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

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

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

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

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

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

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