Acute Cervical Cord Research Articles

Acute central cervical cord injury presenting with only upper extremity involvement.

Twenty-four patients with acute central cervical cord injury with motor and sensory impairment involving only the upper extremities are described; none had any abnormality in the lower extremities. They were all treated conservatively with one exception in whom an anterior decompression was performed. Seventeen had complete recovery of motor function; the remaining 7 had some weakness of the palmar interosseous muscles. The time to recovery was from 2 weeks to 4 months. Sensory recovery took from 4 to 6 months after injury. This type of injury is caused by damage to the anterior and posterior horn cells in the cervical cord.

Hemodynamic Parameters in Patients with Acute Cervical Cord Trauma

The cardiovascular response of the patient with acute spinal cord injury (SCI) is known to be altered secondary to the cord injury. Our current protocol of managing the acute phase of patients with SCI includes invasive hemodynamic monitoring (with arterial line and Swan-Ganz catheter) and support with fluids and dopamine and/or dobutamine, titrated to maintain a hemodynamic profile with adequate cardiac output (to be determined by oxygen consumption and delivery) and a mean blood pressure of > 90 mm Hg. We feel that this protocol provides two benefits: 1) maintaining the mean blood pressure improves the morbidity of these patients by deterring ischemia and accompanying secondary insults; 2) aggressive monitoring and hemodynamic intervention help stabilize the hemodynamic status of these patients and make it possible to consider early surgery in selected cases. Our hypothesis is that the pulmonary vascular bed is more sensitive to the sympathectomized effect of acute complete cervical SCI. We analyzed the demographic, neurologic, and hemodynamic data of 50 consecutive patients during their first week postinjury. All had signs of myelopathy; 31 (62%) were considered clinically complete. Of the 50 patients, 9 (18%) died, 20 did not improve functionally, and 21 improved. The mean heart rate (82.1 +/- 13.3), blood pressure (94.4 +/- 9.4), pulmonary artery pressure (22 +/- 5) and wedge (12.7 +/- 3.4), cardiac index (4.5 +/- 0.9), systemic vascular resistance index (SVRI) (1637 +/- 399), pulmonary vascular resistance index (PVRI) (181 +/- 80), and oxygen transport (694 +/- 156) showed good response to the treatment. Because the measurements were obtained during treatment, they differ from the expected "classic sympathectomized" response, but they provide a database for further analysis of hemodynamic manipulation in SCI. An analysis of the hemodynamic parameters did not differentiate between complete and incomplete lesions or between patients with functional improvement. We determined, on the basis of the initial hemodynamic measurements, that no patient with a clinically complete motor deficit (Frankel Grade A+B) improved of the 10 who had measurements compatible with either: 1) PVRI < 100 with SVRI < 1200; or 2) PVRI < 115 with SVRI < 1300 or PVR/SVR ratio of < 0.08 when SVRI was < 1600. These patients could not have other measurements that showed low SVRI < 1350 with PVRI > 139. At odds with this unique group, 13 of 29 patients with the same clinical picture and without the above physiological criteria of severe hemodynamic deficit eventually improved (P < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Hemodynamic Parameters in Patients with Acute Cervical Cord Trauma

The cardiovascular response of the patient with acute spinal cord injury (SCI) is known to be altered secondary to the cord injury. Our current protocol of managing the acute phase of patients with SCI includes invasive hemodynamic monitoring (with arterial line and Swan-Ganz catheter) and support with fluids and dopamine and/or dobutamine, titrated to maintain a hemodynamic profile with adequate cardiac output (to be determined by oxygen consumption and delivery) and a mean blood pressure of > 90 mm Hg. We feel that this protocol provides two benefits: 1) maintaining the mean blood pressure improves the morbidity of these patients by deterring ischemia and accompanying secondary insults; 2) aggressive monitoring and hemodynamic intervention help stabilize the hemodynamic status of these patients and make it possible to consider early surgery in selected cases. Our hypothesis is that the pulmonary vascular bed is more sensitive to the sympathectomized effect of acute complete cervical SCI. We analyzed the demographic, neurologic, and hemodynamic data of 50 consecutive patients during their first week postinjury. All had signs of myelopathy; 31 (62%) were considered clinically complete. Of the 50 patients, 9 (18%) died, 20 did not improve functionally, and 21 improved. The mean heart rate (82.1 +/- 13.3), blood pressure (94.4 +/- 9.4), pulmonary artery pressure (22 +/- 5) and wedge (12.7 +/- 3.4), cardiac index (4.5 +/- 0.9), systemic vascular resistance index (SVRI) (1637 +/- 399), pulmonary vascular resistance index (PVRI) (181 +/- 80), and oxygen transport (694 +/- 156) showed good response to the treatment. Because the measurements were obtained during treatment, they differ from the expected "classic sympathectomized" response, but they provide a database for further analysis of hemodynamic manipulation in SCI. An analysis of the hemodynamic parameters did not differentiate between complete and incomplete lesions or between patients with functional improvement. We determined, on the basis of the initial hemodynamic measurements, that no patient with a clinically complete motor deficit (Frankel Grade A+B) improved of the 10 who had measurements compatible with either: 1) PVRI < 100 with SVRI < 1200; or 2) PVRI < 115 with SVRI < 1300 or PVR/SVR ratio of < 0.08 when SVRI was < 1600. These patients could not have other measurements that showed low SVRI < 1350 with PVRI > 139. At odds with this unique group, 13 of 29 patients with the same clinical picture and without the above physiological criteria of severe hemodynamic deficit eventually improved (P < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Electrophysiologic changes in lumbar spinal cord after cervical cord injury.

Spontaneous activity on the EMG examination is traditionally ascribed to disease of the lower motor neuron when present in muscles well below the level of para- or quadriplegia despite the absence of any detectable peripheral nerve injury. It is uncertain whether it reflects transient paralysis of transmission (related to clinical spinal shock) or irreversible postsynaptic damage. We performed serial EMG studies of lower extremities and paraspinal muscles on eight young, previously healthy adults, commencing 2 to 9 weeks after acute cervical cord injury. All had stimulated single-fiber EMG (SFEMG) studies at 6-month intervals to determine whether irreversible postsynaptic damage of the anterior horn cell had occurred. MRI and nerve conduction excluded patients with evidence of distal cord injury or peripheral neuropathy. All patients had spontaneous activity in all muscles tested, persisting after spinal shock had resolved. Jitter was present on SFEMG in three of eight patients 6 months after injury. Four of five patients retested 12 months after injury had abnormal jitter, including three who initially had normal SFEMG studies. We conclude that there is electrophysiologic evidence of trans-synaptic distal cord dysfunction following acute spinal cord injury. SFEMG studies suggest that anterior horn cell dropout occurs during the 1st year after injury.

急性期頚髄損傷のＭＲＩ所見

Magnetic resonance imaging (MRI) was performed on 18 patients with acute cervical cord injury using T2-weighted images of a 1.0-T magnet. Three different types of MRI signal patterns were detected in association with these cervical cord injuries. A classification was developed using these three patterns. Type I, seen in six patients, demonstrated a low signal intensity consistent with acute intraspinal hemorrhage. Type II, seen in seven patients, demonstrated a high signal intensity consistent with acute cord edema. Thpe III, seen in five patients, demonstrated no abnormal signal intensity. Type I patterns showed complete quadriplegia except for one and no improvement in their Frankel classification. In comparison, Type II and III patterns improved at least one Frankel classification. MR at 1.0T in extremely useful in the diagnosis of acute cord injury and also demonstrates potential in predicting neurologic recovery.

Myelotomy for Acute Cervical Cord Injury

Four cases of acute cervical cord injury treated by posterior midline myelotomy are described. The initial neurological examinations of these four patients indicated complete cord lesions. On plain neck X-rays, two exhibited anterior dislocation and two showed no bony injury other than ossification of the posterior longitudinal ligament. Myelography via C1/2 lateral puncture showed complete block of the subarachnoid space in two cases, and incomplete block in the other two. Computed tomographic myelography revealed cord swelling in all cases. Posterior midline myelotomy was performed after administration of a steroid and mannitol, or reduction of spinal dislocation. The time from injury to myelotomy ranged from 5 to 21 hours. No patient developed new deficits postoperatively. During long-term follow-up, which ranged from 10 to 19 months, all patients showed improvement in motor function of the upper extremities. Sensory disturbances also diminished to some degree. However, in one patient, who underwent myelotomy 18 hours after injury and had shown progressive neurological deterioration before surgery, the improvement in motor function was only slight. In this case, earlier myelotomy may have been more beneficial. These results support the indication for myelotomy in cases of acute cervical cord injury with cord swelling. Particularly if performed early, this procedure is effective in preventing secondary neurological damage.

Preoperative determination of the level of spinal cord lesions from the killed end potential

To determine preoperatively the level of lesions in acute cervical cord injury, the killed end potential of the spinal cord was recorded with a pair of electrodes placed in the spinal epidural space, one initially being placed rostrally to the lesions for obtaining recordings and the other placed caudally to the lesions for stimulation. The level associated with the largest killed end potential was clearly determined without much difficulty, with sequential recordings on stepwise withdrawal of the recording electrode, in four of five cases investigated. In two cases subjected to surgery, the recording electrode left in place at the level associated with the largest killed end potential was found to be located at, or a few millimeters below, the center of the lesions. This demonstrates the preoperative localizing value of the killed end potential for determining the level of lesions responsible for myelopathy.

Effect of omeprazole on acute gastric stress ulceration in cervical cord transected rats.

Patients with acute paraplegia from trauma have an increased frequency of developing gastric stress ulceration and subsequent hemorrhage. Current treatment of gastric stress ulcer is by antacids or H2 antagonists, but despite such therapy stress ulceration still occurs, probably because these agents are unable to maintain gastric pH above 4. Omeprazole, which blocks the terminal step of acid secretion--the proton pump, can produce long-lasting achlorhydria. This study examined the efficacy of omeprazole in preventing stress ulcer in rats with acute cervical cord transection. Omeprazole was administered intraduodenally at 1.725, 2.625, 3.5, and 17.5 mg/kg, and the ulcer incidence and gastric acid output were measured. Omeprazole produced a dose-dependent inhibition of gastric acid output in the cervical cord transected rat. At the highest dose, complete achlorhydria was achieved. The quantity of gastric ulceration was inversely proportional to the omeprazole dosage with nearly complete prevention of ulceration at the highest dose. In conclusion, omeprazole is very effective in preventing gastric stress ulcers in the spinal cord transected rat. This appears to be related to its potent long-lasting inhibitory effect on gastric acidity.

観血的治療を施行した頚椎・頚髄損傷例の術後合併症について 中・下位頚椎損傷例における

We studied the complications of surgical treatment for acute cervical cord injuries. 193 patients were operated on within one month after the injuries. Operation was performed under general anesthesia. 74 patients sufferd from complete lesion, 29 motor complete and sensory incomplete, 73 incomplete lesion. 17 patients were normal neural status.One patient deteriorated neurologically after the operation, but her paralysis was two segments above the bony damage before the operation. 6 patients died within three months after the operation. But the causes of death did not relate to the operative intervention. 5 patients failed in bone grafts and were reoperated. Respiratory problem, needed prolonged intubation or tracheostomy, existed in thirty patients. 15 suffered from intestinal bleeding.Surgical treatment for acute cervical cord injuries requires attention to the general status after paralysis. Early decompression and rigid fixation gives good condition to paralysed patients.

Acute central cervical cord syndrome caused by minor trauma

tests for bacteria which grow aerobically. Villanova: National Committee for Clinical Laboratory Standards, 1983:1-11 12. Wehrli W. Rifampin: mechanisms of action and resistance. Rev Infect Dis 1983;5:$407-11 13. The Meningococcal Disease Surveillance Group. Analysis of endemic meningoeoccal disease by serogroup and evaluation of chemoprophylaxis. J Infect Dis 1976;134:201-4 14. Khuri-Bulos N. Meningococcal meningitis following rifampin prophylaxis. Am J Dis Child 1973;126:689-91

Cervical cord injury : Irwin J., Abbot R. J., Burt A. A. and Harriman D. (1985) Brain stem signs in acute cervical cord trauma. Paraplegia23, 82

Cervical cord injury : Irwin J., Abbot R. J., Burt A. A. and Harriman D. (1985) Brain stem signs in acute cervical cord trauma. Paraplegia23, 82

Brain stem signs in acute cervical cord trauma

Four cases are reported which illustrate mechanisms by which patients with cervical cord trauma may develop signs of acute brain stem damage. Two patients suffered vertebro-basilar ischaemia as a result of trauma to the vertebral arteries. The remaining two patients developed cavitating lesions within the cervical cord which later dissected rostrally into the brain stem.

Disorder of Serum Electrolyte Concentrations in acute Cervical Spinal Cord Injuries

It is important to grasp sufficiently general and neurological findings in acute cervical cord injuries. In rare cases, It is difficult to grasp exact neurological findings due to disorder of serum electrolyte concentrations. To take an accurate neurological findings, it is necessary to improve serum electrolyte disorder. We examined serum sodium concentration in 85 patients of acute cervical spinal cord injuries. In one case, we could not take accurate neurological findings at the emergency room, probably because of serum electrolyte disorder.

Gastric hypersecretion by intracisteral TRH: Dissociation from hypophysiotropic activity and role of central catecholamine

Y. TACHÉ, D. LESIEGE, W. VALE and R. COLLU, Gastric hypersecretion by intracisternal TRH: dissociation from hypophysiotropic activity and role of central catecholamine, European J. Pharmacol. 107 (1985) 149–155. Intracisternal injection of the TRH analogs, MK 771 (0.01-1 μg) or A 3475 [pGlu-His-(1,3'-dicarboxymethyl)-Pro-NH 2] (0.1-1 μg), dose-dependently stimulated gastric acid secretion in pylorus-ligated rats although A 43475 was devoid of TSH-releasing activity by cultured anterior pituitary cells. Depletion of brain catecholamine by combined administration of the neurotoxic agent, 6-hydroxydopamine, and the catecholamine synthesis inhibitor, α-methyl-ptyrosine, completely abolished intracisternal TRH-induced stimulation of gastric secretion. Blockade of dopamine receptors by intracisternal haloperidol, peripheral depletion of catecholamine by chronic treatment with guanethidine combined with acute adrenalectomy or cervical cord transection at C5 level, did not modify gastric response to TRH. These results suggested that the stimulation of gastric secretion by intracisternal TRH is unrelated to its hypophysiotropic activity and required the integrity of central but not peripheral catecholaminergic system.

Cervical cord injury : Redmund J., Thompson A. and Hutchinson M. (1983) Acute central cervical cord injury due to disco dancing. Br. Med. J.286, 1704

Cervical cord injury : Redmund J., Thompson A. and Hutchinson M. (1983) Acute central cervical cord injury due to disco dancing. Br. Med. J.286, 1704

Points: Acute central cervical cord injury due to disco dancing

Points: Acute central cervical cord injury due to disco dancing

高位けい髄損傷の治療経験

高位けい髄損傷の治療経験

Pulmonary function in acute cervical cord injury.

Measurements of pulmonary function were made on patients within 1 wk, 3 wk, 5 wk, 3 months, and 5 months of spinal cord injury. In patients with functionally complete transection of the cord between segment C5 and C6, the vital capacity was 30% of predicted in the first week after injury. Patients with injuries at C4 had smaller vital capacities. A significant increase in vital capacity occurred within 5 wk of injury with an approximate doubling of vital capacity 3 months after injury. Expiratory flow rates were directly dependent upon vital capacity. There was a high incidence of arterial hypoxemia, in the acute stage, even in patients with adequate ventilatory ability and normocarbia.

Management of neurogenic bladder dysfunctions following acute traumatic cervical central cord syndrome (incomplete tetraplegia) [proceedings

Based on the experience to date with central cord syndrome, most or all of the following conditions should be present before considering transurethral sphincterotomy: (1) minimal neurological recovery within 6 months of injury; (2) four plus spasticity in patients over the age of 50 years; (3) prolonged intermittent catheterisation over 6 months, with persistent residual urine over 300 ml; (4) persistent and repeated use of diazepam, dantrolene sodium to control pelvic floor spasticity; (5) demonstrable detrusor-sphincter dyssynergia.

Programmed management of acute cervical cord trauma

Results in ten patients admitted with the diagnosis of complete traumatic quadriplegia and with fracture-dislocation of the cervical spine are reviewed. Emphasis is placed on aggressive emergency surgical treatment of these lesions such as tracheostomy, laminectomy and cord cooling, incorporated into a detailed protocol of overall management.