Headache in Patients with Cervical Spondylotic Myelopathy.

Purpose: The anatomical mechanisms of cervicogenic headache caused by upper cervical lesions have been reported. However, the pathomechanisms of headache caused by lower cervical spine disorders remain unknown. The purpose of the current study was to clarify the prevalence and pathogenesis of headaches in patients with cervical spondylotic myelopathy (CSM). Methods: In this retrospective study, a questionnaire regarding preoperative and postoperative symptoms was sent to 147 patients with CSM who were surgically treated in our hospital during the previous 10 years. All of the surgical procedures were decompression surgeries between the C3 and C7 levels. Data from 74 patients (50.3%) were available for analysis. Subjects were divided into four groups according to the presence or absence of preoperative and postoperative headache. The severity of pain, severity of neuropathic pain symptoms, depression, severity of myelopathy, and quality of life (QOL) were also evaluated using questionnaires. The scores of these questionnaires were then compared between the four groups. Kruskal-Wallis tests with Dunn-Bonferroni post hoc tests were used for comparisons. Results: Of the patients with CSM, 31% had headaches preoperatively, and 43% of these headaches disappeared postoperatively. Type 4 (preoperative headache-positive/postoperative headache-positive) patients had more severe pain and neuropathic pain symptoms and lower QOL scores compared with type 1 (preoperative headache-negative/postoperative headache-negative) patients. Conclusions: Approximately one-third of all patients with CSM had headaches preoperatively. Headache in patients with CSM may be neuropathic pain. A proportion of headaches in patients with CSM can be treated by decompression surgery.

Abdominal oblique muscle injury at its junction with the thoracolumbar fascia in a high school baseball player presenting with unilateral low back pain.

Abdominal oblique muscle injury is characterized by acute pain and localized tenderness over the lateral trunk. This injury is particularly common among throwing athletes, and usually presents as anterolateral abdominal wall pain. Imaging evidence is scarce in regard to whether oblique muscle injury at its junction with the thoracolumbar fascia can instead present with low back pain. A high school baseball player with unilateral low back pain was referred to us with a different diagnosis.　Careful palpation and magnetic resonance imaging guided our care, and the patient returned to high-level competition after 7 weeks of conservative treatment, with no report of recurrence in the subsequent 12 months. Oblique muscle injury at its junction with the thoracolumbar fascia should be added to the differential diagnosis for throwing athletes with unilateral low back pain following a torque movement.

Four-year follow-up of pregnancy-associated osteoporosis: a case report.

A 22-year-old woman presented with complaints of severe pain in a wide region of the thoracolumbar spine. She developed severe pain in the thoracolumbar spine region 2 months after her first delivery and was referred 1 month later. A lateral thoracic X-ray showed depressed degenerative vertebrae (T7, T9). One month after the initial examination, thoracic sagittal magnetic resonance imaging showed low intensity areas on T1-weighted imaging and iso-high intensity areas on T2-weighted imaging at T5, 7, 8, 9 and 11. Bone mineral density measured by ultrasound was low (%YAM 76%). The bone metabolic markers were high, suggesting accelerated osteoclast activity. These findings prompted a diagnosis of pregnancy-associated osteoporosis. She was asked to stop breastfeeding and to wear a lumbar brace, and treatment with nutritional calcium, activated vitamin D3, and risedronate sodium was started. Her low back pain almost disappeared after treatment. Bone metabolic markers showed normalization 8 months after the initial examination. Risedronate sodium was stopped 2 years and 2 months after the initial examination. Teriparatide treatment was started because her bone mineral density remained low; however, the osteoblast marker P1NP was not increased 5 months after the start of teriparatide treatment.