Spinal Cord Monitoring
Cor J. Kalkman, MD PhD,
The incidence and etiology of postoperative (iatrogenic) spinal cord injury varies with the type of surgery. With neurosurgical removal of intramedullary tumors the lesion typically involves direct mechanical damage to long tract axons. In contrast, after resection of thoraco-abdominal aortic aneurysms there is a high incidence of ischemic spinal cord injury, caused by temporary cross-clamping or permanent interruption of spinal cord blood supply. In particular the anterior horn motor neurons and the spinal motoneuronal system are extremely vulnerable to ischemia. When the aorta is simply cross-clamped and replaced without adjuncts to protect the spinal cord, there is a sigmoid relationship between duration of thoracic aortic cross-clamping and the probability of spinal cord injury. If the time of aortic clamping is less than 30 minutes, the risk of postoperative neurological deficits appears to be small. The probability of paraplegia increases linearly between 30 and 60 minutes of ischemia, to almost 90% after one hour of thoracic occlusion.1 After spine surgery, such as correction of scoliosis, spinal cord injury occurs in 1-2% of cases. Here the injury is probably a combination of mechanical factors and reduced perfusion pressure, for example when instrumentation (laminar hooks, screws or wires) impinges on the cord in combination with low blood pressure. Spinal cord monitoring is based on the premise that rapid detection of spinal cord conduction failure and immediate institution of corrective measures can prevent irreversible ischemic spinal cord injury resulting in paraplegia. These measures may vary from simply increasing blood pressure, to removal of instrumentation (spine surgery), reattachment of segmental arteries in the aortic graft, or refraining from further resection in case of a spinal cord tumor.
The first modality that became available for use in the operating room in the early 80s was monitoring of somatosensory evoked potentials (SSEP). After stimulation of the posterior tibial nerve the ascending signal is conducted non-synaptically via the dorsal columns to the thalamus and then (synaptically) to the somatosensory cortex. SSEPs can be recorded either from the spinal cord (epidural electrodes) or from the scalp. Signal averaging techniques are needed to extract the small evoked signal (0.5-3 µV) from the EEG and background noise; in the operating room typically 200-300 trials are necessary. The SSEP reflects the functional status of the sensory tracts which are mainly located in the dorsal columns. There is a large number of cases series describing the use of this technique for the surgical procedures mentioned above. (refs?). Nuwer et al. (ref 1995) estimated the impact of SSEP monitoring on outcome based on a survey among 173 US spinal surgeons (97.000 cases), of which 153 (88%) used SSEP monitoring. There was a clear relationship between the experience of the team with SSEP monitoring and outcome: experienced teams (>300 cases) had less than half the rate of neurological deficit than those with < 100 cases (>1%). SSEPs accurately predicted 90% of instances of spinal cord compromise during spinal surgery and may have reduced the incidence of permanent neurologic injury by more than 50%. There have been no randomized controlled trials of spinal cord monitoring. Predictably, the major limitation of SSEP is the relative insensitivity to spinal cord ischemia, especially when confined to the anterior part of the cord (anterior spinal artery territory). Therefore, when only SSEP are monitored, ischemia limited to the motor tracts or anterior horn may go undetected, which makes SSEP less suitable for assessment of spinal cord function during procedures where the main mechanism of injury is spinal cord ischemia (thoracic aortic procedures).
Motor evoked potentials Thoraco-abdominal aortic surgery is associated with a high incidence of postoperative paraplegia (10-30%) resulting from temporary interruption of spinal cord blood flow (SCBF) during aortic cross-clamping and permanent alteration of the anatomy of the spinal cord blood supply. A single transcranial electrical or magnetic stimulus applied the motor cortex results in descending volleys in the the cortical spinal tract that can be recorded from an epidural electrode. Large amplitude muscle response are recordable from surface electrodes, provided that the motor neuron pool is sufficiently excitable. As many anesthetics enhance GABA-currents and induce neuronal hyperpolarization, it may be necessary to apply a series of transcranial stimuli in quick succession (e.g. a ‘train’ of 5 pulses, separated by 2 msec) to elicit an action potential. In this way, temporal summation of excitatory postsynaptic potentials allows the hyperpolarized neuron to reach firing threshold.
Because the transcranial motor evoked potential (MEP) recorded from muscle traverses the spinal motorneuron pool in the anterior horn, it is extremely sensitive to an acute reduction of spinal cord blood flow. Experimental and clinical data indicate that myogenic transcranial motor evoked potentials (tc-MEP) disappear within 1-2 minutes after the onset of acute ischemia (residual flow < 25%)[ref]. This technique is sufficiently rapid to allow timely interventions aimed at correcting ischemic conditions and restoration of spinal cord blood flow. In contrast, EP modalities that rely on axonal conduction such as SSEP may require 15 min or more for a significant change after the onset of ischemia. This rapid response time allowed us to devise a surgical protocol in which key decisions during repair of complex thoraco-abdominal aneurysms are based on tc-MEP responses. A.) To maintain spinal cord perfusion during high cross-clamping a system of distal perfusion is used (left atrium to femoral artery bypass). Proximal and distal blood pressures as well as bypass flow are adjusted to maintain tc-MEP at baseline values. In general a distal pressure of 60 mmHg will allow sufficient SCBF to maintain tc-MEPs, but in some patients distal pressures as high as 100 mmHg may be needed. B.) When during staged cross-clamping the tc-MEP signal disappears, critical segmental vessels originate from the excluded segment. An aggressive approach is then used to identify vessels that are either anastomosed directly to the graft or attached via Dacron tube grafts. Finally, the optimal perfusion pressure for the postoperative period is determined based on the pressure/MEP relationship during closure. The experiences during 170 TAAA procedures will be presented. The paraplegia rate was 2.3%. All cases of paraplegia were detected by tc-MEP, but resulted from subsequent inability to revert the ischemia (distal aortic dissection, late thrombosis of attached intercostal vessels). Ther ehave been no randomized trials of MEP monitoring
The recording of MEP signals directly from the pyramidal tracts using epidural electrodes above and below the site of neurosurgical intervention has been shown to be useful during resection of spinal cord tumors. The amplitude of the initial epidural “D-wave” is directly proportional to the number of conductiong axons. Therefore any amplitude decrease signals potential loss of descending tract function.(ref: Deletis)
The success of intraoperative monitoring is critically dependent on anesthetic management. A key issue is that – by nature – almost all anesthetic drugs depress synaptic function both in the cerebral cortex and in the spinal cord grey matter. As a result, progressively increasing concentrations of inhaled or intravenous anesthetics may result in EP changes that are indistinguishable from neuronal ischemia. The goal is to achieve and maintain an anesthetic state that is both appropriate for the patient and the surgical procedure, and that will allow continuous evaluation of neurophysiological activity starting with baseline (anesthetized) values of sufficient amplitude and spectral content. Fluctuations in amplitude or frequency content as a result of changes in anesthetic depth may result in false positive findings. Techniques that maintain constant plasma and CNS concentrations (continuous or target-driven infusions) are therefore preferable to repeated bolus regimens.
For spinal cord monitoring with somatosensory or motor evoked potentials, the margins are quite narrow. While spinal and subcortical responses are relatively resistant to depression by anesthetic drugs, cortical responses are sensitive to volatile agents, and a standard isoflurane/N2O technique may depress amplitudes to such an extent that reliable monitoring becomes impossible. Some authors advocate to use low concentrations of a volatile agent and to eliminate nitrous oxide. Somatosensory evoked potentials can be consistently recorded during total intravenous anesthetic techniques, including propofol/opioid/air, etomidate/opioid, ketamine/midazolam. Neuromuscular blockade improves the signal-to-noise ratio of intraoperative SSEP by removing EMG interference. In contrast, the intraoperative recording of myogenic responses to electrical or magnetic transcranial stimulation is the most demanding in terms of anesthetic management. Unfortunately, propofol, nitrous oxide and inhaled agents all considerably suppress motor transmission, and if neuromuscular blockade can not be omitted it should be tightly controlled. ‘Neurogenic’ MEP (spinal cord stimulation, peripheral nerve recording) are not influenced by high concentrations of inhaled agents (ref) but there is evidence that in the presence of high concentrations of inhaled agents the remaining signal represents non-synaptic retrograde conduction in sensory pathways. The availability of commercial ‘multi-pulse’ stimulators has greatly improved the feasibility of intraoperative monitoring of myogenic transcranial MEP. Anesthetic techniques that are currently used clinically include opioid/ N2O, opioid, ketamine and total intravenous anesthesia using low dose propofol and an opioid. In particular, the very short acting new opioid remifentanil allows the use of higher opioid doses and lower concentrations of hypnotic. This improves EP amplitudes while still allowing rapid wake-up when needed. A special case arises when – despite all these precautions - during a critical monitoring episode, there are signs that the level anesthesia is inadequate. In that situation it is preferable to administer additional opioid, low dose ketamine or an alpha2-agonist such as clonidine, rather than to increase the inhaled concentration or to administer a bolus dose of propofol.