RESUMO
PURPOSE: The research outlines anatomical landmarks that may help surgeons in identifying the lateral antebrachial cutaneous nerve (LABCN) to minimize nerve damage during procedures in the cubital fossa. METHODS: Twenty-eight fresh cadaveric upper extremities were dissected. The course of the LABCN was followed from the emerging point at the biceps brachii tendon (BT) to the mid-forearm. The nerve's relationships with the BT, lateral epicondyle (LE), antebrachial vein, and brachioradialis (BR) muscle were measured and documented. RESULTS: The LABCN emerged lateral to the BT in all specimens and crossed medially at the top of the BT in 50% of the cadavers. It was deep to the forearm superficial fascia in all cadavers. At the level of the LE, the nerve was located at a mean of 6.3 ± 3.1 mm medial to the BR. The LABCN aligns with the medial border of the BR at a mean of 68 mm distal to the interepicondylar line. The mean distance from the LE to the LABCN at the interepicondylar line was 24.5 ± 7.2 mm. The LABCN and antebrachial vein are in the same deep fascia plane, on average 47.6 ± 5 mm (37-55) from the LE. At the elbow joint level, 82.1% of the specimens have two branches for the LABCN, whereas 17.9% demonstrated only a single branch. CONCLUSIONS: Lateral antebrachial cutaneous nerve was situated approximately 6.8 cm distal to the interepicondyle line, positioned at the ulnar edge of the BR, and runs parallel with the antebrachial vein deep to the forearm fascia plane. The nerve crossed over the biceps tendon in 50% of the specimens. These findings suggest that the nerve should be identified 6-7 cm distal to the LE, followed by a proximal dissection. CLINICAL RELEVANCE: This study may help surgeons in identifying LABCN, and reducing the potential risk of LABCN injury.
RESUMO
Neurotrauma is a significant cause of morbidity and mortality worldwide. For instance, traumatic brain injury (TBI) causes more than 30% of all injury-related deaths in the USA annually. The underlying cause and clinical sequela vary among cases. Patients are liable to both acute and chronic changes in the nervous system after such a type of injury. Cerebrovascular disruption has the most common and serious effect in such cases because cerebrovascular autoregulation, which is one of the main determinants of cerebral perfusion pressure, can be effaced in brain injuries even in the absence of evident vascular injury. Disruption of the blood-brain barrier regulatory function may also ensue whether due to direct injury to its structure or metabolic changes. Furthermore, the autonomic nervous system (ANS) can be affected leading to sympathetic hyperactivity in many patients. On a cellular scale, the neuroinflammatory cascade medicated by the glial cells gets triggered in response to TBI. Nevertheless, cellular and molecular reactions involved in cerebrovascular repair are not fully understood yet. Most studies were done on animals with many drawbacks in interpreting results. Therefore, future studies including human subjects are necessarily needed. This review will be of relevance to clinicians and researchers interested in understanding the underlying mechanisms in neurotrauma cases and the development of proper therapies as well as those with a general interest in the neurotrauma field.
