ABSTRACT
Protein energy malnutrition [PEM] leads to impaired myelination with segmental demyelination or even arrested myelination in severe long-standing malnutrition. While many studies have focused on the morphological and biochemical changes in the nervous system associated with malnutrition, few studies have examined the physiological sequelae of these changes. Moreover, the effects of trace elements deficiencies in PEM on the function of the peripheral nerves and the long myelinated central tracts need to be elucidated in these children. In this study, a group of 15 children with nun edematous malnutrition [marasmus] and a group of 15 children with edematous malnutrition [kwashiorkor and marasmus kwashiorkor] aged 8-36 months were compared to a control group of 15 age and sex matched children. All children under the study were evaluated electro-physiologically using somatosensory evoked potentials [SEPs], motor and sensory nerves conduction and needle electromyography [EMG] studies. Serum levels of zinc, copper, selenium and manganese were assessed. The results showed that both ncm edematous and edematous groups had significant reduction of sensory and motor nerves velocities, amplitude and distal latencies with significant delay in the mean cortical SEP and the mean central conduction time compared to the control group. Neuropathic electromyography findings were present in both groups of PEM in the form of fibrillation potentials, positive sharp waves and large polyphonic motor unit action potentials. Serum levels of copper and selenium were significantly related to the motor and sensory conduction deficits, whereas serum levels of zinc and manganese were significantly related to sensory nerve conduction changes only. Copper and zinc levels were significantly lower in patients represented with neuropathic electromyography changes. There was no significant correlation between the serum levels of any of the studied trace elements and the changes in SEPs
Conclusion: the study demonstrated SEPs ,nerve conduction deficits and neuropathic EMG changes in children with PEM. These deficits may be due to more than one factor including protein deficiency, and trace elements deficiencies. The evidence of the latter is documented in the present study and it seems to contribute to these deficits especially in the peripheral nerves