Unilateral aberrant anatomy of the hypoglossal nerve.

PURPOSE: Neck dissection is often performed in patients with oral cancer to both treat and reduce the risk of subsequent neck metastases. Injury to the hypoglossal nerve may result in dysarthria, dysphagia, and profound difficulty with upper airway control. Although surgical landmarks facilitate intra-operative identification of vital structures to be preserved, they should not be an absolute measure, due to anatomical variants. We present a rare case of unilateral aberrant anatomy of the hypoglossal nerve, passing superficial to the internal jugular vein. METHODS: A 70-year-old female presented to the emergency department with an indurated and ulcerated floor of mouth lesion, later confirmed to be a squamous cell carcinoma. She was treated with wide local excision, bilateral selective neck dissection of levels I to III, surgical tracheostomy, anterior mandibulectomy and reconstruction with a left composite radial forearm free flap. RESULTS: A nerve-like structure was identified crossing superficially and perpendicular to the internal jugular vein within the left neck, which was later determined to be an anatomical variant of the hypoglossal nerve. This was carefully dissected and preserved, and the remainder of the surgery completed uneventfully. On the right, the hypoglossal nerve followed its normal anatomical course. The patient made a good recovery and suffered no neurological complications. CONCLUSION: Identification, meticulous dissection and preservation of the hypoglossal nerve is essential in lymphadenectomy involving levels I and II. Detailed knowledge of both normal and variant anatomy is fundamental for surgeons, which will allow for identification and protection of important neurovascular structures, thereby minimising surgical morbidity.

Neuroprotective effect of nerolidol in traumatic brain injury associated behavioural comorbidities in rats.

Traumatic brain injury (TBI) is an insult to the brain from an external mechanical force, leading to temporary/permanent secondary injuries, i.e. impairment of cognitive, physical, and psycho-social functions with altered consciousness. The leading mechanism responsible for neuronal damage following TBI is an increase in oxidative reactions initiated by free radicals generated by the injury along with various other mechanisms. Nerolidol is reported to have potent antioxidant and anti-neuroinflammatory properties. The present study was designed to explore the neuroprotective effect of nerolidol in weight-drop-induced TBI in rats. Animals were injured on the 1st day by dropping a free-falling weight of 200 gm from a height of 1 m through a guide pipe onto the exposed skull. After 14 days of injury, nerolidol (25, 50, and 100 mg/kg, i.p.) treatment was given for the next 14 days. Locomotor activity and motor coordination were evaluated using an actophotometer and rotarod, respectively. Cognitive impairment was observed through the Morris Water Maze and Object Recognition Test. On the 29th day, animals were sacrificed, and their brains were collected for the biochemical estimation. The weight drop model significantly decreased locomotor activity, motor coordination, increased Acetylcholinesterase (AChE) activity, oxidative stress, and induced cognitive deficits in TBI rats. Nerolidol significantly improved locomotor activity, reversed motor incoordination and cognitive impairment, and reduced the AChE activity and oxidative/nitrosative stress. The present study demonstrates the promising neuroprotective effects of nerolidol, which might improve the quality of life of TBI patients.