Poly Neuropathy Beginning Motor, Proximo Distal Myelinic, Symmetrical of The Lower Limbs Revealing A Deficiency in Vitamin D2 Concerning A Clinical Presentation
Received Date: January 19, 2022 Accepted Date: February 19, 2022 Published Date: February 22, 2022
doi: 10.17303/jnnd.2022.10.102
Citation: Halladain Mpung Mansoj (2022) Poly Neuropathy Beginning Motor, Proximo Distal Myelinic, Symmetrical of The Lower Limbs Revealing A Deficiency in Vitamin D2 Concerning A Clinical Presentation. J Neurophysiol Neurol Disord 10: 1-14
Abstract
Study suggests that vitamin D deficiency may contribute to the development of painful neuropathy by playing a role in the pathogenesis of small fiber neuropathy, which particularly affects nociceptive receptors.
Case Presentation
Patient coming for consultation for progressive onset paresthesia over four months with no known pathological history;
General physical examination
Good general condition, good coloration of the mucous membranes, a good state of hydration
Vital parameters
Blood pressure 120/62 mm Hg, Pulse 74 pulses
Weight 70 Kg
Neurological examination
Evidence of neurogenic syndrome in all four limbs
In front of this table the electro neurography was requested
The results of which were in favor of an early motor poly neuropathy, more myelinic, symmetrical in the lower limbs
Several blood tests were requested without particularity and the dosage of vitamin D came back in favor of a deficiency. The management was based on vitamin D supplementation and symptomatic treatment of pain with amendment after a period.of five months
Sensitive Driving Speed
Driving Speed
Wave F
EMG needle
Interpretation
Nerve conduction
• Sensitive parameters: normal
• Motor parameters: decrease in the amplitude of the left SPI,
lengthening of F-wave latencies in the lower limbs
Detection
• Rest: absence of spontaneous activity
• Effort: normal interference plot for the effort provided.
Conclusion
ENMG in favor of an early motor poly neuropathy, proximo distal more myelinic, symmetrical of the lower limbs.
Discussion
Vitamin D, a neurotrophic molecule, is a potent inhibitor of mitosis and a promoter of differentiation in many cells. The receptor for this steroid is expressed in both neurons and glial cells, including Schwann cells (Cornet et al, 1998). It is now well established that vitamin D stimulates the expression of neurotrophins (Cornet et al. 1998 and increases the outgrowth of neurites, when added to cultured hippocampal cells (Brown et al. 2003). Therefore, it can be postulated that the increased axogenesis observed in the current study is due to an increased expression of neurotrophins. However, vitamin D-dependent pathways could also be involved in axonal regeneration. Hence vitamin D deficiency. Results in demyeliation or axonal damage Clinical diagnosis is based on clinical examination, electroneuromyography and nerve conduction study.
Blood and urine test to determine the cause.
The treatment is based on the etiological and symptomatic treatment [1-15].
Conclusion
Secondary poly neuropathy with vitamin D deficiency represents a clinical entity characterized by axonal damage secondary to the deficiency by its role on the nervous system.
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