A flexed neck posture, especially with prolonged sitting, developed in three quadriplegic patients as a manifestation of posttraumatic syringomyelia (PTS). This posture developed at 1, 6, and 20 years after spinal cord injury. All patients complained of increasing weakness of the neck with several hours of sitting, and all required analgesics for aching neck pain. Neck weakness preceded an ascent of the level of sensory or motor deficit in two patients, and followed it in one. Current muscle testing failed to demonstrate weakness of neck extension in any patients, but electromography revealed chronic denervation and reinervation of cervical paraspinal muscles in each patient. Magnetic resonance imaging revealed a syrinx extending from the site of injury to the medulla oblongata in each case. We conclude that a flexed neck posture can represent: (1) a loss of stamina in denervated head support musculature, (2) either a precursor or successor to the conventional signs of PTS, and (3) high cervical syringomyelia.

A 58-year-old man sustained C4–C5 post-traumatic myelopathy with C3–C4 subluxation, slight compression of C3 vertebral body, C4 spinous process fracture and C6 compression fracture. He subsequently developed syringomyelia from C4 to C6, which was shunted into the subarachnoid space. Postoperatively, there was some but insignificant improvement of his symptoms although a postoperative metrizamide spinal computerised tomography showed compelte drainage of the cyst. This patient died 1 year later. Autopsy examination of the spinal cord showed extensive damage of the posterior half of the cord at C3–C4 but the damage was much less extensive from C4 to C6 (where the syrinx was located), affecting mainly the right dorsal column at C4 and the right dorsal column and right anterior horn at C5–C6. In this patient, the syrinx developed in the partially damaged segments of the cord at the level of the spinal fractures and complete drainage of the cyst was not followed by satisfactory relief of his symptoms.

Ischaemic myelopathy is an infrequent but well-known cause of spinal cord injury. While the overall incidence of neurological injury following thoraco-abdominal aortic surgery is low (1-14%), procedures requiring surgical cross-clamping of the aorta have been reported as the major cause of ischaemic cord injury (31%). Little has been reported regarding the clinical and functional outcomes of these injuries. Three patients with a non-penetrating aortic injury who showed evidence of ischaemic cord injury within 72 hours of surgical cross-clamping of the aorta are presented. Data includes functional assessments, muscle strength testing and electromyographic findings. All three patients showed lower thoracic incomplete motor and sensory spinal cord injuries. These findings suggest that, after a period of neurological improvement, a plateau phase is reached at approximately 3 months post injury after which no significant gain in muscle strength is made. All patients were functionally independent and able to ambulate using a straight cane.

Within a 12-year period, 44 (9.4%) of 466 patients had spinal cord injury complicating cervical spondylosis. A history of alcoholic use preceding the accident was obtained in 12 (54.5%) of 22 patients whose cord injury was due to a minor fall. The initial myelopathy was complete in 10 patients and incomplete in 34. Although neurological recovery was seen in the majority of the patients with incomplete cord lesion, complete recovery was unusual and most of the patients were partly or completely wheelchair dependent. No patient developed acute neurological deterioration after injury but seven expired. The mortality rate was much higher in the patients whose initial cord lesion was complete (50% or 5/10) than in those with incomplete myelopathy (5.9% or 2/34). There was no delayed neurological deterioration due to progressive spondylosis of the spine but three patients developed post-traumatic syringomyelia several months to several years after the injury.

In eleven years, 30 (3.2%) of 951 patients with spinal cord injury developed cervical syringomyelia. This condition was found in 22 (4.5%) of 488 posttraumatic tetraplegic and 8 (1.7%) of 463 posttraumatic paraplegic patients; the incidence was about 8 per cent in patients with complete tetraplegia. This study demonstrated the rarer clinical manifestations of syringomyelia, namely autonomic dysfunction, alterations in the sensory level with postural changes, the early occurrence of tendon areflexia and painless motor deterioration. Prolonged F wave latencies were present in all patients with a demonstrable syrinx and a higher protein content was found in the syrinx than in the cisternal fluid. Some of the symptoms and signs in a proportion of the patients treated conservatively remained stable without operative treatment over a number of years. Most of the patients in whom operation was performed for progressive motor weakness or severe pain had good postoperative results although a few developed late sensory or motor changes. There was no benefit in operating on a patient with a small syrinx.

Within a period of 12 years 466 patients with acute spinal cord injury were admitted to our Centre, seven of these having ankylosing spondylitis (AS). A history of alcohol consumption preceding the accident was present in five patients, and in four there was a history of neurological deterioration before their admission. An epidural hematoma was found in one patient and four expired within 3 months of their injury. The incidence of ankylosing spondylitis in cervical cord injury was 1.5%, and an associated epidural hematoma was present in some 14% of the patients. The mortality rate was 57%. There was a high incidence of alcoholic use before the accident. Neurological deterioration commonly occurred before admission.

A patient sustained C7-C8 incomplete myelopathy with dissociated sensory loss after a whiplash injury. Cervical radiograms showed no fracture or dislocation but separation of the C4-C5 and C5-C6 spinous processes and anterior tilting on C5 on C6 vertebral body only in the head-neck flexed position. Complete sensory and motor recovery occurred after neck immobilization. The patient's transient neurologic deficits were probably caused by vascular insufficiency of an anterior radicular artery at the C5-C6 intervertebral foramen.

The incidence and pathological features of colorectal carcinoma in a population of veterans disabled by myelopathy were examined by record review. Thirteen cases of colorectal carcinoma were found among the 1023 such individuals (99 percent male) who were hospitalized and subsequently followed between April 1, 1973 and September 22, 1983. The age adjusted incidence rates ranged from 316 per 100,000 person years in the sixth decade to 1886 per 100,000 person years in the ninth decade of age. These rates were two to six times the highest reported rates for general male populations (P less than 0.05). The location of carcinoma was proximal to the rectosigmoid colon in 62 percent of the 13 paralyzed patients, but in only 12 percent of 31 nonparalyzed male patients with colorectal carcinoma diagnosed at the same hospital in 1977-1979 (P less than 0.001). The stage of the tumor at diagnosis was Dukes Kirklin C in 83 percent of paralyzed patients and 48 percent of the nonparalyzed patients (P less than 0.001). We conclude that colorectal carcinoma is more common, more proximal in location, and more advanced at diagnosis in male subjects with myelopathy than in nonparalyzed male subjects.

The anterior spinal artery syndrome in three patients is described and from the literature 6o additional patients were collected. Motor recovery in the following groups of patients was noted: (1) Partial loss of motor function and pain sensation—70.4 per cent (19/27); (2) Complete motor loss but partial loss of pain—83.3 per cent (5/6); (3) Paresis but pain sensation absent—66.7 per cent (6/9); and (4) Absent motor function and pain—38.9 per cent (7/18). Motor recovery was also found to vary according to aetiology: (A) Unknown cause— 92.9 per cent (13/14); (B) Post-infection or vaccination—88.9 per cent (8/9); (C) Anterior spinal artery occlusion—33.3 per cent (3/9); (D) Spinal cord angioma—20 per cent (2/10); and (E) Aortic lesion—2o per cent (1/5). Patients with sparing of motor function or pain sensation below the lesion do better than those without both functions. Neurological return also varies with the aetiology of the syndrome.

A patient with ankylosing spondylitis sustained C3-C4 vertebral subluxation and C4-C5 myelopathy after a hyperextension trauma. Autopsy showed that several segments below the main cervical cord lesion at the fractured site, there was a second spinal cord lesion at the T1 vertebral level with no corresponding local bony or ligamentous damage. The thoracic cord lesion was probably secondary to traction of the upper thoracic cord, where the blood supply is poor, in a narrow and rigid spinal canal at the moment of extreme hyperextension.

Five patients with vertebral fracture and spinal epidural hematoma (SEH) are described. Another 58-year-old man developed a post-traumatic SEH without bony damage. From the literature, 38 patients (31 male, 4 female, and 3 unknown) were collected. Ankylosing spondylitis or rheumatoid arthritis was noted in 9 of 12 subjects between 50 and 75 years of age. Two groups of patients were identified: Group 1--16 patients with spinal fracture (aged 23 to 63 years), and Group 2--22 patients without spinal fracture (the age was less than 18 years in 12 subjects). In Group 2, a coagulation defect or spinal epidural vascular malformation resulted in a SEH in 6 patients. The preoperative myelopathy was complete in 3 patients each from Group 1 (23.1%) and Group 2 (16.7%). Of the 31 patients operated upon, 9 of the 13 from Group 1 (69.3%) and 6 of the 18 from Group 2 (33.3%) underwent laminectomy within 1 week after the onset of symptoms. Postoperative neurological return was observed in 38.5% (5 of 13) and 88.9% (16 of 18) of these two groups of patients, respectively. Post-traumatic SEHs, predominant in the male population, are often associated with vertebral disease in elderly patients. In the very young patient, there is usually no fracture/dislocation of the spine. A predisposing lesion may be present when spinal fracture is not evident. The prognosis after surgical intervention is better in patients without spinal fracture than in those with vertebral damage, probably because of less contusion to the spinal cord and the presence of very young subjects in the former group of patients.

Two patients sustained acute anterior spinal cord injury associated with a posteriorly displaced bone fragment and herniated cervical disc. Postmortem examination of both spinal cords showed extensive destruction of the cord at the site of injury with sparing of the posterior portion of the dorsal columns; the anterior spinal artery was patent. We conclude that posttraumatic anterior spinal cord syndrome can be caused by damage to the anterior part of the cord without involvement of the anterior spinal artery.

Thirteen patients with motor complete but sensory incomplete lesions following vertebral and spinal cord injuries are described. Sensory dissociation was present with more impairment of pain than touch or proprioception. The loss of pain sensation was complete in seven patients, but was incomplete in the other six subjects four of whom showed major motor recovery. The major point of interest of this study is to show that patients who retain not only touch but also pain sensation have a definitely better prognosis for neurological recovery.

The postoperative progress of 3 patients with spinal epidural hemorrhage, but without spinal fracture or dislocation, is presented. From the literature, 158 cases were collected of spontaneous spinal epidural hematoma treated surgically. Postoperative return of motor function was noted in 95.3%, 87%, and 45.3% of the patients with incomplete sensorimotor, incomplete sensory but complete motor, and complete sensorimotor lesions, respectively. Complete sensorimotor recovery occurred in 41.9%, 26.1%, and 11.3% of these 3 groups of patients, respectively. Recovery following surgical treatment depends on the severity of neurological deficits before treatment. However, the absence of motor or sensorimotor functions preoperatively does not necessarily indicate a poor prognosis.

Complete motor tetraplegia with incomplete sensory loss was caused by spontaneous epidural bleeding from an arteriovenous malformation in the cervical region. There was a family and personal history of cutaneous hemangioma.