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Hyperammonaemic encephalopathy presenting as a stroke mimic with normal liver function tests.
Charles Nye1, Anna Francis2, Shelley Renowden3
1Neurology, North Bristol NHS Trust, Bristol, UK charles.nye@nhs.net.
BMJ Case Reports
|July 10, 2026
Summary
This case study shows that high ammonia levels (hyperammonaemia) can cause reversible brain dysfunction (encephalopathy) mimicking stroke. Early ammonia measurement is crucial for diagnosing unexplained neurological symptoms, even with normal liver tests.
Area of Science:
- Neurology
- Metabolic Disorders
- Gastroenterology
Background:
- Hyperammonaemia can cause encephalopathy mimicking focal neurological deficits.
- Encephalopathy may present with symptoms like aphasia and weakness.
- Normal liver function tests do not exclude hyperammonaemia.
Purpose of the Study:
- To report a case of hyperammonaemia presenting as acute neurological deficits.
- To emphasize the importance of early ammonia level measurement in unexplained encephalopathy.
- To discuss potential causes and management of hyperammonaemia in the absence of overt liver failure.
Main Methods:
- Case report of a man in his 60s with acute neurological symptoms.
- Diagnostic workup included CT brain, CT angiography, MRI brain, and metabolic investigations.
- Treatment involved lactulose, rifaximin, and continuous veno-venous haemofiltration.
Main Results:
- The patient presented with aphasia and right-sided weakness, progressing to altered consciousness.
- MRI revealed symmetrical basal ganglia T1 hyperintensity.
- Metabolic investigation confirmed significant hyperammonaemia (147 µmol/L).
- Treatment led to biochemical and neurological improvement with resolution of deficits.
Conclusions:
- Hyperammonaemia should be considered in cases of unexplained encephalopathy, irrespective of liver function.
- Small bowel bacterial overgrowth is a potential cause of hyperammonaemia without liver failure.
- Prompt diagnosis and management of hyperammonaemia are essential for neurological recovery.
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