The subclavius posticus muscle is a rare aberrant muscle that traverses from the costal cartilage of the first rib posterolaterally to the superior border of the scapula. We report a patient having persistent paralysis of shoulder abduction with wrist and finger extension after a humeral neck fracture. Electromyography (EMG) examination revealed injuries to several upper extremity peripheral nerves, including the radial, axillary, and musculocutaneous nerves. Magnetic resonance imaging (MRI) performed at 10 months post-injury showed severe entrapment of the left brachial plexus by the subclavius posticus muscle at the thoracic outlet. The diagnosis of brachial plexus injury due to a rare abnormal subclavius posticus muscle was typically delayed until the MRI was performed for unexplained multiple peripheral nerve palsy. Resection of the aberrant muscle and brachial plexus decompression did not yield significant improvement in the patient’s radial nerve palsy until 6 months after surgery. Entrapment of the brachial plexus caused by the subclavius posticus muscle can cause symptoms of acute thoracic outlet syndrome following trauma to the upper extremity. In a case of inexplicable multiple peripheral nerve injuries in the upper extremity that are not proportional to the degree of trauma, MRI imaging along with EMG is required.

Chronic pain in painful post-traumatic trigeminal neuropathy, formerly called trigeminal deafferentation pain (TDP) or anesthesia dolorosa, is virtually incurable neuropathic pain. In severe cases, no effective method has yet been established. A 58-year-old woman presented with chronic dysesthetic pain in the right side of her face that had persisted for 8 years. It was caused by percutaneous balloon compression for an unexplained, persistent right gingival pain. The TDP did not respond to any medications or radiosurgery. Considering the typical occipital neuralgia that occurred later, the incomprehensible gum pain was interpreted as referred trigeminal pain from occipital neuralgia. Decompression of the greater occipital nerve improved occipital neuralgia; however, TDP did not respond to internal neurolysis or invasive brain stimulation. The last attempt was made to administer an intrathecal opioid because of pain sufficiently severe to cause suicidal ideation. Trial administration of intrathecal opioids had some effect on pain relief. Although incomplete, the effects of intrathecal morphine infusion were maintained up to 1 year later. Invasive neurosurgical interventions should be cautiously performed for continuous pain in persistent idiopathic facial pain and referred facial pain cases that do not show typical neuralgic pain in primary trigeminal neuralgia because of the risk of TDP.

Although anatomical variation of the sciatic nerve and piriformis muscle at the greater sciatic notch is considered an important cause of piriformis syndrome, there are few reports on the surgical treatment of piriformis syndrome owing to specific anatomical variations of the sciatic nerve and piriformis muscle. In this report, we describe 2 cases of piriformis syndrome caused by a rare type C sciatic nerve variation that were surgically treated using the transgluteal approach. The first patient reported unremitting left hip and leg pain that occurred following blunt trauma to the hip. The second patient complained of chronic pain in the buttocks and right leg, which persisted even after the patient underwent lumbar fusion surgery. Severe sitting pain and sciatica are symptomatic indications for the diagnosis of piriformis syndrome. A rare “C” type sciatic nerve variation was observed on the affected side under magnetic resonance imaging. Transgluteal sciatic nerve decompression provided significant pain relief. If severe sciatic nerve deformation due to a rare sciatic nerve variation can be confirmed with typical findings of piriformis syndrome, the possibility that sciatic nerve entrapment may have occurred in this variation should be considered.

Background: Lymphopenia frequently occurs after concomitant chemoradiation (CCRT) in patients with glioblastoma (GBM) and is associated with worse overall survival (OS). A few studies have tried to identify risk factors for lymphopenia; however, the results were not clear. We aimed to identify potential risk factors for lymphopenia, focusing on the use of dexamethasone to control cerebral edema in patients with GBM. Methods: The electronic medical records of 186 patients with newly diagnosed GBM treated at our institution between 2009 and 2017 were retrospectively examined. Acute lymphopenia was defined as total lymphocyte count less than 1,000 cells/μL at 4 weeks after completion of CCRT.Multivariate logistic regression analysis was used to identify independent risk factors for lymphopenia, and Cox regression analysis was used to identify independent risk factors for OS. Results: Of the 125 eligible patients, 40 patients (32.0%) developed acute lymphopenia. Female sex and median daily dexamethasone dose ≥2 mg after initiation of CCRT were independent risk factors for acute lymphopenia on multivariate analysis. Acute lymphopenia, extent of surgical resection, and performance status were associated with OS; however, dexamethasone use itself was not an independent risk factor for poor OS. Conclusion Female sex, median daily dexamethasone dose ≥2 mg after initiation of CCRT until 4 weeks after completion of CCRT may be associated with acute lymphopenia. However, dexamethasone use itself did not affect OS in patients newly diagnosed with GBM. These results should be validated by further prospective studies controlling for other confounding factors.