Hepatic myelopathy associated with advanced liver cirrhosis.

A 41-year-old man was admitted to our institution with inertia of both lower extremities and walking instability. The patient had been diagnosed with chronic hepatitis B (hepa B) for 10 years, including hepa B virus associated cirrhosis within the last 4 years. The patient had also suffered hepatic encephalopathy within the last 6 months, which resolved following treatment. A month before the current admission, the patient experienced difficulty in moving both lower extremities, which gradually worsened until medical attention was sought. The patient's ability to walk was significantly impaired, with a markedly altered gait and swinging of the upper-body, especially when walking with his eyes closed. The patient reported no numbness or tightness of the lower extremities; furthermore, there was no urinary or fecal incontinence. Physical examination showed the patient had normal levels of consciousness, a spastic gait as described above, and numerous indictors of underlying liver disease including hepatic facies, yellowing of the sclera, palmar erythema and spider angioma, although Kayser-Fleischer rings were absent. Heart and lung function was assessed and found to be normal. The abdomen was distended, the liver was not palpable, and splenomegaly was noted. There was no shifting dullness. Examination of all the limbs revealed no evidence of myotrophy, and the muscular power and tension of the muscles in the upper extremities was normal. Examination of the lower limbs revealed muscle rigidity with normal muscle power. The patellar reflex was present in both lower limbs; similarly, the Babinski reflex was also normal. Deep and light touch sensations were normal. Laboratory blood tests revealed the following results: white blood cell count = 3.1 × 10 9 /L; red blood cell count = 2.85 × 10 12 /L; hemoglobin concentration = 98 g/L; platelet count = 40 × 10 9 /L. Laboratory testing of liver function yielded the following results: alanine aminotransferase activity = 44 IU/L; aspartate aminotransferase activity = 83 IU/L; γ-glutamyl transpeptidase activity = 69 IU/L; the concentration of serum total bilirubin = 57.1 µmol/L, serum albumin = 27.2 g/L, and blood ammonia = 130 µmol/L. The alpha-fetoprotein levels were normal. The patient was positive for hepa B virus surface antigen (HBsAg), and possessed anti hepa B e antigen and anti hepa B c antibodies. Abdominal ultrasound examination revealed changes that were characteristic of liver cirrhosis, the portal vein was widened, and there was embolization in the portal vein. Splenomegaly was also observed. Examination of …