Deep Decompression of the Lateral Femoral Cutaneous Nerve Under Local Anesthesia.

OBJECTIVE: Meralgia paresthetica is a mononeuropathy of the lateral femoral cutaneous nerve (LFCN) caused by compression around the inguinal ligament. We report a surgical alternative for the treatment of meralgia paresthetica under local anesthesia and its outcomes. METHODS: We operated on 12 patients with unilateral meralgia paresthetica whose age at surgery ranged from 62 to 75 years. The mean postoperative follow-up period was 19 months. Microsurgical deep decompression of LFCN was performed with the patient under local anesthesia. Clinical outcomes of surgical treatment were assessed based on the patient's most recent follow-up visit and were classified into 3 categories: complete, partial, or no relief of symptoms. Symptoms of pain or numbness in the anterolateral part of the thigh were evaluated, using a visual analog scale, before surgery and after surgery, i.e., at the most recent follow-up visit. RESULTS: All patients reported symptom improvement: complete relief in 9 patients (75%) and partial relief in 3 patients (25%). In the 3 patients with partial relief, the remaining symptoms did not affect their daily living. Overall, the visual analog scale scores were significantly improved in all patients (P < 0.05), and no patient experienced postoperative recurrence of their symptoms at the time of the last follow-up visit. CONCLUSIONS: Symptoms of meralgia paresthetica can resemble those of a lumbosacral disorder. Microsurgical deep decompression under local anesthesia produces good surgical outcomes. The use of local anesthesia contributes not only to reduction of pain during surgery but also eliminates excessive surgical procedures and reduces the duration of hospital stay.

Surgical treatment of middle cluneal nerve entrapment neuropathy: technical note.

OBJECTIVE The etiology of low-back pain (LBP) is heterogeneous and is unknown in some patients with chronic pain. Superior cluneal nerve entrapment has been proposed as a causative factor, and some patients suffer severe symptoms. The middle cluneal nerve (MCN) is also implicated in the elicitation of LBP, and its clinical course and etiology remain unclear. The authors report the preliminary outcomes of a less invasive microsurgical release procedure to address MCN entrapment (MCN-E). METHODS The authors enrolled 11 patients (13 sites) with intractable LBP judged to be due to MCN-E. The group included 3 men and 8 women ranging in age from 52 to 86 years. Microscopic MCN neurolysis was performed under local anesthesia with the patient in the prone position. Postoperatively, all patients were allowed to walk freely with no restrictions. The mean follow-up period was 10.5 months. LBP severity was evaluated on the numerical rating scale (NRS) and by the Japanese Orthopaedic Association (JOA) and the Roland-Morris Disability Questionnaire (RDQ) scores. RESULTS All patients suffered buttock pain, and 9 also had leg symptoms. The symptoms were aggravated by standing, lumbar flexion, rolling over, prolonged sitting, and especially by walking. The numbers of nerve branches addressed during MCN neurolysis were 1 in 9 patients, 2 in 1 patient, and 3 in 1 patient. One patient required reoperation due to insufficient decompression originally. There were no local or systemic complications during or after surgery. Postoperatively, the symptoms of all patients improved statistically significantly; the mean NRS score fell from 7.0 to 1.4, the mean RDQ from 10.8 to 1.4, and the mean JOA score rose from 13.7 to 23.6. CONCLUSIONS Less invasive MCN neurolysis performed under local anesthesia is useful for LBP caused by MCN-E. In patients with intractable LBP, MCN-E should be considered.

[Chronic Low Back Pain Associated with Gluteus Medius Muscle:A Case Report].

The clinical features and etiology of low back pain(LBP)and buttock pain(BuP)has been poorly understood. We report a case of long-term BuP that was successfully treated with gluteus medius muscle(GMeM)decompression under local anesthesia. A 71-year-old man was referred to our hospital because of long-term BuP and claudication. Left BuP that radiated to the left thigh was observed. The pain was mostly triggered by palpation at the middle of the iliac crest and greater trochanter. Lumbar and pelvic radiograms showed no significant lesions. Lumbar magnetic resonance imaging revealed a mild lumbar spinal canal stenosis at the L4/L5 segment. Based on the evidence of a trigger point and pain relieved after GMeM block injection, we made a diagnosis of GMeM pain. Although several GMeM block injections relieved his pain, the analgesic effect was transient and the claudication remained. Then, we decided to perform GMeM decompression. We made a 5-cm-long skin incision across the trigger point on the buttock. After confirming a wide exposure of the gluteal aponeurosis over the GMeM, we cut and opened it for sufficient GMeM decompression, and the GMeM expansion was confirmed. After surgery, his symptoms immediately improved. No evidence of recurrence was observed 6 months after his treatment. For the treatment of LBP and BuP, GMeM pain would be considered a causative factor. We report that it can be treated with a less invasive surgical technique, which would contribute to good clinical outcome.

Low back pain due to middle cluneal nerve entrapment neuropathy.

PURPOSE: The etiology of low back pain (LBP) is complicated and the diagnosis can be difficult. Superior cluneal nerve entrapment neuropathy (SCN-EN) is a known cause of LBP, although the middle cluneal nerve (MCN) can be implicated in the elicitation of LBP. METHODS: A 76-year-old woman with a 4-year history of severe LBP was admitted to our department in a wheelchair. She complained of bilateral LBP that was exacerbated by lumbar movement. Her pain was severe on the right side and she also suffered right leg pain and numbness. Based on palpation and nerve blocking findings we diagnosed SCN-EN and MCN entrapment neuropathy (MCN-EN). RESULTS: Her symptoms improved with repeated SCN and MCN blocking; the MCN block was the more effective and her symptoms improved. As her right-side pain around the MCN -EN with severe trigger pain recurred we performed microscopic right MCN neurolysis under local anesthesia. This led to dramatic improvement of her LBP and leg pain and the numbness improved. At the last follow-up, 7 months after surgery, she did not require pain medication. CONCLUSIONS: The MCN consists of sensory branches from the dorsal rami of S1-S4. It sandwiches the sacral ligament between the posterior superior and inferior iliac spine as it courses over the iliac crest. Its entrapment at this hard orifice can lead to severe LBP with leg symptoms. An MCN block effect is diagnostically useful. Less invasive MCN neurolysis under local anesthesia is effective in patients who fail to respond to observation therapy.

Acute Poststroke Depression Is Associated with Thalamic Lesions and Clinical Outcomes: A Case-Control Study.

BACKGROUND: We investigated the role of acute-phase stroke lesions and patient characteristics in poststroke depression (PSD) and its effect on the clinical outcome. PATIENTS AND METHODS: Five and 30 days after admission, 175 patients self-reported their depressive symptoms on the Patient Health Questionnaire-9. We compared the clinical characteristics and outcomes in patients with (n = 41) and without PSD (n = 134). Stroke severity was assessed with the National Institutes of Health Stroke Scale (NIHSS); the modified Rankin Scale (mRS) was used to determine the functional outcome. RESULTS: There was no significant difference between patients with and without PSD in the age, gender ratio, lesion side, and the history of hypertension, diabetes mellitus, alcohol and tobacco use, and previous stroke. Thalamic lesions were significantly associated with PSD (P = .03), although there was no significant difference in both the NIHSS score and the final mRS score of patients with thalamic lesions. Backward stepwise logistic regression analysis showed that a higher NIHSS score and thalamic lesions were independent predictors of PSD. Total hospitalization was significantly longer in patients with PSD. At the time of admission, the NIHSS score was significantly higher in patients who developed moderate to severe PSD than in those with mild PSD or without PSD. CONCLUSIONS: PSD in the acute phase was associated with thalamic lesions and severe stroke. Hospitalization was significantly longer in patients with PSD and their functional disability was more severe, suggesting that PSD played a role in the unsatisfactory results of poststroke rehabilitation.

Treatment of low back pain elicited by superior cluneal nerve entrapment neuropathy after lumbar fusion surgery.

OBJECT: Low back pain (LBP) attributable to fusion failure, implant failure, infection, malalignment, or adjacent segment disease may persist after lumbar fusion surgery (LFS). Superior cluneal nerve (SCN) entrapment neuropathy (SCNEN) is a clinical entity that can produce LBP. We report that SCNEN treatment improved LBP in patients who had undergone LFS. METHODS: Between April 2012 and August 2015, we treated 8 patients (4 men and 4 women ranging in age from 38 to 88 years; mean age, 69 years) with SCNEN for their LBP after LFS. Our criteria for the diagnosis of SCNEN included a trigger point over the posterior iliac crest 7 cm from the midline and numbness and radiating pain in the SCN area upon compression of the trigger point. Symptom relief was obtained in more than 75% of patients within 2 h of inducing a local nerve block at the trigger point in the buttocks. The mean postoperative follow-up period was 28 months (range, 9-54 months). RESULTS: LBP was unilateral in 3 and bilateral in 5 patients. The senior author (T.I.) operated all patients for SCNEN under local anesthesia because they reported recurrence of pain after the analgesic effect of repeat injections wore off. This led to a significant improvement of their LBP. CONCLUSIONS: SCNEN should be considered in patients reporting LBP after LFS. Treatment of SCNEN may be a useful option in patients with failed back surgery syndrome after LFS.

Neurovascular bundle decompression without excessive dissection for tarsal tunnel syndrome.

Tarsal tunnel syndrome (TTS) is an entrapment neuropathy of the posterior tibial nerve and its branches in the tarsal tunnel. We present our less invasive surgical treatment of TTS in 69 patients (116 feet) and their clinical outcomes. The mean follow-up period was 64.6 months. With the patient under local anesthesia we use a microscope to perform sharp dissection of the flexor retinaculum and remove the connective tissues surrounding the posterior tibial nerve and vessels. To prevent postoperative adhesion and delayed neuropathy, decompression is performed to achieve symptom improvement without excessive dissection. Decompression is considered complete when the patient reports intraoperative symptom abatement and arterial pulsation is sufficient. The sensation of numbness and/or pain and of foreign substance adhesion was reduced in 92% and 95% of our patients, respectively. In self-assessments, 47 patients (68%) reported the treatment outcome as satisfactory, 15 (22%) as acceptable, and 7 (10%) were dissatisfied. Of 116 feet, 4 (3%) required re-operation, initial decompression was insufficient in 2 feet and further decompression was performed; in the other 2 feet improvement was achieved by decompression of the distal tarsal tunnel. Our surgical method involves neurovascular bundle decompression to obtain sufficient arterial pulsation. As we use local anesthesia, we can confirm symptom improvement intraoperatively, thereby avoiding unnecessary excessive dissection. Our method is simple, safe, and without detailed nerve dissection and it prevents postoperative adhesion.