In order to determine the influence of early ambulation and other factors on headaches occurring after lumbar myelography we randomised 207 patients (127 men and 80 women) into two groups. Following the investigation, we allowed the 101 patients (65 men and 36 women) in group A to sit or stand freely, while we confined the 106 patients (62 men and 44 women) in group B to bed for 20 hours. The nine patients in group B who could not maintain bed rest were excluded.

There was no significant difference between the two groups as regards the prevalence of spinal headache (8.9% in group A v 14.4% in group B). Patients who reported headaches, however, were significantly more likely to be women (18.7%) than men (7.3%), be younger (mean age 45 years v 56 years), have a higher cerebrospinal pressure before removal of fluid (mean values 172 v 137 mm H₂O) and a lower systolic (mean values 120 v 134 mmHg) and diastolic blood pressure.

We conclude that, although other factors may be associated with headaches, late ambulation is not effective in preventing spinal headaches after lumbar myelography.

Degenerative changes of the knee often cause loss of extension. This may affect aspects of posture such as lumbar lordosis. A total of 366 patients underwent radiological examination of the lumbar spine in a standing position. The knee and body angles were measured by physical examination using a goniometer. Limitation of extension of the knee was significantly greater in patients whose lumbar lordosis was 30° or less. Lumbar lordosis was significantly reduced in patients whose limitation of extension of the knee was more than 5°. It decreased over the age of 70 years, and the limitation of extension of the knee increased over the age of 60 years. Our study indicates that symptoms from the lumbar spine may be caused by degenerative changes in the knee. This may be called the ‘knee-spine syndrome’.

In patients who underwent autogenous iliac bone grafting we studied prospectively injury to the lateral femoral cutaneous nerve (LFCN) in relation to the size (length, depth, width) of the graft. We also examined the neurological deficit, by questioning them about numbness and/or pain in the lateral thigh.

The risk of injury was significantly higher in those in whom the depth of the graft was more than 30 mm. With regard to the length of the graft the incidence of nerve injury was 20% when the graft was 45 mm long or more, 16% when it was between 30 mm and 45 mm long, and 8% when it was less than 30 mm long. We should inform patients of the possibility of such injury, and take size into consideration when harvesting grafts from the ilium.

Based on a study using a retrograde neurotracer, we have previously found that the dorsal portion of the L5/6 disc in the rat is multisegmentally innervated by dorsal root ganglia (DRG) from the level of T13 to L6, and that sensory nerve fibres from DRG of T13, L1 and L2 pass through the paravertebral sympathetic trunks. In this study in newborn rats, we injected crystals of 1,1′-dioctadecyl-3,3,3′,3′-tetramethylinedocarbocyanine perchlorate (DiI) into the DRG of T13, L1 and L2 and showed DiI-labelled sensory nerve fibres in the dorsal portion of the discs from the level of T13/L1 to L5/6. Our results show that the dorsal portion of the lumbar discs is innervated by the DRG from levels T13 to L2.

We have examined the process of fusion of the intertransverse processes and bone graft in the rabbit by in situ hybridisation and evaluated the spatial and temporal expression of genes encoding pro-α1 (I) collagen (COL1A1), pro-α1 (II) collagen (COL2A1) and pro-α1 (X) collagen (COL10A1).

Beginning at two weeks after operation, osteogenesis and chondrogenesis occurred around the transverse process and the grafted bone at the central portion of the area of the fusion mass. Osteoblasts and osteocytes at the newly-formed woven bone expressed COL1A1. At the cartilage, most chondrocytes expressed COL2A1 and some hypertrophic chondrocytes COL10A1. In some regions, co-expression of COL1A1 and COL2A1 was observed. At four weeks, such expressions for COL1A1, COL2A1 and COL10A1 became prominent at the area of the fusion mass. From four to six weeks, bone remodelling progressed from the area of the transverse processes towards the central zone. Osteoblasts lining the trabeculae expressed a strong signal for COL1A1. At the central portion of the area of the fusion mass, endochondral ossification progressed and chondrocytes expressed COL2A1 and COL10A1.

Our findings show that the fusion process begins with the synthesis of collagens around the transverse processes and around the grafted bone independently. Various spatial and temporal osteogenic and chondrogenic responses, including intramembranous, endochondral and transchondroid bone formation, progress after bone grafting at the intertransverse processes. Bone formation through cartilage may play an important role in posterolateral spinal fusion.

We studied 23 patients with spondylolysis of the fifth lumbar vertebra (L5) and 20 with spondylolytic spondylolisthesis at this level. All were more than 40 years of age. The transverse processes at L5 were significantly wider in the former group than in the latter. We also dissected 56 cadavers to study the morphological relationship between the transverse process of L5 and the iliolumbar ligament, and found that the wider transverse process is associated with increased width of the posterior band of the iliolumbar ligament.

If a patient with pars defects has wide transverse processes at L5, the lumbosacral junction may be stabilised by wide posterior bands of the iliolumbar ligament and the fifth lumbar vertebra by the ligament, preventing anterior displacement.

We have studied fracture-dislocation of the fifth lumbar vertebra in seven patients and reviewed 50 previously reported cases. Based on this information, we have classified the injury into five types: type 1, unilateral lumbosacral facet-dislocation with or without facet fracture; type 2, bilateral lumbosacral facet-dislocation with or without facet fracture; type 3, unilateral lumbosacral facet-dislocation and contralateral lumbosacral facet fracture; type 4, dislocation of the body of L5 with bilateral fracture of the pars interarticularis; and type 5, dislocation of the body of L5 with fracture of the body and/or pedicle, with or without injury of the lamina and/or facet.

Conservative treatment of fracture-dislocation of L5 is generally not effective because the lesion is fundamentally unstable. Planning of the operation should be made on the basis of the various types of injury.

It has been thought that lumbar intervertebral discs were innervated segmentally. We have previously shown that the L5-L6 intervertebral disc in the rat is innervated bilaterally from the L1 and L2 dorsal root ganglia through the paravertebral sympathetic trunks, but the pathways between the disc and the paravertebral sympathetic trunks were unknown.

We have now studied the spines of 17 rats to elucidate the exact pathways. We examined serial sections of the lumbar spine using immunohistochemistry for calcitonin gene-related peptide, a sensory nerve marker. We showed that these nerve fibres from the intervertebral disc ran through the sinuvertebral nerve into the rami communicantes, not into the corresponding segmental spinal nerve.

In the rat, sensory information from the lumbar intervertebral discs is conducted through rami communicantes. If this innervation pattern applies to man, simple decompression of the corresponding nerve root will not relieve discogenic pain. Anterior interbody fusion, with the denervation of rami communicantes, may be effective for such low back pain.

The afferent pathways of discogenic low-back pain have not been fully investigated. We hypothesised that this pain was transmitted mainly by sympathetic afferent fibres in the L2 nerve root, and in 33 patients we used selective local anaesthesia of this nerve.

Low-back pain disappeared or significantly decreased in all patients after the injection. Needle insertion provoked pain which radiated to the low back in 23 patients and the area of skin hypoalgesia produced included the area of pre-existing pain in all but one. None of the nine patients with related sciatica had relief of that component of their symptoms.

Our findings show that the main afferent pathways of pain from the lower intervertebral discs are through the L2 spinal nerve root, presumably via sympathetic afferents from the sinuvertebral nerves. Discogenic low-back pain should be regarded as a visceral pain in respect of its neural pathways. Infiltration of the L2 nerve is a useful diagnostic test and also has some therapeutic value.

We carried out MRI studies of 74 patients with end-plate and vertebral bone-marrow changes associated with degenerative lumbar disc disease. Abnormalities were classified into type A, with decreased signal intensities, and type B, with increased signal intensities on T1-weighted spin-echo images. Twenty-seven (73%) of the 37 patients with type-A changes had low back pain, in contrast to only four (11%) of the 37 patients with type-B changes. Lateral flexion-extension radiographs showed hypermobility in 26 patients (70%) with type-A changes, and in only six (16%) with type-B changes. Type-A changes correlated with segmental hypermobility and low back pain, while type-B changes were more common in patients with stable degenerative disc disease.

We studied the use of gadolinium diethylenetriaminepentaacetic acid-enhanced MRI in the detection of pathological changes in the nerve roots of 25 patients with unilateral sciatica due to lumbar disc herniation. Enhancement was observed in the affected nerve roots within the root sleeve at the caudal edge of the herniation and was classified into three categories: grade 0, none; grade 1, enhancement restricted to a focal region within the sleeve; and grade 2, diffuse and homogeneous. The grade of enhancement correlated well with the severity of the sciatica, and was considered to be due to a disruption of the blood-nerve barrier, leading to oedema.