Deficit histology

Renal osteodystrophy is a complex disorder with several pathogenic factors. Histological evidence of bone disease is common in early renal failure and deficits in calcitriol synthesis seems to be an important factor in the pathogenesis of secondary hyperparathyroidism in early CRF. The most common component is osteitis fibrosa manifested as subperiosteal resorption of bone. This is due to decreased excretion as well as increased secretion of parathyroid hormone. In CRF small increments of serum phosphorus cause small decreases in serum calcium. 

An animal study of the histological and physiological effects of intrathecal lidocaine at varjdng concentrations from 3 to 20% showed the presence of lesions in the posterior roots and columns characterized by axonal degeneration (261). The lesions were severe at higher concentrations, but even at the lower concentration of 7.5% there were mild lesions that did not correlate with the presence of neurofunctional deficit. 

A 7-year-old boy with Duchenne muscular dystrophy and attention deficit hyperactivity disorder (ADHD) developed acute hepatic failure, with features of autoimmune hepatitis (2). The only medications he had taken were pemoline (56 mg/day) and cjrproheptadine (2 mg/day). Pemoline was withdrawn after 8 months as the presumed cause of his raised transaminases. Two weeks later he developed an altered mental state, jaundice, and encephalopathy. The histological features of the liver and his autoimmune antibody panel were consistent with autoimmune hepatitis. He was treated with corticosteroids and azathioprine and recovered. 

Kanthasamy et al. (1994) also performed neurochemical as well as histological evaluations as a function of KCN exposure. Compared with controls, reduced dopamine levels were observed in the striatum and hippocampus, and fewer dopamine neurons were detected in the basal ganglia of KCN-treated animals. These findings are important in the context of the observed motor impairment, because toxicant-induced basal ganglia disruption has been associated with locomotor deficits (Langston, Ballard, Terrud, Irwin, 1983). 

Until recently, olfaction has received limited attention in pathological conditions in man. Recent interest in the human olfactory system has been brought about, in part, by neuropathological investigations that described the presence of histological lesions in olfactory-related structures in Alzheimer s disease (Reyes et al. 1987 Pearson et al. 1985 Esiri and Wilcock, 1984), a condition clinically characterized by progressive intellectual decline and behavioral abnormalities. Other clinical studies have shown that olfactory deficits occur in patients with Alzheimer s disease (Doty and Reyes, 1987 Doty et al. 1988), Parkinson s disease (Doty et al. 1988) and schizophrenia. 

The deficit induced by amygdala lesions at the age of 500 days was similar to that induced by lead, in that there was an increase in time to make eight correct choices in comparison to controls by either kind of treatment. Testing for retention also revealed similar behaviour between lead-exposed and lesioned animals. This outcome must be considered preliminary as the histological examination is not yet complete. In addition to the deficit exhibited by lesioned and lead-treated rats, and in contrast to all previous age points, there was a significant (p < 0.05) difference between permanently and maternally exposed rats at this age in the acquisition part. 

Because imtreated mice develop hindlimb paralysis as early as 12 days after onset, a time point of 10 days was chosen for tissue conparisons. At diis time, control mice have lost significant motor fiinction whereas drug-treated mice appear virtually the same as on the first day of onset Histological examinations of spinal cord sections from cohort mice revealed better preservation of normal architecture and more neurons in Mn porphyrin-treated mice this qualitative conclusion was verified quantitatively via counts of spinal cord neurons. Porphyrin-treated mice had 3489 ISO neruons/20 serial sections relative to 2131 151 for untreated controls. Previous studies in both mice and humans have suggested that approximately 50% of spinal motor neurons must be lost before noticeable muscle weakness is seen. Once that threshold has been crossed, subsequent l( s of even a few percent of the remaining motor neurons translates into significant new motor deficits. 

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