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Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin
Published on: March 26, 2015
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[Reversible hepatic myelopathy: a case report]
Daisuke Hirozawa1, Kei Fukada, Takahide Yaegaki
1Department of Neurology, Osaka General Medical Center.
Rinsho Shinkeigaku = Clinical Neurology
|April 8, 2014
Summary
This case study shows that ammonia-lowering therapy can reverse early-stage hepatic myelopathy in alcoholic liver cirrhosis patients. Successful treatment improved gait and nerve function, challenging the need for immediate liver transplantation.
Area of Science:
- Neurology
- Hepatology
- Gastroenterology
Background:
- Alcoholic liver cirrhosis can lead to hepatic myelopathy, a neurological complication.
- Hepatic myelopathy symptoms include gait disturbances and sensory deficits.
- Traditionally, liver transplantation is considered the primary treatment for hepatic myelopathy.
Observation:
- A 42-year-old female with alcoholic liver cirrhosis presented with spastic gait and lower extremity sensory issues.
- Elevated serum ammonia and abnormal tibial somatosensory evoked potentials (SEP) supported the diagnosis.
- Other causes of myelopathy were excluded.
Findings:
- Ammonia-lowering therapy with lactulose was administered orally.
- The patient showed significant improvement in spastic gait.
- Tibial SEP abnormalities resolved, with N30 and P38 potentials emerging post-treatment.
Implications:
- This case suggests that ammonia-lowering therapy is a viable treatment option for early-stage hepatic myelopathy.
- Early intervention with lactulose may prevent the progression of neurological deficits.
- This finding offers a less invasive therapeutic alternative to liver transplantation in select cases.
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