Synthes spine drill instrumentation.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R G Fessler.
Explore the source record for details and available documents.
The introduction of microdiscectomy to lumbar spine surgery has resulted in a significant decrease in postoperative pain and length of hospital stay. Intraoperative application of long-acting local anesthetic agents has been used for many general and neurosurgical procedures for the management of postoperative pain. In addition, many surgeons routinely use intraoperative corticosteroids during lumbar discectomy to reduce traumatic nerve root inflammation. However, the efficacy of intraoperative long-acting local anesthetic agents and corticosteroids for reduction of postoperative discomfort has not been reported for lumbar discectomy. This study evaluated 32 patients at a university-based Veterans Administration hospital undergoing lumbar microdiscectomy. All 32 patients presented with radicular symptoms and had radiographic confirmation of a herniated nucleus pulposus. These patients were divided into three groups. Group 1 (12 patients) received 160 mg intramuscular Depo-Medrol (methylprednisolone acetate) and 250 mg intravenous Solu-Medrol (methyl-prednisolone sodium succinate) at the start of the operation. A macerated fat graft soaked in 80 mg Depo-Medrol was placed over the affected nerve root following discectomy. In addition, 30 ml of 0.25% bupivacaine was infiltrated into the paraspinal musculature at skin incision and during closure. Group 2 (10 patients) received 30 ml of 0.25% bupivacaine infiltrated into the paraspinal musculature at skin incision and at closure. In this group of patients, a saline-soaked fat graft was placed over the affected nerve root. Group 3 (10 patients) acted as a control group, undergoing lumbar microdiscectomy without corticosteroids or bupivacaine. Patients receiving bupivacaine and corticosteroids (Group 1) had a statistically significantly shorter hospital stay (1.4 days) compared to the control group (4.0 days) (p = 0.0004, Mann-Whitney U-test). Patients in Group 1 required less postoperative narcotic analgesia than the other groups. Finally, a larger percentage of patients in Group 1 reported complete relief of back and radicular pain on postoperative Day 1 compared to other groups. Postoperative complications and functional outcome were not different between the groups. These results indicate that the combination of long-acting anesthetic agents and corticosteroids can reduce postoperative discomfort and subsequently the length of postoperative hospital stay.
Explore the source record for details and available documents.
Because of the protean nature of thoracic disc disease, surgeons should maintain a high order of suspicion of a thoracic disc herniation in the patient with unexplained localized back or torso pain and sensorimotor deficits. These patients should have MR imaging performed as a screening test, and, if suspicious for a thoracic disc herniation, confirmatory myelogram and postmyelogram CT imaging. Though the natural history is anecdotal, there appears to be a tendency for myelopathic symptoms and signs to be progressive, warranting surgical intervention. For radicular dysfunction or localized back pain, a conservative therapeutic plan is recommended. If intractable pain is demonstrated, and the diagnosis is certain, then surgical intervention is recommended. Once surgical intervention is recommended the surgical approach needs to be individualized according to the surgeon's skills and experience and the specifics of the patient's pathology. Appropriate surgical decision-making depends on an understanding of the variety of surgical options and their advantages and disadvantages, and an understanding of the biomechanical factors of the spine of the individual patient. Surgical concepts important to successful thoracic disc removal are (1) minimal spinal cord manipulation, (2) preservation of the neurovascular supply whenever possible, (3) minimal manipulation of the intercostal nerve, and (4) preservation of maximal bony and ligamentous attachments allowable for adequate exposure. Lastly it is recommended that the posterior longitudinal ligament be removed to ensure complete spinal cord decompression.
Epidural lipomatosis is a condition in which excess adipose tissue is deposited circumferentially about the spinal cord in the epidural space. It is most frequently seen in patients on chronic steroid treatment for a variety of medical problems and can present as nonspecific back pain, radiculopathy, or frank spinal cord compression. Diagnosis and treatment have generally relied on multi-level decompressive laminectomy after myelography and computed tomography. The immunocompromised state and the reported postoperative mortality (22%) of these patients, however, suggests that nonoperative therapy may be preferable whenever possible. Five cases of epidural lipomatosis are reported, and previous literature is reviewed for presentation, evaluation, and treatment of this condition.
Twenty-seven cases of craniovertebral junction compression treated with transoral surgery were reviewed to assess the influences of pathological processes and surgical interventions on spinal stability. All patients presented with signs and symptoms of spinal-cord or brain-stem dysfunction. Pathology included rheumatoid arthritis in 11 patients, congenital osseous malformations in 11, spinal fractures in two, plasmacytoma in one, osteomyelitis in one, and a gunshot injury in one. Instability was defined as clear radiographic evidence of mobile subluxation in conjunction with clinical assessment. Of 19 patients (70%) requiring internal fixation, nine underwent upper cervical fusion and 10 had occipitocervical fusion. When instability occurred, all subluxations were at the C1-2 level. There were no occipito-atlantal subluxations. Eight patients (30%) had preoperative instability of the craniovertebral junction due solely to their pathology, 11 patients (40%) suffered instability after transoral surgery, and eight (30%) were without clinical or radiographic evidence of instability (mean follow-up period 14 months). Craniovertebral junction instability predominated among patients with rheumatoid arthritis: 91% required fusion and 45% presented with pre-existing instability. Among individuals with congenital osseous malformations, 45% required fusion and only one patient (9%) had pre-existing instability. Patients who required subsequent posterior decompression of a Chiari malformation were at risk for developing instability; three of four became unstable after posterior decompression. Transoral resection of the dens, the anterior arch of C-1, and the lower clivus does not fully destabilize the spine; however, this operation may potentiate incipient pathological instability. The primary determinants of instability are the extent of pathological bone destruction, ligamentous weakening, and operative bone removal. Long-term follow-up monitoring is needed after transoral surgery to detect cases of late instability.
A total of 104 patients underwent transpedicular spinal instrumentation using the Cotrel-Dubousset (71 cases) or the Texas Scottish Rite Hospital (33) screw-rod system. Surgery was performed for lumbar vertebral column instability secondary to fractures (28 cases), spondylolisthesis (29), tumors (four), vertebral osteomyelitis (two), or postoperative causes (41). Pseudoarthrodesis due to failure of a prior fusion was present in 37 cases. The 55 men and 49 women (mean age 47 years, range 18 to 87 years) all presented with severe back pain. Signs or symptoms of neural compression were noted in 96 patients. Surgery consisted of neural decompression, internal fixation, and autogenous iliac bone grafting. Spondylolistheses were fused in situ, without reduction; otherwise, major spinal deformities were corrected. A total of 516 pedicle screws were placed. The mean extent of fusion was 2.7 motion segments (range one to six motion segments). A 96% fusion rate was obtained with a mean follow-up period of 20 months. There were no operative deaths. Major complications included one spinal epidural hematoma, three isolated nerve root deficits (two transient, one permanent), and three wound infections (two deep, one superficial). Instrument failure eventually developed in 18 patients; nine were asymptomatic with a solid fusion and did not require further treatment and the other nine were symptomatic or had a pseudoarthrosis and required operative revision. Pedicle screw-rod fixation offers biomechanical advantages compared to other forms of internal fixation for the lumbar spine. It enables short-segment fixation with preservation of lumbar lordosis and adjacent normal motion segments. This technique provides a highly successful method to obtain arthrodesis, even with prior pseudoarthrosis.
Explore the source record for details and available documents.
The upper thoracic vertebrae are difficult to approach surgically because of the narrowing of the thoracic inlet, the proximity of the brachial plexus, and the parascapular shoulder musculature. A novel lateral parascapular extrapleural approach to the upper thoracic vertebrae is described. The parascapular shoulder musculature (trapezius, levator scapulae, and rhomboid muscles) is reflected off the spinous processes to the scapula as a musculocutaneous flap, preserving the neurovascular supply. The paraspinal musculature is mobilized and retracted, and the upper dorsal ribs are removed with caution to avoid injury to the C-8 and T-1 nerve roots. The rami communicantes are transected, and the sympathetic chain is displaced anterolaterally. The T2-4 vertebrae can be approached unobstructed. The T-1 nerve root obstructs posterolateral access to the T-1 vertebra, necessitating an inferolateral approach underneath the T-1 nerve root axilla. Four patients with compressive myelopathy from upper thoracic vertebral metastases underwent neural decompression, vertebral reconstruction, and posterior spinal fixation with this approach. Their postoperative neurological status was either unchanged or improved. Complications included radiographic pleural effusion and superficial wound dehiscence; one patient required posterior spinal reinstrumentation for progressive kyphosis. One patient developed pneumonia 7 days postoperatively which was unresponsive to appropriate treatment. It is believed that the anatomical limitations to this region have been overcome, and that excellent exposure of the T1-4 vertebrae for neural decompression and vertebral reconstruction can be performed safely. A major advantage is that posterior spinal fixation can be carried out simultaneously.
A case of infection of the superior sagittal sinus with Petriellidium boydii is reported. This relatively common fungal pathogen rarely invades the central nervous system. Immunological compromise and poor personal hygiene seem to be common attributes shared by this patient and the 4 previous patients reported to have suffered invasion of the central nervous system by this organism. This report is unique in that it is the first demonstrating apparent hematogenous dissemination of this organism to the central nervous system.
The feasibility of employing the rat as an experimental model for investigation of full-dose heparin anticoagulation was assessed. Striking similarities were found to exist between rats and humans regarding baseline-activated partial thromboplastin time (APTT) values, and dosage per kilogram of heparin required to produce an APTT value of 1 1/2-3 times normal, the clinical definition of full-dose heparinization. Based upon these similarities, it appears that the rat can effectively serve as an experimental model for investigating the effects of heparin in humans.
The risk of hemorrhagic complications with anticoagulation therapy in patients following intracranial surgery has prevented investigation of the potential use of heparin in the early postoperative period. The authors have evaluated the safety of anticoagulation therapy following experimental craniotomy in male Holtzman rats. The dose and schedule of heparin administration, which elevated and maintained the activated partial thromboplastin time (APTT) within the therapeutic range of 1 1/2 to 3 X control APTT, was alternating doses of 400 and 500 IU/kg injected subcutaneously every 6 hours. This schedule was initiated 2, 4, 7, 10, and 14 days after craniotomy and was continued for 72 hours thereafter. The results demonstrated that the incidence of intracerebral hemorrhage declined as the postoperative interval prior to initiation of anticoagulation increased. If anticoagulation therapy was initiated during the first 7 postoperative days, the risk of intracerebral hemorrhage was high (mean 14.7%): however, if an additional 3 to 7 days elapsed prior to initiation of anticoagulation, the incidence of intracerebral hemorrhage dropped significantly (mean 0%) (p less than 0.05). These results suggest that anticoagulation therapy can be safely initiated 10 to 14 days after craniotomy.
Beta-Endorphin-like immunoreactivity in cerebrospinal fluid was assayed in 11 patients receiving electrical stimulation of the brain for chronic pain. Immunoreactivity increased dramatically after contrast ventriculography prior to stimulation. No further elevations were observed after stimulation. The magnitude and time course of elevations were identical after placement of electrodes either in the thalamus or in the periventricular gray matter. These results suggest that previous findings of stimulation-induced elevation of beta-endorphin-like immunoreactivity in cerebrospinal fluid are attributable to an artifact of contrast ventriculography.
Electrolytic lesions of the medial (MR) or dorsal (DR) raphe nucleus significantly antagonized serum prolactin elevations produced by 5-hydroxytryptophan (5-HTP) in rats pretreated with fluoxetine or citalopram, (serotonin (5-HT) uptake blockers). Lesioned animals in which total blockade of serum prolactin elevations was observed also had total blockade of 5-HT accumulation in the median eminence. However, the increase in serum prolactin levels produced by 5-HTP plus 5-HT reuptake blockade in lesioned rats was not significantly different from sham-operated rats if as little as 15-20% of control median eminence accumulation was present. Serum prolactin elevations produced by quipazine, a direct acting 5-HT agonist, were not significantly affected by MR lesions. On the basis of these results, we suggest that: (1) serum prolactin elevations following 5-HT reuptake blockade plus 5-HTP are correlated with 5-HT concentration in the median eminence; (2) lesion-induced antagonism of 5-HTP-induced prolactin elevation is critically dependent upon complete blockade of median eminence 5-HT accumulation; and (3) 5-HT neurons arising from cell bodies located in the MR and DR are necessary for endogenous serotonergically mediated effects on prolactin secretion in the rat.
Intraoperative ultrasound can aid the biopsy of deep intracranial lesions. It is, perhaps, less clear whether ultrasound could be useful in functional neurosurgery, where the target is not abnormal in echogenicity. As an example, we chose to investigate in a dog model the periventricular gray target, which is frequently the choice for the placement of electrodes to control intractable pain. Autopsies showed the placement of our electrodes with less than 1 mm of error in four of five brains and a 1.5-mm error in the fifth brain. The largest error was seen to occur on the video screen and was due to our failure to tighten the guide properly. The potential advantages of this technique over conventional stereotaxis include the avoidance of: ventricular catheterization, the injection of contrast agent into the ventricles, the necessity for a stereotactic frame, and multiple x-ray exposures. Also, with real time scanning the surgeon has instant visual confirmation of electrode placement and can observe quickly any significant hematoma formation.
Much interest has recently been focused on the possible role of the endogenous opiates in the perception of pain in humans. Several investigators have examined the levels of these substances in human cerebrospinal fluid (CSF) in attempts to identify the mechanisms by which electrical stimulation of the brain might induce analgesia. Most of these CSF samples were collected at the time of ventriculography or myelography. In the present study, the levels of beta-endorphin in the CSF of 22 patients undergoing myelography were examined before and after the injection of a contrast agent. beta-Endorphin increased an average of 356% (p less than 0.0005) 15 to 20 minutes following the injection of contrast material into the lumbar subarachnoid space. Thus, routine myelography may have a profound effect on the levels of beta-endorphin measured by radioimmunoassay in human CSF, and great care must be taken in interpreting the significance of changes seen in beta-endorphin levels in CSF collected from patients at the time of myelography or ventriculography. The effect of the injection of contrast material on beta-endorphin immunoreactivity must be distinguished from the postulated effects of any analgesia-inducing therapy.
Six adult dogs were implanted stereotaxically with chronic indwelling Medtronic platinum-tipped electrodes in the left ventromedial hypothalamic area (VMH); two dogs with electrodes placed in the subcortical white matter served as controls. Following 24 hours of food deprivation, VMH-stimulated dogs delayed their next meal for a period ranging from 1 to 18 hours. When not stimulated, however, each dog ate immediately upon receiving its food and consumed greater than average daily intake (p less than 0.005). The two control dogs ate immediately upon receiving food regardless of whether they were stimulated or not. Dogs that received 1 hour of VMH stimulation every 12 hours for 3 consecutive days maintained an average daily food intake of 35% of normal baseline levels (range 13% to 51%), and water consumption averaged 50% of baseline intake (range 29% to 67%). Both of these results were statistically significant (p less than 0.01). After cessation of stimulation, food and water intake returned to normal within 6 to 9 days, with no observable "rebound hyperphagia." The two animals that received subcortical electrodes showed no change in food or water intake with stimulation. Blood pressure, pulse, respiration, temperature, and gross behavior were not altered during or after stimulation. These results suggest that the use of electrical stimulation of the VMH may be a useful modality for regulating food intake, and deserves further examination as a potential alternative therapy for human morbid obesity.
An effect of metrizamide, a contrast medium, on results of beta-endorphin radioimmunoassay was examined. We found that 1, 5, and 10 microL of the medium added to 100 microL of standard containing 0 to 500 pg of beta-endorphin shifted the standard curve to the left in proportion to the metrizamide concentration. Three other contrast media showed a similar effect at low concentrations of beta-endorphin. This effect of contrast media artificially increased results in radioimmunoassay of beta-endorphin in cerebrospinal fluid, the mean overestimate being 121.9% (range, 0 to 435%). For plasma samples, this effect of contrast media resulted in an average 11.7% overestimate of beta-endorphin (range, -16% to 41%). These observations bring into question the validity of a previous suggestion that an increase in beta-endorphin in cerebrospinal fluid after intracerebral electrical stimulation is the mechanism for stimulation-produced analgesia.