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M G Fehlings

Publications and source records attributed to M G Fehlings.

At least 55 records · Page 3Linked to original sources
PubMed1998

A review of the pathophysiology of cervical spondylotic myelopathy with insights for potential novel mechanisms drawn from traumatic spinal cord injury.

Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction. Despite advances in diagnosis and surgical treatment, many patients still have severe permanent neurologic deficits caused by this condition. An improved understanding of the pathophysiology of cervical spondylotic myelopathy, particularly at a cellular and molecular level, may allow improved treatments in the future. A detailed review of articles in the literature pertaining to cervical spondylotic myelopathy was supplemented by an analysis of relevant mechanisms of spinal cord injury. The pathologic course of cervical spondylotic myelopathy is characterized by early involvement of the corticospinal tracts and later destruction of anterior horn cells, demyelination of lateral and dorsolateral tracts, and relative preservation of anterior columns. Static and mechanical factors and ischemia are critical to the development of cervical spondylotic myelopathy. Free radical-and cation-mediated cell injury, glutamatergic toxicity, and apoptosis may be of relevance to the pathophysiology of cervical spondylotic myelopathy. To date, research in cervical spondylotic myelopathy has focused exclusively on the role of mechanical factors and ischemia. Fundamental research at a cellular and molecular level, particularly in the areas of glutamatergic toxicity and apoptosis may result in clinically relevant treatments for this condition.

Cervical Vertebrae↗
PubMed1998

Predictors of hospital mortality and mechanical ventilation in patients with cervical spinal cord injury.

PURPOSE: The objective of this study was to identify predictors of death and mechanical ventilation in patients with traumatic cervical spinal cord injury. METHODS: From 1981 to 1994, 72 patients with traumatic cervical spinal cord injury resulting in neurological deficits were identified in this retrospective study. For each patient, neurological and associated injuries, physiological variables, complications, hospital mortality and the need for mechanical ventilation were recorded. Univariate and multivariate logistic regression analyses were done to identify predictors of mortality and the need for mechanical ventilation. RESULTS: Fifteen patients (21%) died in the first three months after injury. Univariate analyses identified age, heart disease, neurological level at C4 and above, GCS < or = 13, forced vital capacity and cough, to be associated with mortality. Multivariate logistic regression identified age (P = 0.01), neurological level (P = 0.03) and GCS (P = 0.05) as independent predictors of mortality. In 41 patients (57%), the lungs were mechanically ventilated. Univariate analyses identified. The following predictors of the need for mechanical ventilation: neurological level at C5 and above, complete cord lesions, copious sputum, pneumonia and lung collapse. Multivariate logistic regression identified copious sputum (P = 0.01) and pneumonia (P = 0.01) as independent predictors of the need for mechanical ventilation. CONCLUSION: Age, neurological level and GCS are independent predictors of mortality in patients with traumatic cervical spinal cord injury. Copious sputum and pneumonia are independent predictors of the need for mechanical ventilation.

Adolescent↗
PubMed1998

Relationship between severity of spinal cord injury and abnormalities in neurogenic cardiovascular control in conscious rats.

Abnormal sympathetic tone after spinal cord injury (SCI) initially results in hypotension and is subsequently associated with autonomic dysreflexia characterized by paroxysmal hypertension and bradycardia in response to noxious or visceral stimuli. To evaluate the effect of a clinically relevant compression model of SCI on cardiovascular control in the early postinjury period, we monitored arterial pressure (AP) and heart rate under control resting conditions and after visceral stimulation (colon distension) in conscious rats for 1 week after clip compression injury of the cord at T5. Rats were randomly allocated into 4 groups (n = 8 each): sham-operated, 20, 35, and 50 g injuries. Only the 50 g injury was associated with significant hypotension (73 +/- 4 mmHg) at 1 day post-SCI when compared to sham-injured rats (91 +/- 3 mmHg). In control rats, colon distention caused a transient pressor response of 16 +/- 3 mmHg and tachycardia. In rats with 20 g 35 g, and 50 g injuries, colon distension 1 day after SCI increased AP by 8 +/- 2, 15 +/- 3, and 21 +/- 1 mmHg, respectively. The hypertensive response correlated with injury severity (r = 0.75; p < 0.0001) and was associated with bradycardia. By 7 days after SCI, only rats with 50 g cord injuries experienced hypertension with reflex bradycardia with visceral stimulation. These data show that dysfunctional cardiovascular control after SCI is correlated with the severity of injury. Mild and moderate compressive SCI result in transient cardiovascular abnormalities which normalize by 1 week. In contrast, more severe injuries are associated with neurogenic hypotension and autonomic dysreflexia.

Animals↗
PubMed1998

Role of group I metabotropic glutamate receptors in traumatic spinal cord white matter injury.

Metabotropic glutamate receptors (mGluRs) participate in glutamate neural transmission, but their role in the pathophysiology of spinal cord injury (SCI) has not been explored. Accordingly, we examined the role of group I mGluRs, which are linked to phospholipase C, in mediating SCI using an in vitro model. A dorsal column segment was isolated from the spinal cord of adult rats, maintained in vitro, and injured by compression for 15 sec with a clip having a 2 g closing force. Under control conditions after SCI, the compound action potential (CAP) amplitude was reduced to 69.1 +/- 5.4% of baseline. Blockade of group I mGluR receptors with MCPG, 4CPG, or AIDA resulted in improved recovery of CAP amplitude (82.2 +/- 2.0%, 86.2 +/- 3.9%, and 86.0 +/- 2.5% of baseline, respectively). The group I/II agonist trans-ACPD and selective group I agonist DHPG exacerbated the posttraumatic reduction of CAP amplitude. The phospholipase C inhibitor U-73122 improved recovery of CAP amplitude after traumatic spinal cord axonal injury. Western blotting and immunocytochemistry demonstrated the presence of mGluR1alpha-immunopositive astrocytes and the absence of mGluR5 in spinal cord white matter. These studies are consistent with the hypothesis that activation of group I mGluR receptors after SCI exacerbates posttraumatic axonal injury through a phospholipase C dependent mechanism. The presence of mGluR1alpha labeling on astrocytes suggests a role for these cells in the pathophysiology of SCI. Additional studies in vivo, are required to further clarify the role of mGluRs in acute traumatic SCI.

Age Factors↗
PubMed1998

Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1-year follow up. Results of the third National Acute Spinal Cord Injury randomized controlled trial.

OBJECT: A randomized double-blind clinical trial was conducted to compare neurological and functional recovery and morbidity and mortality rates 1 year after acute spinal cord injury in patients who had received a standard 24-hour methylprednisolone regimen (24MP) with those in whom an identical MP regimen had been delivered for 48 hours (48MP) or those who had received a 48-hour tirilazad mesylate (48TM) regimen. METHODS: Patients for whom treatment was initiated within 3 hours of injury showed equal neurological and functional recovery in all three treatment groups. Patients for whom treatment was delayed more than 3 hours experienced diminished motor function recovery in the 24MP group, but those in the 48MP group showed greater 1-year motor recovery (recovery scores of 13.7 and 19, respectively, p=0.053). A greater percentage of patients improving three or more neurological grades was also observed in the 48MP group (p=0.073). In general, patients treated with 48TM recovered equally when compared with those who received 24MP treatments. A corresponding recovery in self care and sphincter control was seen but was not statistically significant. Mortality and morbidity rates at 1 year were similar in all groups. CONCLUSIONS: For patients in whom MP therapy is initiated within 3 hours of injury, 24-hour maintenance is appropriate. Patients starting therapy 3 to 8 hours after injury should be maintained on the regimen for 48 hours unless there are complicating medical factors.

Activities of Daily Living↗
PubMed1997

Role of NMDA and non-NMDA ionotropic glutamate receptors in traumatic spinal cord axonal injury.

We examined the role of glutamatergic mechanisms in acute injury to rat spinal cord white matter. Compound action potentials (CAPs) were recorded from isolated dorsal column segments in vitro. Under control conditions (Ringer's solution), the CAPs decreased to 71.4 +/- 2.0% of preinjury values after compression injury with a clip exerting a closing force of 2 g. The combination of the NMDA receptor blocker APV (50 microM) and the AMPA/kainate (KA) receptor blocker CNQX (10 microM) resulted in significantly improved recovery of CAP amplitude postinjury; however, the NMDA receptor antagonist APV alone did not enhance postinjury recovery, and infusion of NMDA (10 microM) did not affect recovery of the CAPs. In contrast, the AMPA/KA receptor blockers NBQX (10 microM) or CNQX (10 microM) significantly enhanced the recovery of CAP amplitude postinjury. The agonists AMPA (100 microM) or KA (100 microM) resulted in significant attenuation of CAP amplitude postinjury. Coapplication of AMPA/KA plus NBQX and CNQX was also associated with improved functional recovery. After incubation with AMPA and KA, Co(2+)-positive glia were visualized in spinal cord white matter. Similar results were seen after compressive injury but not in control cords. Immunohistochemistry and Western blot analysis demonstrated AMPA (GluR4)- and KA (GluR6/7 and KA2)-positive astrocytes in spinal cord white matter. In summary, non-NMDA ionotropic glutamate receptors seem to be involved in the pathophysiology of traumatic spinal cord injury. The presence of AMPA (GluR4) and KA (GluR6/7 and KA2) receptors on periaxonal astrocytes suggests a role for these cells in glutamatergic white matter injury.

Animals↗
PubMed1997

Assessment of a new ultrafiltration blood processing system.

PURPOSE: To report our clinical experience with a new blood processing device which uses ultrafiltration. We assessed safety and efficacy by evaluating: 1 ) the quality and the quantity of intraoperative shed blood processed and reinfused to the patient 2) homologous blood requirements 3) clinical status of the patient post-transfusion. METHODS: With Ethics Committee approval, the ultrafiltration device was used in six consenting patients undergoing major elective spinal surgery. Blood samples for haematology and biochemistry tests were collected from patients post-induction of anaesthesia (baseline), 1 hr and 24 hr post-autotransfusion. Volumes of blood collected and processed, and all autologous and homologous transfusions were recorded. Patients were assessed post-operatively for any adverse effects. RESULTS: Five patients had donated blood preoperatively. One patient required homologous blood products in addition to autologous blood. In two patients, the filtration cartridge became blocked and required changing midprocessing. No patient sustained device-related complications. One patient had postoperative haematuria which resolved spontaneously within two hours. CONCLUSION: The ultrafiltration device was safe and effective in reducing homologous blood requirements in six patients undergoing elective spinal surgery. Further evaluation of the ultrafiltration device will be necessary, especially in view of the blockage of the filtration cartridge.

Blood Transfusion, Autologous↗
PubMed1997

A new model of acute compressive spinal cord injury in vitro.

A novel in vitro method of spinal cord injury was developed to facilitate the study of cellular and molecular mechanisms underlying neural trauma. A 3-cm length of thoracic spinal cord was removed from the adult Wistar rat. A strip of dorsal column and its associated dorsal horn gray matter was excised and pinned in an in vitro recording chamber where it was constantly perfused with oxygenated Ringer's solution at either 25 degrees C or 33 degrees C. Injury was performed by compressing the dorsal column segment in vitro with a modified aneurysm clip (closing force 2.0 g) for 15 s. Microelectrode and sucrose gap recordings were generated to characterize the physiological effects of compressive injury. Longitudinal thin sections of control and injured dorsal column segments were examined by electron microscopy. At 25 degrees C, injured axons were characterized by a significant reduction in amplitude of the compound action potential (CAP) to 76.9 +/- 2.4% (P < 0.0005) and an increase in response latency to 112.5 +/- 2.5% (P <0.005). At 33 degrees C, the effects of injury on the CAP amplitude were accentuated (P< 0.0001). With the K+ channel blocker, 4-AP (1 mM), there was broadening of the CAP of injured axons and a delay in repolarization of the axonal resting membrane potential, suggesting myelin disruption with exposure of paranodal K+ channels. Ultrastructurally, injured dorsal column segments showed considerable axonal and myelin pathology including splaying of the myelin sheath and vesicular degeneration.

4-Aminopyridine↗
PubMed1997

Serial recording of somatosensory and myoelectric motor evoked potentials: role in assessing functional recovery after graded spinal cord injury in the rat.

Accurate functional outcome measures are essential in assessing therapeutic interventions after experimental spinal cord injury (SCI). We examined the hypothesis that serial recording of somatosensory (SSEP) and myoelectric motor evoked potentials (mMEPs) would provide complementary information to standard methods of behavioral analysis in a rat model of SCI and would allow objective discrimination of functional recovery in sensory and motor tracts. Clip compression injury of varying severity (sham, 23 g, 34 g, 56 g) and transections were performed at T1 in adult rats. SSEPs were recorded from the right sensorimotor cortex (SMC) after stimulation of the contralateral hind paw; mMEPs were recorded from the paraspinal, quadriceps, and the tibialis anterior muscles after anodal stimulation of the SMC. The inclined plane and Tarlov techniques were used to assess clinical neurological function. All outcome measures were assessed weekly prior to and up to 6 weeks following injury. Changes in clinical neurological function as assessed by the inclined plane and Tarlov methods varied with increasing injury severity (R = -0.72 and R = -0.73, respectively). SSEP latency was strongly correlated with injury severity (R = 0.92) and with clinical behavioral scores (R = -0.93 for inclined plane). The tibialis anterior mMEP correlated significantly, though weakly, with changes in inclined plane (R = 0.49) and Tarlov scores (R = 0.41). Although the mMEPs were sensitive to the presence of SCI, these recordings did not discriminate between severities of injury. We conclude that serial recording of SSEPs but not myoelectric MEPs correlates closely with the extent and temporal course of clinical neurological recovery after graded SCI in the rat.

Animals↗
PubMed1997

The effect of the sodium channel blocker QX-314 on recovery after acute spinal cord injury.

There is evidence that elevated intracellular sodium ([Na+]i) activity potentiates spinal cord injury (SCI) and the hypoxic/ischemic cell death. In this study, we examined the effect of QX-314, a potent Na+ channel blocker, on recovery after SCI in vivo. QX-314 (2.0 and 10 nmol) or vehicle was microinjected (2 microL) into the injury site 15 min after SCI. Injury was performed by compression of the spinal cord at C7-T1 for 1 min with a modified aneurysm clip exerting a closing force of 35 g. Neurological function was assessed 1 day after injury and weekly thereafter until 6 weeks by the inclined plane method and by the modified Tarlov technique. After 6 weeks of injury, the origin of descending axons at the injury site was determined by retrograde labeling with fluorogold (FG), and a computer-assisted morphometric assessment of the injury site was performed. There was a significant improvement in counts of retrogradely labeled neurons in the red nucleus and rostral ventrolateral medulla (RVLM) in rats treated with either 2 nM (1338 +/- 366 and 28.8 +/- 16) or 10 nM (1390 +/- 511 and 46.3 +/- 31) QX-314 as compared to vehicle (902 +/- 403 and 13.8 +/- 8). There was a trend to increased neuronal counts in the sensorimotor cortex (170.8 +/- 226.8) and vestibular nuclei (1096.2 +/- 970.2) with QX-314 (10 nM) as compared to the vehicle-treated group. There was no significant difference in the extent of neurological recovery between the control and treated groups. Our results suggest that the Na+ channel blocker QX-314 partially preserves the integrity of descending motor axons after SCI. However, in this study, the effects were insufficient to result in sustained improvements in behavioral neurological function.

Anesthetics, Local↗
PubMed1997

Occipital condyle fractures.

OBJECTIVE: Occipital condyle fractures (OCFs) are infrequently recognized. Three recent cases of OCF in our center prompted a review of the incidence, clinical presentation, diagnosis, and treatment of this entity. METHODS: A retrospective review of medical records and radiographic results was performed for 93 of 316 consecutive patients who were victims of trauma, who presented at the Toronto Hospital during a 13-month period, and who had undergone computed tomography of the occiput. RESULTS: A review of the literature regarding OCF revealed that cranial nerve deficits occurred in 31% of the patients with OCFs; of those, the deficits were delayed in 38%. Three new cases of OCF, with neck pain but without cranial nerve deficits, have been reported. The cervical spine x-rays revealed nothing abnormal in 96% of the reported cases. In our retrospective review, asymptomatic OCF was revealed by computed tomography for 1 of the 93 patients. CONCLUSION: OCF is a diagnostic challenge. We suggest that computed tomographic scans of O-C2 be obtained in the following circumstances: presence of lower cranial nerve deficits, associated head injury or basal cranial fracture, or persistent severe neck pain despite normal radiographic results. We propose a new classification system for the management and treatment of OCF based on the stability of the O-C1-C2 joint complex reflected by the presence of displacement of the condyle, computed tomographic or radiographic evidence of O-C1-C2 instability, and magnetic resonance evidence of ligamentous injury. OCFs are divided into the following types: Type 1 (stable), undisplaced fracture; Type 2A (stable), displaced fracture with no ligamentous instability; and Type 2B (unstable), displaced fracture with ligamentous instability.

Aged↗
PubMed1997

Multilevel anterior cervical corpectomy and fibular allograft fusion for cervical myelopathy.

This study was conducted to determine the safety and efficacy of multilevel anterior cervical corpectomy and stabilization using fibular allograft in patients with cervical myelopathy. Thirty-six patients underwent this procedure for cervical myelopathy caused by spondylosis (20 patients), ossified posterior longitudinal ligament (four patients), trauma (one patient), or a combination of lesions (11 patients). The mean age (+/- standard deviation) of the patients was 58 +/- 10 years and 30 of the patients were men. The mean duration of symptoms before surgery was 30 +/- 6 months and 11 patients had undergone previous surgery. Prior to surgery, the mean Nurick grade of the myelopathy was 3.1 +/- 1.4. Seventeen patients also had cervicobrachial pain. Four vertebrae were removed in six patients, three in 19, and two in 11 patients. Instrumentation was used in 15 cases. The operative mortality rate was 3% (one patient) and two patients died 2 months postoperatively. Postoperative complications included early graft displacement requiring reoperation (three patients), transient dysphagia (two patients), cerebrospinal fluid leak treated by lumbar drainage (three patients), myocardial infarction (two patients), and late graft fracture (one patient). One patient developed transient worsening of myelopathy and three developed new, temporary radiculopathies. All patients achieved stable bone union and the mean Nurick grade at an average of 31 +/- 20 months (range 0-79 months) postoperatively was 2.4 +/- 1.6 (p < 0.05, t-test). Cervicobrachial pain improved in 10 (59%) of the 17 patients who had preoperative pain and myelopathy improved at least one grade in 17 patients (47%; p < 0.05). Twenty-six surviving patients (72%) were followed for more than 24 months and stable, osseous union occurred in 97%. These results show that extensive, multilevel anterior decompression and stabilization using fibular allograft can be achieved with a perioperative mortality and major morbidity rate of 22% and with significant improvement in pain and myelopathy.

Aged↗
PubMed1996

Changes in pharmacological sensitivity of the spinal cord to potassium channel blockers following acute spinal cord injury.

In this investigation we studied changes in the pharmacological sensitivity of dorsal column white matter to a variety of K+ channel blockers, including 4-aminopyridine (4-AP), following acute spinal cord injury (SCI) in vitro using a modified aneurysm clip. Compound action potentials (CAPs) were recorded extracellularly with microelectrodes and by the sucrose gap recording technique. With acute trauma, injured axons showed significantly enhanced sensitivity to 4-AP in comparison to uninjured controls as early as 10 min following injury. Microelectrode derived field potential recordings showed a significantly greater increase in a delayed positive component (P2) of the CAP at both 1 and 5 mM 4-AP in injured as compared to noninjured axons. Sucrose gap recordings showed an increase in CAP area and amplitude of injured axons with 1 mM 4-AP at 22 degrees C. The relative improvement in CAP area and amplitude with 4-AP was even more pronounced (P < 0.05) at higher temperatures (37 degrees C). As shown by sucrose gap, 4-AP also caused a delay in repolarization of the CAP and depolarization of the resting membrane potential of acutely injured axons. TEA (0.1 mM and 10 mM), when infused alone and with CsCl (10 mM), produced similar effects on injured and intact axons. In conclusion, the results of this study show an altered sensitivity of the spinal cord to 4-AP following acute SCI. In contrast, TEA and CsCl exhibit no difference in their effects on low frequency axonal conduction between injured and noninjured axons. The data suggest that acute traumatic myelin disruption following SCI causes axonal dysfunction partly due to abnormal activation of 4-AP-sensitive 'fast' K+ channels.

4-Aminopyridine↗
PubMed1996

Mechanisms of secondary injury to spinal cord axons in vitro: role of Na+, Na(+)-K(+)-ATPase, the Na(+)-H+ exchanger, and the Na(+)-Ca2+ exchanger.

There is evidence that intracellular Na+ entry potentiates hypoxic-ischemic cell death by causing cytotoxic cell edema, intracellular acidosis, and gating of Ca2+ entry by reverse activation of the Na(+)-Ca2+ exchanger. In this study, we examined the role of Na+ in mediating traumatic injury to spinal cord axons. Dorsal column segments from adult rats (n = 87) were isolated and maintained in an in vitro recording chamber while being superfused with oxygenated Ringer's solution (95% O2/5% CO2, 25 degrees C). Selected experiments (n = 10) also were done at 33 degrees C. Compound action potentials (CAP) were recorded from microelectrodes. Injury was performed by compression of the dorsal column segment for 15 sec with a modified aneurysm clip exerting a closing force of 2 gm. With injury, the CAP decreased to 72.1 +/- 9.6% of baseline values. Removal of extracellular Na+ and replacement with the impermeant cation N-methyl-D-glucamine enhanced recovery of the CAP to 98.3 +/- 18.3% (p < 0.05) of baseline. The Na+ channel blockers tetrodotoxin and procaine also improved recovery of the CAP to 96.3 +/- 23.7% (p < 0.05) and 82.8 +/- 4.6% (p < 0.05) of baseline values, respectively. In contrast, increasing Na+ permeability with veratridine resulted in greater attenuation of CAP amplitude after 1 hr of trauma (60.1 +/- 8.4%, p < 0.05). Similarly, prevention of extrusion of Na+ from the intracellular compartment by inhibiting the Na(+)-K(+)-ATPase pump with ouabain resulted in greater attenuation of CAP amplitude at 1 hr after trauma (56.7 +/- 3.6%, p < 0.05). The Na(+)-H+ exchange blockers amiloride (100 microM) and harmaline (100 microM) significantly improved recovery after injury to 89.6 +/- 17.0% (p < 0.05) and 85.7 +/- 7.2% (p < 0.05) of baseline, respectively. However, administration of the Na(+)-Ca2+ exchange blockers benzamil (100 or 500 microM) and bepridil (50 microM) was ineffective. In summary, reduction of extracellular Na+ confers neuroprotection after spinal cord injury in vitro. Intracellular sodium rises appear to be mediated by voltage-gated Na+ channels. Blockade of the Na(+)-H+ exchanger also is neuroprotective, possibly by reducing intracellular acidosis. Furthermore, prevention of extrusion of intracellular Na+ by the Na(+)-K(+)-ATPase pump exacerbates the effects of compression trauma. However, reverse operation of the Na(+)-Ca2+ exchanger does not explain the injurious effects of Na+ in traumatically injured CNS white matter.

Animals↗
PubMed1996

Initial stabilization and medical management of acute spinal cord injury.

Despite intensive preventive efforts, acute spinal cord injury remains a significant public health problem. The pathophysiology of this type of injury involves both the primary, or initial, mechanical injury and secondary injury mechanisms such as ischemia, lipid peroxidation and intracellular calcium influx. Initial management includes immobilization of the injured spine, maintenance of the airway, systemic oxygen delivery and treatment of neurogenic shock. All patients with acute spinal cord injury should receive an intravenous bolus of methylprednisolone, 30 mg per kg, within eight hours of injury, followed by an infusion of 5.4 mg per kg per hour for 23 hours. Transfer to a regional acute spinal cord injury unit for definitive management should be accomplished as soon as the patient's condition is stabilized.

Acute Disease↗
PubMed1995

Intradural metastasis mimicking nerve sheath tumor.

STUDY DESIGN: This is a case report. OBJECTIVE: This is an unusual case of a 69 year-old man with metastatic carcinoma to the C8 and T1 intradural roots, with extension through the intervertebral foramen of C7-T1 mimicking a nerve sheath tumor clinically and radiologically. This report reviews the clinical features, radiology, pathology, and pathogenesis of these metastatic lesions. SUMMARY OF BACKGROUND DATA: Nerve sheath tumors are the most common primary spinal tumors. In contrast, metastasis to the spinal nerve roots is very rare. Metastatic tumors may clinically simulate other diseases and, as in this case, a nerve sheath tumor. METHODS: A review and discussion of the case facts are presented. RESULTS: Metastatic carcinoma to C8 and T1 nerve roots was diagnosed intraoperatively during C7-T1 laminectomy and partial tumor debulking. The patient had a satisfactory recovery, with symptomatic relief of painful radiculopathy, but with no improvement in motor strength. CONCLUSION: Metastasis to spinal nerve roots can clinically mimic other diseases. As in this case, the proper diagnosis may be possible only at surgery.

Aged↗
PubMed1995

Use of sensory-evoked potentials recorded from the human occiput for intraoperative physiologic monitoring of the spinal cord.

STUDY DESIGN: This is a report of a prospective case series. OBJECTIVE: The purpose of this study was to determine whether evoked potential activity recorded from occipital scalp electrodes in humans is similar to that recorded in animals, and to evaluate the independence of this activity from the classical somatosensory-evoked potential. SUMMARY OF BACKGROUND DATA: Intraoperative somatosensory-evoked potentials can be of limited usefulness in predicting spinal cord injury because they are transmitted primarily through the dorsal columns, and therefore do not reflect integrity of important ventral pathways. It recently has been shown in animal studies that a sensory-evoked potential recorded from the cerebellum is mediated via ventral tracts and is useful as an adjunct to the somatosensory-evoked potential in spinal cord monitoring. METHODS: Twenty-five patients undergoing spinal or posterior fossa surgery were consecutively entered into the study. Evoked responses were recorded transcranially from over the cerebellar hemispheres and from the vertex. Recordings were made directly from the surface of the cerebellar hemispheres in seven of these patients. RESULTS: Waveforms could be recorded and reproduced in all but one of the patients. The overall appearance of the occipital recordings was similar to the appearance of responses obtained in animals. The mean latency of the first negative peak recorded from the ipsilateral occiput was 33.0 msec (standard deviation, 3.7 msec) compared with 52.4 msec (standard deviation, 6.1 msec) for the somatosensory-evoked potential. In addition, the amplitude of this response (0.35 microV; standard deviation, 0.20 microV) was independent of the amplitude of the somatosensory-evoked potential (0.76 microV; standard deviation, 0.69 microV). In five cases, one evoked potential could be recorded in the absence of the other. Recordings from the surface of the cerebellum were of the same morphology, but of greater amplitude than the transcranial recordings. CONCLUSION: Evoked responses can be reliably recorded from over the occiput and show characteristics independent of the classical somatosensory-evoked potential. These responses are very similar to the cerebellar-evoked potential recently characterized in animals and may provide a method for assessing the physiologic integrity of the ventral tracts of the spinal cord in humans.

Animals↗