Eda ÇOBAN KILIÇ, Mehmet Ali ALDAN, Elmir XANMEMMEDOV, Pakize Nevin SUTLAS, Dursun KIRBAŞ

Subclinic hepatic encephalopathy presented with progressive cognitive impairment

Hepatik ensefalopati (HE), karaciğer fonksiyon bozukluğuna bağlı olarak hastalarda nöropsikiyatrik belirtilerin gelişimi ile karakterize bir tablodur. Altmış iki yaşındaki erkek hasta, son bir yıl içinde gelişen unutkanlık yakınması nedeni ile nöroloji polikliniğine başvurdu. Nörolojik ve sistemik muayenesinde zaman oryantasyonu bozukluğu dışında özellik yoktu. Kraniyal MR’da, bilateral globus pallidusta, T1 ağırlıklı incelemede hiperintens, T2 ve FLAIR ağırlıklı incelemelerde bilateral ak maddede hiperintens lezyonlar ve difüzyon kesitte ADC’de karşılığı olmayan bilateral sentrum semiovalede difüzyon kısıtlılığı gösteren alanlar gözlendi. EEG’de her iki hemisferde biyoelektrik aksama ve yavaş dalga paroksizmal aktiviteleri mevcuttu. Laboratuvar incelemelerinde karaciğer fonksiyon testlerinde bozukluk, serum amonyak düzeyinde yükseklik tespit edildi. Batın ultrasonunda splenomegali, batın tomografisinde karaciğerde siroz bulguları mevcuttu. Detaylı nöropsikiyatrik muayene sonucunda ciddi bilişsel bozukluk saptandı. Hastada kronik karaciğer hastalığı zemininde gelişen HE tablosu düşünüldü. HE’nin özellikle yaşlı hastalarda progresif kognitif yıkıma neden olabilecek subklinik bir tablo olarak akılda tutulması gerektiği bu olgu sunumu ile vurgulanmaya çalışıldı.

Progresif kognitif bozuklukla prezante olan subklinik hepatik ensefalopati olgusu

Hepatic encephalopathy reflects a spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction. A 62 year old male was admitted to our neurology policlinic with progressive cognitive impairement lasting for a year. No abnormality was detected in his systemic and neurological examination except time disorientation. His cranial MRI demonstrated high signal intensity in the bilateral globus pallidus on T1-weighted images and high signal intensity along the hemispheric white matter on FLAIR-T2-weighted images. Also diffusion restriction was seen in bilateral centrum semiovale. Laboratory data showed thrombopenia, increased transaminase and gamma glutamyl transferase, decreased albumin levels. The plasma ammonia level was high. Abdominal echosonography and CT revealed atrophic cirrhotic liver and splenomegaly. EEG was associated with low-frequency waves in both hemispheres. His detailed neuropsychiatric evaluation revealed severe cognitive impairment. In combination with laboratory and radiological data, hepatic encephalopathy was suspected. In conclusion, in a 62 year old male without any pathologic systematic or neurological examination findings, subclinic hepatic encephalopathy can be seen with progressive cognitive impairment. By presenting this case, we aimed to keep in mind the diagnosis of subclinic hepatic encephalopathy especially in elderly people with progressive cognitive impairment.

PDF

___

1. Akın P, Erten B. Hepatik ensefalopati. İstanbul Üniversitesi Cerrahpaşa Tıp Fakültesi Sürekli Tıp Eğitimi Etkinlikleri 2002; 28:111-120 (Article in Turkish).
2. Khan F, Ashalatha R. Acquired (Non-Wilsonian) hepatocerebral degeneration. Neurology India 2004; 52:527.
3. Arnold SM, Els T, Spreer J, Schumacher M. Acute hepatic encephalopathy with diffuse cortical lesions. Neuroradiology 2001; 43:551-554.
4. Ferenci P, Lockwood A, Mullen K, Tarter R, Weissenborn K, Bleir A. Hepatic encephalopathy: definition, nomenclature, diagnosis and quantification-final report of the working party at the 11th World Congresses of Gastroenterology, Vienna, 1998. Hepatology 2002; 35:716-721.
5. Weissenborn K. Diagnosis of encephalopathy. Digestion 1998; 59:22-24.
6. Ortiz M, Jacas C, Cordoba J. Minimal hepatic encephalopathy: diagnosis, clinical significance and recommendations. J Hepatol 2005; 42:45-53.
7. Norenberg MD. Astroglial dysfunction in hepatic encephalopathy. Metab Brain Dis 1998; 13:319-335.
8. Rovira A. MR imaging findings in hepatic encephalopathy. AJNR Am J Neuroradiol 2008; 29:1612-1621.
9. Brunberg JA, Kanal E, Hirsch W, Van Thiel DH. Chronic acquired hepatic failure: MR imaging of the brain at 1.5 T. AJNR Am J Neuroradiol 1991; 12:909-914.
10. Matsusue E, Kinoshita T, Ohama E, Ogawa T. Cerebral cortical and white matter lesions in chronic hepatic encephalopathy: MR-pathologic correlations. AJNR Am J Neuroradiol 2005; 26:347-351.
11. Rovira A, Mínguez B, Córdoba J, Aymerich FX. Decreased white matter lesion volume and improved cognitive function following liver transplantation. Hepatology 2007; 46:1485-1490.
12. Ziylan YZ, Uzum G, Bernard G, Diler AS, Bourre JM. Changes in the permeability of the blood-brain barrier in acute hyperammonemia: Effect of dexamethasone. Mol Chem Neuropathol 1993; 20:203-218.