Trigger areas nerve decompression for refractory chronic migraine.

BACKGROUND: Chronic migraine refractory to medical treatment represents a common debilitating primary neurovascular disorder associated with great disability, high financial costs, reduced rates of productivity and impaired health-related quality of life. OBJECTIVE: To demonstrate the feasibility of scalp (trigger areas) nerve decompression as a treatment alternative in the management of refractory CM patients METHODS: From January 2005 to January 2020, we retrospectively collected data of 154 patients diagnosed with chronic migraine that underwent trigger site nerve decompression. These trigger areas were divided according the nerve compromise as frontal (supraorbital nerve), temporal (auriculotemporal nerve), occipital (greater occipital nerve). Following extensive clinical evaluation, the surgical treatment was performed after under local anesthesia and required the release of the affected nerve from surrounding connective tissue adhesions, and vascular conflicts. RESULTS: Of the total amount of patients, 91 (59.09%) patients underwent auriculotemporal nerve decompression, 27 (13.63%) cases supraorbital nerve decompression, 15 (9.74%) patients greater occipital nerve decompression, and the remaining 21 (13.63%) patients had more than one procedure of nerve decompression. At 1-year follow or latest follow-up, 96 (62.2%) patients were considered as cured, 29 cases (18.83%) reported improvement of their symptoms, 21 (13.64%) patients considered only a partial symptomatic remission and 5 (3.25%) patients reported no change or failed surgical treatment. CONCLUSION: Nerve decompression of trigger site areas (frontal, temporal, occipital) by removal of tissue, muscles and vessels in patients with medically refractory CM is a feasible alternative treatment modality with a high success of up to 80.5.

Kinetics of apoptosis and expression of apoptosis-related proteins in rat CA3 hippocampus cells after experimental diffuse brain injury.

The present study examined kinetics of apoptosis and expression of apoptosis-related proteins Bcl-2, Bax, and caspase-3 in the CA3 hippocampus cells after diffuse brain injury (DBI) induced experimentally in rats. Percentage of apoptotic cells and expressions of above proteins were examined by flow cytometry and immunohistochemistry. Substantial neuronal apoptosis was documented in the CA3 hippocampus cells after DBI (22.26 ± 2.97% at 72 h after DBI vs. 2.92 ± 0.88% in sham-operated animals). Expression of Bc1-2 decreased, while expression of Bax and caspase-3 increased after DBI, with caspase-3 expression peaking after that of Bax (72 vs. 48 h, respectively). Further, the Bc1-2/Bax expression ratio decreased prior to increase of caspase-3 expression. In conclusion, cell apoptosis and altered expressions of Bcl-2, Bax, and caspase-3 are present in the CA3 region of hippocampus after experimental DBI. Changes in the Bc1-2/Bax expression ratio may facilitate activation of caspase-3 and aggravate neuronal apoptosis after brain injury.