Pain sensitivity as a correlate of clinical status in individuals with chronic low back pain.

STUDY DESIGN: A cross-sectional study of baseline correlates of clinical pain and functional status in consecutive patients being treated for chronic low back pain. OBJECTIVES: To determine if an individual's global pain sensitivity, measured by experimental pain threshold to pressure at various regions of the body, is associated with baseline measures of clinical pain and physical functioning. SUMMARY OF BACKGROUND DATA: Previous studies have demonstrated that in individuals with chronic low back pain, clinical pain and functional status are significantly associated with demographic, structural, and psychosocial factors. However, a large portion of variance remains unexplained. Because pain sensitivity (tenderness) has been shown to occur as a continuum in the population, the authors sought to determine if such sensitivity might be associated with clinical status in chronic low back pain, beyond what is known regarding demographic, structural, and psychosocial factors. METHODS: Forty-five patients with chronic low back pain were assessed for a variety of demographic, structural, and psychosocial factors, which previously have been shown to contribute to clinical status. In addition, all patients underwent testing for pain tolerance and threshold at various areas of the body. RESULTS: Age, degree of structural abnormality observed on magnetic resonance imaging, and depressive symptoms were all significantly correlated with either clinical pain or functional status. Pain sensitivity, the target of this investigation, accounted for significant proportions of variance in functional status and pain, even after controlling for demographic, structural, and psychosocial variables. CONCLUSIONS: These pilot data suggest that an individual's experimental pain threshold (a measure of tenderness) is associated with baseline functional status and pain in cases of chronic low back pain and may represent an important domain warranting further investigation.

A clinical and neuropathologic study of silk suture as an embolic agent for brain arteriovenous malformations.

PURPOSE: To evaluate the safety and efficacy of silk suture as an agent for preoperative embolization of cerebral arteriovenous malformations. METHODS: Clinical and histopathologic results were analyzed in six patients who underwent embolization of cerebral arteriovenous malformations using silk suture in combination with other agents. RESULTS: Three of the patients treated with silk hemorrhaged after embolization, and two of these patients died. Neuropathologic analysis of four patients showed acute perivascular inflammation, sometimes quite severe. CONCLUSIONS: The inflammatory response to silk may explain its effectiveness in producing vascular occlusion. However, a fulminate vasculitis theoretically can predispose to delayed hemorrhage. Other problems with silk include the pressure required to inject the agent and the inability to determine the final site of deposition of the silk. Although other embolic agents may share some of these potential difficulties, we feel that the disadvantages outweigh the advantages of silk as an embolic agent.

Effect of lidocaine after experimental cerebral ischemia induced by air embolism.

To investigate possible approaches to the treatment of neural damage induced by air embolism and other forms of acute cerebral ischemia, somatosensory evoked potentials (SEP's) were measured after cerebral air embolism in the anesthetized cat. Air was introduced into the carotid artery in increments of 0.08 ml until the SEP amplitude was reduced to approximately 10% or less of baseline values. Either a saline or lidocaine infusion was begun 5 minutes after inducing cerebral ischemia. In the saline-treated group, SEP amplitude was reduced to 6.7% +/- 1.6% (mean +/- standard error of the mean) of baseline, with a return to 32.6% +/- 4.7% of baseline over a 2-hour period. In the lidocaine-treated group, SEP amplitude was reduced to 5.9% +/- 1.5%, with a return to 77.3% +/- 6.2% over a 2-hour period. The results suggest that lidocaine administration facilitates the return of neural function after acute cerebral ischemia induced by air embolism.

Updated assessment and current classification of spinal meningeal cysts.

The classification of spinal meningeal cysts (MC's) in the literature is indistinct, confusing, and in certain categories histologically misleading. Based on a series of 22 cases, the authors propose a classification comprising three categories: spinal extradural MC's without spinal nerve root fibers (Type I); spinal extradural MC's with spinal nerve root fibers (Type II); and spinal intradural MC's (Type III). Although water-soluble myelography may disclose a filling defect for all three categories, computerized tomographic myelography (CTM) is essential to reveal communication between the cyst and the subarachnoid space. Communication demonstrated by CTM allows accurate diagnosis of a spinal MC and rules out other mass lesions. Magnetic resonance imaging appears useful as an initial study to identify an intraspinal cystic mass. Final characterization is based on operative inspection and histological examination for all three categories.

Delayed postoperative dural arteriovenous malformations. Report of two cases.

The authors present two cases of dural arteriovenous malformations (AVM's) that developed at the site of previous suboccipital craniectomies. No other cases of delayed postoperative dural AVM's have been reported. Congenital and acquired dural AVM's are discussed, with reference to the similarity between postoperative dural AVM's and traumatic dural AVM's. Embolization is recommended in selected cases where the arterial supply is primarily from the external carotid system.

Reduction of experimental intracranial hypertension by lidocaine.

Previous animal studies in our laboratory revealed that acute cerebral ischemia induced by air embolism is accompanied by a sharp and pronounced rise in both systemic blood pressure and intracranial pressure. To investigate possible approaches to the treatment of severe intracranial hypertension, we produced cerebral air embolism in anesthetized, ventilated cats by the infusion of air into the vertebral artery. Untreated animals consistently experienced severe acute intracranial hypertension. Pretreating the animals with lidocaine greatly attenuated the intracranial hypertension caused by air embolism. Lidocaine given after the injury was also effective in reducing intracranial pressure. Our results suggest that lidocaine may be a useful agent for reducing intracranial hypertension associated with ischemic or traumatic injuries to the brain.

Reactivation of herpesvirus in neurosurgical patients.

The authors are presenting seven patients who had operations between July 1984 and July 1985 and who developed herpes infections postoperatively. Four of the patients developed their infections in a dermatomal distribution that correlated with the nerve roots manipulated at operation. A spectrum of localized herpes reactivation is demonstrated in this series. The use of corticosteroids and other associated variables are discussed. Like reactivation of herpes simplex after trigeminal nerve operation, we believe reactivation of herpes simplex and herpes zoster can occur in operation of the cervical, thoracic, or lumbosacral spine.

Identification of a retained surgical sponge using magnetic resonance imaging.

We report a patient who had a spinal abscess due to a retained surgical sponge. Through the use of magnetic resonance imaging, the sponge was identified. Postoperative foreign body complications are discussed.

Effects of collagenase and chymopapain on spinal nerves and intervertebral discs of cynomolgus monkeys.

In order to test the safety and efficacy of Nucleolysin, a collagenase for intradiscal chemotherapy, laminectomies were performed on the L2-3 intervertebral discs of four groups of three young adult Cynomolgus monkeys. One primate from each group was injected with half the recommended human dose of Nucleolysin, chymopapain, or the same volume of sterile water. The remaining half of the human dose of each drug or equal volume of sterile water was equally divided and placed upon the right L-3 and L-4 nerve roots at their vertebral foramina. The right L-4 nerve root was first compressed for 10 seconds with an aneurysm clip. These procedures were done to simulate inadvertent contact of enzyme with spinal nerves in patients undergoing chemonucleolysis. After 4 weeks of observation, the 12 primates were humanely killed and examined post mortem. The effects of both enzymes were limited to those tissues with which they came in direct contact. Complete digestion of the nucleus pulposus of all enzyme-injected intervertebral discs was observed. Variable portions of the anulus fibrosus (from 2.3% to 57.4%) were also dissolved. Direct contact of Nucleolysin with lumbar nerve roots caused minor perineural reaction and no more intraneural changes than seen in sterile water controls. Chymopapain induced mild to severe perineural skeletal muscle necrosis and fibrosis with perineural arterial lesions as well as a degenerative neuropathy which was more marked in the traumatized nerve. The results of this study suggest that Nucleolysin and chymopapain are approximately equally effective on intervertebral discs, and that Nucleolysin is less injurious to spinal nerve roots and perineural tissue at the doses used.

Selective conventional arteriography and computed tomography with and without contrast infusion: minimal requirements for the assessment of transient ischemic attacks.

The authors report two unusual cases referred for extracranial bypass surgery. These patients presented with symptoms of transient ischemic attacks (TIAs) and demonstrated the necessity of conventional selective angiography and computed tomography (CT), with and without contrast infusion, as part of the preoperative assessment. The authors discuss how digital subtraction angiography alone is inadequate and how CT without contrast enhancement may fail to visualize lesions that may exhibit TIA-like symptoms. In the face of the multiplicity of preoperative tests used to evaluate patients with TIA symptoms, the authors stress the importance of selective conventional angiography and CT with and without contrast administration.

Effect of intravenous lidocaine on experimental spinal cord injury.

A series of experiments was conducted to study the effect of systemic intravenous administration of lidocaine on neurological recovery after acute experimental spinal cord injury in cats. The spinal cord was injured by the rapid inflation of an epidural balloon at T-6. The physiological integrity of the spinal cord ceased within 2 seconds in all animals, as demonstrated by acute disappearance of the somatosensory evoked response (SER). There was essentially no return of the SER in the five untreated animals when monitored for 4 hours post-injury. All of the pathological specimens from these animals revealed severe central cord hemorrhage. Intravenous lidocaine was begun 15 minutes after the injury in five animals. Three of these animals had significant return of the SER. The pathological specimens from the lidocaine-treated animals revealed either mild or moderate central cord hemorrhage. The results of this experiment suggest that systemic lidocaine administration has a significant beneficial effect in the treatment of acute spinal cord injury.

Protective effect of lidocaine in acute cerebral ischemia induced by air embolism.

To investigate possible approaches to the prevention and treatment of neural damage induced by air embolism and other forms of acute cerebral ischemia, a model was used in which cerebral air embolism was produced by infusion of air (0.4 ml) into a vertebral artery of chloralose-anesthetized cats. Neurological function was assessed by measuring cortical somatosensory evoked responses in a group of 10 untreated animals and in a group of eight animals pretreated with intravenous lidocaine (5 mg/kg). In the untreated group, the primary somatosensory amplitude was reduced to 28% +/- 9% (mean +/- standard error) of the value before air embolism, with a return to 60% +/- 8% 1 hour and 73% +/- 12% 2 hours after embolism. In the group pretreated with lidocaine, the primary somatosensory amplitude was reduced to 68% +/- 9% of the value before air embolism, with a return to 92% +/- 3% 1 hour and 97 +/- 2% 2 hours after embolism. Pretreatment with lidocaine also greatly attenuated the acute hypertension and the increase in intracranial pressure following air embolism. These results demonstrate that pretreatment with intravenous lidocaine significantly reduces the neural decrement and increases the recovery of neural function after acute cerebral ischemia induced by air embolism.

Computed tomography of an optic chiasm glioma in an elderly patient.

A 75-year-old white woman, otherwise healthy, developed progressively reduced visual acuity primarily in her left eye over 2 months. A computed tomography scan of the head demonstrated a moderately large, round, circumscribed, benign-appearing suprasellar mass that was enhanced with infusion of contrast medium. At craniotomy, a glioma of the optic chiasm that extended into the left optic nerve was observed.

The cutting-edge microvascular needle. A scanning electron microscopic study.

The authors have compared the vascular endothelial damage caused by blunt-tipped microvascular needles as reported previously with that of sharp cutting-edged needles of comparable size. The same four distinct vascular lesions were found with cutting-edged needles as with the blunt-tipped needles. Even though one experimenter made all of the lesions, and all of the tissue was handled in the same fashion, there was much variation in the extent of the intimal damage. Overall, cutting-edged needles produced slightly less intimal tearing and platelet aggregation than blunt-tipped needles, but the difference was not striking.

Cardiovascular effects of cerebral air embolism.

This study was conducted to determine whether air distributed to the cerebral circulation alone could cause acute cardiovascular dysfunction and thus be a potential mechanism for sudden death following arterial air embolism. Cardiovascular measurements were made in anesthetized, ventilated cats during infusion of air into a vertebral artery. Cerebral air embolism was found to induce an acute hypertensive response accompanied by severe cardiac arrhythmias. Interruption of the autonomic nervous system was found to abolish the cardiac arrhythmias but not to affect significantly the acute hypertensive response following cerebral air embolism. These results suggest that potentially lethal cardiac arrhythmias can occur from air distributed solely to the cerebral circulation, and that these arrhythmias are mediated by the autonomic nervous system. The results also indicate that acute hypertension can occur from cerebral air embolism, but that this response is not solely mediated by the autonomic nervous system.