Why do tremors occur after overt hepatic encephalopathy?

Question

Hello doctor,

I am 39, and I was diagnosed with cirrhosis secondary to Wilson's disease about four years ago. I had my first episode of overt hepatic encephalopathy two months ago. I am on Penicillamine for Wilson's disease, and my copper levels have been reasonably controlled. My hepatologist thinks the overt hepatic encephalopathy was precipitated by a gastrointestinal bleed from a peptic ulcer - my hemoglobin dropped to 6.8 g/dL, and I needed three units of blood.

I am now on Pantoprazole, and the ulcer has healed on endoscopy. My current ammonia is 84 µmol/L on Lactulose 20 mL twice daily. But my neurologist is concerned because I still have persistent neurological symptoms such as hand tremors and word-finding difficulties, even though the acute overt hepatic encephalopathy has resolved. She is unsure whether these residual symptoms are from the OHE or from the neurological manifestation of Wilson's disease itself because Wilson's can also cause neurological damage. My ophthalmologist confirmed that Kayser-Fleischer rings are still visible.

My MELD score is 17, and the transplant team has done a preliminary evaluation. I am also a teacher and have been on medical leave for three months; the cognitive symptoms are making it impossible to return to work. Is there any specific neurological rehabilitation for post-OHE cognitive issues, and how do we separate the Wilson's disease neurological damage from the overt hepatic encephalopathy effects?

Please help.

Answer 1

Hi,

Welcome to icliniq.com.

I understand your concern.

Your situation is understandably challenging because both Wilson’s disease and hepatic encephalopathy can affect the brain and cause overlapping neurological symptoms.

In cirrhosis related to Wilson’s disease, toxin buildup, especially ammonia, can temporarily impair brain function during episodes of overt hepatic encephalopathy (OHE). The gastrointestinal bleed you experienced was a well-known trigger, and treatment with Lactulose to maintain two to three soft bowel movements daily is appropriate to help prevent recurrence. Persistent symptoms such as tremor or difficulty finding words after recovery from OHE are not uncommon. Some patients experience residual cognitive slowing for weeks to months while the brain gradually recovers.

However, Wilson’s disease itself can also produce neurological manifestations due to copper deposition in the brain, which may cause tremor, coordination problems, or speech difficulties. Continued therapy with Penicillamine helps reduce copper accumulation and prevent further neurological injury. Distinguishing between the two causes usually involves a combination of neurological examination, brain imaging (often MRI), and copper studies. MRI (magnetic resonance imaging) patterns or progression despite good copper control may suggest Wilson-related neurological involvement, while fluctuating symptoms linked to ammonia levels or liver function often point toward encephalopathy.

Regarding recovery, structured cognitive and neurological rehabilitation can be helpful. Programs involving speech therapy, memory exercises, and occupational therapy may improve concentration, language function, and daily cognitive performance after OHE. Since your MELD (model for end-stage liver disease) score is 17 and transplant evaluation has begun, ongoing monitoring by a hepatology and transplant team is important. In advanced Wilson-related cirrhosis, liver transplantation can correct the metabolic defect and often improves both liver function and encephalopathy.

Close coordination between hepatology and neurology will help determine whether your remaining symptoms are more related to Wilson’s disease or residual encephalopathy and guide the most appropriate rehabilitation and treatment plan.

I hope this information helps you.

Feel free to reach out in case of further queries.

Thank you.