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Effect of protein calorie malnutrition on peripheral nerves. A clinical, electrophysiological and histopathological
Insights
Protein calorie malnutrition (PCM) in children impairs peripheral nerve function, with nerve conduction abnormalities worsening with PCM severity. Severe PCM shows retarded myelination and demyelination, impacting nerve structure and function.
Area of Science:
- Pediatric Neurology
- Nutritional Neuroscience
- Peripheral Nerve Disorders
Background:
- Protein calorie malnutrition (PCM) is a significant global health issue affecting children.
- Peripheral nerve dysfunction is a known complication of severe malnutrition.
- Understanding the specific neuropathological changes in PCM is crucial for diagnosis and management.
Purpose of the Study:
- To investigate the peripheral nerve abnormalities in children with varying degrees of protein calorie malnutrition (PCM).
- To correlate nerve conduction studies with sural nerve biopsy findings in relation to PCM severity.
- To elucidate the morphological basis of impaired peripheral nerve function in pediatric PCM.
Main Methods:
- Studied 43 children (7-62 months) with mild to severe PCM.
- Performed motor and sensory nerve conduction studies.
- Analyzed sural nerve biopsies for myelinated fiber density, size spectrum, internodal length, and light microscopy.
Main Results:
- Reduced motor nerve conduction velocity and sensory conduction abnormalities were found in both mild/moderate and severe PCM groups.
- Abnormalities correlated with PCM severity, hypotonia, and hyporeflexia.
- Severe PCM showed impaired myelinated fiber development, persistent small fibers, and significant segmental demyelination (approx. 50%), unlike mild/moderate PCM.
Conclusions:
- Retarded myelination and segmental demyelination are likely the primary morphological causes of peripheral nerve dysfunction in pediatric PCM.
- Short internodes on large diameter fibers may also contribute to impaired nerve function.
- These findings highlight the neurotoxic effects of PCM on peripheral nerve development and integrity.
Abstract:
Forty-three children (aged 7 to 62 months) with protein calorie malnutrition (PCM) were studied; 13 had mild to moderate PCM and 30 severe PCM. A reduction of motor nerve conduction velocity and abnormalities of sensory conduction were present in both groups. The abnormality of motor nerve conduction was directly related to the severity of PCM and the presence of hypotonia and/or hyporeflexia. Sural nerve biopsies from both groups were studied for myelinated fibre density, fibre size spectrum, relationship of internodal length with diameter and qualitative light microscopic changes. The biopsies from children with mild to moderate PCM were characterized by a normal developmental change in myelinated fibres with an increasing proportion of medium and large size fibres, a transition from a unimodal to a bimodal distribution and an appropriate relationship of internodal length to fibre diameter. Evidence of mild segmental demyelination was observed in only one patient of this group. In contrast, in the biopsies from children with severe PCM, the normal developmental pattern for myelinated fibre size distribution was impaired with a persistence of small myelinated fibres, and there was a failure of internodal segments on large fibres to elongate with increase in age and significant segmental demyelination in about 50 per cent of cases. Retarded myelination and segmental demyelination probably form the morphological basis for impaired peripheral nerve function in PCM. Short internodes on large diameter fibres may also contribute to this effect.