Middle cluneal nerve entrapment sites in the surgical field.

INTRODUCTION: Middle cluneal nerve (MCN) entrapment around the sacroiliac joint elicits low back pain (LBP). For surgical decompression to be successful, the course of the MCN must be known. We retrospectively studied the MCN course in 15 patients who had undergone MCN neurolysis. METHODS: Enrolled in this retrospective study were 15 patients (18 sides). We inspected their surgical records and videos to determine the course of the entrapped MCN. The area between the posterior superior- and the posterior inferior iliac spine was divided into areas A-D from the rostral side. The MCN transit points were identified at the midline and the lateral edge connecting the posterior superior- and posterior inferior iliac spine. Before and 6 months after surgery, the patients recorded the degree of LBP on the numerical rating scale and the Roland-Morris Disability Questionnaire. RESULTS: We decompressed 24 MCNs. The mean number was 1.3 nerves per patient (range 1-2). The MCN course was oblique in the cranio-caudal direction; the nerve tended to be observed in areas C and D. In six patients (40%), we detected two MCN branches, they were in the same area and adjacent. Postoperatively, LBP was improved significantly in all patients. CONCLUSION: Between the posterior superior- and the posterior inferior iliac spine, the MCN ran obliquely in the cranio-caudal direction; it was prominent in areas on the caudal side. In six (40%) patients, we decompressed two adjacent MCNs. Our findings are useful for MCN decompression surgery.

Long-term outcome after surgery for middle cluneal nerve entrapment neuropathy.

PURPOSE: Entrapment of the middle cluneal nerve (MCN-E) can elicit low back pain (LBP). Patients whose LBP responds only transiently to the analgesic effects of MCN blockage may be candidates for surgery. This study addresses its long-term efficacy. METHODS: We initially subjected 34 MCN-E patients (48 sides) to surgical release. Of these, 4 were excluded from this study because their follow-up was shorter than 24 months. The mean age of the 30 included patients was 71.5 years; the mean postoperative follow-up period was 40.4 months. Clinical outcomes were assessed on the Numerical Rating Scale (NRS) for LBP and the Roland Morris Disability Questionnaire (RDQ) before surgery and at the latest follow-up visit. RESULTS: The 30 patients (44 sides) reported severe LBP, leg symptoms were elicited by 32 sides. A mean of 1.4 MCN branches were surgically released, 32 sides were addressed by neurolysis, 7 by neurectomy, and 5 underwent both procedures due to the presence of 2 nerve branches. There were no complications. In the course of a mean follow-up of 26.3 months, MCN-E elicited recurrent symptoms on 6 sides; all had undergone neurolysis or neurectomy and a second operation improved the symptoms. All patients showed significant improvement at the last follow-up visit. Postoperatively both their NRS for LBP and their RDQ scores were improved (pre- vs. postoperative scores, p < 0.05). CONCLUSIONS: While surgical release of MCN-E is expected to yield long-term symptom relief, on 6 of 32 sides (18.8%) treated by neurolysis the patients reported pain recurrence. Whether neurectomy effectively prevents the recurrence of MCN-E in the long term requires further study.

[Microneurosurgical Treatment for Refractory Entrapment Neuropathy of Suprascapular Nerve:A Case Report].

Suprascapular nerve entrapment is rarely treated by neurosurgeons in Japan. However, it is often observed in post-stroke patients and in cases of accessory nerve injury as a complication of posterior fossa craniotomy. We report a case of suprascapular nerve entrapment due to superior transverse scapular ligament, which was successfully diagnosed and surgically treated. The patient was a 66-year-old female who used be a janitor. She complained of dysesthesia around the shoulder. The diagnosis was made based on the characteristic neurological findings including pain around the scapula, supraspinatus muscle weakness, and favorable but temporary response to suprascapular nerve block. After undergoing conservative management for one and a half year, she decided to undergo the nerve decompression surgery. The surgical treatment was performed under microscope with neuromonitoring. Following surgery, the painful area was dramatically reduced. We believe that suprascapular nerve disorders can be treated with careful neurological evaluation by neurosurgeons.

Ganglia-Induced Tarsal Tunnel Syndrome.

BACKGROUND: Tarsal tunnel syndrome (TTS) is a common entrapment neuropathy that is sometimes elicited by ganglia in the tarsal tunnel. METHODS: Between August 2020 and July 2022, we operated on 117 sides with TTS. This retrospective study examined data from 8 consecutive patients (8 sides: 5 men, 3 women; average age 67.8 years) with an extraneural ganglion in the tarsal tunnel. We investigated the clinical characteristics and surgical outcomes for these patients. RESULTS: The mass was palpable through the skin in 1 patient, detected intraoperatively in 1 patient, and visualized on MRI scanning in the other 6 patients. Symptoms involved the medial plantar nerve area (n = 5), lateral plantar nerve area (n = 1), and medial and lateral plantar nerve areas (n = 2). The interval between symptom onset and surgery ranged from 4 to 168 months. Adhesion between large (≥20 mm) ganglia and surrounding tissue and nerves was observed intraoperatively in 4 patients. Of the 8 patients, 7 underwent total ganglion resection. There were no surgery-related complications. On their last postoperative visit, 3 patients with a duration of symptoms not exceeding 10 months reported favorable outcomes. CONCLUSIONS: Because ganglia eliciting TTS are often undetectable by skin palpation, imaging studies may be necessary. Early surgical intervention appears to yield favorable outcomes.

Impact of Dynamic Change of Meandering of Parallel Artery to the Idiopathic Tarsal Tunnel Syndrome.

In idiopathic tarsal tunnel syndrome (TTS), walking seems to make symptoms worse. The findings imply that an ankle movement dynamic component may have an impact on the etiology of idiopathic TTS. We describe how the ankle movement affects the nerve compression caused by the surround tissue, particularly the posterior tibial artery. We enrolled 8 cases (15 sides) that had TTS surgery after tarsal tunnel (TT) MRI preoperatively. Dorsiflexion and plantar flexion were the two separate ankle positions used for the T2* fat suppression 3D and MR Angiography of TT. Based on these findings, we looked at how the two different ankle positions affected the posterior tibial artery's ability to compress the nerve. Additionally, we assessed the posterior tibial artery's distorted angle. We divided the region around the TT into four sections: proximal and distal to the TT and proximal half and distal half to the TT. Major compression cause was posterior tibial artery. Most severe compression point was proximal half in the TT in all cases without one case. In each scenario, the nerve compression worsens by the plantar flexion. The angle of the twisted angle of the posterior tibial artery was significantly worsened by the plantar flexion. In idiopathic TTS, deformation of posterior tibial artery was the primary compression component. Nerve compression was exacerbated by the plantar flexion, and it was attributable with the change of the distorted angle of the posterior tibial artery. This could be a contributing factor of the deteriorating etiology by walking in idiopathic TTS.

Anterolaterally Projecting Clinoid Segment Aneurysm Causing Oculomotor Palsy, with an Anatomical Review of the Clinoid Segment of the Internal Carotid Artery.

We describe a rare case of an anterolaterally projecting clinoid segment aneurysm of the internal carotid artery (ICA) causing oculomotor palsy. A 76-year-old woman was referred to our facility because of right oculomotor palsy that had been found just before surgery to remove bilateral cataracts. Neuroimaging revealed that the patient had an aneurysm at the clinoid segment that projected anterolaterally, eroding the anterior clinoid process. The aneurysm was thought to be compressing the oculomotor nerve, which runs at the upper part of the lateral wall of the cavernous sinus, thereby causing oculomotor palsy. Endovascular coiling of the aneurysm was successfully performed, and the oculomotor palsy was alleviated postoperatively. Anatomically, there exists the carotid collar between the arterial wall of the clinoid segment and the anterior clinoid process, containing the clinoid venous plexus in it. Hence, the anterolateral wall of the clinoid segment, although protected by a stiff bony structure, has an anatomical base that allows it to protrude centrifugally. Once protrusion occurs, the bone may be eroded by remodeling caused by the aneurysm's pulsed beating.