Attention already has been drawn to the possible causative role of aluminum intoxication in so-called dialysis dementia or encephalopathy (see Chap. 39). Removal of aluminum from the water used in renal dialysis has practically eliminated this disorder. It should be noted that the neuropathologic changes in experimental aluminum intoxication (see later) are not those observed in dialysis dementia. Perl and colleagues have reported the accumulation of aluminum in tangle-bearing neurons of patients with Alzheimer disease and in the Guamanian Parkinson–dementia–ALS complex. However, analysis of neuritic plaques by nuclear microscopy, without using chemical stains, failed to demonstrate the presence of aluminum (Landsberg et al). The significance of these findings remains to be determined. Longstreth and colleagues described a progressive neurologic disorder consisting of intention tremor, incoordination, and spastic paraparesis in 3 patients who had worked for more than 12 years in the same pot room of an aluminum smelting plant. Similar cases clearly attributable to aluminum intoxication have not been reported, however.
Organic compounds of tin may seriously damage the nervous system. Diffuse edema of the white matter of the brain and spinal cord has been produced experimentally with triethyltin. Presumably, this was the basis of the mass poisoning produced by a triethyltin-contaminated drug called Stalinon. The illness was characterized by greatly elevated intracranial pressure and by a spinal cord lesion in some cases (Alajouanine et al). Trimethyltin intoxication is much rarer; seizures are the main manifestation. Experimental studies in rats have shown neuronal loss in the hippocampus, largely sparing the Sommer sector, with later involvement of neurons in the pyriform cortex and amygdala (see review by LeQuesne).
A stereotyped episodic encephalopathy has been associated with bismuth intoxication, usually arising from the ingestion of bismuth subgallate. Large outbreaks have been reported in Australia and France (Burns et al; Buge et al). The onset of the neurologic disturbance is usually subacute, with a mild and fluctuating confusion, somnolence, difficulty in concentration, tremulousness, and sometimes hallucinations and delusions. With continued ingestion of bismuth, there occurs a rapid (24 to 48 h) worsening of the confusion and tremulousness, along with diffuse myoclonic jerks, seizures, ataxia, and inability to stand or walk. These symptoms regress over a few days to weeks when the bismuth is withdrawn, but some patients have died of acute intoxication. High concentrations of bismuth were found in the cerebral and cerebellar cortices and in the nuclear masses throughout the brain. These concentrations can be recognized as hyperdensities on a CT scan (Buge et al).