Rob D. Dickerman

Intra-ocular pressure changes during maximal isometric contraction: does this reflect intra-cranial pressure or retinal venous pressure?

Recent publications have suggested that intra-ocular pressure (IOP) may be an indirect assessment of intra-cranial pressure (ICP). Both IOP and ICP have similar physiologic pressure ranges and similar responses to changes in intra-abdominal, intra-thoracic and aortic pressure. Previous studies have demonstrated the relationships between retinal arterial pressure and aortic pressure, intra-ocular pressure and retinal venous pressure, intra-cranial pressure and retinal venous pressure. Power athletes routinely utilize the Valsalva maneuver during weightlifting. In fact there are reports of stroke, cerebral hemorrhage, subarachnoid hemorrhage, conjunctival, foveal and retinal hemorrhage, retinal detachment, hiatal hernia and pneumothorax associated with weightlifting. These events are thought to occur secondary to the extreme pressure elevations that occur in the intra-abdominal, intra-thoracic, intra-cranial, intra-ocular and vascular compartments. To date no human studies have examined the IOP changes that may occur with heavy resistance exercise. Therefore, we recruited power athletes (n = 11), who had participated in prior studies, from the local metropolitan area. The athletes had blood pressure status, drug screening and medical histories performed during previous investigations. Intra-ocular pressure was measured by noncontact tonometry at rest and during maximal isometric contraction. All subjects resting IOP were within normal ranges (mean 13 +/- 2.8 mmHg). Intra-ocular pressures were significantly (p < 0.0001) elevated in each subject during maximal contraction (mean 28 +/- 9.3 mmHg). One subjects IOP reached 46 mmHg during maximal contraction. Linear regression analysis demonstrated a significant linear relationship (r = 0.62, p < 0.0001) in the net change of IOP from rest to maximal contraction for each subject. This study demonstrates that IOP elevates to pathophysiologic levels during resistance exercise. The findings of conjunctival hemorrhages in two subjects further supports IOP being reflective of retinal venous pressure. The enormous pressures generated by power athletes during weightlifting leads to elevations in ICP which obstruct venous outflow leading to hemorrhage and elevations in IOP. The question remains as to whether these intermittent bursts of elevated IOP can lead to long-term pathological sequelae.

Anabolic steroid-induced hepatotoxicity: is it overstated?

OBJECTIVE There have been numerous reports of hepatic dysfunction secondary to anabolic steroid use based on elevated levels of serum aminotransferases. This study was conducted to distinguish between serum aminotransaminase elevations secondary to intense resistance training and anabolic steroid-induced hepatotoxicity in elite bodybuilders. DESIGN This was a case-control study of serum chemistry profiles from bodybuilders using and not using anabolic steroids with comparisons to a cohort of medical students and patients with hepatitis. PARTICIPANTS The participants were bodybuilders taking self-directed regimens of anabolic steroids (n = 15) and bodybuilders not taking steroids (n = 10). Blood chemistry profiles from patients with viral hepatitis (n = 49) and exercising and nonexercising medical students (592) were used as controls. MAIN OUTCOME MEASURES The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (GGT), and creatine kinase (CK) levels. RESULTS In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Creatine kinase (CK) was elevated in all exercising groups. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT. CONCLUSION Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated, because no exercising subjects, including steroid users, demonstrated hepatic dysfunction based on GGT levels. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. For these reasons, when evaluating hepatic function in cases of anabolic steroid therapy or abuse, CK and GGT levels should be considered in addition to ALT and AST levels as essential elements of the assessment.

Left Ventricular Wall Thickening Does Occur in Elite Power Athletes with or without Anabolic Steroid Use

Reports on the occurrence of left ventricular wall thickening in resistance-trained athletes have rejected the possibility for this physiological adaptation to occur without concomitant anabolic steroid abuse. Others have concluded short bursts of arterial hypertension that occur with maximal weight lifting are not sufficient to induce left ventricular wall thickening, and left ventricular wall thickness ≥13 mm should not be found in pure resistance-trained athletes. Therefore, we examined 4 elite resistance-trained athletes by two-dimensional echocardiography. In addition, we retrospectively examined the individual left ventricular dimensions of 13 bodybuilders from our previous echocardiographic studies. All 4 elite resistance-trained athletes had left ventricular wall thicknesses beyond 13 mm. One of the elite bodybuilders has the largest left ventricular wall thickness (16 mm) ever reported in a power athlete. Retrospectively, 43% of the drug-free bodybuilders and 100% of the steroid users had left ventricular wall thickness beyond the normal range of 11 mm. In addition, 1 drug-free subject and 3 steroid users were beyond the critical mark of 13 mm. No subjects demonstrated diastolic dysfunction. In contrast to previous reports, we have demonstrated that left ventricular wall thicknesses ≥13 mm can be found routinely in elite resistance-trained athletes. The use of anabolic steroids concomitant with intensive resistance exercise does appear to augment left ventricular size without dysfunction. Anabolic steroids may accelerate left ventricular wall thickening indirectly by increasing strength, thus augmenting the pressor response.

Testosterone, Sex Hormone-Binding Globulin, Lipoproteins, and Vascular Disease Risk:

Background That men have a higher risk of coronary heart disease has implicated testosterone as a risk factor. Lipoprotein levels have been reported to be altered by androgens, thus increasing the risk of coronary heart disease, myocardial infarction, and sudden death. The increasing abuse of anabolic steroids and reports of cases of sudden death and myocardial infarction among bodybuilders have raised concerns about an increase in cardiovascular risk for this population. Methods Twelve competitive bodybuilders were recruited for a comprehensive study on the cardiovascular risks associated with use of anabolic steroids. Six competitive heavyweight bodybuilders ingesting self-directed regimens of anabolic steroids (steroid group) and six competitive heavyweight drug-free bodybuilders were used for cardiovascular risk assessment. Apolipoproteins A-I and B, total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, triglyceride, testosterone, and sex hormone-binding globulin levels were determined in each athlete. Results Total, HDL and LDL cholesterol, apolipoproteins A-I and B, and triglyceride levels were significantly lower in members of the steroid group. As expected, testosterone level was significantly higher in members of the steroid group; sex hormone-binding globulin level was significantly lower. Apolipoprotein and lipoprotein levels were lower in members of the steroid group, whereas the total: HDL cholesterol ratio was significantly higher for members of the steroid group. Conclusions Consistently with previous reports, androgens were associated with decreases in HDL cholesterol and apolipoprotein A-I levels. However, androgens were also associated with reduced LDL cholesterol and apolipoprotein B levels. Despite the significantly higher total: HDL cholesterol ratio, the low serum total cholesterol levels (within the fifth percentile) and low plasma triglyceride levels in members of the steroid group raise questions concerning the exact role of androgens in increasing risk of cardiovascular disease.

Failure rate of frontal versus parietal approaches for proximal catheter placement in ventriculoperitoneal shunts: revisited

Early studies on ventriculoperitoneal shunt malfunctions demonstrated that proximal catheter obstruction was the most common cause for shunt malfunction and choroid plexus was the primary culprit for catheter obstruction. Subsequently, several studies were performed using stereotactic and endoscopic guidance systems to assist with optimal placement of proximal shunt catheters. Surgeons collectively agree that optimum placement of the proximal catheter tip is away from choroid plexus in the frontal horn. To achieve this catheter placement, neurosurgeons typically choose a frontal or parietal approach. Two previous studies comparing parietal and frontal shunt failure rates in the pediatric population have different conclusions. Thus, we decided to compare proximal catheter failure rates of frontal versus parietal approaches on 117 patients (ages ranging from 1 month to 80 years) who had undergone ventriculoperitoneal shunt placement at our institution. Statistical analysis demonstrated a significantly higher malfunction rate in the patients less than 3 years of age and a lower overall malfunction rate in patients shunted for normal pressure hydrocephalus. Surprisingly, there was no significant difference between the two surgical approaches. Thus, we concluded after reviewing the literature, that regardless of the initial surgical approach, the most important variable in shunt malfunction appears to be the final destination of the catheter tip in relation to the choroid plexus.

Middle cerebral artery blood flow velocity in elite power athletes during maximal weight-lifting

Abstract Cerebral blood flow velocity (CBFV) has been shown to significantly increase during dynamic exercise (running) secondary to increases in cardiac output. Static exercise (weight-lifting) induces supraphysio- logical arterial pressures up to 450/380 mmHg, and thus may alter CBFV. Catastrophic brain injuries such as stroke, cerebral hemorrhage, subarachnoid hemorrhage, retinal hemorrhage and retinal detachment have been associated with weight-lifting. A recent study has shown that intra-ocular pressure HOP), which is an indirect measure of intracranial pressure, elevates to pathophysiologic levels during weight-lifting. Recent CBFV studies instituting Valsalva have demonstrated decreases in CBFV from 21%-52%. To date, no studies have examined CBFV during maximal weight-lifting to elucidate the cerebrovascular responses to extreme pressure alterations. We recruited nine elite power athletes, including a multi-world record holder in powerlifting, for a transcranial Doppler study of middle cerebral artery blood flow velocity at rest and during maximal weight-lifting. All subjects’ resting blood flow velocities were within normal ranges (mean 64.4 ± 9.5 cm seer). Blood flow velocities were significantly (p < 0.0001) decreased in all subjects during maximal lifting (mean 48.4 ±10.1 cm sec2). Linear regression analysis demonstrated a significant inverse linear relationship in the net change of blood velocities from rest to maximal lift for each subject (r =0.8585, p < 0.001). This study demonstrates that blood flow velocities are significantly decreased during heavy resistance training. The drop in CBFV during weight-lifting was significantly less than previous Valsalva studies, which likely reveals the cardiovascular, baroreflex, and cerebrovascular system adaptations occurring in these elite power athletes. [Neurol Res 2000; 22: 337-340]

Anterior and posterior lumbar interbody fusion with percutaneous pedicle screws: comparison to muscle damage and minimally invasive techniques.

Study Design. Retrospective analysis of patients whom underwent one-level anterior lumbar interbody fusion or posterior lumbar interbody fusion with percutaneous pedicle screws. Objective. To determine which minimally invasive fusion technique, anterior or posterior lumbar fusions, induces the least amount of muscle damage. Summary of Background Data. Creatine phosphokinase is recognized as a good marker for muscle damage occurring in patients after spine surgery. Minimally invasive fusions are known to reduce the amount of muscle damage. Which surgery induces the least amount of muscle damage is yet to be determined. Minimally invasive spine surgery is becoming increasing popular due to the benefits of less muscle damage, shorter hospital length and quicker recovery. Lumbar fusions are one of the most common surgeries and is becoming less invasive with the use of percutaneous pedicle screws. Methods. Seventy-four patients whom underwent either anterior or posterior lumbar interbody fusions with percutaneous pedicle screws had preoperative and postoperative creatine kinase levels. Statistical analysis then compared the average change between the 2 groups. Results. Minimally invasive anterior lumbar interbody fusions with percutaneous pedicle screws had significantly less muscle damage (P < 0.05) than minimally invasive posterior lumbar interbody fusions with percutanoues screws. Conclusion. Minimally invasive anterior lumbar interbody fusions with percutaneous pedicle screws cause significantly less muscle damage than minimally invasive posterior lumbar interbody fusions with percutaneous screws. Furthermore minimally invasive anterior lumbar body interbody fusions demonstrated near the same amount of muscle damage to previously published literature on lumbar microdikectomies.

New method of pediatric cranioplasty for skull defect utilizing polylactic acid absorbable plates and carbonated apatite bone cement.

Cranial defect repair in the pediatric population requires a variety of special considerations. The pediatric skull has a dynamic nature that prohibits the use of rigid fixation, which is commonly applied in the adult population. A technique using a combination of polylactic acid plates and carbonated apatite bone cement has been devised by our group. Skull defects of varying sizes were repaired in 34 pediatric patients. Patients were examined on postoperative day 3 and at 3 months via three-dimensional computed tomography scans. Patients have been followed up to 60 months after surgery without complications or failures to date. This method benefits the pediatric patients undergoing cranioplasty by minimizing the insertion of long-term foreign bodies and allows the possibility for transformation of this construct into viable tissue.

Reactivation of dormant lumbar methicillin-resistant Staphylococcus aureus osteomyelitis after 12 years

The adequate treatment of methicillin-resistant Staphylococcus aureus (MRSA) osteomyelitis has intrigued clinicians for some time. As the resistance of these pathogens, coupled with the increase in community-acquired cases, continues steadily to rise, clinicians are finding it useful to employ multi-modal approaches for efficacious treatment. The authors present a single case report of a patient with recurrent MRSA osteomyelitis, lumbar paraspinal and epidural abscess. He was found to have decreased muscle strength and was hyporeflexic in the involved extremity. Serum testing demonstrated MRSA bacteremia. Neuroimaging studies revealed evidence of paraspinal abscess and a presumed herniated nucleus pulposus at the L5/S1 interspace with significant nerve root compromise. Despite antimicrobials, his symptoms persisted, necessitating surgical exploration. At surgery, paraspinal and epidural abscesses were encountered and debrided; however, no herniated disc was visualized. This case demonstrates the diagnostic and therapeutic dilemmas with which these lesions present. We postulate that the MRSA osteomyelitis/discitis pathogens were walled off in the disc space and subsequently inoculated the soft tissues with ensuing bacteremia. We concur that antimicrobial treatment should be the first line of therapy for these patients; however, surgical debridements and cautious spinal instrumentation should be employed where appropriate.

Atraumatic vertebral artery dissection after cervical corpectomy: a traction injury?

Study Design. Case report with review of the literature. Objectives. Presented is the first case of vertebral artery dissection secondary to intraoperative traction in cervical spine surgery. The pathogenesis and management of vertebral dissection in the immediate postoperative period are reviewed in detail. Summary of Background Data. Vertebral artery dissection is commonly associated with direct trauma, atraumatic or spontaneous. There are numerous reports of direct injury to the vertebral artery with cervical spine surgery, and it is a well-recognized risk. Cervical traction is also used routinely for improved placement of intervertebral devices/grafts. This is the first report of vertebral artery dissection occurring intraoperatively secondary to traction. The postoperative management is reviewed in detail. Methods. Case study with extensive review of the literature. Results. The patient underwent C6 corpectomy without intraoperative complications. Intraoperative wake-up test was normal. The patient remained intubated overnight for airway precautions. On postoperative day 1, the patient was lethargic and not following commands. Emergent CT of the brain and cervical spine revealed multiple posterior circulation infarcts with normal cervical spine and no hematoma. A stat angiogram revealed vertebral dissection. Medical management was initially attempted; however, infarcts continued, eventually requiring posterior fossa craniectomy/decompression and sacrificing the vertebral at the O-A junction. Conclusions. This is the first report of vertebral artery dissection occurring secondary to traction in cervical spine surgery. Surgeons must be aware that traction, even when performed appropriately, is not without risks. Anomalous vertebral arteries, osteophytes, and numerous other anatomic variants can lead to vertebral injury with traction.