Post-surgical left oculomotor nerve neuromyotonia: Cause or coincidence?

Abstract

Ocular neuromyotonia (ONM) is characterized by episodes of binocular diplopia usually triggered by an eye movement requiring contraction of the affected extraocular muscle. It consists of an involuntary, sometimes painful contraction of one or more extraocular muscles. It is most often secondary to radiotherapy of the para-sellar region, although other aetiologies have been reported. Some cases do not have a clearly identified aetiology and are classified as idiopathic. Most cases of ONMs are unilateral but bilateral ONMs have also been described.1–4 We report a case of left ONM in a 55-year-old female patient, several weeks after simultaneous surgical resection of two meningiomas, situated on the right side (Simpson II). The particularity of this case is linked to its puzzling presentation, its similarity with spasm of the near reflex and the putative mechanism through which surgery might have precipitated the symptoms.

Ocular neuromyotonia: a review of diagnosis and treatment

“…Cases of ONM have been reported with impingement by internal carotid artery aneurysm [19], posterior cerebral artery [20,21], and a loop of a dolichoectatic basilar artery [10]. Postsurgical remodeling and subsequent neurovascular contact has also been reported to lead to ONM [18]. Recently, it has been postulated that most idiopathic cases of ONM in the literature result from vascular compression that went undetected by routine computed tomography or MRI scans [22] similar to the proposed mechanism in hemifacial spasm.…”

“…Vascular compression represents a third cause of ONM. In every case of ONM without history of radiotherapy or TED, vascular compression must be considered [18]. Cases of ONM have been reported with impingement by internal carotid artery aneurysm [19], posterior cerebral artery [20,21], and a loop of a dolichoectatic basilar artery [10].…”

Neuromuscular hyperexcitability syndromes

“…Secondary acquired PNHS also exist and originate from a diverse spectrum of disorders damaging peripheral nerves, such as polyneuropathies (especially in the context of irradiation) and toxins (insecticide, toluene, lead, etc.) [7 ▪ ,8 ▪ ,9]. There is no consensus on the diagnostic process to follow in secondary PNHS, but an autoimmune and paraneoplastic screening similar to that in primary PNHS is indicated.…”