Traditional wisdom teaches that “good surgeons know how to operate, better ones when to operate, and the best when not to operate”.¹ When treating patients with chronic facial pain, prudent application of this aphorism draws not only from experience but also from rigorous scientific investigation. Lang et al (pages1506–9 of this issue) have strengthened the base of scientific evidence that informs the clinical decision not to recommend microvascular decompression for persistent idiopathic facial pain (PIFP).

Suboccipital microvascular decompression of the trigeminal nerve root is well established for the treatment of trigeminal neuralgia. Postoperatively, immediate relief ranges from 91% to 97% and long term efficacy from 53% to 70%, with an estimated annual recurrence rate of 3.5%.² Of the treatments effective for alleviating the pain of trigeminal neuralgia, microvascular decompression uniquely addresses the underlying pathology, which is generally presumed to arise from vascular compression of the trigeminal nerve root entry zone. Redundant turns in senescent blood vessels commonly abut the trigeminal nerve root. Neurovascular contact may progress, in the susceptible patient, to pulsatile indentation, focal demyelination, aberrant discharges, and ephaptic neural transmission. These disturbances culminate in paroxysmal crescendos, particularly if nociceptive inhibition is inadequate. Lancinating or electrical pain strikes fleetingly and repetitively in response to normally non-painful afferent stimuli, such as oral movement or light touch at a remote facial trigger zone.

But then, not all facial pains behave as trigeminal neuralgia, and craniotomy is not without risks. Although no controlled clinical trial has shown benefit from microvascular decompression in atypical, non-paryoxysmal trigeminal distribution pain,^2–4 microvascular decompression is occasionally tried for the individual patient with terrible intractable unexplained pain. Severely affected patients consult many physicians and may be willing to undergo invasive procedures of uncertain benefit.³ In such cases, magnetic resonance imaging (MRI) may suggest a rationale for surgical intervention should it happen to disclose a vessel coursing alongside the trigeminal nerve root. Recent advances in MRI spatial resolution have brought into view more of these neurovascular liaisons. Finer imaging detail, however, alone cannot distinguish the pathological from the incidental. Systematic clinical correlations are required for the sake of diagnostic clarity and treatment validity.

Lang et al utilised highly sophisticated MRI with 3D reconstruction to assess 12 subjects with PIFP. Radiologists blinded to the laterality of the pain evaluated the images for neurovascular contact, which was frequent, occurring in nine subjects. Of distinct interest is the fact that the presence of neurovascular contact did not differ between the symptomatic and asymptomatic sides, discounting any causal relationship to pain. None of the PIFP patients had morphologies of grooving, distortion, or deviation of the trigeminal root, which are considered more specific for trigeminal neuralgia.

Visualisation of neurovascular contact, it must be concluded, is a non-specific finding that should not itself be used as a convenient way of establishing a diagnosis or opting for surgery in the patient with PIFP. Satisfactory outcomes for patients are still best guided by clinical criteria, in particular, the temporal pattern, pain characteristics, and triggering factors.