Dennis G. Vollmer's research while affiliated with Washington University in St. Louis and other places

A biomechanical study of human cadaveric thoracic vertebral bodies was conducted using several anterior fusion options subjected to axial loads. This study emphasized the contribution of the endplate to resistance of graft subsidence. To determine the importance of the vertebral endplate in resisting subsidence of various constructs into the vertebral body; the relative efficacy of potential alternative graft constructs such as iliac crest, ribs, humerus, and titanium mesh cage; and the importance of bone mineral content, vertebral level, and cross-sectional graft area on construct subsidence. As the fixation length of anterior and posterior spinal constructs is reduced, load sharing of the anterior column has become more important to reduce failure of the shorter devices. Several alternative graft constructs and surgical techniques have been used for reconstruction of the anterior column. There exist little comparative data as to whether any of these constructs are superior and whether the vertebral endplate contributes significantly to the integrity of the construct. Sixty-three isolated human cadaveric vertebral bodies from T3 to T12 were used to test seven different constructs in direct axial load onto prepared endplates with an electrohydraulic testing device. These constructs were: 1) titanium mesh cage (17 x 22 mm) on intact endplate, 2) C-shaped humerus on intact endplate, 3) tricorticated iliac graft in "tee configuration" on intact endplate, 4) tricorticated iliac graft in cancellous trough, 5) triple rib strut graft, 6) single rib on endplate, and 7) single rib on cancellous body. Dual X-ray absorptiometry assessment of bone mineral content was performed. A uniaxial load was applied with force and displacement data collected to determine maximal load to "failure" of the vertebral body. Preservation of vertebral endplate did not significantly increase the resistance to graft subsidence. The titanium cage construct provided the greatest resistance to axial load. Preservation of the vertebral endplate may not offer a significant biomechanical advantage in reconstructing the anterior column. Several alternative constructs are mechanically equivalent.

Intraoperative transligamentous ultrasonography was used in a variety of different thoracic surgical procedures for spinal cord compression secondary to neoplastic disease. The utility and practicality of intraoperative transligamentous ultrasonography for thoracic intraspinal disease was evaluated. Because intraoperative localization and evaluation of targeted levels in the thoracic spine using radiographs is often difficult or imprecise, alternative or complementary techniques may be helpful. Intraoperative transligamentous ultrasound, performed before laminectomy, via an interlaminar window, has not been widely used for thoracic intraspinal pathology. A standard 7.5-MHz hand-held probe, used in conjunction with a Codman OR 330 ultrasound machine, was used to evaluate the practicality of intraoperative transligamentous ultrasound in the thoracic spine. A clear sonographic window, permitting visualization of the spine and the intraspinal contents, can frequently be found. However, densely calcified ligamentum flavum or overlapping laminas do not allow effective insonation. Four illustrative cases are presented. Transligamentous ultrasound before laminectomy can be used for localization and evaluation of intraspinal disease in many patients. Overlapping laminas or calcified ligamentum flavum can impede adequate sonographic visualization, but in these cases adequate intraoperative transligamentous ultrasound evaluation is usually possible through a small laminotomy. Evaluation of intraspinal lesions and localization of the correct surgical level is facilitated by dynamic real time sonographic imaging.

Several different types of resections are performed for medically intractable mesiobasal temporal lobe epilepsy (TLE). Although the amount of neocortical and amygdalar resection varies, most surgeons agree that removal of at least a portion of the hippocampus is critical for seizure control. We describe a preliminary cadaveric investigation of the feasibility of endoscopic hippocampectomy. A transsquamosal approach through the middle temporal gyrus permitted easy access to the pes hippocampus through the temporal horn of the lateral ventricle but made access to the body and tail of the hippocampus difficult. A posterior approach, through the occipital horn of the lateral ventricle, as in placement of an occipital ventricular catheter, permitted a clearer view of the entire hippocampus from the trigone to the pes hippocampus. Using this technique, we identified the choroid plexus and fissure, calcar avis, collateral trigone, collateral eminence, and uncal recess of the temporal horn. Transventricular endoscopy, through an occipital approach to the temporal horn, permits clear visualization of the pertinent intraventricular anatomy necessary to perform a hippocampectomy. With further developments in neuroendoscopic technology, this approach may provide a surgical strategy for patients with medically intractable epilepsy of well-defined mesiobasal origin.

Hearing preservation during the posterior fossa surgery depends on many factors, including tumor size and site of origin. In many cases, regardless of the presumed tumor origin, the severity of the pure-tone loss or decline in speech discrimination on preoperative testing prompts the surgeon to choose a surgical approach (translabyrinthine or transcochlear) that negates the chance for postoperative functional hearing in the involved ear. We describe a 41-year-old woman with unilateral severe sensorineural hearing loss who experienced a remarkable recovery of hearing after combined retrolabyrinthine and retrosigmoid removal of a 4 cm petrous ridge meningioma using intraoperative cochlear monitoring. Despite the tumor size, early intraoperative loss of wave I and proximity of the tumor to the porus, complete tumor removal was accomplished with preservation of the cochleovestibular bundle. Three weeks postoperatively, the patient noted marked subjective improvement and speech audiometry demonstrated an improvement in word recognition, from 0% to 86%. This improvement has remained 1 year postoperatively, with no evidence of persistent tumor on repeat MRI scan. The case report illustrates the possibility of not just hearing preservation but improvement after removal of even large posterior fossa meningiomas that do not directly invade the cochlear nerve itself.

The reactivity of rabbit basilar artery and penetrating arteriolar microvessels was studied in vitro using an isometric-tension measurement technique and an isolated perfused arteriole preparation, respectively. Comparisons were made between reactivities of normal vessels and those obtained from animals subjected to experimental subarachnoid hemorrhage (SAH) 3 days prior to examination. Subarachnoid hemorrhage produced significant increases in basilar artery contraction in response to increasing concentrations of serotonin (5-hydroxytryptamine) (10 ⁻⁹ to 10 ⁻⁵ M) and prostaglandin F 2α (10 ⁻⁹ to 10 ⁻⁵ M) when compared to normal arteries. In addition, SAH attenuated the relaxing effect of acetylcholine following serotonin-induced contraction and of adenosine triphosphate after KCl-induced basilar artery contractions. In contrast to the changes observed in large arteries, cerebral microvessels did not demonstrate significant differences in spontaneous tone or in reactivity to a number of vasoactive stimuli including application of calcium, serotonin, and acetylcholine. On the other hand, small but significant changes in arteriolar responsiveness to changes in extraluminal pH and to application of KCl were noted. Findings from this study suggest that intracerebral resistance vessels of the cerebral microcirculation are not greatly affected by the presence of subarachnoid clot, in contrast to the large arteries in the basal subarachnoid space. The small changes that do occur are qualitatively different from those observed for large arteries. These findings are consistent with the observation of significant therapeutic benefit with the use of calcium channel blockers without changes in angiographically visible vasospasm in large vessels. It is likely, therefore, that calcium antagonists may act to decrease total cerebrovascular resistance at the level of the relatively unaffected microcirculation after SAH without changing large vessel diameter.

To better understand the relationship between patient age and clinical outcome following traumatic coma, the data for 661 patients, aged 15 years or older at the time of receiving a nonpenetrating head injury, were analyzed. All patients were prospectively followed and the information was entered into the Traumatic Coma Data Bank. This information was statistically analyzed to determine trends and interactions between patient age and other prognostic indicators. Older patients had higher rates of mortality overall; vegetative survival was seen in 4.8% to 8.0% of patients and did not exhibit a trend related to age. Injury severity, as assessed by motor score or Glasgow Coma Scale score, did not significantly differ according to age. The injury mechanism was age-related, with a greater frequency of falls and pedestrian accidents in older patients. Multiple injury was less frequent in older patients. Medical complications and systemic trauma were considered to be the primary cause of death in less than 25% of patients, with the exception of those between 45 and 55 years of age. When the data were studied in univariate fashion, no factor was identified that accounts for the adverse effect of age on head-injury outcome. Multivariate logistic regression, performed to assess the combined effect of multiple variables on outcome, failed to eliminate patient age as an independent predictor. Based upon this analysis, it is likely that the effect of age on outcome following head injury is dependent upon an alteration in the pathophysiological response of the aging central nervous system to severe trauma and not an increased incidence of non-neurological complications or other clinical parameters.

This study was performed to examine the effect of the dihydropyridine calcium antagonist, nicardipine, on vasospasm after experimental subarachnoid hemorrhage (SAH) in the rabbit. The study was carried out in two parts: 1) effect of intravenous nicardipine (n = 45) and 2) effect of intracisternal nicardipine (n = 21). SAH was induced by injecting 5 ml of autologous arterial blood into the cisterna magna. In the intravenous study, there were five groups: 1) SAH without treatment; 2) SAH with vehicle (saline); 3) SAH and intravenous infusion of low-dose nicardipine (0.01 mg/kg/h); 4) SAH and intravenous infusion of high-dose nicardipine (0.15 mg/kg/h); and 5) controls without SAH. The intravenous infusions were started immediately after SAH and continued for 48 hours until death. In the intracisternal study, there were three groups: 1) SAH without treatment; 2) SAH with intracisternal administration of nicardipine (0.37 mg/h); and 3) controls without SAH. Intracisternal infusions were begun 70 hours after SAH and continued for 2 hours until death. After perfusion-fixation, the basilar artery was removed and processed for morphometric analysis. In the intravenous study, vessels from animals subjected to SAH were significantly narrowed when compared with controls, although after high-dose nicardipine vessel caliber was slightly larger than in the other SAH groups. Animals given intracisternal nicardipine showed a nonsignificant reduction of caliber as compared with controls: only 12% decrease in diameter and 22% decrease in luminal area. In the rabbit SAH model, nicardipine had a very modest effect on vasospasm at the doses tested.

The majority of patients seeking medical care after head trauma have sustained injuries of mild or moderate severity, i.e., GCS scores of 13 to 15 or 9 to 12, respectively. Mortality rates under these circumstances are generally low; however, serious complications must be detected and treated early. The initial evaluation involves determination of level of consciousness and examination for the presence of focal neurologic deficits. Skull radiography has a limited role in the management of mild and moderate head injuries, but consideration must be given to local factors such as the availability of cranial CT. CT scanning is a safe, noninvasive, and generally cost-effective means of assessing patients at risk for developing intracranial complications. The role of MR imaging in evaluating minor head injuries is not yet established. Patients with an altered level of consciousness require hospitalization in essentially all cases. Selected patients with a GCS score of 15 also benefit from overnight hospitalization and observation. After mild and moderate head injury, significant neuropsychologic deficits are frequent, but are generally finite in their duration. Postconcussive symptoms are also generally self-limited. Although objective evidence suggests that structural brain damage results from mild injuries, the relationship between postconcussional symptoms and structural damage is unclear. Persistent postconcussional symptomatology probably arises from a combination of physiogenic and psychogenic causes. It is possible that early patient education and reassurance will reduce the incidence of prolonged postconcussional symptomatology.

The pathogenesis of cerebral vasospasm occurring after subarachnoid hemorrhage (SAH) is unknown. Several lines of experimentation have suggested a free radical mechanism in the etiology of vasospasm. Iron is an important catalyst in the generation of free radicals and lipid peroxides in response to tissue injury. We hypothesize that the elaboration of iron from the subarachnoid clot might result in enhanced generation of free radicals and lipid peroxidation. If so, then treatment with deferoxamine, an iron-chelating compound, might reduce the formation of free radicals and thereby ameliorate vasospasm. This hypothesis was examined in a rabbit model of experimental cerebral vasospasm. New Zealand White rabbits were divided into the following experimental groups: control (normal) animals (n = 7), control animals treated with deferoxamine (n = 3), animals subjected to SAH and killed on Day 2 (n = 7), animals subjected to SAH on Day 2 and treated with deferoxamine (n = 9), animals subjected to SAH killed on Day 3 (n = 7), and animals subjected to SAH on Day 3 and treated with deferoxamine (n = 7). Deferoxamine treatment (50 mg/kg/8 hours) was begun 16 hours before the induction of SAH and continued until the animals were killed by perfusion fixation. The basilar artery caliber was assessed using morphometric techniques. The diameter of the basilar arteries in the control animals was 0.64 +/- 0.02 mm. Deferoxamine treatment alone did not alter the artery diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Whipple's disease is infrequently considered in the differential diagnosis of patients presenting with progressive neurological deterioration. This is in part a result of the relative rarity of this entity and in part due to the more frequent initial presentation of the disease with gastrointestinal, musculoskeletal, or cardiovascular symptoms. A case is described in which the neurological symptoms of progressive dementia and weakness were seen in the relative absence of non-neurological symptomatology. The diagnosis of Whipple's disease was made from a brain biopsy. The neuropathology of Whipple's disease of the central nervous system is described and the importance of considering it as a treatable entity in the differential diagnosis of progressive neurological deterioration, despite the absence of systemic symptomatology, is stressed.