Acute spinal cord transection causes spinal shock that is characterized by complete paralysis, hyporeflexia, loss of sensation, and muscle hypotonia caudal to the lesion. Spinal cord injury (SCI) disrupts or disinhibits the suprasegmental influence over segmental interneurons mediating presynaptic inhibition. The hyporeflexia associated with spinal shock may be due to an increase in the efficacy of presynaptic inhibition [12]. Over time, presynaptic activity decreases, resulting in enhanced spinal reflexes [13]. Observations in cats indicate that rostral acute SCI causes postsynaptic caudal lumbar motor neuron changes. In cats, rostral acute SCI causes hyperpolarization of caudal lumbar segment motor neurons [14–17]. Immediately following rostral spinal cord transection, the monosynaptic reflexes from the medial and lateral gastrocnemius, soleus, posterior biceps, and semitendinous muscles are reduced in amplitude or completely absent. During the 6 h following transection there is some recovery of reflex activity [18]. When using cold as a model for acute reversible spinal cord transection, hyperpolarization of caudal motor neurons occurs within 30 s and monosynaptic reflex amplitudes are gradually decreased. These changes persist during the application of cold. Rewarming restores reflex amplitudes to original values in 30 s, and the resting motor neuron membrane potential back to the original value in 1 min [14–16].

The hyperpolarization of motor neurons following spinal cord transection or cooling is thought to be secondary to decreased suprasegmental facilitation of motor neurons, which usually keeps them in a slightly hypopolarized state [14–17]. Fusimotor drive is also depressed early after acute spinal cord injury, for gamma motor neurons are also hyperpolarized [19]. H-reflexes and F-responses reflect the level of excitation of a large percentage of the motor neuron pool in the spinal cord gray matter [20, 21]. These recordings may be very helpful in detecting intraoperative spinal cord ischemic insults, since the level of gray matter excitability is depressed more with ischemia than is posterior column function. In animals the dorsal horn potential that is generated by postsynaptic gray matter activity disappears within 3–5 min after cessation of spinal cord perfusion. Posterior column potentials persist for 12–15 min [22].

Changes in spinal cord electrophysiologic signal processing can be used to help understand the electrophysiologic mechanisms occurring during acute SCI [23]. Changes in serial, parallel, and oscillatory processing, hyperpolarization, inhibition, and disinhibition may be observed.

Spinal nerve roots are more susceptible to injury than are peripheral nerves [24]. Spinal nerve roots are susceptible to injury by two mechanisms. The first is that proximally the dorsal and ventral roots split into rootlets and minirootlets [25]. The area where this split occurs is the central-peripheral transitional region, which is the point where the nerve root is more susceptible to mechanical injury. The axons at this point are enclosed by a thin root sheath, cerebrospinal fluid and meninges, and lack the protective covering of epineurium and perineurium that is present in peripheral nerve [26]. The second mechanism of injury is that there is an area of hypovascularity at the junction of the proximal and middle one-third of the dorsal and ventral roots. This is the point of anastomosis between the central vasa corona and peripheral segmental vessels. At this point, the nerve roots are more susceptible to mechanical injury [25].

The relationship between compression and traction forces on nerve conduction is well described in peripheral nerves and nerve roots [24, 27, 28]. The conduction abnormalities are coupled to the perfusion of the nerve root [24, 28]. A 3-mm retraction distance (pressure around 70 g/cm²) caused the intraneural blood flow to decrease to 20 % of initial value [28]. If nerve root dysfunction is recognized in the reversible phase, permanent injury can be avoided. Compression and traction may produce a mechanical effect on the nerve tissue in addition to compromising the blood supply to the nerve. Physiologic block is the first sign of nerve dysfunction and can be reversed in seconds.

When more axons in the nerve are blocked, the latency of the averaged nerve action potentials may increase and the amplitude may decrease. A more intense or prolonged compression or traction may produce myelin deformation at the edges of compression and prolongation of the nerve action potential latencies [28]. Further mechanical loading may produce a conduction block from segmental demyelination with reductions in action potential amplitudes. With injury, reversible functional changes precede more severe morphologic nerve changes such as neurapraxia (segmental demyelination) and axonotmesis (Wallerian degeneration). Although both these morphologic changes may be reversible in weeks to months, perineural and intraneural scarring may result and propagate further nerve damage [26, 27, 29, 30].

The mechanosensitivity of normal and abnormal dorsal root ganglia and axons has been defined in human and animal models [24]. In a cat model, rapidly applied mechanical forces induce short-duration (200 ms) impulses in normal nerve root. Static mechanical forces do not induce impulses in normal nerve root. Rapidly and statically applied mechanical forces induce long periods (15–30 s) of repetitive impulses in irritated or in regenerating nerves in continuity. Minimal acute compression of normal dorsal root ganglion induces prolonged (5–25 min) repetitive firing of nerve [31]. Mechanically induced trains of nerve action potentials can desynchronize afferent 1a nerve action potentials during H-reflex recordings and decrease the H-reflex amplitude. When interpreting intraoperative motor nerve root studies, it is important to understand the pathophysiologic mechanisms of nerve root injury and to understand the response of normal and pathologic nerve to not only different types of mechanical force, but also to electrical stimulation.

Following electrical stimulation of a mixed sensory–motor peripheral nerve, the compound motor action potential (CMAP) or M-wave is recorded from the peripherally innervated muscle. The M-wave is the result of orthodromic motor conduction from the point of stimulation to the muscle. In addition to the short latency M-wave, three late responses can be recorded: H-reflex, F-response, and A-wave (axon reflex). The mechanisms responsible for generating F-responses and A-waves are different from H-reflexes [32]. When recording intraoperative H-reflexes, the F-response and A-wave should not be confused with H-reflexes.

The F-response is not a reflex. After supramaximal stimulation of a mixed peripheral nerve, antidromic motor nerve impulses are conducted proximally to the ventral horn where they activate from 1 to 5 % of the motor neurons. This is followed by orthodromic conduction through motor fibers, and the F-response is recorded from muscle. The F-response is of low amplitude, and the latency, configuration, and duration vary from one stimulus to the next. This variability occurs because each time the motor neuron pool is activated, a different population of 1–5 % of the motor neuron pool is activated that have different conduction characteristics [33]. Both afferent and efferent components of the F-response follow the same motor neurons. The subpopulation of the motor neuron pool activated by the F-response and H-reflex are not the same [34]. F-response persistence is a measure of the excitability of the motor neuron pool. Persistence is the number of recorded F-responses divided by the number of stimuli. Clinically, a persistence less than 50 % is considered to be abnormal [35] (Fig. 8.2).

The A-wave is a late motor response that is present with constant latency, configuration, and amplitude. Low-intensity stimulation elicits the A-wave, and it is usually blocked by higher intensity of stimulation. A-wave latency is between the CMAP and the F-response latency or exceeds the F-response latency. It may also appear with a latency between the M-wave and H-reflex latency or the latency may exceed the H-reflex latency. A-wave amplitude is less than the H-reflex amplitude. The A-wave should not be confused with the H-reflex or F-response. The A-wave is generated by peripheral nerve changes rather than changes in the central nervous system signal processing. The physiology of the A-wave is that there is peripheral neural damage with the presence of a collateral sprout from a proximal point of damaged motor nerve. The collateral sprout innervates muscle. When the antidromic impulse reaches the point of damage, a portion of the electrical impulse proceeds distally along the collateral sprout, and a small portion of the muscle is activated. Depending on the nerve stimulated, A-waves may be normal or abnormal (Fig. 8.3) [32].

See Chap. 7 for a discussion of H-reflex testing.

To record reflexes intraoperatively, it is critical that the anesthetic technique does not significantly inhibit the activity of suprasegmental spinal cord function, spinal interneurons, and segmental motor neurons. Also, adequate neuromuscular junction (NMJ) transmission must be present. Reflexes and F-responses are usually monitored during the recording of SSEPs, tcMEPs, EEG, and free-run EMG. The anesthetic technique used must allow for the recording of all these signals with maximum sensitivity (see Chap. 19 for a discussion of general anesthesia monitoring) [2, 55–60].

The technique used varies depending on the surgical procedure, patient’s age, medical history, and the presence of a pre-existing neurologic deficit. Frequently, total intravenous anesthesia (TIVA) with constant infusion of propofol and fentanyl and other opioids are used. Bolus injections of these agents should be avoided to prevent suppression of recordings and if nitrous oxide is used it should not exceed 50 vol.% [61]. Ketamine may serve an adjunctive role to reduce propofol utilization. High dose of ketamine may suppress tcMEP amplitudes [58]. Ketamine is an excitatory agent and increases SSEP, tcMEP, and H-reflex amplitudes [62].

Dexmedetomidine can be used to supplement propofol during TIVA. Suggested therapeutic levels (0.5–0.7 μg/kg/h) suppress MEP amplitudes but not SSEP amplitudes [63, 64]. One study found that 0.6 μg/kg/h did not suppress SSEP, tcMEPs, and visual evoked potentials [65]. Subtherapeutic doses of less than 0.5 μg/kg/h combined with propofol do not suppress tcMEPs [66, 67].

The author studied the effect of dexmedetomidine on intraoperative SSEPs, tcMEPs, EEG, H-reflexes, and F-responses in 17 patients during correction of scoliosis. After completion of distraction and fixation, a loading dose of 1 μg/kg of dexmedetomidine was added to the fentanyl and propofol technique and this was followed by an infusion of 0.5 μg/kg/h to the end of surgery. No muscle relaxants were used. The addition of dexmedetomidine had no effect on SSEPs or EEG but the effect on motor signals was variable. Lower extremity tcMEP amplitudes decreased from 0 to 100 % (mean, 86 ± 16.6 %), F-response amplitudes decreased from 0 to 100 % (mean, 58 ± 12.5 %), and H-reflex amplitudes decreased from 0 to 100 % (mean, 71 ± 13.9 %). Because of the variable and at times pronounced effects on motor signals, it was recommended that dexmedetomidine not be used to monitor tcMEPs, H-reflexes, or F-responses [68].

NMJ-blocking agents should be avoided other than using short-acting agents for intubation. NMJ function needs to be carefully monitored. The most common technique is the train-of-four (TOF) response . Another technique is the T1 % response. T1 % = first unblocked response/control response × 100. NMJ monitoring should be conducted on muscles that may be affected by the surgical procedure.

The effects of propofol on the soleus H-reflex were studied in 33 patients. No NMJ-blocking agents were used. H-reflexes were recorded before administration of anesthetics and after an initial dose of 2 mg/kg over 1 min followed by a continuous infusion at a rate of 167 μg/kg/min for 10 min. Measurements were also made after infusing propofol to a blood level of 6 and 9 μg/mL. The initial dose of 2 mg/kg decreased the H-reflex amplitude and H:M ratio. The following 10-min infusion did not further decrease these values. The 6-μg/mL injection did not change the H-reflex amplitude and H:M ratio. The 9-μg/mL injection decreased the amplitude and H:M ratio. They recommended that the propofol induction dose be 1.0–2.5 mg/kg and this should be followed by an infusion from 100 to 200 μg/kg/min. They concluded that the immobility during propofol anesthesia is not caused by a depression of spinal motor neuron circuit excitability. Propofol does not decrease axon conduction peripherally nor transmission at the neuromuscular junction [69].

Soleus H-reflexes were used to determine the level of motor neuron excitability intraoperatively. In ten normal human volunteers, 1.0–1.5 % enflurane was found to decrease H-reflex amplitudes from 35 to 100 % of baseline values [70].

The effect of isoflurane alone and isoflurane with N₂0 on the soleus H-reflex was studied under general anesthesia in 25 patients. No NJM-blocking agents were used. Twenty-three of these patients had consistently measurable stable H-reflexes with baseline amplitudes varying from 3.43 to 11.97 mV. The addition of 0.68 % isoflurane decreased the amplitude to 48 % of the baseline. Increasing the isoflurane to 1.37 % decreased the amplitude to 33.8 % of baseline. The combination of 0.81 % isoflurane with 30 % N₂0 decreased the amplitude to 66.2 % of baseline. The combination of 0.37 % isoflurane with 70 % N₂0 decreased the amplitude to 30.4 % of the baseline. They reported that increasing isoflurane concentration results in decreased H-reflex amplitude. Increasing the N₂0 concentration results in decreased H-reflex amplitude. They concluded that the H-reflexes may be recorded with a combination of isoflurane and N₂0. The H-reflex is maximally stable within the range of anesthetic concentrations used to achieve surgical immobility [55].

The effect of isoflurane and N₂0 on spinal motor neuron excitability was studied in eight adult patients by monitoring soleus H-reflexes and abductor hallucis F-responses. No NMJ-blocking agents were used. H-reflex amplitude was decreased to 48.4 ± 18.6 % of the baseline with 0.6 minimum alveolar concentration (MAC) isoflurane and to 33.8 ± 19.1 % with 1.2 MAC isoflurane. MAC is defined as the alveolar concentration of an anesthetic agent that prevents movement in 50 % of patients in response to a painful stimulus. F-response amplitude and persistence decreased to 52.2 ± 22.8 % and 44.4 ± 26.0 % of the baseline at 0.6 MAC isoflurane and to 33.8 ± 26.0 % and 21.7 ± 22.8 % at 1.2 MAC. With 1.0 MAC isoflurane, the H-reflex amplitude was decreased by 32.5 ± 19.2 %, 33.3 ± 20.8 %, and 30.4 ± 23.5 % of baseline levels at 30, 50 and 70 % nitrous oxide, respectively [71].

In 12 adult patients, a comparison of the effects of isoflurane on tcMEPs and F-responses were studied. Anesthesia was maintained with 60 % N₂0, 100 μg/kg/min of propofol and supplementary fentanyl, 0.5–1.0 μg/kg. Recordings were made before and after adding 0.5 % isoflurane. Baseline tcMEP amplitudes (median, 205 μV, 25th–75th percentiles, 120–338 μV), F-response amplitudes (median, 100 μV, 25th–75th percentiles, 64.2–137.5 μV) and F-response persistence (59 ± 29 %) were decreased to 0.0 μV (0–15 μV), 49 μV (12.4–99.6 μV), and 30 ± 31 %, respectively, by 0.5 % isoflurane. The tcMEPs were suppressed more than the F-responses. No NMJ-blocking agents were used [72].

Soleus H-reflexes and abductor hallucis F-responses were monitored to determine the effect of hyperventilation and hypoventilation on motor neuron excitability during isoflurane anesthesia. H-reflex and F-responses were recorded before and after changing the end-tidal CO₂ (ETCO₂) concentration. Anesthesia was maintained with 0.8 % isoflurane and no muscle relaxants were used. An ETCO₂ of 25 mmHg decreased the preanesthetic H-reflex amplitude from 6.8 ± 2.7 mV to 4.0 ± 2.0 mV and to 2.0 ± 2.2 mV at an ETCO₂ of 45 mmHg. F-response persistence decreased from the preanesthetic value of 100 % to 77 % ± 24 % at an ETCO₂ of 25 mmHg and to 61 ± 19 % at an ETCO₂ of 45 mmHg. They concluded that hyperventilation and hypoventilation effects motor neuron excitability and may affect the probability of patient movement during surgery [73].

Volunteers were sedated with a constant level of propofol (2 mg/L) and to a constant level of sevoflurane (0.8 vol.%). Soleus H-reflexes were used to study the depressive effects of these agents individually. The amount of depression was found to be dependent on the size of the H-reflex and is different at different stimulus intensities, indicating a varying effect of propofol and sevoflurane on motor neurons of different size. H-reflex depression is more for both agents at a lower intensity of stimulation than at a higher intensity of stimulation, indicating that smaller motor neurons are depressed more than larger motor neurons. In contrast, excitability of motor neurons by supraspinal effects affects the larger before smaller motor neurons [74]. From a practical standpoint, if H-reflexes are being recorded with a low stimulus intensity and injury occurs that effects the larger motor neurons, this injury could be missed because only the function of the smaller motor neurons would be monitored. The smaller motor neuron population would already be suppressed by the anesthesia, further decreasing the sensitivity for detecting injury. A higher intensity of stimulation would activate small and large motor neurons, allowing the monitoring of a greater percentage of the motor neuron pool.

Studies of the normal and abnormal electrophysiology of the spinal cord CPG components in humans and animals have resulted in the understanding of the mechanisms involved in acute complete and partial SCI in humans. How H-reflex and F-response changes correlate with the patient’s postoperative status is derived from the publications discussed as follows.

Soleus H-reflexes and abductor hallucis F-responses were recorded in 32 patients during spinal cord surgery. In six patients, an abrupt fall in H-reflex amplitude beyond 3 SD from the baseline or significant drop in F-response persistence coincided to perturbation or injury to the spinal cord. Transient suppression occurred in four patients with less than a 50 % drop in H-reflex amplitude or abductor hallucis F-response persistence. These patients did not develop a new postoperative neurologic deficit. Suppression exceeded 90 % of the baseline values and persisted through surgery in two patients. Both patients had profound postoperative neurologic deficits. The author concluded that rostral SCI suppresses H-reflexes and F-responses and the degree of suppression reflects the severity of injury. The mechanism responsible for these changes is thought to be hyperpolarization of caudal motor neurons, which occurs within seconds of injury [75].

H-reflexes were recorded in the lower extremities in 31 patients during spinal surgery. A significant change in amplitude was considered significant if it exceeded 3 SD of the mean postanesthetic baseline. In six patients, a significant decrease in H-reflex amplitude occurred. The onset of H-reflex suppression coincided with a potentially injurious event in each case. In one case involving a cervical myelotomy, a large syrinx collapsed during decompression, producing immediate fluctuation in the H-reflex amplitude. The amplitude recovered to the baseline level 9 min later. Postoperatively, no neurologic deficit was noted. Another case involved mechanical reduction of a T-8 spinal fracture. Increased variability in H-reflexes developed with manipulation of the spine before reduction. The first attempt to reduce the fracture produced a transient fall in H-reflex amplitude . The second attempt at reduction produced a pronounced reduction in amplitude to less than 10 % of baseline. H-reflexes remained suppressed until the end of surgery and postoperatively the patient had severe motor and sensory deficits in both legs that were not present preoperatively. A third case involved a cervical myelotomy for decompression of a posttraumatic syrinx.

During surgery, cervical cord hemorrhage occurred and was followed by reduction H-reflex amplitude. The amplitude steadily declined and the H-reflexes disappeared and remained absent. Postoperatively, the patient had profound weakness in both lower extremities. The changes in these patients demonstrated that H-reflex changes occur immediately at the time of spinal injury. H-reflex changes may be reversible and reflect the severity of SCI [4].

H-reflexes may indicate intact spinal cord function with changes in SSEPs. Soleus H-reflexes and tibial SSEPs were monitored in a patient during T7–T12 laminectomy for spinal stenosis. During laminectomy, the left SSEP became absent and the right amplitude was significantly transiently reduced. No H-reflex changes occurred. Postoperatively, no lower extremity motor deficits were present and no new sensory deficits [76].

Spinal cord function was monitored in 278 pediatric spine with gastrocnemius H-reflexes and SSEPs. Combined H-reflex and SSEP monitoring improved the reliability for detecting spinal cord compromise compared with either procedure alone. H-reflexes changed more than SSEPs. The changes reflected changes in spinal cord gray matter function related to acidosis and changes in hematocrit and blood pressure [77].

In a clinical setting, soleus H-reflexes and abductor halluces F-responses were recorded in 14 patients following SCI that resulted in either partial injury without spinal shock or injury with spinal shock. Deep tendon reflexes following tap of the Achilles tendon and patellar tendons were also evaluated. Patients were evaluated within 24 h of injury and on day 10, 20, and 30 after injury. F-responses were absent in patients with spinal shock, reduced in persistence in patients with acute injury without spinal shock, and normal in persistence in patients with chronic injury. F-response changes persisted up to 2 weeks following SCI. H-reflexes were absent or markedly suppressed in patients with spinal shock within 24 h of injury but recovered to normal amplitude within several days of the injury. Deep tendon reflexes were proportionally more depressed in spinal shock than H-reflexes. This demonstrated dissociation between electrically and mechanically induced reflexes during spinal shock . The observation that the stretch reflex is more depressed than the H-reflex is consistent with depressed fusimotor drive with SCI [19].

A 63-year-old woman with a large T8–9 herniated disk that was causing spinal stenosis with cord compression was treated with a bilateral T8–9 laminectomy with left far lateral costovertebral exposure for disk removal. She presented clinically with right T8 dermatomal and bilateral lower extremity pain. Baseline intraoperative tibial SSEPs were bilaterally normal. Baseline lower extremity tcMEPs were present. Baseline lower extremity H-reflexes and F-responses were present bilaterally. During removal of the calcified disk, the lower extremity tcMEPs became absent. The left vastus medialis H-reflex became absent and the left tibialis anterior, gastrocnemius, and abductor hallucis H-reflex amplitudes were decreased 47, 61, and 97 %, respectively. The right tibialis anterior, gastrocnemius, and abductor hallucis H-reflex amplitudes were decreased 75, 88, and 97 %, respectively. The F-responses were present with 35 % of the stimuli on the left and with 30 % of the stimuli on the right. Baseline F-responses were present bilaterally with each stimulus. There were no changes in the tibial SSEPs. Postoperatively, the patient’s lower extremity sensory function was normal. The lower extremity pain was gone but pain was still present in the right T8 distribution. The lower extremities were weak; she could not stand and could not perform coordinated lower extremity functions. Her strength improved and she was able to walk with assistance on discharge 12 days after surgery. The 1.9 to 8.4 % [78, 79] of the motor neuron pool activated by transcranial electrical stimulation was lost. The 24–100 % [20] of the motor neuron pool activated by the H-reflexes was decreased from 47 to 100 %. The 1.0–5.0 % [21] of the motor neuron pool activated by the F-responses was deceased by 65 and 70 %. The pattern of change in these motor systems in this patient indicates that these techniques may activate the same, different, or overlapping populations of the motor neuron pool. Since the tcMEPs became absent and there was preservation of some H-reflex and F-response function, perhaps H-reflex and F-response changes are better predictors of postoperative motor function than are tcMEPs. The H-reflex and F-response changes correlated with the patient’s postoperative motor function while the tcMEPs did not [80].