Value of Intraoperative Neuromonitoring in Spinal Tuberculosis Surgery: Case Report of Neurological Compromise with Normal Imaging

Abstract

Spinal tuberculosis (TB), also known as Pott's spine, remains a significant cause of spinal deformity and neurological compromise, particularly in endemic regions. Surgical correction of chronic deformities is associated with significant risks, including spinal cord injury. Intraoperative neurophysiological monitoring (IONM) has become an essential tool to minimize neurological complications. We report a case of an adolescent boy with longstanding thoracolumbar kyphosis due to spinal TB, where IONM identified true positive motor pathway compromise during deformity correction, despite intraoperative C-arm imaging confirming correct pedicle screw placement. Surgery was halted, and staged completion was planned. Postoperative neurological deficits confirmed the predictive validity of IONM. This case highlights the indispensable role of IONM in surgical decision-making, particularly in complex TB-related deformities where imaging alone may be insufficient to prevent neurological injury.

 

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Keywords

Pott's spine - spinal tuberculosis - intraoperative neuromonitoring - kyphotic deformity - spinal cord injury

Background

Tuberculosis (TB) has been known to medicine for centuries, with early descriptions appearing in ancient Indian texts like the Sushruta Samhita, where it was called Yakshama. Spinal TB, commonly referred to as Pott's spine after Sir Percival Pott who first described it in the 18th century, remains one of the most serious forms of skeletal TB.[1] Even today, despite effective antitubercular therapy (ATT) and significant progress in surgical techniques, spinal TB continues to be a major clinical challenge due to its potential to cause progressive spinal deformity and neurological deficits.[2]

Spinal TB accounts for almost 50% of extrapulmonary skeletal TB cases, with the thoracic vertebrae, particularly the paradiscal region being the most commonly affected. When left untreated, the infection can cause destruction of the vertebral bodies, leading to angular kyphosis and, in severe cases, compression of the spinal cord. This not only compromises spinal stability but also poses a serious risk to neurological function.[3] Surgical management in such cases focuses on decompression of the spinal cord, correction of the deformity, and stabilization. However, these procedures often carry high risk especially in chronic, rigid deformities and have the potential for iatrogenic neurological injury.[4]

A newer and increasingly important tool in spine surgery is intraoperative neuromonitoring (IONM), which allows real-time assessment of spinal cord function during surgery. While IONM is widely used in scoliosis surgeries for idiopathic and congenital cases, its application in spinal TB case particularly those with severe kyphosis is relatively underreported.[1] In TB-related deformities, the spinal cord is often more vulnerable due to chronic compression, scarring, adhesions, and altered vascular anatomy. In this context, the use of multimodal IONM including motor evoked potentials (MEPs), somatosensory evoked potentials (SSEPs), and electromyography (EMG) can help detect early signs of spinal cord compromise, enabling the surgical team to respond before permanent damage occurs.[5]

This case report highlights the integration of IONM in the management of an adolescent boy with severe thoracic kyphosis secondary to spinal TB. The case illustrates how neuromonitoring provided critical intraoperative information that was not evident on imaging, ultimately influencing surgical decision-making and patient outcome. This report emphasizes the emerging role of IONM in high-risk spinal TB surgeries and supports its broader adoption in similar complex deformity corrections.

 

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Case Presentation

A right-handed, school going adolescent boy aged 15 years presented with history of progressive upper back deformity, bilateral lower limb weakness more pronounced on the right side, decreased sensation below the L2 dermatome, and lower back pain. Symptoms were insidious in onset and of progressive nature with the development of spinal deformity in the past 2 years.

He had been diagnosed with spinal TB involving thoracic vertebrae D9 to D11 one year prior and had completed a full course of ATT. Over the past few months, he noted increasing difficulty in ambulation and numbness in both feet. On examination, power in the upper limbs was normal. Motor strength was reduced in both lower limbs, with Medical Research Council grades of ⅗ in right hip flexors, ⅘ in left hip flexors, and ⅘ in bilateral knee flexors and right knee extensors. The motor strength was 5/5 in left knee extensor. Sensory examination revealed loss of sensation below L2. Reflexes were exaggerated with bilateral knee jerks at 3 + , ankle jerks at 4 + , ankle clonus, and bilateral extensor plantar responses, consistent with an upper motor neuron lesion as documented in our clinical examination. Written informed consent was obtained from the patient's parents for the procedure and for publication of this case report.

Investigations and Treatment Plan

Magnetic resonance imaging (MRI) of the spine, as shown in [Fig. 1], revealed healed paradiscal TB lesions at D9 to D11, associated with severe angular kyphosis measuring 65 degrees and spinal cord compression at the apex of the deformity. There were no signs of active infection, and laboratory markers including erythrocyte sedimentation rate) (15 mm/hr) and C-reactive protein (3.2 mg/L) were within normal limits.

Fig. 1 Magnetic resonance imaging of the spine showing healed paradiscal tuberculosis (TB) lesions at D9 to D11, associated with severe angular kyphosis measuring 65 degrees and spinal cord compression at the apex of the deformity.

A multidisciplinary team discussion considered both one-stage and staged correction approaches. Given the severity and chronicity of the deformity, the surgical team initially planned for a single-stage procedure with the understanding that intraoperative findings might necessitate modification to a staged approach. The patient and family were thoroughly counseled regarding the high risk of neurological deterioration estimated at 15 to 20% based on current literature for similar deformities[6] despite all precautions. The surgical plan involved decompression osteotomy from thoracic D9 to lumbar L1 vertebrae, pedicle screw fixation from D2 to D8 and from D12 to L5, and subsequent rod placement to correct the kyphosis under continuous IONM using SSEPs, MEPs, and EMG. The planned correction aimed to reduce kyphosis by approximately 30 degrees (from 65 to 35 degrees), as literature suggests that attempting greater correction in chronic TB deformities substantially increases neurological risk.[7] [8]

 

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Intraoperative Outcome

Under total intravenous anesthesia using remifentanil (0.1–0.2 μg/kg/min) and propofol (100–150 μg/kg/min), with patient in prone position, incision of 40 cm was made. Superficial fascia and muscles of the back dissected and soft tissue covering the vertebrae were cleared. Under C-arm guidance, pedicle screws were placed at the junction of transverse process, lamina and superior auricular facet from D2 to D8 and from D12 to L5 vertebrae. Multimodal IONM was employed to monitor spinal cord integrity throughout the procedure. Baseline recordings were established after positioning but before incision. MEPs were recordable in abductor pollicis brevis (baseline amplitude: right 650 μV, left 720 μV), rectus abdominis (baseline amplitude: right 320 μV, left 310 μV), and abductor hallucis (baseline amplitude: right 210 μV, left 240 μV), as shown in [Fig. 2]. Despite multiple attempts and optimization techniques, baseline SSEPs was not consistently recordable, likely due to preexisting posterior column dysfunction.

Fig. 2 Motor evoked potential (MEP) intraoperative neuromonitoring (IONM) recoding during surgery in abductor pollicis brevis (bilateral hand), rectus abdominis, and abductor hallucis (bilateral foot) at 12.57 p.m. (2 hours after surgery initiation). Baseline recordings are shown in red color.

The surgical procedure proceeded in a sequential manner with careful IONM throughout. During the initial 2 hours, pedicle screw placement was completed from D2 to D8 and D12 to L5 without any changes in IONM signals. This was followed by decompression osteotomy spanning D9 to L1, where bone fragments compressing the spinal cord were successfully removed, again with no alterations in neurological monitoring parameters.

The deformity correction phase commenced at hour 3 with initial rod placement and the first correction maneuver, achieving approximately 15 degrees of correction without any associated IONM changes. However, during the fourth hour of surgery, while attempting the second correction phase to reach the target 35-degree correction, a sudden and complete loss of MEP signals occurred. This neurological compromise manifested specifically during bilateral rod compression maneuvers at the thoracolumbar junction, as the surgical team attempted to correct the remaining 15 degrees of kyphosis from 50 degrees to the target 35 degrees.

The MEP signal loss was immediate and complete for lower extremity muscles, while upper extremity and truncal monitoring remained largely preserved. Specifically, MEPs remained recordable from the abductor pollicis brevis with amplitudes unchanged from baseline, and from the rectus abdominis with amplitudes decreased by only 25% but still present. In contrast, lower limb muscles demonstrated complete (100%) loss of distal MEP signals, as illustrated in [Fig. 3]. The temporal relationship between the neurological compromise and the deformity correction forces, rather than hardware placement or decompression procedures, strongly suggests that the signal loss was directly related to the mechanical stresses imposed during the correction maneuvers at the thoracolumbar junction.

Fig. 3 Motor evoked potential (MEP) intraoperative neuromonitoring (IONM) recoding during surgery showing sudden drop in MEP signals (bilateral foot) at 3.45 p.m. and complete drop at 3.50 p.m.

The surgical team immediately initiated a standardized IONM alarm protocol. All corrective forces were released, mean arterial pressure was increased from 75 to 85 to 90 mm Hg, hematocrit was confirmed at 32%, and high-dose methylprednisolone (30 mg/kg bolus) was administered intravenously. After 15 minutes of these interventions, repeat stimulation showed no recovery of lower limb MEPs. Anesthesia was maintained with stable parameters throughout the procedure with minimum alveolar concentration between 0.2 and 0.3, and hemodynamic parameters remained stable with no episodes of hypotension. C-arm fluoroscopy confirmed correct screw placement with no breach into the canal. Due to persistent loss of MEPs despite corrective measures, the surgical team halted the procedure and decided to stage the rod fixation. X-ray showing the screw placement has been shown in [Fig. 4].

Fig. 4 X-ray showing pedicle screw placement.

 

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Postoperative Outcome

The patient was monitored closely postoperatively and was managed with intravenous methylprednisolone as per the high-dose spinal cord injury protocol, receiving a 30-mg/kg bolus for 2 days followed by a continuous infusion at 5.4 mg/kg/hour. Despite these measures, neurological examination revealed a significant deterioration in motor and sensory function compared with the preoperative status. Power in both upper limbs remained intact at 5/5; however, the lower limbs showed complete motor paralysis, with 0/5 strength in hip flexors and knee extension bilaterally. Sensory examination demonstrated a marked loss of sensation below the T9 dermatome on the right and T8 on the left. Deep tendon reflexes were absent in both knees and ankles, and plantar responses were also absent bilaterally. These findings were suggestive of new-onset postoperative spinal cord injury likely secondary to intraoperative cord handling or vascular compromise.

Urgent postoperative MRI performed within 12 hours showed increased T2 signal intensity in the spinal cord at the apex of correction, suggesting cord edema, but no evidence of hematoma or mechanical compression requiring immediate surgical intervention. Based on these findings, cord injury was likely due to vascular compromise or stretch injury rather than direct mechanical compression. Despite the poor initial neurological outcome, a decision was made to proceed with the second stage of surgery on postoperative day 2 for rod fixation and stabilization to prevent further deformity progression and potential worsening of neurological status from instability. This decision was made after thorough discussion with the patient's family and the hospital ethics committee. The second procedure involved minimal manipulation of the deformed segment and was performed purely for stabilization. No additional deformity correction was attempted. Postoperative imaging confirmed a final kyphosis of approximately 45 degrees, representing a 20-degree correction from the original 65-degree deformity.

At 2 weeks' follow-up, the patient showed minimal neurological recovery with return of trace movement (⅕) in hip flexors bilaterally but remained wheelchair-dependent. He was enrolled in an intensive rehabilitation program and continues to be followed.

 

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Discussion

Correcting spinal deformity in TB, especially when it is longstanding and severe, is one of the more challenging areas in spine surgery. In chronic cases, the spinal cord is often already compromised, tethered by fibrous tissue, surrounded by scarring, and adapted to a shortened and deformed spinal column. Any sudden correction of this alignment puts the spinal cord at significant risk of injury, even when surgery appears to go well.[6] IONM becomes crucial in these cases as it allows the surgical team to track spinal cord function in real time.[9] [10] The management of IONM signal loss during spinal deformity correction requires a systematic, time-sensitive approach. Based on established protocols from major spine centers and our institutional experience, the following stepwise protocol has been described [11] [12]:

• Immediate actions (0–2 minutes): (1) Document time of signal loss and surgical maneuver being performed. (2) Verify equipment function and electrode placement. (3) Communicate with the anesthesia team to optimize physiological parameters. (4) Halt all corrective maneuvers and release applied forces.

• Physiological optimization (2–5 minutes): (1) Increase mean arterial pressure by 10 to 15 mm Hg (target 85–90 mm Hg) through vasopressor administration. (2) Ensure adequate oxygenation (SpO2 > 95%) and ventilation. (3) Maintain normothermia (36–37°C). (4) Check hematocrit (target > 30%) and consider transfusion if indicated. (5) Reduce anesthetic depth if possible while maintaining adequate anesthesia.

• Pharmacological intervention (5–10 minutes): (1) Administer high-dose methylprednisolone (30 mg/kg intravenous bolus) as per spinal cord injury protocol. (2) Consider mannitol (0.5–1 g/kg) if intracranial pressure elevation is suspected. (3) Ensure adequate perfusion pressure maintenance.

• Reassessment (10–15 minutes): (1) Repeat IONM testing after optimization measures. (2) Document response to interventions. (3) Consider intraoperative imaging if hardware malposition is suspected. (4) Evaluate for technical factors affecting monitoring.

• Decision making (15–30 minutes): (1) If signals recover partially or completely: proceed with extreme caution and significantly reduced correction goals. (2) If signals remain absent despite optimization: strongly consider staging the procedure. (3) Document decision rationale thoroughly for medicolegal purposes. (4) Communicate with patient's family regarding intraoperative findings.

This protocol is consistent with recommendations from the Scoliosis Research Society and International Society for Spinal Cord Monitoring, emphasizing that immediate response to IONM changes can potentially prevent or minimize permanent neurological deficits. [9] [13]

In the present case, the first and only sign of spinal cord distress came from IONM, specifically the loss of MEPs. Imaging showed that all screws were placed correctly, and nothing appeared to be wrong structurally. Yet, after surgery, the patient had a sudden and complete loss of motor and sensory function in the lower limbs. This confirmed that the IONM signal loss was “true positive.”

This case highlights how functional monitoring like MEPs can sometimes reveal problems before they become obvious in other ways. In TB spine cases, MEPs are especially useful because they detect injuries to the anterior spinal cord pathways, exactly where damage from stretching or reduced blood flow is most likely to occur.[7] Unlike imaging, which shows anatomy, MEPs reflect real-time function, providing the only warning before permanent injury occurs. Studies have shown that MEPs have a sensitivity of 92% and specificity of 98.9% for detecting motor pathway compromise in spinal deformity surgery.[10]

The literature suggests that kyphosis correction in healed TB should generally not exceed 30 to 40% of the original deformity angle to minimize cord stretch.[8] In our patient, we had attempted approximately 30% correction (20 degrees out of 65 degrees) when MEP signals were lost, suggesting this patient's spinal cord had even lower tolerance for correction than anticipated. Thus, our case demonstrates that even using a conservative correction target (30 degrees rather than attempting full correction), neurological injury can still occur in chronic TB kyphosis. One likely explanation for the poor outcome is spinal cord stretch injury. In chronic cases, the cord becomes adapted to a shortened position. When surgeons straighten the spine, even modestly, it can stretch the cord beyond its tolerance. Another possibility is vascular compromise. The radicular vessels supplying the thoracic cord are particularly vulnerable during deformity correction, and even transient ischemia can cause permanent damage.[14] The postoperative MRI findings of cord edema without compression support a vascular or stretch etiology rather than direct mechanical injury.

Recent studies have emphasized that patients with preoperative neurological deficits, as in our case, have an increased risk of postoperative neurological deterioration even with IONM use.[12] Thuet et al demonstrated that adult spinal deformity patients with preoperative neurological deficits had a 4.2-fold increased risk of postoperative neurological complications compared with those without preoperative deficits. This finding is particularly relevant to TB spine cases, where chronic compression often results in baseline neurological compromise.

A critical reflection on our management reveals several important considerations for future similar cases: (1) The decision to proceed with a second surgery for stabilization despite neurological deterioration was based on preventing potential instability-related complications, though the optimal timing for such intervention remains debatable. (2) While our IONM protocol detected cord compromise, the permanent deficit suggests that earlier intervention might be warranted at the first sign of signal change, rather than waiting for the standard 15-minute reassessment. (3) Future cases might benefit from even more conservative correction targets, potentially accepting suboptimal radiographic correction to preserve neurological function.

This case also reminds us that while IONM is a powerful tool, it is not perfect. In patients who already have weak signals because of prior damage, it can be hard to detect new problems in time. MEPs and SSEPs can be influenced by anesthetic factors, patient's body temperature, or their overall condition during surgery. And sometimes, damage happens gradually or after monitoring ceases.[13] However, multimodal monitoring approaches combining MEPs, SSEPs, and EMG have been shown to improve the sensitivity and specificity of neurological monitoring in complex deformity cases.[11]

Most studies[14] [15] [16] agree that using IONM reduces the chances of serious injury, especially in high-risk cases. It helps surgeons make more informed decisions during the operation and has been shown to improve outcomes overall. A systematic review by Pastorelli et al demonstrated that IONM use in spinal deformity surgery reduced the incidence of permanent neurological deficits from 0.7 to 0.17%.[10] But as this case shows, even with all precautions, complications can still occur, especially in patients with longstanding, severe deformities due to infection like TB.

The lessons from this case emphasize the importance of careful planning, understanding the individual patient's anatomy and disease history, and correcting deformities gradually rather than all at once. Future approaches might benefit from advanced imaging such as posture-sensitive MRI to help predict which patients are at highest risk, and potentially consider more conservative correction strategies including multiple staged procedures with gradual correction.[16] Future research should focus on determining optimal staging strategies, identifying reliable predictors of neurological risk beyond conventional imaging, and developing standardized protocols for responding to IONM changes in deformity correction surgery. A multidisciplinary approach combining surgical expertise, advanced imaging, neurophysiological monitoring, and rehabilitation remains essential to managing these challenging cases and minimizing devastating complications.

 

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Conclusion

Surgical correction of tuberculous kyphosis poses significant neurological risks, especially in chronic cases with spinal cord fibrosis and tethering. This case demonstrates that IONM can successfully detect real-time cord distress but may not always prevent postoperative deficits, particularly in longstanding severe deformities. Although we employed a relatively conservative correction target and responded promptly to IONM changes using a standardized protocol, the patient still experienced significant neurological deterioration, highlighting the extreme vulnerability of the chronically compressed spinal cord in TB kyphosis and emphasizes several key principles such as: (1) deformity correction must be approached with extreme caution and potentially in multiple stages; (2) even minor correction can exceed the spinal cord's physiological tolerance in some cases; and (3) while IONM is invaluable, surgeons should maintain a high index of suspicion and extremely conservative correction goals in chronic TB kyphosis cases. The implementation of standardized IONM alarm protocols and aggressive neuroprotective measures remains essential in minimizing, though not eliminating, the risk of devastating neurological complications in these challenging cases.

 

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Conflict of Interest

None declared.

Note

The manuscript has been read and approved by all the authors, that the requirements for authorship as stated earlier in this document have been met, and that each author believes that the manuscript represents honest work.

Authors' Contributions

Y.K., A.K., and N.S. were directly involved in the patient's care. N.S. and Z.T. contributed to drafting the manuscript, sourcing and editing clinical images, compiling investigation results, preparing original diagrams and algorithms, and critically revising the work for important intellectual content. Y.K. and A.K. gave final approval of the manuscript. Y.K., as the clinician in charge of the patient's care, supervised the preparation of the manuscript, obtained informed consent from the patient/guardian/family members, and takes overall responsibility for the integrity of the content.

• References

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Publikationsverlauf

Artikel online veröffentlicht:
17. September 2025