Paracetamol-induced acute renal failure in the absence of fulminant liver damage.

phenothiazines.Although the first patient had no visual impairment or apraxia, computed tomographic appearances were compatible with parieto-occipital infarcts in arterial boundary zones and may have been due to hypotension.3The paroxysms of muscle spasms, tachycardia, sweating, and rage were probably due to brain-stem dysfunction analogous to the "rage reaction" produced experimentally in animals by diencephalic damage or stimulation.4The akinetic mutism, catatonic posturing, and disordered eye movements in the second patient indicated a lesion of the upper brain stem affecting the basal ganglia.5Despite systemic hypotension the clinical features described above are not those expected from lesions in arterial boundary zones but are more in keeping with damage to basal ganglia and diencephalic structures, which are lairly resistant to hypotension.Asphyxic anoxia may affect basal ganglia, and hypoxia may have caused such damage in our cases.In addition, anaphylaxis may cause vasoconstriction or increased vascular permeability, and these mechanisms may have produced lesions in the well-vascularised structures of the brain stem and basal ganglia.I thank Dr G D Schott for helpful suggestions,