[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