A 29-year-old male petrol station pump attendant was admitted with ataxia and clinical evidence of a sensorimotor polyneuropathy which developed over the preceding 3 months. He had cognitive dysfunction, hearing loss, and cerebellar clinical abnormalities that came on slowly over the three years. He had a fifteen-year history of sniffing mostly glue, occasionally paint thinners, and, in the recent two years, gasoline. Magnetic resonance brain imaging showed abnormalities of the cerebral cortex, cerebral white matter, corpus callosum, hippocampus, brainstem and cerebellar atrophy, hypointensities of basal ganglia, red nuclei, and substantia nigra as previously described in toluene sniffing. Abstinence for six months led to partial clinical improvement. Clinicians need to be aware of this preventable entity which has peculiar radiological findings which are being increasingly accepted as typical.

Background: Aluminium encephalopathy results from exposure to aluminium from occupational, recreational, and environmental sources. Movement disorders, cerebellar ataxia, pyramidal tract signs, dementia, microcytic anemia and bone disease are typical manifestations. Case Report: A 55-year-old woman had clinical manifestations, persistent hyperaluminemia without magnetic resonance imaging (MRI) scan changes of toxic encephalopathy following a prolonged exposure to marine grade paints containing 30% aluminium. Chelation therapy with ethylenediaminetetraacetic acid (EDTA) demonstrated decreased levels of aluminemia and significant neurological improvement over time. Discussion: This diagnosis should be entertained in patients with movement disorders, cerebellar ataxia, pyramidal signs, and dementia of unknown etiology. Highlights: Aluminium encephalopathy (AE) is a neurological syndrome caused by aluminium neurotoxicity. Manifestations include cognitive impairment, motor dysfunction, microcytic anemia and bone disease. This case illustrates AE with hyperaluminemia associated with chronic exposure to industrial paints and clinical and biochemical reversibility after chelation therapy with ethylenediaminetetraacetic acid. Movement disorders are highlighted.

We report our experience with seven cases of thyrotoxicosis associated with hypokalaemic periodic paralysis seen over a 25-year period in Trinidad, West Indies, an ethnically diverse island. All the cases were males, one was a Chinese, two were of East Indian and four of African descent, with a mean age 31.4 years (range 22-54 years). Early diagnosis and appropriate treatment led to the prompt resolution of the symptoms. Although rare in the Caribbean region, clinicians should be aware of the features of this potentially fatal but readily remediable complication of thyrotoxicosis.