Neuroanesthesia and Neuromonitoring Flashcards

During resection of a spinal cord arteriovenous malformation, motor evoked potentials (MEPs) suddenly disappear bilaterally after a bolus of rocuronium 0.3 mg/kg is given to treat patient movement. The surgeon requests confirmation that signal loss is pharmacological rather than ischaemic. Which finding BEST distinguishes neuromuscular blockade from a true cord lesion?

Answer: Preserved D-wave amplitude on direct spinal cord epidural recording

The D-wave is recorded from a direct epidural electrode placed on the spinal cord and reflects descending corticospinal tract activity proximal to the neuromuscular junction. It is therefore entirely unaffected by neuromuscular blocking agents. Preserved D-wave amplitude with absent muscle MEPs conclusively indicates the signal loss is peripheral (NMJ block) and not a spinal cord ischaemic event. Sugammadex reversal (A) could help but takes time and confounds the surgical field assessment. Preserved SSEPs with absent MEPs (B) can occur with true anterior cord syndrome. A pre-bolus TOF > 0.9 (C) only tells you about the baseline state, not the current degree of block at time of loss.

A 58-year-old patient undergoing elective clipping of an unruptured anterior communicating artery aneurysm has mean arterial pressure (MAP) maintained at 75 mmHg intraoperatively. The neuromonitoring technician reports a 60% reduction in bilateral SSEP amplitude 8 minutes after temporary clip application to the A1 segment. The neurosurgeon estimates 4 more minutes of clip time are needed. Which intervention has the STRONGEST evidence for extending ischaemic tolerance at this point?

Answer: Intravenous thiopental 3–5 mg/kg to achieve burst suppression on EEG

Barbiturate burst suppression (thiopental or propofol) reduces cerebral metabolic rate of oxygen (CMRO₂) by up to 50–60% and is the most evidence-supported pharmacological neuroprotectant for temporary clip ischaemia during aneurysm surgery. The IHAST trial definitively showed intraoperative hypothermia to 33°C offered no benefit over normothermia for good-grade aneurysm surgery (ruling out D). Induced hypertension (B) improves collateral flow but is second-line and less potent than metabolic suppression when collaterals are anatomically limited by the clip. Mannitol (A) reduces ICP/oedema but does not directly address ischaemic neuronal metabolism.

An awake craniotomy for left temporal glioma resection is proceeding under dexmedetomidine sedation. During language mapping, the patient becomes acutely dysphasic and develops focal clonic movements of the right hand consistent with cortical spreading seizure. Propofol 50 mg IV terminates the seizure. However, 20 minutes later the patient is fully awake but refuses to cooperate with language testing, stating 'I don't want to do this anymore.' Which is the MOST appropriate next step?

Answer: Pause resection, allow a minimum 10-minute recovery period, then reattempt testing with simplified tasks

After a cortical spreading seizure and propofol rescue, the cortex undergoes a refractory period during which mapping is unreliable (false positives are common). Best practice is to pause resection for at least 10 minutes, allow the patient to recover fully, and reattempt with simplified, validated language tasks (e.g., object naming before sentence completion). Midazolam (A) will impair cortical function and invalidate mapping. Converting to GA (B) eliminates the key safety feature of the procedure. Cold irrigation (D) has evidence for aborting intraoperative seizure activity but does not address the patient's psychological distress or the cortical refractory period, and is not the priority at this point.

During posterior fossa surgery in the sitting position, a patient develops sudden loss of auditory brainstem response (ABR) waves III–V with preserved wave I, coinciding with a decrease in end-tidal CO₂ from 4.2 to 3.1 kPa. Venous pressure at the right atrium reads –2 cmH₂O. What is the MOST likely cause of this ABR pattern?

Answer: Venous air embolism causing brainstem ischaemia

In the sitting position, a sudden drop in ETCO₂ is a classic sign of significant venous air embolism (VAE) — air entrainment reduces pulmonary perfusion and CO₂ delivery to the lungs. The ABR pattern of preserved wave I (cochlear nerve, peripheral) with loss of waves III–V (pontine and midbrain generators) indicates brainstem ischaemia rather than cochlear ischaemia (which would abolish wave I as well). VAE in the sitting position can rapidly compromise posterior fossa venous drainage and brainstem perfusion. Surgical retraction (B) typically produces more gradual asymmetric changes. Hypocapnia (C) alone would reduce cochlear blood flow symmetrically but is less likely to cause rapid brainstem ischaemia at this CO₂ level. AICA occlusion (D) causes ipsilateral wave loss, not bilateral loss.

A patient with traumatic brain injury has an ICP of 28 mmHg and MAP of 88 mmHg. Cerebral perfusion pressure (CPP)–guided therapy is being used. The intensivist calculates the pressure reactivity index (PRx) from a continuous 5-minute correlation between ICP and MAP waveforms and obtains a value of +0.42. What does this PRx value indicate, and what is the CORRECT interpretation for optimising CPP target?

Answer: Impaired autoregulation; the CPP should be adjusted toward the patient's optimal CPP (CPPopt) identified from the U-shaped PRx vs CPP curve

PRx is the moving Pearson correlation coefficient between slow-wave MAP and ICP. A positive PRx (+0.42) indicates impaired cerebrovascular pressure reactivity — ICP is passively tracking MAP rather than being buffered, signifying loss of autoregulation. The correct clinical action is not simply to raise or lower CPP arbitrarily, but to identify the individual patient's CPPopt — the CPP value at the nadir of a U-shaped PRx vs CPP curve (where PRx is most negative, indicating best autoregulation). Targeting CPPopt has been associated with improved outcomes in TBI research (Rao et al., Steiner et al.). Answer A is wrong because +0.42 (positive) signals impaired, not intact, autoregulation. Answer B oversimplifies — reducing CPP when autoregulation is impaired can worsen ischaemia. Answer C quotes a guideline floor but does not capture the nuanced CPPopt concept.

A patient undergoes carotid endarterectomy (CEA) under regional anaesthesia (cervical plexus block). Intraoperatively, after carotid cross-clamping, the surgeon notes ipsilateral stump pressure of 38 mmHg. The patient develops ipsilateral hand weakness and slurred speech. A shunt is inserted. Which of the following intraoperative EEG changes would have been the EARLIEST indicator of cerebral ischaemia in this patient had EEG monitoring been in use?

Answer: Attenuation of beta activity (13–30 Hz) followed by loss of fast frequency activity in the ipsilateral hemisphere

The EEG signature of acute focal cerebral ischaemia follows a stereotyped sequence: within 10–30 seconds of significant flow reduction, there is first attenuation and loss of fast (beta) frequencies, followed by progressive slowing with emergence of theta and eventually delta activity. The earliest detectable change is loss of the high-frequency beta band — this precedes the appearance of slow waves. Bilateral synchronous spike-wave (C) is an epileptiform pattern, not ischaemic. Diffuse bilateral theta (D) is non-specific and typically a later or contralateral stress response. Delta waves (A) appear but are a later manifestation of established ischaemia, not the earliest indicator. Recognising early beta attenuation is clinically critical as it offers a narrow window (20–30 s) for shunt insertion before irreversible injury.