High-Risk Cutaneous Squamous Cell Carcinoma without Palpable Lymphadenopathy: Is There a Therapeutic Role for Elective Neck Dissection?

PURPOSE: The beneficial role of elective neck dissection (END) in the management of high-risk cutaneous squamous cell carcinoma (CSCC) of the head and neck remains unproven. Some surgical specialists suggest that END may be beneficial for patients with clinically node-negative (N0) high-risk CSCC, but there are few data to support this claim. We reviewed the available literature regarding the use of END in the management of both CSCC and head and neck SCC (HNSCC). METHODOLOGY: The available medical literature pertaining to END in both CSCC and HNSCC was reviewed using PubMed and Ovid Medline searches. RESULTS: Many surgical specialists recommend that END be routinely performed in patients with N0 HNSCC when the risk of occult metastases is estimated to exceed 20%; however, patients who undergo END have no proven survival benefit over those who are initially staged as N0 and undergo therapeutic neck dissection (TND) after the development of apparent regional disease. There is a lack of data regarding the proper management of regional nodal basins in patients with N0 CSCC. In the absence of evidence-based data, the cutaneous surgeon must rely on clinical judgment to guide the management of patients with N0 high-risk CSCC of the head and neck. CONCLUSIONS: Appropriate work-up for occult nodal disease may occasionally be warranted in patients with high-risk CSCC. END may play a role in only a very limited number of patients with high-risk CSCC.     

Goldenhar’s Syndrome associated with congenital cyanotic heart disease

A case of Goldenhar’s Syndrome in a 10 year old girl is reported. The unusual features are the absence of epibulbar dermoid which is one of the major hallmarks of the Syndrome and the presence of an associated Cyanotic Heart disease.     

Central Sensitization Theory of Migraine: Clinical Implications

The clinical science of migraine headache continues to evolve. Theories of the pathophysiology of migraine have progressed from the early vascular basis of migraine to more complex current theories that emphasize the centrality of neuronal dysfunction. The most recently articulated theory of migraine is the central sensitization hypothesis, which proposes that altered processing of sensory input in the brainstem, principally the trigeminal nucleus caudalis, could account for many of the temporal and symptomatic features of migraine, as well as its poor response to triptan therapy when such treatment is initiated hours after the onset of pain. Both preclinical and clinical data support the central sensitization theory. A critical clinical implication of this theory is that drugs that are capable of either aborting or arresting the process of central sensitization, most prominently dihydroergotamine, may have a unique role in the treatment of migraine. An additional, and highly practical, implication is based upon the finding that cutaneous allodynia—pain arising from innocuous stimulation of the skin, as in hair brushing or the application of cosmetics—is an easily identifiable marker of central sensitization. Thus, the presence or absence of cutaneous allodynia can be integrated into the routine clinical assessment of migraine and utilized as a determinant of treatment. Future basic and clinical research on central sensitization is likely to be of ongoing importance to the field.