Histopathological and toxicological analyses confirmed a clinical diagnosis of selenium (Se) intoxication in pigs from a farm in Spain. After an initial episode of diarrhoea, animals presented both dermatological and neurological signs; the most obvious sign was a marked hind limb paresis. Cutaneous lesions consisted on diffuse alopecia, multifocal skin necrosis and coronary band necrosis of the hooves. Central nervous system lesions involved the cervical and lumbar intumescences of the spinal cord and consisted of a severe, bilateral symmetrical poliomyelomalacia of the ventral horns; pons and medulla oblongata also presented lesions of polioencephalomalacia. Analyses of feed and sera from clinically affected pigs revealed a marked increase in Se concentration. Clinical investigations indicated that a failure in Se dosage in feed was the cause of the toxicosis.

Huntington's disease (HD) is characterized by the presence of hyperkinesias, but bradykinesia is also present in most patients. We studied the motor performance of 18 patients with genetically proven HD (age, 38.5 +/- 10 y; clinical stage, 1.7 +/- 1.7; (CAG) triplet length, 49.2 +/- 6.8 triplets; all but three patients were free from neuroleptics) and compared with a control group (n = 18) and with a typical Parkinson's disease (PD) group (n = 20). Motor study included the four timed tests commonly used for PD: Pronation-supination (PS), finger dexterity (FD), movement between two points (MTP) and walking test (WT). Tests were done at 9 AM. The PD group was studied in "off" condition, with no medication given for 12 hours. The HD group was slower than the controls on all tasks (all tests significant, p < 0.01, Mann-Whitney U test) and even slower than PD group (for FD, p < 0.05). A significant correlation was found between each test and clinical stage (for PS, r = 0.84; for FD, r = 0.75; for MTP, r = 087, and for WT, r = 0.77, Pearson). Severe bradykinesia was present in HD, and motor impairment is related to clinical stage.

We report a new case of non-reentrant supraventricular tachycardia, associated with tachycardia-induced cardiomyopathy fully reversible after radiofrequency (RF) ablation, together with striking features of apparent concomitant Mobitz type 1 atrioventricular (AV) block in both AV node pathways. Further analysis of the conduction patterns during the incessant non-reentrant tachycardia raised unresolved hypothesis about the involved mechanisms and further interrogations on AV node physiology.

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