Uremic Encephalopathy Associated with Bilateral Basal Ganglia and Cerebellar Lesion in a Non-diabetic Hemodialysis Patient.
- Author:
Soung Rok SIM
1
;
Sang Hun LEE
;
Jae Hoon JAHNG
;
Jae Yun LIM
;
You Kyoung CHOI
;
Ki Sun BAE
;
Woo Il PARK
;
Ki Joong KIM
;
Kyung Yul LEE
;
Hyeong Cheon PARK
;
Sung Kyu HA
Author Information
1. Department of Internal Medicine, College of Medicine, Yonsei University, Seoul, Korea. hask1951@yumc.yonsei.ac.kr
- Publication Type:Case Report
- Keywords:
Bilateral basal ganglia;
Cerebellar vermis;
Metabolic acidosis;
Non-dia betic ESRD;
Uremic encephalopathy
- MeSH:
Acidosis;
Ataxia;
Basal Ganglia*;
Brain;
Central Nervous System;
Dysarthria;
Follow-Up Studies;
Humans;
Hypoglycemia;
Hypokinesia;
Magnetic Resonance Imaging;
Middle Aged;
Myalgia;
Neurologic Manifestations;
Polycystic Kidney, Autosomal Dominant;
Renal Dialysis*;
Rhabdomyolysis;
Risk Factors;
Tomography, X-Ray Computed
- From:Korean Journal of Nephrology
2006;25(6):1061-1066
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Involvement of central nervous system is a well- known compication in uremic patients. However, development of acute extrapyramidal symptoms with bilateral basal ganglia involvement (acute basal ganglia syndrome), especially in non-diabetic hemodialysis patient is very rare. We report a case of acute basal ganglia syndrome in a non-diabetic hemodialysis patient. A 45-year-old man with autosomal dominant polycystic kidney disease (ADPKD) on chronic hemodialysis treatment for the last 4 years was admitted due to generalized myalgia. On admission, the patient was found to have rhabdomyolysis and intractable metabolic acidosis. Nine days after admission, he suddenly developed dysarthria, lateralizing ataxia, and bradykinesia. Brain MRI demonstrated low and high signals in bilateral basal ganglia and cerebellar vermis in T1-weighted and T2-weighted images, respectively. Intensified hemodialysis treatment combined with general supportive therapy resolved the severe metabolic acidosis and the neurologic manifestations gradually improved. Follow up brain CT scan taken 3 months later showed decreased size of initial low attenuation lesions in bilateral basal ganglia and cerebellar vermis. Although no definite pathophysiology is yet established, severe metabolic disorder is believed to play an important role in development of acute basal ganglia syndrome. Correction of metabolic acidosis and hypoglycemia in our patient lead to improvement in neurologic manifestations and organic brain lesions. Our case suggests that severe metabolic acidosis and hypoglycemia in uremic patient may act as risk factors for acute basal ganglia syndrome even in non-diabetic patient.
