1 ction of cellular/viral factors leading to a metabolic encephalopathy.

2 lications were stroke (41%) and severe toxic/metabolic encephalopathy (37%).

3 esemble the symptoms of human TANGO2-related metabolic encephalopathy and arrhythmias, a hereditary d

4  as stroke, transient ischemic attack, toxic-metabolic encephalopathy, and other.

5  support the notion that HAD is a reversible metabolic encephalopathy fueled by viral replication.

6 ases, including head and spinal cord trauma, metabolic encephalopathies, multiple sclerosis and other

7 nd three in the trastuzumab emtansine group [metabolic encephalopathy, neutropenic sepsis, and acute

8 rivascular macrophages and microglia drive a metabolic encephalopathy, we reasoned that COP-1 could b