FRCA Notes

Neurophysiological Monitoring

The intermediate curriculum asks for knowledge of 'monitoring of spinal cord function under general anaesthesia' and 'operative spinal cord monitoring'.

It also asks for knowledge of 'the indications for using neurophysiological monitoring to benefit patients requiring neurosurgery/neuro-critical care'.

Resources

  • Intra-operative neurophysiological monitoring is employed to minimise the risk of injury to nerve pathways during neurosurgical and spinal procedures
  • It helps diagnose nerve injury but also allows salvage of neural tissue before damage is irreversible

  • Mechanisms of such injury include:
    • Direct mechanical disruption of nerves or spinal cord from surgical instrumentation
    • Thermal injury from surgical coagulation
    • Pressure injury e.g. from patient positioning
    • Ischaemic injury from local or global hypoperfusion of the spinal cord

The ideal monitor

  • High sensitivity and specificity
    • False negatives can lead to unnoticed damage
    • False positives can lead to unnecessary intervention
  • Fast response time to changes in patient condition
  • Detects tissue injury early enough to allow therapeutic intervention and reversal of damage
  • Aids clarification of physiological targets
  • Provides prognostic value for subsequent care

Classification

  • Free-running signals (i.e. detection of spontaneous activity);
    • EEG
    • Free-running EMG

  • Measurement of evoked electrical response of a specific neural pathway
    • Somatosensory evoked potential (SSEP)
    • Motor evoked potential (MEP) a.k.a. provoked EMG
    • Brainstem auditory evoked potential (BAEP)


Type of Surgery Monitoring
Intracranial surgery involving cortical/subcortical pathways and their blood supply MEP | SSEP | VEP | EEG | Language mapping and monitoring
Vascular surgery involving cranial blood supply e.g. AVM resection MEP | SSEP
Posterior fossa/CPA/brainstem surgery BAEP | MEP | SSEP | Corticobulbar MEP | Brainstem reflexes
Surgery involving spinal cord e.g. decompression, scoliosis, spinal trauma, tAAA repair MEP | SSEP | EMG
Functional neurosurgery e.g. movement disorder surgery EEG | SSEP | MEP | EMG | ± language mapping
Surgery close to peripheral nerves e.g. thyroid, parotid EMG
Microvascular decompression for trigeminal neuralgia EMG | BAEP | SSEP | MEP | Corticobulbar MEP | Brainstem reflexes


  • Transcutaneous stimulus is applied at large mixed sensorimotor nerves at a level which activates large-diameter, fast-conducting Ia muscle afferent and group II cutaneous nerve fibres
  • Such nerves inlcude the posterior tibial nerve (L4 - S2), ulnar nerve (C8 - T1) and median nerve (C6 - T1)

  • The impulse is transmitted via ascending sensory tracts (via dorsal columns and thalamocortical pathways)
    • Blood supply via paired posterior spinal arteries

  • The impulse is detected using peripheral (Erb's point), epidural or scalp electrodes
  • Typically smaller amplitude than MEPs
  • Not significantly affected by therapeutic levels of volatile agents

  • Injury indicated by either:
    • Decreased amplitude >50%
    • Increased latency >10%

  • Stimuli applied to the motor cortex, either:
    • Transcranially through the scalp
    • Directly through electrical stimulation of the brain

  • The impulse is transmitted via descending corticospinal / corticobulbar tracts
    • Blood supply via the single anterior spinal artery

  • Detected using epidural/intrathecal or muscle electrodes
    • Epidural or IT electrodes measure either D-waves (direct; negative peaks) or I-waves (indirect; positive peaks)

    • Muscles used typically include tibialis anterior, abductor hallucis, vastus medialis or the thenar muscles
    • Electrodes measure effect as compound muscle action potentials; CMAPs

  • Warning of impending injury is indicated by a 50% reduction in amplitude, or the need to increase the stimulation strength/frequency
  • Injury is indicated by complete loss (absence) of CMAPs
    • Transient loss may not indicate nerve injury

Corticobulbar MEPs

  • Corticobulbar MEPs assess integrity of pathways to the orofacial muscles: orbicularis oculi and oris/mentalis/masseter/soft palate/vocal cords/trapezius/tongue
  • The primary motor cortex is stimulated unilaterally, in a similar fashion to standard MEPs, and signal recorded at the facial muscles

Brainstem evoked potentials

  • Monitor the vestibulocochlear nerve and brainstem function
  • Acoustic stimulus delivered by a device at the ear canal
  • Response recorded by an electrode placed at the mastoid or ear lobe
  • As with MEPs, a 50% reduction in signal amplitude or increase in stimulation strength/frequency is a warning of potential nerve injury

Visual evoked potentials

  • Retinal stimulation with flashing red or white light
  • Scalp or cortical electrodes measure activity in calcarine cortex

Free-running EMG

  • Demonstrates muscle activity in response to nerve manipulation
  • An 'A train' firing pattern may indicate axonal damage

Stimulated EMG

  • A mapping technique to locate nerves in the surgical field
  • A nerve is stimulated and the CMAP recorded

Language mapping

  • Direct cortical stimulation (using low frequencies via a bipolar probe) in the awake patient is the gold standard
  • It is applied at cortical and subcortical levels to delineate the essential sites involved in language function
  • A high frequency, monopolar train-of-five stimulation technique is an alternative which may reduce seizure incidence

Blink reflex

  • Allows continuous monitoring of the trigemino-facial pathways of the brainstem

Laryngeal adductor reflex

Trigeminal–hypoglossal reflex

  • Assesses the functional integrity of the trigeminal–hypoglossal brainstem pathways

Masseter reflex

  • Stimulation of trigeminal afferents below the zygomatic arch
  • Measured over masseter muscle
  • Assesses sensory and motor components of the trigeminal brainstem pathways

Temperature

  • 15% reduction in central neuronal conduction for every 1'C reduction in temperature
  • Effects are additive; pathways involving multiple synapses are effected to a greater extent
  • Seen as:
    • Decreased amplitude and increased latency of evoked potentials
    • Reduction in state of awareness on EEG
  • BAEP are relatively resistant to hypothermia

  • Hyperthermia also has effects
    • Increased temperature as high as 39֯֯'C reduces SSEP latency by 5-7%
    • Increases beyond 39'C increases latency and can result in neuronal damage

  • → Maintain temperature within ±2'C of starting temperature

Carbon dioxide

  • Hypocapnoea may impair intra-operative neuromonitoring signal acquisition due to cerebral vasoconstriction
  • Hypercapnoea up to a PaCO2 of 6.7kPa has no effect on SSEP or MEP

  • → Maintain normal PCO2 levels

Tissue oxygen delivery

  • Progressive hypoxia will cause increased latency and reduced amplitude of SSEP until eventual signal loss
  • Cortical areas are more sensitive than subcortical areas due to higher tissue metabolic activity
  • This may be caused by reductions in haematocrit; a haematocrit of 10-15% will increase latency and reduce amplitude of evoked potentials

  • → Maintain tissue oxygenation and aim haematocrit of ≥ 0.3

Hypotension

  • SSEPs and MEPs are affected by reductions in MAP below the autoregulatory threshold
  • BAEPs may, again, be more resistant to this effect
  • The effect is amplified by hypotension in combination with other deranged physiology e.g. hypoxia
  • Patients with pre-existing abnormalities of cerebral perfusion or impaired autoregulation are more vulnerable to these effects
  • Extremely transient reductions in MAP (e.g. adenosine for aneurysm clipping) is not known to affect MEP/SSEP signals

  • → Maintain an appropriate MAP based on individual patient factors

Positioning

  • Ensure patient positioning isn't compromising vascular flow or causing nerve compression e.g. neck flexion during posterior fossa surgery

  • In general, anaesthetics exhibit dose-dependent suppression of evoked potential signals
  • MEPs are more sensitive than SSEPs, while BAEPs and EMG are relatively resistant (except for NMBA and the latter)

Drug Effect on SSEP Effect on MEP Other
Propofol (at common doses) - - -
Barbiturates No effect even at high doses Suppressed Reduce VEP, no effect on BAEP
Benzodiazepines Unchanged at pre-med. dose - Slow EEG waves
Volatile agents Suppressed at >1 MAC (and as low as 0.3 MAC) Suppressed at >0.5 MAC Initial increase EEG followed by dose-dependent reductions and suppression at >1.5MAC
Nitrous oxide Suppressed Suppressed -
Opioids Unpredictable SSEP depression
Boluses show ↑ depression vs. infusions		 Dose-dependent myogenic MEP depression, but no effect on neurogenic MEP -
Ketamine Enhanced Enhanced
Suppressed at >1mg/kg bolus doses		 ↑ EEG activity ± seizures
NMBAs - Prevent CMAP recording, but not MEP transmission
NB effect on MEP may outlast effect on NMJ		 Obliterate EMG monitoring
Dexmedetomidine Minimal effect from 0.3–0.5μg/kg/hr infusion Effects at 0.5μg/kg/hr More research needed overall


  • Any loss of neuromonitoring should be promptly communicated by the neurophysiologist and a multidisciplinary approach to treatment taken
  • The use of a checklist to guide the multidisciplinary response has been advocated

Management

  • Neurophysiologist
    • Investigate technical reasons as to why there may be a loss of signal e.g. electrodes, artefact
    • Repeat tests to rule out false positive
    • Optimise stimulating parameters and settings
    • Assess whether signal change is focal (often surgical) or global (often anaesthetic)

  • Surgeon
    • Stop any manipulation
    • Assess surgical field
    • Evaluate ± reverse recent interventions
    • Consider use of saline wash or papaverine
    • Consider need for further imaging ± whether to proceed with surgery

  • Anaesthetist
    • Check depth of anaesthesia and for residual neuromuscular blockade
    • Ensure adequate perfusion pressure by raising MAP (e.g. >70mmHg or 10-20% increase above baseline) and optimise other physiological factors (see above)
    • Ensure no drug cause such as volatile agent >0.5MAC, use of ɑ2-agonists, use of NMBA or propofol accumulation
    • Check positioning for vascular or neurological compromise

  • If measures fail to improve the signal loss; urgent imaging, a wake-up test or curtailing the procedure may be required

  • Stimulation of muscles for mastication
    • Bite injury/airway occlusion
    • Bite blocks required

  • Patient movement if high current used, especially during MEP
    • Can cause surgical interference
    • Can interfere with monitoring e.g. saturations, arterial line

  • Bleeding from electrode placement sites

  • Sharps injuries from multiple electrodes