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Editor,—Aneurysms of the posterior communicating artery classically present with a painful progressive palsy of the third cranial nerve producing ptosis, ophthalmoparesis, and mydriasis. We present a case in which aneurysmal compression of the third nerve produced a variable ptosis and ophthalmoparesis without pupillary involvement in association with intermittent hyperfunction of the ipsilateral third nerve innervated muscles.
A 73 year old woman with a history of hypertension and ischaemic heart disease was referred to the eye department with a 3 week history of intermittent diplopia which she described as inconsistently horizontal, vertical, or oblique, and a 2 week history of right retro-orbital pain and difficulty in opening her right eye. The diplopia and ptosis were often worse in the mornings.
On examination the corrected visual acuities were right 6/6 and left 6/9. There was a very variable and apparently fatiguable right ptosis which was occasionally replaced by right upper lid retraction (Fig 1). The results of ocular motility testing were inconsistent, ranging from 4 prism dioptres of exotropia to 25 prism dioptres of esotropia in the primary position with between 3 and 7 prism dioptres of left hypertropia. There was variable limitation of elevation and depression of the right eye and occasional right upper lid retraction on downgaze. On upgaze, the deviation reversed to become a right hypertropia due to right superior rectus overaction (Fig 1).
Magnetic resonance imaging and angiography were performed showing a 6–7 mm diameter saccular aneurysm arising from the intracranial internal carotid artery at the level of the posterior communicating artery. Attempted embolisation of the aneurysm failed owing to a focal stenosis at the origin of the right internal carotid artery and the patient underwent uneventful clipping of the aneurysm instead. There was a rapid improvement in the ophthalmoparesis following clipping and 6 weeks postoperatively all the neurological signs had resolved.
The early recognition of oculomotor nerve compression by a posterior communicating artery aneurysm is essential given that the mean interval between the onset of diplopia and bleeding is 4 weeks in patients who develop a subarachnoid haemorrhage.1 Although the retro-orbital pain was typical, this case is unusual for two reasons. Firstly the ptosis and ophthalmoparesis were notably variable (Fig 1). Secondly, episodes of right upper lid retraction, esotropia, and hypertropia were observed (Fig 1). Although modest variability of symptoms (for example, intermittent diplopia2) has previously been described, we can find no reports in the literature of such marked fluctuations in ptosis due to third nerve compression. Furthermore, in this case upper lid retraction and, on eye movement testing, esotropia and hypertropia—that is, excessive activity in third nerve innervated muscles, was observed.
A similar phenomenon of co-existing inappropriate neural discharge and block is seen in hemifacial spasm3 where compression of the seventh nerve by abnormal vessels produces hemifacial spasm and mild facial weakness. Although there is some controversy as to whether it is the mechanical irritation of the facial nerve or secondary hyperexcitability of the facial nerve nucleus that is responsible for hemifacial spasm,4 5 it is now accepted by most authors that compression of the facial nerve is the causative factor.4-6 A precise intraoperative correlation between decompression of the facial nerve and electromyographic disappearance of abnormal facial muscle activity has been demonstrated7although the facial weakness has been reported to take longer to resolve.5 An analogous situation of aneurysmal compression causing alternating ophthalmoparesis and third nerve hyperactivity in the case reported here is suggested by the similar course of resolution to that seen following decompression of the facial nerve for hemifacial spasm—the third nerve hyperactivity resolved immediately following clipping of the aneurysm while the ophthalmoparesis improved rapidly but took several weeks to resolve fully. The degree of third nerve hypofunction was, however, much greater than the mild facial weakness seen in hemifacial spasm and may have been due to the greater degree of compression of the third nerve in this case.
This case is important for two reasons. Firstly, this is the first report of compression of the third cranial nerve producing alternating oculomotor hypo- and hyperfunction as a result of a compressive lesion. Secondly, it emphasises the importance of excluding compression by intracranial aneurysm in a patient with variable signs which could be explained by a partial third nerve palsy.
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