Superior oblique myokymia: Magnetic resonance imaging support for the neurovascular compression hypothesis

Yousry, Indra; Dieterich, Marianne; Naidich, Thomas P.; Schmid, U. D.; Yousry, Tarek

doi:10.1002/ana.10118

Cited by 93 publications

(32 citation statements)

References 38 publications

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“…12 More recently, microvascular compression of the trochlear nerve has also been proposed as a cause of SOM. 13 This theory has received support from ultrathin section MRI scanning 14 and from a report of successful treatment of SOM with microvascular decompression. 15 Patient 19, who subsequently developed hemifacial spasm ipsilateral to her SOM, is particularly interesting in this regard.…”

Section: Discussionmentioning

confidence: 98%

Superior oblique myokymia: Efficacy of medical treatment

Williams

Purvin

Kawasaki

2007

Journal of American Association for Pediatric Ophthalmology and

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Section: Discussionmentioning

confidence: 98%

Superior oblique myokymia: Efficacy of medical treatment

Williams

Purvin

Kawasaki

2007

Journal of American Association for Pediatric Ophthalmology and

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“…Vascular loops impinging on the IV cranial nerve are thought to be one of the causes of this syndrome, which often remains idiopathic [27,48].…”

Section: ■ Paroxysmal Oscillopsiamentioning

confidence: 99%

Vision and vertigo

Bronstein

2004

Journal of Neurology

150

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This review deals with two syndromes, oscillopsia and visual vertigo. Oscillopsia is the illusion of oscillation of the visual surroundings. For diagnosis purposes one should ask, when does the oscillopsia occur? If oscillopsia is only present during head (or whole body) movements, the likely underlying cause is a bilateral defect in the vestibulo-ocular reflex (VOR). The more common causes are post meningitic vestibular damage, gentamicin ototoxicity or bilateral idiopathic vestibular failure. When oscillopsia develops after specific head positions, it is usually due to a positional nystagmus, usually the result of brainstem-cerebellar disease. When the oscillopsia is largely unrelated to head movements, one should ask, is it fairly constant or is it in attacks (paroxysmal)? If the oscillopsia is constant it is usually due to the presence of a clinically observable nystagmus; the most common is downbeat nystagmus but the most visually disabling is pendular nystagmus. If the oscillopsia comes in brief attacks it is usually due to a paroxysmal nystagmus as observed in irritative VIII nerve and brainstem lesions. However, the most common cause of paroxysmal oscillopsia is a non organic condition called voluntary nystagmus. Treatment of oscillopsia is often pharmacological but disappointing; the best chance of success is carbamazepine for paroxysmal disorders secondary to structural vestibular nerve/nuclear lesions.Visual vertigo should not be confused with oscillopsia. It can be defined as dizziness provoked by visual environments with large size (full field) repetitive or moving visual patterns. Patients with visual vertigo report discomfort in supermarkets and when viewing movement of large visual objects, eg crowds, traffic, clouds or foliage. Visual vertigo is present in many patients with a history of a peripheral vestibular disorder, particularly those who are visually dependent (ie subjects who use vision preferentially for postural and space orientation control). Patients with visual vertigo benefit from the addition to their standard vestibular rehabilitation of optic flow (optokinetic) stimuli and exercises involving visuo-vestibular conflict.

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“…11,12,14,[21][22][23] In 1983 Bringewald 24 first postulated that SOM could result from vascular compression of the trochlear nerve and others have subsequently confirmed this hypothesis. [25][26] Since none of the patients in our series had magnetic resonance imaging performed in the manner necessary to document this finding, we cannot comment on whether any of our patients had neurovascular compression.…”

Section: Discussionmentioning

confidence: 91%