Common Late-Onset Subcortıcal Cerebral Hemorrhage Following Excessive Alcohol Consumption: A Case Report

Abstract

50 year old male patient who was suffering from cooperation disorder and bilaterally blindness was admitted to our emergency service. He was addicted to alcohol and had excessive alcohol consumption the day before. Cranial nonenhanced CT was normal. T2 weighed MR imaging performed at 1,5 T unit showed high signal intensity in bilateral putaminal foci.In this localization diffusion-weighed images(DWI) were hyperintense due to restricted diffusion and low ADC values. After two weeks, drowsiness and confusion were appeared suddenly. Cranial nonenhanced CT was showed extensive subcortical white matter and basal ganglia abnormalities consistent with edema and hemorrhagic changes. The patient was transferred to intensive care unit and died after one day. In methanol intoxication, cerebral and intraventricular hemorrhage, cerebellar necrosis, diffuse cerebral edema, bilateral subcortical white matter necrosis and edema were defined It should also be known that 2 or 3 weeks after ingestion of methyl alcohol, the deterioration of the patient\'s general situation is responsible for cerebral subcortical hemorrhage. We have also thought that patients\' mortality and morbidity can be reduced with radiological imaging due to early diagnosis. Key words: Cerebral subcortical hemorrhage, CT, methanol intoxication, MRI

Keywords

• Cerebral subcortical hemorrhage, CT, methanol intoxication, MRI

Common Late-Onset Subcortıcal Cerebral Hemorrhage Following Excessive Alcohol Consumption: A Case Report

Öz

Bilateral körlük ve kooperasyon bozukluğu olan 50 yaşındaki erkek hasta acil servisimize başvurdu. Olgu, alkol bağımlısıydı ve bir gün öncesinde aşırı alkol tüketimi mevcuttu. Yapılan kontrastsız kranial BT incelemesi normaldi. 1,5T MR cihazında yapılan T2 ağırlıklı görüntülemede, bilateral putamen lokalizasyonunda yüksek sinyal intensitesi izlendi. Difüzyon ağırlıklı görüntülerde bu lokalizasyonlarda, difüzyon kısıtlılığı nedeniyle hiperintensiteler ve düşük ADC değerleri mevcuttu. İki hafta sonrasında hastada, aniden baş dönmesi ve konfüzyon ortaya çıktı. Yapılan kontrastsız kranial BT’de, bazal ganglionlarda ve yaygın subkortikal beyaz cevherde ödem ve hemoraji izlendi. Hasta yoğun bakım ünitesine alındı ve bir gün sonra öldü. Metanol intoksikasyonunda, serebral ve intraventriküler hemoraji, serebral ödem, bilateral subkortikal beyaz madde nekrozu görülebilir. Metil alkol alımın takiben 2-3 hafta sonrasında ani genel durum bozukluğundan serebral subkortikal hemoraji sorumludur. Erken teşhis nedeniyle radyolojik görüntüleminin, hastanın mortalite ve morbiditesini azaltabileceğini düşünmekteyiz

Anahtar Kelimeler

• Serebral subkortikal kanama, BT, metanol zehirlenmesi, MR

References

1. Wyngaardcn JB, Smith LU, Bcnnct SC. Cecil textbook of medicine. Philadelphia, Saunders 1992:113.
2. Phang PT. Passcrini L, Mielke B ct al. Brain hemorrhage associated with methanol poisoning. Crit Care Med 1988; 16:137-40.
3. Koopmans RA, Li DKB, Paty DW. Bazal ganglia lesions in methanol poisoning: MR appearance. J Comput Assist Tomogr 1988;12:168-9.
4. Kuteifan K, Oesterle H, Tajahmady T, et al. Necrosis and haemorrhage of the putamen inmethanol poisoning shown onMRI. Neuroradiology 1998;40:158-60.
5. Server A, Hovada K.E, Nakstad P. Hj, Conventional and Diffusion – Weighted MRI in the Evaluation of Methanol Poisoning, A Case Report. Acta Radiologica 2003;44:691–5.
6. Deniz S, Oppenheim C, Lehericy S, et al. Diffusion- weighted magnetic resonance imaging in a case of metha- nol intoxication. Neurotoxicology 2000; 21: 405–8.
7. Glazer M, Dross P. Necrosis of the putamen caused by methanol intoxication:MR findings. AJR 1993;160:1105–6.