Spinal cord injury in a 14-year-old male secondary to cervical hyperflexion with exercise.

STUDY DESIGN: Case report. OBJECTIVES: To present an interesting case of a 14-year-old male with acute paresis of upper extremities and progressive difficulty with lower extremities. The patient is a competitive wrestler and was performing his daily abdominal workout 'sit-ups' with hands interlocked behind his head. During the end and immediately following his abdominal workout, he felt progressive weakness in his upper extremities. He was rushed to the hospital within an hour and seen in the emergency room and admitted to the neurology service for a presumed thromboembolic event. SETTING: New York, USA. RESULTS: The patient was negative for any hematologic disease or coagulopathy. Magnetic resonance imaging was negative for any mass effect on the spinal cord and neurological examination revealed bilateral upper extremity paraparesis 3/5 and lower extremity spasticity and propioceptive dysfunction. The patient was treated with corticosteroids and rigid collar, follow-up examination at 3 months revealed resolution of symptoms. DISCUSSION/CONCLUSION: The pathophysiology of central cord syndrome is thought to be primarily secondary to a hyperextension injury, which causes buckling of the ligamentum flavum and increasing spinal cord diameter which leads to cord compression. This syndrome is more commonly seen in the spondylotic elderly. This case involves a teenager with normal canal diameter; however, combining aggressive exercise with extreme cervical hyperflexion, one can plausibly account for an acute ischemic event or repetitive microinjury to the spinal cord.

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.

Prophylaxis to avert exacerbation/relapse of multiple sclerosis in affected patients undergoing surgery. Surgical observations and recommendations.

To provide the neurological and neurosurgical communities with case evidence of postoperative multiple sclerosis (MS) relapse, literature review to support operative stress-induced relapse and recommendations for perioperative prophylaxis to prevent relapse in patients undergoing surgery. Two case studies are presented with recommendations based on an extensive review of the medical literature and personal experience to support perioperative prophylactic suggestions. Both patients fully recovered to preoperative functional status after treatment. We now routinely implement perioperative prophylaxis to MS patients undergoing surgery at our institution with no complications to date. Perioperative prophylaxis in patients with MS undergoing surgery can prevent relapse. It is of utmost importance that the surgical community realizes that prophylactic treatment is available and should be utilized during elective and emergent surgical situations.

Sudden death secondary to fulminant intracranial aspegillosis in a healthy teenager after posterior fossa surgery: the role of corticosteroids and prophylactic recommendations.

Postoperative complications from corticosteroids in neurosurgical patients are not uncommon. Too often the deleterious immunosuppressive effects of corticosteroids are overlooked in neurosurgery patients and can lead to serious and lethal infections. EXPERIMENTAL DESIGN: case report of a 16-year-old healthy male who presented for elective resection of a recurrent juvile pilocytic astrocytoma of the posterior fossa 4 years after initial resection. SETTING: major University institutional practice. INTERVENTION/RESULTS: a standard suboccipital craniotomy with gross total resection. Postoperatively, the patient suffered from posterior fossa syndrome and diminished gag reflex requiring nasogastric feeds with progressive improvement. While awaiting transfer to a rehabilitation center on postoperative day 12 he suffered a sudden temperature spike followed by neurological decline. A stat computed tomography scan of the brain revealed a diffuse miliary process with severe cerebral edema. Sputum and cerebrospinal fluid cultures identified Aspergillus. Despite immediate therapy to combat the malignant cerebral edema, the patient died within 24 hours of onset of the symptoms. Corticosteroids are used routinely in neurosurgery to combat cerebral edema without much consideration for the immunosuppressive effects. This case demonstrates how the immunosuppressive effects of corticosteroids can lead to a fulminant lethal fungal infection. Neurosurgeons should be aware of the anticatabolic medications now available to combat the deleterious side effects of corticosteroids.

Intramedullary inflammatory mass dorsal to the Klippel-Feil deformity: error in development or response to an abnormal motion segment?

STUDY DESIGN: Case study on a 45-year-old female with progressive weakness and paresthesias in her lower extremities and a magnetic resonance image of an intramedullary mass at the level of C5-6 and a Klippel-Feil (KF) deformity ventral to the lesion. OBJECTIVE: Present an interesting case of an intramedullary mass coexisting with a ventral KF deformity with review of the medical literature on intramedullary masses and cervical spine biomechanics. SETTING: New York city, New York, USA. METHODS: Case study with discussion of neurosurgical and neuropathological findings and review of the literature. RESULTS: The patient underwent open neurosurgical excisional biopsy of the intramedullary mass which revealed a non-neoplastic inflammatory mass that slowly resolved with medical management. CONCLUSIONS: While no definitive etiology was found in this case we offer two interesting mechanisms: (1) maldevelopment of the cervical spine or (2) this inflammatory mass is in response to an abnormal motion at the level of the Klippel-Feil.

Isolated intracranial infection with Mycobacterium avium complex.

UNLABELLED: Mycobacterium avium-M. complex (MAC) has been linked to devastating respiratory and systemic illnesses in patients, especially in those who are immunosuppressed. The purpose of this study is to describe a case of isolated central nervous system (CNS) infection with MAC. This is a single case report of a patient with isolated intracranial mycobacterial infection. SETTING: the patient was treated and the immunohistochemical investigations were undertaken at the National Institutes of Health in Bethesda, Maryland, USA. INTERVENTION: the patient initially was treated with a cocktail of antimycobacterial medications. However, because his disease was refractory, he underwent a suboccipital craniotomy and evacuation of his cerebellar mass. The patient was determined to have a low production of interferon-gamma (INF-gamma) and tumor necrosis factor-alpha (TNF-alpha) when compared to normal values. Despite extensive radiographic imaging studies and biopsies, there was no evidence of another focus of MAC infection in this patient. We conclude that intracranial infectious lesions in patients such as ours should be treated with conventional systemic antibiotic regimens as the first-line of therapy. We suggest neurosurgical intervention in medically refractory cases of intracranial infections.

Evaluation of aminotransferase elevations in a bodybuilder using anabolic steroids: hepatitis or rhabdomyolysis?

The use of anabolic steroids among competitive athletes, particularly bodybuilders, is widespread. Numerous reports have noted "hepatic" dysfunction secondary to anabolic steroid use based on elevated serum aminotransferase levels. The authors' objective was to assess whether primary care physicians accurately distinguish between anabolic steroid-induced hepatotoxicity and serum aminotransferase elevations that are secondary to acute rhabdomyolysis resulting from intense resistance training. Surveys were sent to physicians listed as practicing family medicine or sports medicine in the yellow pages of seven metropolitan areas. Physicians were asked to provide a differential diagnosis for a 28-year-old, anabolic steroid-using male bodybuilder with an abnormal serum chemistry profile. The blood chemistries showed elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) levels, and normal gamma-glutamyltransferase (GGT) levels. In the physician survey (n = 84 responses), 56% failed to mention muscle damage or muscle disease as a potential diagnosis, despite the markedly elevated CK level of the patient. Sixty-three percent indicated liver disease as their primary diagnosis despite normal GGT levels. Prior reports of anabolic steroid-induced hepatotoxicity that were based on aminotransferase elevations may have overstated the role of anabolic steroids. Correspondingly, the medical community may have been led to emphasize anabolic steroid-induced hepatotoxicity and disregard muscle damage when interpreting elevated aminotransferase levels. Therefore, when evaluating enzyme elevations in patients who use anabolic steroids, physicians should consider the CK and GGT levels as essential elements in distinguishing muscle damage from liver damage.

Secondary partial empty sella syndrome in an elite bodybuilder.

The pituitary gland is a hormone-responsive gland and is known to vary in size depending on the hormonal status of the patient and the multifaceted positive and negative feedback hypothalamic-pituitary-gonadal axis. Partial empty sella syndrome with an atrophied pituitary gland is seen in primary neuroendocrinopathies such as growth hormone deficiency, primary hypothyroidism, central diabetes insipidus and hypogonadism. Partial empty sella has also been shown to occur in patients with elevations in intracranial pressure. Secondary partial empty sella syndrome with significant pituitary gland atrophy from negative feedback inhibition of long-term exogenous hormonal use has not been previously reported. We are reporting on a case of partial empty sella syndrome occurring in an elite bodybuilder with a long history of exogenous abuse of growth hormone, testosterone and thyroid hormone. The pathophysiological mechanisms of secondary partial empty sella syndrome from exogenous hormone use and the possibility for elevations in intracranial pressure contributing to this syndrome will be discussed.

The hiccup reflex arc and persistent hiccups with high-dose anabolic steroids: is the brainstem the steroid-responsive locus?

Hiccups have been classified as a neurologic reaction triggered by a multitude of factors. There are only a few reports of persistent hiccups associated with oral and intravenous corticosteroid use in the medical literature. It has been proposed that corticosteroids lower the threshold for synaptic transmission in the midbrain and directly stimulate the hiccup reflex arc. There is a recent report of progesterone-induced hiccups, which were thought to occur secondary to the glucocorticoid-like effects of progesterone on the brainstem. We report the first case of anabolic steroid-induced hiccups occurring in an elite power lifter. The hiccups occurred within 12 hours of the individual increasing his doses of oral anabolic steroids and persisted for 12 consecutive hours until medical attention was sought. In this report the pathophysiology of anabolic steroid-induced hiccups is discussed, and the postulated relationships of steroids and the hiccup reflex arc reviewed.

Bilateral median neuropathy and growth hormone use: a case report.

A male elite bodybuilder suffered bilateral median nerve neuropathy during a self-administered course of growth hormone (GH). Nerve conduction velocities revealed bilateral median neuropathy consistent with carpal tunnel syndrome (CTS). This is the first case of GH-induced CTS occurring in an athlete. Contrary to earlier studies, this report demonstrates that GH-induced CTS is not an age-related phenomenon and alerts physicians to include GH abuse as a possible etiology of median neuropathy in athletes.

Somatic von Hippel-Lindau gene mutations detected in sporadic endolymphatic sac tumors.

Endolymphatic sac tumors (ELSTs) occur sporadically or in association with an autosomal dominantly inherited tumor syndrome, von Hippel-Lindau (VHL) disease. In VHL disease, a germline mutation of the VHL tumor suppressor gene is inherited, and loss of function of the wild-type allele occurs through genetic deletion with subsequent development of neoplastic growth. Genetic alterations associated with sporadic ELSTs are less well understood. In this study, we used tissue microdissection to selectively analyze neoplastic cells from four sporadic ELSTs. In two cases, we detected somatic mutations involving VHL gene exons 1 and 2, respectively. Additionally, one of these cases revealed deletion of the VHL gene locus. Two cases did not reveal VHL gene mutation; one of these two cases showed VHL gene deletion. These results suggest that mutations and allelic deletions of the VHL tumor suppressor gene play a role in the tumorigenesis of sporadic ELSTs.

The upper range of lumbar spine bone mineral density? An examination of the current world record holder in the squat lift.

Weight-bearing exercise is known to improve bone mineral density, however, excessive forces exerted on the lumbar spine can be pathologic. Cadaveric studies have calculated a hypothetical "critical compression force" at which the lumbar spine would suffer collapse. In addition, recent studies have suggested that bone density correlates with strength. Thus far studies have failed to examine elite power athletes to determine the possible upper range for bone mineral density and critical compression force. Therefore, we recruited the current world record holder in the squat lift, with a record squat lift >469 kg, for an examination of lumbar spine bone mineral density. The subject had dual energy x-ray absorptometry (DEXA) and magnetic resonance imaging (MRI) performed of the lumbar spine. The subject also had serum chemistries, cell blood count and testosterone levels performed. DEXA scan revealed the highest bone mineral density reported to date. MRI revealed normal alignment, no evidence of disc herniation or compressive disc disease. There was no frank or neural foraminal canal stenosis. The estimated compressive force generated on his lumbar spine during the squat lift of > 469 kg doubles the previously reported critical compression force. This case study supports the previously described relationship between strength and bone density and redefines the upper limits of bone density in strength athletes.