Cervical spondylotic myelopathy in the young adult: A review of the literature and clinical diagnostic criteria in an uncommon demographic

Background: Cervical spondylotic myelopathy (CSM) is typically encountered in the elderly population. Significant inconsistencies currently exist regarding the definition of the disorder, the true incidence of CSM in younger populations, and the established diagnostic criteria. Objective: To highlight the lack of standardization in the definition and diagnosis of CSM. Methods: A PubMed literature search was conducted spanning the years 2001 to 2011. The search was limited by the following terms: 1) English language, 2) Adults (19-44 years old), and 3) “cervical spondylotic myelopathy.” Each article was reviewed to determine if the presence of the definition of CSM existed in the article. The clinical characteristics used to make the diagnosis of CSM were recorded for each article. Cochran’s Q statistic was used to determine whether some clinical characteristics were more frequently used than others. Results: 93 papers were reviewed in detail and 16 case reports, reviews, and articles concerning less than three patients were excluded, resulting in 77 articles in the final analysis. The most common clinical definitions were gait disturbance (22/77 articles (28.6%)), upper limb paresthesias or sensory disturbance (21/77 (27.3%)), and clumsy hands (15/77 (19.5%)). Hyperreflexia, spasticity, and pathologically increased reflexes were identified as diagnostic criteria in a minority of patients. Conclusion: The literature employs a wide range of neurologic signs and symptoms to make the diagnosis of CSM, with a majority of studies failing to rely on strict diagnostic criteria. The clinician should not discount CSM as an explanation for the aforementioned findings, as it is well-reported in the literature among the ages 18-44

Prevention and Management of Bleeding During Endoscopic Approaches to Skull Base Pathologies

The rate of serious permanent morbidity and mortality with endonasal approaches has declined secondary to increased knowledge of the pertinent anatomy, advanced neuroimaging and navigation techniques, better surgical instruments, and improved exposure and reconstruction strategies.1-3 Although rare, vascular injury remains a potentially serious complication. However, with limited systematically-collected and reported data, the exact incidence rate of vascular injuries is difficult to determine. In terms of arterial injuries, the incidence based on reported series likely ranges from 0.3%-9% (Table 1),4-11 with higher rates most commonly associated with chordomas and chondrosarcomas involving the clivus. Venous injury is comparatively less severe and easier to manage. As a result, there is a comparatively lower impetus to publish epidemiological data and management strategies for these injuries. The consequences of arterial injury include fatal hemorrhage, vessel occlusion or thromboembolism causing infarction, development of a pseudoaneurysm (PA), carotid-cavernous fistula (CCF), subarachnoid hemorrhage (SAH), and vasospasm.6,7,9 Surgical expertise and detailed knowledge of the neurovascular anatomy is critical to the avoidance and management of vascular injuries. Pages: 20-2

Catecholamines—Crafty Weapons in the Inflammatory Arsenal of Immune/Inflammatory Cells or Opening Pandora’s Box§?

It is well established that catecholamines (CAs), which regulate immune and inflammatory responses, derive from the adrenal medulla and from presynaptic neurons. Recent studies reveal that T cells also can synthesize and release catecholamines which then can regulate T cell function. We have shown recently that macrophages and neutrophils, when stimulated, can generate and release catecholamines de novo which, then, in an autocrine/paracrine manner, regulate mediator release from these phagocytes via engagement of adrenergic receptors. Moreover, regulation of catecholamine-generating enzymes as well as degrading enzymes clearly alter the inflammatory response of phagocytes, such as the release of proinflammatory mediators. Accordingly, it appears that phagocytic cells and lymphocytes may represent a major, newly recognized source of catecholamines that regulate inflammatory responses