A 79-year-old male patient presented with subacute limb-girdle weakness five weeks after the first infusion of immune checkpoint inhibitor (ICI) pembrolizumab, an adjuvant therapy after excision of a melanoma with sentinel node removal. The patient showed selective neck extension weakness, complete bilateral ptosis, ophthalmoplegia and type II respiratory failure. Bloodwork disclosed elevated creatine kinase (2985 U/l (normal range 46–171)) and high-sensitivity cardiac troponins (979 ng/ml (normal range ≤ 45)). A thoracic cardio-echogram showed hypokinesia of the apex, secondary to a myocardial infarction in 2011. A cardiac MRI was not performed because of orthopnoea and need for continuous non-invasive ventilation (BiPAP). An EMG disclosed myopathic changes in proximal upper limb muscles, without signs of a neuromuscular junction disorder on repetitive nerve stimulations performed at ulnar, nasal and (clinically weak) trapezius muscles. A stimulated single fibre EMG performed in the right orbicularis oculi muscle showed a normal mean jitter (18 μs). Anti-acetylcholine receptor and anti-MuSK antibodies were negative. A pyridostigmine trial showed no clinical improvement. A brain MRI showed marked patchy, pathological contrast enhancement of extraocular muscles, findings consistent with myositis (Fig. 1). Differentiation from physiological contrast-enhancement of extraocular muscles was based on thickening of the muscles and infiltration of the surrounding fatty tissues (Fig. 1) [1]. A diagnosis of an ICI-induced myositis was made, with possible concomitant myocarditis.
Fig. 1
Brain and orbital MRI findings in a patient with ICI-induced myositis and a healthy control individual. Coronal fat saturated T1 Space sequence after gadolinium administration and axial fat saturated FLAIR image in a patient with myositis (a-b) and in a control individual (c-d). Image a shows thickening and increased contrast enhancement of the left superior rectus-levator palpebrae muscle complex (arrow) compared to the right-hand side. Furthermore, infiltration and enhancement is seen in the surrounding orbital fat (star in a). Image b through the orbit at the level of the rectus superior muscle (b) shows a marked increase of signal intensity around the muscle indicating inflammatory oedema (arrow). These findings are not present in the control patient, where uniform thickness and enhancement of the extraocular muscles is seen (arrow in c), as well as normal hypointense orbital fat surrounding the muscles (star in c and d). Note that hyperintense artefacts coming from the maxillary sinus often surround the rectus inferior muscles (arrowheads in a and c), this should not be interpreted as inflammatory changes
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