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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.

✓ 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.

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.

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.

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

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.

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.

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 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.

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.

✓ The pathological changes occurring in the thoracic spinal cords of 41 cats were studied by light microscopy at 4 hours, 4 weeks, and 4 months after graded transdural trauma. Alterations characteristic of a vascular injury proportionate to the magnitude of the original trauma which results in tissue hypoxia, destruction, and reparation were identified at each interval studied. In more severely injured animals these changes consisted of an initial hemorrhagic infarction followed by the removal of necrotic parenchyma and the development of an adhesive arachnoiditis and intramedullary cavitation. A comparison of the findings in the present investigation with what has been described in postmortem studies of spinal cord injured patients indicates that the response of the spinal cord to non-disruptive trauma is similar in both cases.

✓ The spinal cord of anesthetized cats was subjected to impact trauma of different intensities to determine how changes in trauma magnitude affect the formation and distribution of edema. All animals underwent a laminectomy to expose the cord segments corresponding to the T5–7 vertebrae. Fourteen cats were injected with fluorescein-labeled albumin, and then subjected to 260, 360, 500, or 700 gm-cm injury to the spinal cord. They were sacrificed at 8 hours after trauma. Twelve cats were injected with fluorescein-labeled dextrans of 20,000, 40,000, 70,000, or 150,000 molecular weight (MW) prior to 500 gm-cm injury, and sacrificed 8 hours after trauma. Serial cord sections from both groups were studied by fluorescence microscopy. In nine cats, sections of cord were removed 8 hours after trauma of 260, 360, or 500 gm-cm impact, and 1-cm sections were assayed for dry weight. Extravasated tracers were present in areas of hemorrhage at the site of impact in all animals. Extension of tracers and increases in tissue water rostrally and caudally from the site of impact were observed consistently with time only in animals receiving 500 or 700 gm-cm trauma. The distance of migration was similar for all tracers. The longitudinal distribution of increased tissue water was consistent with the distribution of fluorescent markers. The findings indicate that the longitudinal extension of posttraumatic edema is directly related to the amount of initial trauma.

✓ A scale has been developed for assessment of the severity of spinal cord injury and the prognosis for recovery. Based on neurological examination, this scale employs numerical grading of selected functions below the level of the injury. The scale is adaptable to prospective as well as retrospective studies, and provides a reliable estimation of prognosis and, therefore, a means of comparing the effectiveness of differing treatment modalities. In relation to a group of 37 patients with cervical spinal cord injury treated under one protocol and assessed within 24 hours and again at 1 year from injury, a descriptive model of the patterns of recovery has been obtained. Relative recovery of the initial deficit measured as a “percentage recovery ratio” is presented as an analytical tool for comparison of effectiveness of different methods of therapy.

The potential of ependymomas to spread throughout the intracranial subarachnoid space is well documented, though the incidence is disputed. This relates in part to the time required for such metastases to produce symptoms. The diagnosis of such spread, however, is important for therapeutic management. This report demonstrates the effectiveness of computerized tomography in diagnosing spread of ependy moma throughout the basal cisterns and cerebral fissures.

Sensory and motor function scales using a comprehensive neurological examination in emergency departments were developed during a 5-year prospective study of the epidemiology of acute spinal cord injury. Cross-classification of the scales on 133 patients identified 18.8 per cent who had severe motor impairment but minimal or no sensory loss. This discrepancy was not associated with older age or comorbidity but these patients tended to have a higher prevalence of fracture dislocations, hyperesthesia and Brown-Sequard Syndrome. The discrepancy between sensory and motor function was almost certainly due to the pathology of the cord lesion. Overall, motor function was more likely than sensory function to show improvement during the acute hospitalisation. This was especially true for patients admitted with good sensory but poor motor function. These patients need to be delineated soon after injury if we are to fully understand the aetiology of spinal cord injury and appropriately manage and evaluate different therapeutic modalities.