Diyabetes mellitusda santral ve periferik sinir iletim anormallikleri

AMAÇ: Santral ve periferik sinir sisteminde hasara neden olan diyabetes mellitusta, elektrofizyolojik olarak santral ve periferik sinir iletim zamanının ölçülerek etkilenmenin düzeyinin belirlenmesi amaçlanmıştır. YÖNTEM: Diyabetes mellitus tanısı ile takip edilen 25 hastada elekronörografik incelemede N. medianus ve N. tibialis posterior sinirlerin uyarımı ile somatosensoryel uyarılmış potansiyel (SUP) çalışmaları gerçekleştirilmiştir. Median sinir uyarımı ile kortikal N19 potansiyelleri yanısıra Erb potansiyelleri (N9-N11) ve spinal komponentleri ile santral iletim zamanı ölçümü yapılmıştır. N. Tibialis posterior uyarımı ile P37 potansiyeli değerlendirildi. Elde edilen veriler yaşları ve boyları uyumlu 24 sağlıklı kontrol grubu ile karşılaştırıldı. BULGULAR: Diyabetes mellitus tanılı 19 olguda duysal ağırlıklı mikst tip polinöropati saptanırken, 6 olguda anlamlı anormallik tesbit edilemedi. Kontrol grubu ile karşılaştırıldığında bütün SUP komponentlerinin pik latanslarında gecikme tesbit edildi. Santral iletim zamanı 6 hastada hesaplanamadı, 12 hastada gecikmiş olarak bulundu. SONUÇ: Diyabetin periferik somatosensoryel yol kadar, santral iletim fonksiyonlarını da etkilediği görülmüştür.

Central and peripheral conduction nerve abnormalities in diabetes mellitus

PURPOSE: To investigate the degree of being affected by measuring central and peripheral nerve conduction time, electrophysiologically in diabetes mellitus that is making damage in central and peripheral nervous system. MATERIAL and METHODS: Somatosensory evoked potentials are recorded by stimulating median nerve and posterior tibial nerve in 25 subjects with diabetes mellitus. By stimulating median nerve, cortical N19 potentials, Erb potentials (N9-N11) and spinal components and also central conduction time are measured. P37potentials are studied by stimulating posterior tibial nerve. The results of diabetic group are compared with the results of 24 age and height-matched normal subjects. RESULTS: While sensory dominant polyneuropathy was detected in 19 subjects with diabetes mellitus, there was not any abnormality in 6 subjects. The peak latancies of all SEP components were delayed when compared with control group. While central conduction time could not be obtained in 6 subjects, it was delayed in 12 subjects. CONCLUSIONS: Diabetes affects central conductive functions as well as peripheral somatosensory pathways.

___

  • 1. Abbruzzese G, Schenone A, Scramuzza G, et al. Impairment of central motor conduction in diabetic patients. Electromyogr Clin Neurophysiol 1993;89:335-340.
  • 2. Cracco J, Castells S, Mark E. Spinal somatosensory evoked potentials in juvenil diabetes. Ann. Neurol. 1984;15:55-58.
  • 3. Dyck PJ, Karnes JL, O’Brien P, et al. The spatial distrubition of fiber loss in diabetic polyneuropathy suggests ischemia. Ann. Neurol. 1986;19:440-449.
  • 4. Gupta PR, Dorfman LJ. Spinal somatosensory conduction in diabetes. Neurology 1981;31:841-845.
  • 5. Handevidt F. Peripheral neuropathy in person with Diabetes. Clinical Excellence for Nurse Practitioners 2001;5:17-19.
  • 6. Krendel DA. Vascular inflamation in proximal diabetic neuropathy. J Neurol 1998;245:748.
  • 7. Laika SH, Shirakura K, Kato K, et al. Discriminant analysis of different levels of diabetic neuropathiesrecorded by somatosensory-evoked potentials. International Congress Series 2004;1256:479-483.
  • 8. Liveson JA, Ma DM. Somatosensory evoked responses. In: Craven RH, Wissler BM, Shapiro G, Morrone SR (eds) Laboratuary for clinical neurophysiology. F.A.Davis Company-Philadelphia. 1992, p. 278-323.
  • 9. Llewelyn JG, Thomas PK, King RHM. Epineural microvasculitis in proximal diabetic neuropathy. J Neurol 1998;245:159-165.
  • 10. Maetzu C, Villosalada C, Cruz Martinez A. Somatosensory evoked potentials and central motor pathways conduction after magnetic stimulation of the brain in diabetes. Electromyogr Clin Neurophysiol 1995;35:443-448.
  • 11. Pozzessere G, Rizzo PA, Vale E, et al. Early detection of neurological involvement in IDDM and NIDDM. Multimodal evoked potentials versus metabolic control. Diabetes care 1988;11:473-480.
  • 12. Said G, Bigo A, Améri A, et al. Uncommon early—onset neuropathy in diabetic patients. J Neurol 1998;245:61-68.
  • 13. Suzuki C, Ozaki I, Tonasaki M, et al. Peripheral and central conduction time abnormalities in diabetes mellitus. Neurology 2000;54:1932-1937.
  • 14. Thompson PD, Day BL, Rothwell JC, et al. The interpretation of electromyographic responses to electrical stimulation of the motor cortex in diseases of the upper motor neurone. J Neurol. Sci 1987;80:90-110.
  • 15. Van der Kamp W, Maertens de Noordhout A, Thompson PD, et al. Correlation of phasic muscle strength and corticomotoneuron conduction time in multiple sclerosis. Ann Neurol. 1991;29:6-12.
  • 16. Varsik P, Kucera P, Buranova D,et al. Is the spinal cord lesion rare in diabetes mellitus? Somatosensory evoked potentials and central conduction time in diabetes mellitus. Medical science monitor : International medical Journal of Experiment and Clinical Research. 2001;7:712-715 (abstract). 17. Verma A, Bisht MS, Ahuja GK. Involvement of central nervous system in diabetes mellitus. JNNP 1984;47:1-416.