{'fraction_non_alphanumeric': 0.02347255781843286, 'fraction_numerical': 0.0075940628236106315, 'mean_word_length': 5.662068965517242, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Fourth nerve palsy associated with almost complete absence of the superior oblique muscle.

Apreviously healthy 46-year-old woman presented to our neuro-ophthalmology clinic with recent spontaneous onset of painless vertical binocular diplopia. She complained of no other neurological symptoms and there was neither history of recent trauma nor systemic illness. Examination revealed a left-sided hypertropia, with right-sided head tilt. A Bielschowsky head tilt confirmed a left superior oblique palsy. Results of a neurological examination were otherwise entirely normal. Negative investigations included a Tensilon test, autoantibody screen, and lumbar puncture for oligoclonal bands. Magnetic resonance imaging (MRI) of the brain and orbits revealed a virtually absent left superior oblique muscle (Fig. 1). No structural lesions were identified in the region of the trochlear nucleus. Isolated trochlear nerve palsy is the commonest cause of acquired vertical strabismus in adults, the majority of patients regaining adequate superior oblique muscle function. Where trauma and other differential causative mechanisms are excluded, a diagnosis of hitherto latent congenital superior oblique muscle palsy, with acute decompensation of vertical fusion, can be considered. Such patients generally become symptomatic during some intercurrent event such as systemic illness. Despite appropriate investigation, the cause often remains unknown; in these cases, and where recovery is not forthcoming, neuroimaging for structural lesions affecting the trochlear nerve may be warranted.1,2 In our case, although the ipsilateral muscle belly reduction suggests an acquired neurogenic disorder with subsequent muscle atrophy, given the short history, an acutely decompensating, latent congenital superior oblique muscle palsy with acute decompensation of vertical fusion cannot be ruled out. Markedly atrophic or hypoplastic muscle bellies have been demonstrated by MRI in both congenital and acquired palsies of the superior oblique muscle,3,4 though it remains unclear if the muscle shrinkage observed in the former is a primary defect, a progressive denervational process, or a combination. It has been previously shown that denervation of a striated muscle results in loss of up to 80% of bulk because of wasting of individual fibres.5 Conflict persists as to whether there is a significant difference in the reduction in muscle bulk between congenital and acquired palsies of the superior oblique muscle, though one study recorded mean reductions in muscle volume, compared with the fellow eye, of 45% (range, 0%–98%) and 66% (range, 30%–95%), respectively.4 With further studies, MRI may prove useful in determining changes in muscle bulk and thus potentially differentiating congenital from acquired palsies. Fourth nerve palsy associated with almost complete absence of the superior oblique muscle