Putaminal hemorrhagic necrosis can represent an early consequence of cerebral hypoxia in general but it is most often seen after carbon monoxide intoxication. However, this finding can also happen in isolated methanol intoxication [1]. In our case, we cannot differentiate whether putaminal lesions were due to hypoxemia or specific methanol toxicity. In fact, formic acid formation secondary to methanol poisoning, can inhibit cytochrome oxidase activity in the mitochondria, leading to histotoxic hypoxia with predilection for the brain and the visual pathway [2, 3]. Reports have described an association between extensive white matter demyelination and basal ganglionic damage after hypoxia [4]. This damage is explained in our case probably by the delay of resuscitation and therefore brain hypoxia. In fact, hypoxia causes necrosis and edema in different regions in the brain. Cerebral cortex, hippocampus, cerebral cortex as well as caudate nucleus, putamen and globus pallidus are considered as vulnerable zones in the brain [5]. Putamen is prone to develop injuries because of its high metabolic demand and its crucial place in vascular perfusion’s boundary zones [6].

The extension of these lesions depends on hemodynamic and metabolic patient characteristics but mostly the duration of hypoxia. Individuals older than 30 years like our patient are at greater risk of delayed demyelination [7].

Evolution varies from recovery to death. In our case the patient did not demonstrate neurological recovery.

As for other methanol intoxication MRI findings, optic nerve damage can be assessed by enhanced T1 fat-saturated (FatSat) images and diffusion-weighted images showing a bilateral mild contrast enhancement and restricted diffusion in the retrobulbar segment of the optic nerves [8]. In our case, there was no restricted diffusion in the optic nerves.

Our case is interesting because it represents severe methanol intoxication associated with a severe hypoxic ischemic brain injury. MRI was crucial for the diagnosis of this damage. We attest the lack of a 2^nd control MRI after antidote therapy which could have given us a thorough understanding of the injury evolution in our patient.