Transbrachioradialis Approach to the Radial Tunnel: An Anatomic Study of 5 Potential Compression Sites.

BACKGROUND: Recent anatomic studies have failed to demonstrate a single utilitarian approach to intraoperative identification and surgical release of all 5 potential sites of posterior interosseous nerve (PIN) compression in the radial tunnel. This study examines if a single incision brachioradialis-splitting approach without the use of additional anatomic windows is capable of adequately exposing the entire length of the radial tunnel, including all 5 sites of PIN compression to allow for adequate release. METHODS: Ten fresh frozen cadaver forearms (6 female, 4 male) were dissected utilizing a curvilinear 7 cm incision over the brachioradialis. The muscle belly was split via simple blunt retraction, exposing the radial tunnel. The PIN was identified and mobilized at 5 compression sites: radiocapitellar joint (RCJ), radial recurrent vessels (Leash of Henry), fibrous medioproximal edge of extensor carpe radialis brevis, arcade of Frohse, and distal edge of supinator. RESULTS: The PIN was identified and effectively released in all specimens without difficulty from this single approach. All 5 sites of compression were visible and accessible through the brachioradialis-split approach. Specifically, there was no difficulty in identifying and releasing the PIN at the distal edge of supinator. CONCLUSIONS: Radial tunnel syndrome is defined as PIN compression within the radial tunnel spanning from the fibrous RCJ to the distal edge of the supinator. A single brachioradialis-splitting approach is adequate for complete visualization and release of all compression sites of the radial tunnel. Utilizing this technique allows for surgical access and ease as well as minimizing necessity for additional windows or multiple incisions.

Reduced expression of conditioned fear in the R6/2 mouse model of Huntington's disease is related to abnormal activity in prelimbic cortex.

Prefrontal cortex (PFC) dysfunction is common in patients with Huntington's disease (HD), a dominantly inherited neurological disorder, and has been linked to cognitive disruption. We previously reported alterations in neuronal firing patterns recorded from PFC of the R6/2 mouse model of HD. To determine if PFC dysfunction results in behavioral impairments, we evaluated performance of wild-type (WT) and R6/2 mice in a fear conditioning and extinction behavioral task. Fear conditioning and extinction retrieval were similar in both genotypes, but R6/2s exhibited less fear during extinction by freezing less than WTs. A fear reinstatement test after extinction retrieval indicated that faster extinction was not due to poor memory for conditioning. During initial extinction and extinction retrieval training, neuronal activity was recorded from prelimbic (PL) cortex, a subregion of PFC known to be important for fear expression. In WTs, a large number of neurons were activated by the conditioned stimulus during initial extinction and this activation was significantly impaired in R6/2s. Notably, there was no genotype difference in PFC activity during extinction retrieval. Thus, altered extinction is likely a result of reduced fear expression due to impairments in PL activation. Collectively, our results suggest that PFC dysfunction may play a key role in R6/2 cognitive impairments.