[15].
The clinical symptoms of MERS syndrome are nonspecific and diverse. The most common manifestation is fever which was the prodromal symptom in our patient [16]. Fever may precede or accompanies neurological symptoms. Other general clinical symptoms including headache and digestive tract disturbances (vomiting and diarrhea)[10, 17] have been also reported. Consciousness disturbance, seizures, behavior changes, drowsiness, confusion, acute urinary retention, and delirium may also be the common neurological symptoms associated with MERS [10; 18, 19, 20]. In our case, gastro-intestinal involvement and consciousness disturbance were predominant.
Typically, MRI features show reversible hyperintense signals on T2‐ weighted images, fluid‐attenuated inversion recovery images (FLAIR), and diffusion‐weighted images (DWI) in the splenium of the corpus callosum (SCC) (classified in MERS type I) [16]. Sometimes, radiologic abnomalies can extend to other areas of the corpus callosum and adjacent periventricular white matter in a symmetrical pattern (classified in MERS type II). Our patient was a MERS type II case.
Yuan et al, in their review reported that the total of 29 patients recovered completely within a month [6, 19]. In rare cases, patients, especially those with type II lesions on MRI, may develop neurological sequelae and lesions may persist on MRI for months even if their size diminishes [21].
Several mechanisms have been proposed for the pathogenesis of MERS but this is still unclear. There are several hypotheses, including intramyelinic edema [18], hyponatemia [17],and oxidative stress [22], neuroaxonal damage[23], autoimmune processes [24], and cytotoxic edema [25]. The possible explanation for this is intramyelinic edema resulting from separation of myelin layers[26, 27] and local infiltration of inflammatory cells