Search PubMed⌕ Search

Biomedical subjects

D K Resnick

Publications and source records attributed to D K Resnick.

48 records · Page 3Linked to original sources
PubMed1997

Biomechanics of the thoracolumbar spine.

The thoracolumbar spine is the principal load-bearing structure of the body. As such, it is subject to a wide variety of forces that can be described by biomechanical principles. Forces act through vectors, depending on the direction of force and the relative location of the instantaneous axis of rotation. Patterns of failure due to supraphysiologic loading or through the loss of structural integrity may be predicted based on the applied force vectors and the stabilization components lost. An understanding of these forces and their effects on the spine is crucial for the safe and efficacious treatment of spinal deformities.

Biomechanical Phenomena↗
PubMed1996

Rosai-Dorfman disease presenting with multiple orbital and intracranial masses.

Rosai-Dorfman disease is an idiopathic histocytic proliferative disorder typically characterized by painless cervical adenopathy, fever, and weight loss. Extranodal manifestations are responsible for presentation in approximately 25% of patients. Orbital involvement has been described in about 10% of patients. There have been only 16 reported cases of Rosai-Dorfman disease presenting with an intracranial mass. We report an unusual case of a patient presenting with bilateral orbital tumors as well as multiple intracranial masses. Clinical, magnetic resonance imaging, and histopathological features are discussed.

Adult↗
PubMed1996

Microvascular decompression for trigeminal neuralgia in patients with multiple sclerosis.

BACKGROUND: Microvascular decompression (MVD) of the trigeminal nerve is a well-established procedure for the treatment of idiopathic trigeminal neuralgia. Multiple sclerosis (MS) has long been considered a contraindication for this procedure, due to the known polycentric nature of the disease. Medical treatment followed by percutaneous procedures provide relief for the great majority of these patients. There exists a small subgroup of patients with trigeminal neuralgia who are diagnosed with MS only after a microvascular decompression procedure has been performed. Furthermore, management of the patient with known MS whose pain continues to recur, despite maximal medical therapy and multiple percutaneous procedures, can be exceedingly difficult. METHODS: Five patients with MS, three who had undergone multiple unsuccessful percutaneous procedures and two in whom the diagnosis of MS had not been established, underwent exploration of the cerebellopontine angle. Three patients underwent MVD alone, and two (both with known MS) underwent MVD and partial section of the trigeminal nerve. RESULTS: Patients who underwent microvascular decompression alone did not have satisfactory relief of pain. Patients who underwent partial sectioning of the nerve did better. CONCLUSIONS: Patients with MS and symptoms of typical trigeminal neuralgia may benefit from exploration of the cerebellopontine angle and partial sectioning of the nerve. MVD alone fails to provide adequate or reliable relief of pain.

Adult↗
PubMed1996

The relationship of blood velocity as measured by transcranial doppler ultrasonography to cerebral blood flow as determined by stable xenon computed tomographic studies after aneurysmal subarachnoid hemorrhage.

Transcranial doppler (TCD) ultrasonography is often used to guide the management of patients with subarachnoid hemorrhage (SAH). However, the correlation between increased blood velocity as measured by TCD ultrasonography and angiographic vasospasm was established before the routine use of hypervolemia/hemodilution and administration of nimodipine and did not address blood flow. The relationship of blood velocity as measured by TCD ultrasonography and local cerebral blood flow (LCBF) in SAH managed with these modalities is unknown. Patients presenting with aneurysmal SAH between January 1992 and September 1993 who underwent TCD ultrasonography and xenon computed tomographic (Xe/CT) LCBF studies within 12 hours were retrospectively studied. Fifty patients underwent a total of 94 paired studies, encompassing 709 vascular territories. All were treated with nimodipine and hypervolemia/hemodilution. Hematocrit, blood pressure, and partial carbon dioxide pressure were similar at the time of TCD ultrasonography and Xe/CT measurement of LCBF. When LCBF in the middle cerebral artery (MCA) was < or = 31 ml/100 g/min, the corresponding peak systolic velocity measured by TCD ultrasonography was 119 cm/s, whereas those > 31 ml/100 g/min had a velocity of 169 cm/s (P = 0.006). High LCBF was associated with high velocity in all vascular territories, reaching significance in all but the internal carotid artery. At the time of each study, 41 neurological examinations were focal and 53 were nonfocal. The Xe/CT measurement of LCBF in the MCA contralateral to a deficit was significantly less than in territories without corresponding clinical deficits (P = 0.01), whereas peak systolic velocities in the MCA were not significantly different (P = 0.71). Territories with increases in blood velocity in the MCA of > 50 cm/s/24 h did not have statistically different LCBF (P = 0.183). Our results suggest that increased blood velocity revealed by TCD ultrasonography correlates with increased LCBF and not with ischemia. No difference in LCBF was found in territories with and without rapid increases in blood velocity in the MCA. Furthermore, although focal neurological deficits corresponded with decreased contralateral LCBF in the MCA, increased velocity did not correlate with neurological findings. Therapeutic decisions based solely on blood velocity revealed by TCD ultrasonography might be inappropriate and potentially harmful. Xe/CT studies of LCBF are useful in guiding the management of SAH.

Aneurysm, Ruptured↗
PubMed1995

Surgical management of the cloverleaf skull deformity.

The cloverleaf skull deformity, or Kleeblattschädel, is a rare malformation caused by synostosis of multiple cranial sutures. This anomaly has been reported to carry a dismal prognosis both in terms of neurological outcome as well as cosmetic appearance if treatment is delayed. Due to the paucity of data concerning the results of early operative intervention, it remains uncertain whether aggressive craniofacial decompressive/reconstructive procedures are effective in ameliorating the effects of the malformation on both neurological development and cosmetic appearance. This paper reports the treatment and outcome of 7 children with the cloverleaf skull malformation treated at our institution between 1981 and 1993. All children underwent an initial decompressive craniectomy with the removal of at least 50% of the cranial vault for relief of high intracranial pressure in early infancy. Our first 4 patients underwent near total calvariectomy whereas the 3 children treated subsequently have undergone a staged approach with anterior followed by posterior craniectomies with bone morcellation and replacement. Subsequent reconstructions, intended to further improve the cosmetic appearance, were performed later in infancy or in early childhood. Follow-up ranges from 17 months to 9 years, with a mean of 61 months. Long-term results are reported with regard to neurological outcome as well as normalization of skull shape in terms of both the cephalic indices and general cosmetic appearance. Of the 4 children initially treated with total calvariectomy, only 1 child is neurologically normal and has a good cosmetic appearance. One child is severely impaired neurologically following a sagittal sinus thrombosis suffered during a secondary reconstructive procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Cephalometry↗
PubMed1995

Microvascular decompression for glossopharyngeal neuralgia.

Glossopharyngeal neuralgia is an uncommon cause of facial pain with a relative frequency of 0.2 to 1.3% when compared with trigeminal neuralgia. It is characterized by intermittent, lancinating pain involving the posterior tongue and pharynx, often with radiation to deep ear structures. Since its first description in 1910 by Weisenburg, a variety of destructive procedures have been performed to provide relief in patients whose pain was refractory to medical treatment. These procedures all necessitated the sacrifice of the glossopharyngeal nerve and, in most cases, also involved the destruction of at least part of the vagus nerve as well. In 1977, Laha and Jannetta reported good results in four patients who underwent microvascular decompression of the glossopharyngeal and vagus nerves for glossopharyngeal neuralgia. Since 1971, 40 patients have undergone microvascular decompression of the glossopharyngeal and vagus nerves for treatment of typical glossopharyngeal neuralgia. This procedure provided excellent immediate results (complete or > 95% relief of pain) in 79%, with an additional 10% having a substantial (> 50%) reduction in pain. Long-term follow-up (mean, 48 mo; range, 6-170 mo) reveals excellent results (complete or > 95% reduction in pain without any medication) in 76% of the patients and substantial improvement in an additional 16%. There were two deaths at surgery (5%) both occurring early in the series as the result of hemodynamic lability causing intracranial hemorrhage. Three patients (8%) suffered permanent 9th nerve palsy. (ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Isolated toxoplasmosis of the thoracic spinal cord in a patient with acquired immunodeficiency syndrome. Case report.

Toxoplasmosis and lymphoma are the two most common causes of intraparenchymal cerebral mass lesions in patients with acquired immunodeficiency syndrome (AIDS). The clinical and radiographic features of the intracranial lesions have been well described. Because of the high frequency of toxoplasmosis in the AIDS population, common therapy for patients presenting with intracranial mass lesions consists of an empirical trial of anti-Toxoplasma chemotherapy, with biopsy reserved for cases demonstrating features considered to be more consistent with lymphoma, or for lesions that do not improve despite adequate anti-Toxoplasma treatment. A similar treatment algorithm does not exist for intramedullary lesions of the spinal cord. The authors describe a patient who presented with paraparesis resulting from an isolated thoracic intramedullary lesion. An open biopsy of the lesion revealed characteristic structures containing Toxoplasma tachyzoites. The clinical and radiographic presentation of the lesion is discussed, the available literature is reviewed, and a treatment strategy for spinal cord lesions in AIDS patients is proposed.

Acquired Immunodeficiency Syndrome↗
PubMed1994

The effect of hypothermia on the incidence of delayed traumatic intracerebral hemorrhage.

Hypothermia has been shown to cause coagulation abnormalities, primarily related to platelet dysfunction. We reviewed coagulation function and the incidence of delayed traumatic intracerebral hemorrhage in a series of 36 patients with severe head injuries (Glasgow Coma Scale 3-7) enrolled in a prospective, randomized, clinical trial of therapeutic moderate hypothermia. Patients were randomized to a normothermic group (n = 16) or to a group cooled to 32 to 33 degrees C within 6 hours of injury (n = 20). Prothrombin times, partial thromboplastin times, and platelet counts were obtained in the emergency room and then again within 24 hours of randomization. Delayed traumatic intracerebral hemorrhage occurred in 6 of 20 (30%) hypothermic patients and 5 of 16 (31%) normothermic patients. In the hypothermic group, 9 of 17 patients had an increased prothrombin time during hypothermic therapy, as opposed to 11 of 16 in the normothermic group during the corresponding time period. The partial thromboplastin time was prolonged in 2 of 17 hypothermic patients and 2 of 16 normothermic patients. Three patients in the hypothermic group and one in the normothermic group developed thrombocytopenia (a platelet count of less than 100,000). There were no significant differences between the two groups in the incidence of delayed traumatic intracerebral hemorrhage, in measured coagulopathy, or in the mean values of measured coagulation parameters. Although the possibility of a hypothermia-induced coagulopathy has not yet been excluded, the short-term use of hypothermia does not appear to increase the risk for intracranial hemorrhagic complications in head injuries.

Adolescent↗
PubMed1993

Delayed pulmonary perforation. A rare complication of tube thoracostomy.

Tube thoracostomy is a standard therapy for a number of pulmonary disorders. The procedure is associated with a certain incidence of morbidity related to the technique of insertion, the patient population selected, and the length of time the tube remains in place. Complications of tube placement previously described include empyema, residual pneumothorax, lung perforation, placement of the tube in the chest wall, diaphragmatic perforation, perforation of intraabdominal organs (such as spleen, liver and stomach), unilateral pulmonary edema, bronchopleural fistula, hemothorax, cardiogenic shock and Horner syndrome. A case of a delayed pulmonary perforation developing several days after placement of a chest tube is described with a discussion of the clinical and radiographic findings associated with this complication. A possible pathophysiologic mechanism by which this complication may have occurred is proposed.

Aged↗
PubMedDate not supplied

Selective cyclooxygenase 2 inhibition lowers spinal cord prostaglandin concentrations after injury.

BACKGROUND CONTEXT: Prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) concentrations are elevated in the injured spinal cord for hours to days after injury. Treatment of animals with a selective cyclooxygenase-2 (COX-2) inhibitor has been shown to improve functional outcome in an animal model. PURPOSE: We sought to characterize the effects of COX-2 inhibition on prostaglandin concentrations in the spinal cord after injury. STUDY DESIGN/SETTING: A drug study was performed using 76 male Long Evans rats. OUTCOME MEASURES: PGE2 and TxB2 concentrations were measured by enzyme immune assay. METHODS: Fifty-six rats were subject to spinal cord injury, and 4 rats served as sham controls. Twenty eight rats received 3 mg/kg of celebocid by means of an orogastric tube within 20 minutes after injury, and 28 received vehicle alone. The animals were sacrificed at time points between 2 and 72 hours after injury, and PGE2 and TxB2 levels were measured. A second study was performed using transcardiac saline perfusion in order to reduce intragroup variance in measured PGE2 and TxB2 levels. Sixteen animals underwent spinal cord injury. Animals were sacrificed at 4 and 24 hours after injury, and PGE2 and TxB2 levels were measured. RESULTS: PGE2 and TxB2 concentrations were elevated after injury in all animals. Administration of celebocid resulted in a delayed reduction of PGE2 and TxB2 concentrations in the initial drug study. These results were not statistically significant. Transcardiac perfusion with normal saline reduced the intragroup variance. Using this technique, administration of celebocid resulted in a statistically significant reduction in PGE2 and TxB2 concentrations in the injured cord segment 4 and 24 hours after injury. CONCLUSION: Administration of a selective COX-2 inhibitor after injury results in a decrease of PGE2 and TxB2 concentrations in the injured spinal cord. Transcardiac perfusion after sacrifice reduces measured variance, probably through reducing the contribution of blood-borne prostaglandins.

Animals↗
PubMedDate not supplied

Regional and temporal changes in prostaglandin E2 and thromboxane B2 concentrations after spinal cord injury.

BACKGROUND CONTEXT: Inflammatory metabolites of arachidonic acid likely play a significant role in secondary injury after spinal cord trauma. PURPOSE: We sought to characterize the regional and temporal alterations in prostaglandin concentrations after injury in a rat model. STUDY DESIGN/SETTING: Prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) concentrations were measured in cerebrospinal fluid (CSF) and in different parts of the injured spinal cord at various time points after spinal cord injury. OUTCOME MEASURES: PGE2 and TxB2 levels were measured by means of an enzyme immune assay. METHODS: Forty-six adult Long Evans rats were subject to spinal cord injury using the NYU impactor. Animals were divided into three groups. Fourteen animals were used in a pilot study to determine the timing and location of PGE2 production after spinal cord injury. These animals were sacrificed, and samples of injured cord, rostral cord and CSF were assayed for PGE2 concentration. The remaining 32 animals were used to establish the time course of prostaglandin production. Twenty-eight animals were subjected to a spinal cord injury, and four animals served as sham-operated controls. These animals were sacrificed at predetermined time points 2 to 72 hours after injury, and the injured segments of spinal cord were harvested. RESULTS: Both PGE2 and TxB2 concentrations increased immediately after injury in the injured segment. PGE2 concentrations increased faster and more dramatically in the injured segment of spinal cord than in CSF or noninjured segments. Elevations in PGE2 and TxB2 concentrations were persistent for 72 hours after injury. CONCLUSION: Elevated concentrations of arachidonic acid metabolites can be detected in the injured segment of the spinal cord for at least 72 hours after injury. Concentration changes are detected earlier and are more dramatic in the injured cord segment than in rostral segments or the CSF.

Animals↗