitize hypoxic tumor cells, a treatment protocol was instituted at Yale University Medical Center and affiliated hospitals, using large dose fraction irradiation therapy in conjunction with the hypoxic cell sensitizer metronidazole. Nineteen patients with biopsy-confirmed, previously untreated, cerebral grade IV glioblastoma multiforme were, following surgery, irradiated once a week at 600 rad per fraction, 3.5 to 4 hours after ingestion of metronidazole, 6 gm/m2. A total of 7 treatments were employed, with all patients maintained on antiseizure medications and corticosteroids. Metronidazole levels were determined prior to each treatment and patients were followed closely clinically and with serial computerized tomography (CT) scans. The treatment was well tolerated, in general, with no untoward side effects related to the high dose fraction irradiation. The majority of the patients experienced varying degrees of gastrointestinal upset lasting up to several hours following metronidazole administration. Three patients died of pulmonary emboli. One patient experienced moderately severe ototoxicity. A median survival of 9.4 months was obtained for all 19 patients, suggestive of a prolongation of survival compared to historical controls treated with conventionally fractionated radiation or with unconventional radiation fractionation schemes and metronidazole or misonidazole.

✓ Intracranial pressure (ICP) and cerebral perfusion pressure were monitored in 12 patients who were comatose secondary to hypoxic (five cases) or hypotensive (seven cases) nontraumatic cerebral insults. Patients who were hypotensive but not hypoxic developed significant increased ICP. In patients who were comatose from hypoxic cerebral insults without hypotension, ICP was normal. When an increase in ICP was diagnosed, patients were managed aggressively so as to improve cerebral perfusion and lower ICP. Although a functional salvage rate of 25% was obtained, this may reflect the severity of the initial cerebral insult rather than the effect of treatment. In order to prevent the potential deleterious effects of raised ICP, it is concluded that monitoring ICP and maintaining adequate perfusion may be warranted in comatose patients who have suffered nontraumatic diffuse ischemic but not purely hypoxic cerebral insults.

✓ The microscopic appearance of the primate spinal cord within a 4-hour interval following the delivery of a direct force sufficient to produce a transitory paraplegia was investigated by light microscopy. The resulting hemorrhagic lesion involved primarily the central gray matter and was attributed to the direct effect of the trauma on the vessels in the gray matter with a consequent impairment of blood supply to the injured area. Chromatolysis, vacuolation, and alterations in cytoplasmic density and stainability were observed within the neurons. The edematous changes in the white matter, which were more marked in the internal layers relative to the external layers, appeared minimal and explain in part why the paraplegia was transient.

Percutaneous fine-needle aspiration and biopsy techniques have proved to be a safe, accurate and effective means of obtaining cytological diagnosis (Holm et al, 1979). Recently neurosonographic biopsy techniques have been widely used in conjunction with open brain biopsies (Grode et al, 1983; Knake et al, 1983; Rubin et al, 1980). Ultrasound has been used to evaluate sonographic echogenicity, size, and configuration of mass lesions as well as their relationship to the cerebral ventricles and other vital structures. The ability of ultrasound to localise precisely a deeply situated intracranial lesion intra-operatively has reduced patient morbidity, operative time and cost of surgery. We report our experience with the use of a sonographically guided percutaneous approach in the evacuation of a cerebral cyst and discuss the technique, advantages, disadvantages and future applications.

The. he plight of civilian patients in the United States who sustain injuries to the spinal cord, resulting in a permanent paralysis, has been a dismal one. To the existing 125,000 individuals chronically paralyzed in this manner, between 5,000 and 10,000 people are added each year. Most of these additional patients are young, being between the ages of 18 and 25, of which 84% are young men. Compounding the personal tragedy of a group that remains largely depressed and nonproductive is the recent estimate by the Armed Forces that caring for each spinalcord injured patient from the time of his injury to his death costs $900,000. Recently, though, interest has been rekindled in basic research concerning the morphologic, physiologic, biochemical, and vascular events occurring in the spinal cord within minutes and hours of an injury that produces either a transient or a permanent paralysis. The initial stimulus for much of

SummaryGlucose and lactate content in dog brain were measured before and during arrest of circulation in a standard preparation. Comparison with other studies of the same model allowed the guarded conclusion that the cerebral lactate level in dogs after 10 min of severe hypoxia may be indicative of an irreversible state. Lactate concentration rose and glucose levels fell during a 10-min period of ischemia. The increase in lactate concentration was sufficient to account for about one-fourth of the decrease in glucose content by way of anerobic glycolysis.

Acute traumatic epidural hematoma may develop secondary to an arterial or venous bleed. The computed tomography (CT scan) appearance of the hematoma depends on the source and severity of bleeding, the interval between injury and CT scan, and the degree of clot organization or breakdown. We report the emergency evaluation, CT scan evolution, and clinical management of one such acute venous epidural hematoma.