Toshiyuki Dokai

Surgical outcomes and prognostic factors of cervical spondylotic myelopathy in diabetic patients

BackgroundThere have been a few reports on the surgical outcomes of cervical myelopathy in diabetic patients; however, those studies included ossification of the posterior longitudinal ligament. This study investigated whether surgical outcome of expansive laminoplasty (ELAP) for diabetic patients with cervical spondylotic myelopathy (CSM) differs from that for non-diabetic patients and determined prognostic factors in diabetic patients.MethodsWe retrospectively reviewed 78 patients with CSM after excluding the cases with other medical conditions, which could affect surgical outcome from 222 consecutive patients who had undergone ELAP between 2000 and 2008 in our hospital. The patients were divided into two groups: diabetic patients (Group 1) and non-diabetic patients (Group 2). We evaluated differences in age, gender, pre- and postoperative Japanese Orthopaedic Association (JOA) score, recovery rate (RR), symptom duration, and postoperative complications between the two groups. In Group 1, the correlation between RR and factors indicating the severity of diabetes mellitus was assessed.ResultsThere were 13 patients in Group 1 and 65 in Group 2. There was no significant difference in age, gender, JOA score before or after surgery, or symptom duration between the two groups. Group 1 showed poorer recovery of sensory and motor function in the lower extremities. A negative correlation was observed between RR and the preoperative hemoglobin A1c (HbA1c) level in Group 1.ConclusionsDiabetic patients experienced benefits from ELAP similar to non-diabetic patients. A negative correlation between RR and preoperative HbA1c level suggests that strict blood sugar control is recommended before surgery.

Spinal subdural haematoma concurrent with cranial subdural haematoma: Report of two cases and review of literature.

Subdural haematomas co-existing in the cranium and spine are considered extremely rare. We report 2 cases demonstrating the condition described here with a review of literature. One of these 2 patients was the first case in which the spinal lesion was found before the cranial lesion. A 66-year-old man without trauma presented with paraparesis accompanied by severe leg pain. The patient was diagnosed as having spinal subdural haematoma extending from L1 to S1 vertebral levels with magnetic resonance images (MRI). Two days after admission, the patient developed disorientation and abnormal behavior; therefore, computed tomography (CT) of brain was performed, and chronic cranial subdural haematoma was observed. A 60-year-old man who developed headache showing gradually progressive was diagnosed as having cranial subdural haematoma on CT. Three days after admission, he became insomnolent due to severe low back pain radiating to ankle. On MRI, subdural haematoma was found extending from L3/4 to S2 vertebral levels. Only brain surgery was performed for all cases by the neurosurgeons. Paraparesis and severe leg pain, which were derived from spinal lesions, showed recovery approximately 2 weeks after onset and spinal subdural haematoma was completely resolved on MRI obtained 2 or 5 months after onset, respectively. There is a possibility that the incidence of spinal subdural haematoma concurrent with cranial subdural haematoma could be underestimated because the doctor had not obtained CT or MRI of the brain. Doctors should aware of such a condition and check patients with spinal subdural haematoma for neurological signs derived from brain lesions. Spontaneous resolution of spinal subdural haematoma was observed; therefore, surgery for this condition should be indicated only for patients with moderate or severe paraparesis or paraparesis deteriorated.

Posterior occipitocervical fixation under skull-femoral traction for the treatment of basilar impression in a child with Klippel–Feil syndrome

We present the case of a 15-year-old boy with symptoms due to Klippel-Feil syndrome. Radiographs and CT scans demonstrated basilar impression, occipitalisation of C1 and fusion of C2/C3. MRI showed ventral compression of the medullocervical junction. Skull traction was undertaken pre-operatively to determine whether the basilar impression could be safely reduced. During traction, the C3/C4 junction migrated 12 mm caudally and spasticity resolved. Peri-operative skull-femoral traction enabled posterior occipitocervical fixation without decompression. Following surgery, cervical alignment was restored and spasticity remained absent. One year after surgery he was not limited in his activities. The surgical strategy for patients with basilar impression and congenital anomalies remains controversial. The anterior approach with decompression is often recommended for patients with ventral compression of the medullocervical region, but such procedures are technically demanding and carry a significant risk of complications. Our surgical strategy was an alternative solution. Prior to a posterior cervical fixation, without decompression, skull traction was used to confirm that the deformity was reducible and effective in resolving associated myelopathy.

Significance of Stabilometry for Assessing Postoperative Body Sway in Patients with Cervical Myelopathy

Study Design Prospective study. Purpose To examine the changes in body sway using stabilometry in patients who underwent cervical laminoplasty for cervical myelopathy. Overview of Literature Although the patients of cervical myelopathy complain body sway there are few report to examine body sway objectively. Methods Patients who received treatment for cervical myelopathy between October 2010 and February 2013 were included. Twenty-one patients underwent cervical laminoplasty (myelopathy group). Body sway was assessed using stabilometry, wherein patients stood on a stabilometer with their eyes closed for 30 seconds. The Romberg ratio, outer peripheral area (OPA) with eyes closed (cm2), and total locus length per unit area (L/A) with eyes closed (/cm) were examined. Examinations were performed preoperatively (at baseline) and at 8 weeks postoperatively. Examination results of patients in the myelopathy group were compared with those of 17 healthy individuals (control group). Clinical symptoms were evaluated using the Japanese Orthopaedic Association scale score (JOA score) and the timed up and go (TUG) test. Results In the myelopathy and control groups, the mean baseline Romberg ratio, OPA, and L/A were 2.3±1.2, 8.9±5.5 cm2, and 14.2±5.3/cm and 1.4±1.0, 4.3±2.8 cm2, and 23.7±10.1/cm, respectively. Eight weeks after laminoplasty, only L/A showed significant improvement from baseline in the myelopathy group (23.2±10.1 to 16.8±7.9; p=0.03). The Romberg ratio and OPA showed improvement in the myelopathy group, but the changes were not statistically significant. JOA scores and TUG test results in this group significantly improved from baseline to 8 weeks after laminoplasty (12.7 to 13.4 and 10.8 to 8.0 seconds, respectively; both p<0.05). Conclusions L/A is a useful parameter for measuring body sway to assess the recovery of body sway after laminoplasty.

Spinal Cord Venous Infarction Presumed to be Caused by a Lumbar Vertebral Body Malformation after Vertebral Complession Fracture

We report a case of a 81-year-old woman with a subacute bilateral legs palsy due to venous congestion of the spinal cord caused by an arteriovenous fistula in the first lumbar vertebra which fractured previously. We diagnosed her spinal infarction only by MRI. She recovered from leg palsy at first. So we waited and saw her symptom. But after that leg palsy repeated with short interval and gradually her palsy was getting worse and became completed palsy. We performed selective spinal angiography and found out arteriovenous fistula in first lumbar vertebra fractured previously. We estimated that vertebral fracture might make arteriovenous fistula in vertebral body and this fistula caused venous congestion spinal cord. Spinal cord venous infarctions due to venous congestion with lumbar vertebral body malformation is a very rare. Therefore we delayed to diagnose and this delay caused to permanent neurological deficits.