Journals / Epilepsi / 2017 / Cilt: 23 - Sayı: 2

Rezonans Görüntüleme Bulguları: Olgu Sunumu

Hiperglisemi ile İndüklenen Non-Konvülzif Status Epileptikus ve Kraniyal Manyetik

Journal
Epilepsi
Pages
84–90
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

This study aimed to report and discuss the cranial MRI findings of a patient with NKH who was diagnosed with nonconvulsive status epilepticus in the light of the literature.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Nonketotic hyperglycemia (NKH) usually involves frequent seizures up to 25%, and these seizures are the first finding of diabetes mellitus in 50% of the patients.
📊
Key Findings & Data:The most common seizure type is reported as epilepsia partialis continua (EPK), and some occipital lobe seizures and aphasic seizures may also be seen in these patients.
💡
Conclusion & Impact:This study aimed to report and discuss the cranial MRI findings of a patient with NKH who was diagnosed with nonconvulsive status epilepticus in the light of the literature.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Nonketotic hyperglycemia (NKH) usually involves frequent seizures up to 25%, and these seizures are the first finding of diabetes mellitus in 50% of the patients. The most common seizure type is reported as epilepsia partialis continua (EPK), and some occipital lobe seizures and aphasic seizures may also be seen in these patients. The recovery from seizures by the correction of hyperglycemia. The cranial magnetic resonance imaging (MRI) findings associated with both status epilepticus (SE) and seizures induced by hyperglycemia have been described; however, their significance and underlying mechanisms have not been understood. Although consensus has been reached on the acute treatment of SE, insufficient information is available on the long term or maintenance treatment, especially in SEs with acute symptoms. This study aimed to report and discuss the cranial MRI findings of a patient with NKH who was diagnosed with nonconvulsive status epilepticus in the light of the literature.

Özet

Non-ketotik hiperglisemide (NKH) %25’e varan sıklıkta nöbetler görülür ve hastaların %50’sinde nöbetler diyabet hastalığının ilk bulgusudur. En sık epilepsiya parsiyalis kontinua (EPK) görülürken, oksipital lob kaynaklı nöbetler ve afazik nöbetler de görülebilir. Nöbetler hiperglisemi-nin düzeltilmesi ile düzelir. Hem status epileptikus (SE) ile hem de hiperglisemi ile indüklenen nöbetlerle ilişkili kraniyal manyetik rezonans görüntüleme (MRG) bulguları tanımlanmıştır ama bunların önemi ve altında yatan mekanizmalar anlaşılamamıştır. Status epileptikusun akut tedavisi üzerinde konsensus sağlanmış olsa da özellikle akut semptomlu SE’lerde idame tedavisinin nasıl düzenleneceği konusunda yeterli bilgi bulunmamaktadır. Bu yazıda, NKH’si olan, non-konvülzif status epileptikus (NKSE) tanısı konan ve kraniyal MRG bulguları olan bir hasta sunuldu, literatür eşliğinde tartışıldı.

🔖

Cite This Article

ATMACA, M. Ç., ATMACA, M. M. (2017). Rezonans Görüntüleme Bulguları: Olgu Sunumu. Epilepsi, Cilt: 23 - Sayı: 2, 84–90. https://ajindex.com/articles/156700

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (18)

  1. Ong B, Bergin P, Heffernan T, Stuckey S. Transient seizure-rela-ted MRI abnormalities. J Neuroimaging 2009
  2. 19(4):301–10. 49. Hong KS, Cho YJ, Lee SK, Jeong SW, Kim WK, Oh EJ. Diffusion changes suggesting predominant vasogenic oedema during partial status epilepticus. Seizure 2004
  3. 13(5):317–21. 48. Scott RC, King MD, Gadian DG, Neville BG, Connelly A. Pro-longed febrile seizures are associated with hippocampal vasogenic edema and developmental changes. Epilepsia 2006
  4. 47(9):1493–8. 47. Szabo K, Poepel A, Pohlmann-Eden B, Hirsch J, Back T, Sedlac-zek O, et al. Diffusion-weighted and perfusion MRI demonstra-tes parenchymal changes in complex partial status epilepticus. Brain 2005
  5. 128(Pt 6):1369–76. 46. Yogarajah M, Duncan JS. Diffusion-based magnetic reso-nance imaging and tractography in epilepsy. Epilepsia 2008
  6. 49(2):189–200. 45. Di Bonaventura C, Bonini F, Fattouch J, Mari F, Petrucci S, Carnì M, et al. Diffusion-weighted magnetic resonance imaging in patients with partial status epilepticus. Epilepsia 2009
  7. 50 Suppl 1:45–52. 44. Miki T, Seino S. Roles of KATP channels as metabolic sensors in acute metabolic changes. J Mol Cell Cardiol 2005
  8. 38(6):917–25. 43. Olsen RW, Avoli M. GABA and epileptogenesis. Epilepsia 1997
  9. 38(4):399–407. 42. Treiman DM. GABA ergic mechanisms in epilepsy. Epilepsia 2001
  10. 42 Suppl 3:8–12. 41. Harden CL, Rosenbaum DH, Daras M. Hyperglycemia presen-ting with occipital seizures. Epilepsia 1991
  11. 32(2):215–20. 40. Duckrow RB, Beard DC, Brennan RW. Regional cerebral blood flow decreases during hyperglycemia. Ann Neurol 1985
  12. 17(3):267–72. 39. Singh BM, Strobos RJ. Epilepsia partialis continua associated with nonketotic hyperglycemia: clinical and biochemical pro-file of 21 patients. Ann Neurol 1980
  13. 8(2):155–60. 38. Pisani F, Oteri G, Costa C, Di Raimondo G, Di Perri R. Ef-fects of psychotropic drugs on seizure threshold. Drug Saf 2002
  14. 25(2):91–110. 37. Wieser HG. Temporal lobe or psychomotor status epilepti-cus. A case report. Electroencephalogr Clin Neurophysiol 1980
  15. 48(5):558–72. 36. Wieser HG, Hailemariam S, Regard M, Landis T. Unilateral limbic epileptic status activity: stereo EEG, behavioral, and cognitive data. Epilepsia 1985
  16. 26(1):19–29. 35. Seshia SS, McLachlan RS. Aura continua. Epilepsia 2005
  17. 46(3):454–5. 34. Mauguière F. Scope and presumed mechanisms of hallucinati-ons in partial epileptic seizures. Epileptic Disord 1999
  18. 1(2):81–91. 33. Elliott B, Joyce E, Shorvon S. Delusions, illusions and halluci-nations in epilepsy: 1. El