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Hemifacial spasm is a distressing, common, and well defined condition, which is difficult to treat. It is characterised by clonic and tonic contractions of the muscles supplied by the facial nerve, is intermittent, and is usually worsened by fatigue or emotional upsets.
A clinical picture similar to that of hemifacial spasm is also seen in trigeminal neuralgia, another condition for which widely varying pathophysiological bases, including vascular compression, have been proposed.1
In our case postmortem exploration of the posterior cranial fossa disclosed a strikingly abnormal relation between the anterior inferior cerebellar artery and VIIth cranial nerve. Such abnormal vascular anomalies around the facial nerve are repeatedly reported in the literature, and they seem to be closely correlated with hemifacial spasm.2
We took the cadaver of a man who had died aged 51, from the dissection material held by the First Department of Anatomy at the University of Vienna.
A square 2 cm×2 cm was drilled in the centre of the skull cap. formalin:water (1:5; 30 ml) was injected subdurally. The cadaver was left in the cold room for 24 hours. Then a mixture of phenol:formalin:water (3:1:10) was introduced into the femoral artery about 5 cm below the inguinal ligament through a 3 mm diameter cannula. Before preparation the cadaver remained in this phenol:formalin:water mixture for about 6 to 8 months.
The vascular anomaly reported was noted when the brain was moved carefully backwards. The brain, which was otherwise normal, was then dissected out of the cranial cavity. The external radius of the anterior inferior cerebellar artery was determined by a digital gauge.
During the exploration of the posterior cranial fossa of the cadaver, we encountered an unusual course of the right anterior inferior cerebellar artery (1.20 mm diameter), which arose from the lower third of the basilar artery and passed through the facial nerve 1.5 cm from the cerebellopontine angle, forming a ring around the nerve about 0.5 cm proximal to the point of penetration and compressing it at several points (fig 1).
The anterior inferior cerebellar artery first ran vertically downwards closely following the basilar and the right vertebral arteries. Then it took a horizontal course until it made a V shaped angle before penetrating the seventh cranial nerve. After it had passed through the facial nerve, with about one third of the fibres above it and two thirds below, its course made a ring around the seventh cranial nerve and disappeared between the cerebellum and the pons into the deep tissue. Along its course a branch went off to the choroid plexus of the fourth ventricle.
The cause and treatment of hemifacial spasm remain controversial. Whereas some theories postulate a cerebral or brain stem mechanism for its origin, others suggest that the causative lesion is within the facial nerve, either within the posterior fossa or at a more distal location.
Our unusual finding lends support to the neurovascular compression theory to explain the aetiology of this disorder as we would like to point out the unusual nature of this anatomical variety of the anterior inferior cerebellar artery.
During an investigation of the posterior cranial fossa, we became aware of an abnormal relation between a vessel and a nerve, which is not described in the current textbooks and encyclopedias. Although there is much literature reporting a close relation between the symptom “facial tic” and vessel variety3 4; our variety—that is, with both transfixion of the facial nerve and an arterial loop around the same nerve—has not been described in the specialist literature, nor has it been mentioned in the most recent review of variants.
Several authors have provided illustrations of a loop formed by the anterior inferior cerebellar artery, but without elaborating further on the topographic relation between the artery and the internal acoustic meatus or the seventh and eighth cranial nerves. It has been asserted that this vessel seldom appears on radiographs.
Typical hemifacial spasm is caused by vessels on the anterocaudal side of the nerve, whereas atypical hemifacial spasm is caused by vessels on the posterior rostral side.5
The relevant aspect of this article lies in its emphasis on the connection between the neurological symptoms and this anatomical variety of a nerve.
The deceased had begun to experience intermittent symptoms of varying intensity in his face at the age of 49. These symptoms took the form of uncontrollable twitching at the right corner of his mouth, ipsilateral hearing impairment, retroauricular cramps, and retroauricular sensory impairment. According to the case history, the deceased had undergone a full otorhinolaryngological examination and pure tone speech audiometry during his lifetime. Thus, it was possible to diagnose the perceptive unilateral acoustic hypoacousia on the right. Early auditory evoked potential studies had also been performed showing an increase in latency and a decrease in amplitude without any deterioration of morphology of the waves. It had not been possible to use MR for the diagnosis as he had a pacemaker in place. None of these symptoms responded to therapy with botulinum toxin.
In our case the compression of the facial nerve at several points could have led to irritation of the region supplied by the posterior auricular nerve and in this way to the symptoms described above.
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