Ketamine’s Impact on Intraoperative Neurophysiological Monitoring: Absence of Data in Postpolio Syndrome

Dear Editor, Intraoperative neurophysiological monitoring (IONM) is widely used during spinal surgery to detect early compromise of neural pathways and reduce the risk of permanent neurological injury. Transcranial motor evoked potentials (TcMEPs) assess the functional integrity of descending motor tracts, while somatosensory evoked potentials (SSEPs) evaluate ascending sensory pathways. Together, they provide complementary information regarding spinal cord and nerve root function.1-3 However, the quality of evoked potentials is influenced by both anesthetic technique and underlying neurological disease. Postpolio syndrome (PPS), a late complication of poliomyelitis, is characterized by progressive weakness, fatigue, and wasting due to chronic anterior horn cell degeneration.4 Several studies have shown that ketamine can preserve or even enhance TcMEP amplitudes, presumably by increasing cortical excitability, facilitating spinal motor neuron responsiveness, and augmenting excitatory glutamatergic transmission.5-7 Ketamine’s effect in PPS has not been defined. This study evaluates whether ketamine can improve TcMEP responses in patients with PPS undergoing spinal surgery. Four male patients with established PPS, aged 34–42 years, underwent posterior lumbar fusion between August 2019 and June 2021 at a tertiary care centre in Bengaluru, Karnataka, India Table 1. All patients were diagnosed based on the March of Dimes criteria, including a confirmed history of paralytic poliomyelitis, partial neurological recovery, a prolonged period of functional stability, and the subsequent development of new or progressive weakness and/or fatigue not explained by other conditions. Patients exhibited progressive muscle weakness and atrophy over time, leading to musculoskeletal imbalance and low back pain Figure 1. Alternative neurological, rheumatological, or thyroid causes of limb weakness were excluded.8Table 1: Demographic details of the patientsFigure 1: Patients with postpolio syndrome with right-sided lower limb atrophy and intraoperative neurophysiological monitoring electrodes placed in the limbsGeneral anesthesia was induced with fentanyl (2 μg/kg) and propofol (1 mg/kg), with atracurium (0.5 mg/kg) administered for tracheal intubation. Anesthesia was maintained using propofol (100 μg/kg/min) and fentanyl (1 μg/kg/h), titrated to maintain a bispectral index between 30 and 40. No additional neuromuscular blocking agents were given. Physiological parameters were maintained within normal ranges. TcMEPs were elicited using transcranial electrical stimulation via scalp electrodes placed anterior to C3 and C4, with recordings obtained from selected upper- and lower-limb muscles. SSEPs were elicited by posterior tibial nerve stimulation. Baseline recordings were obtained after confirmation of recovery from neuromuscular blockade. A ketamine bolus of 1 mg/kg was administered intravenously, and evoked potentials were reassessed at 3 and 6 min. Baseline TcMEPs were recordable in all patients but demonstrated markedly reduced amplitudes in chronically weak muscles, particularly the quadriceps, which frequently showed inconsistent responses. Distal muscles such as the tibialis anterior and flexor hallucis longus produced more reliable signals Figure 2. SSEPs were present bilaterally, with reduced amplitudes but preserved latencies Figure 3.Figure 2: Transcranial motor evoked potential of the patient before (red) and after giving (green) inj. ketamine bolusFigure 3: Somatosensory evoked potential in patients with postpolio syndromeFollowing ketamine administration, no improvement in TcMEP amplitude or consistency was observed in either affected or relatively preserved muscles. SSEPs remained unchanged. All patients remained hemodynamically stable, and no new postoperative neurological deficits were identified. This case series highlights both the feasibility and the limitations of IONM in patients with PPS. Despite significant preoperative weakness, TcMEPs and SSEPs could be obtained in all patients, supporting the use of multimodal monitoring in this population. However, the consistently low amplitudes observed in affected muscles underscore the impact of chronic lower motor neuron loss on motor evoked potential generation. The ability to obtain baseline TcMEPs and SSEPs, despite marked preoperative weakness (<4/5), is clinically relevant, as it shows that multimodal IONM is technically feasible in PPS. While quadriceps responses were often unreliable or low amplitude, consistent TcMEPs could be elicited from more distal muscles such as the tibialis anterior and flexor hallucis longus. This aligns with previous work showing that TcMEPs are more likely to be recordable from muscles with preserved strength, even in neuromuscular disorders.9,10 The preserved SSEP responses, even though of lower amplitude, suggest that dorsal column sensory pathways are relatively spared in PPS, as expected from its anterior horn cell pathology. These findings support the continued use of IONM during spinal procedures in PPS, particularly when neural structures are at risk. The failure of ketamine to enhance TcMEP responses in PPS contrasts with reports from other surgical populations. Ketamine has been shown to improve TcMEP amplitudes in children, patients with neuromuscular scoliosis, and individuals undergoing complex spinal deformity correction.5-7 These effects are attributed to increased cortical excitability, reduced inhibitory neurotransmission, and enhanced spinal motor neuron responsiveness. In patients with PPS, however, the primary limitation is not insufficient cortical drive but a markedly reduced pool of functional anterior horn cells capable of transmitting the signal to muscle. TcMEPs represent the summated activity of multiple motor units. In PPS, surviving motor neurons are often enlarged through collateral reinnervation, but their number is substantially reduced. As degeneration progresses, even these compensatory motor units are lost. Under such circumstances, pharmacological enhancement of cortical excitability is unlikely to translate into increased compound muscle action potentials. This explains why ketamine failed to improve TcMEPs in both severely affected and relatively preserved muscles in our cohort. These findings have important practical implications. Ketamine is sometimes empirically administered when TcMEPs are weak or absent, with the expectation of signal augmentation. In patients with disorders characterized by anterior horn cell degeneration, such as PPS, this strategy may be ineffective. Instead, emphasis should be placed on alternative optimization measures, including minimizing anesthetic depth, avoiding neuromuscular blockade, maintaining physiological stability, and selecting multiple distal muscle recording sites where residual motor units may be better preserved. The limitations of this study include its small sample size, retrospective design, and evaluation of only a single ketamine dose. While higher doses might theoretically produce greater cortical facilitation, they also carry the risk of potential suppression of evoked potentials and neurotoxicity.11 Prospective studies with larger cohorts and comparative evaluation of other facilitatory agents are warranted. Multimodal IONM is feasible in patients with PPS undergoing spinal surgery. However, ketamine does not appear to enhance TcMEP amplitudes in this population, likely due to irreversible lower motor neuron loss. Careful anesthetic and technical optimization remain essential for effective monitoring in patients with chronic motor neuron disease. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.