錐体路症状を伴うアルコール性小脳変性症—アルコール性脊髄症との関連について

Alcoholic Cerebellar Degeneration with Pyramidal Sign : In Relation to Alcoholic Myelopathy

　錐体路症状を伴うアルコール性小脳変性症の2例を報告した。第1例は，46歳女性，アルコール依存症。約8年間の大酒後に歩行障害が出現し，約2カ月で完成。錐体路症状，失調性歩行，下肢の失調などを認め，CTとMRIで小脳虫部と小脳半球背側部の萎縮を示した。第2例は，58歳男性，大酒家。約40年の大酒後に歩行障害が出現し，約4カ月で完成。錐体路症状，失調性歩行を認め，CTとMRIで小脳虫部の萎縮を示した。2例ともに入院後軽度の神経症状の改善を示したが，失調性歩行，腱反射亢進は持続している。我々の2例は，本邦では稀とされるアルコール性小脳変性症で，アルコール性脊髄症との関連を考える上でも興味ある症例である。

Two cases of alcoholic cerebellar degeneration with pyramidal sign were reported. Patient 1 with alcohol dependence syndrome was a 46-year-old woman. After the alcohol abuse of about eight years, she complained of gait disturbance. The gaitdisturbance progressively worsend in about two months and she could not ambulate freely by her-self. Neurological examination revealed nystagmus, ataxic and spastic gait, slight weakness and spas-ticity of the lower extremities, hyperreflexia of the extremities, bilateral Babinski's signs, and incoor-dination of the lower extremities. Examination of liver function and serum B12 was normal. Cranial CT scan and MRI revealed atrophy of the cerebellar vermis and dorsal part of the cerebellum. Though neurological signs slightly improved after the admission to our hospital and the abstinence from alcohol abuse, ataxic gait and hyperreflexia of the extremities have continued. Patient 2 was a 58-year-old man. He was a heavy drinker, but was not a patient with alcohol dependence syndrome. After the heavy drinking of about 40 years, he complained of gait disturbance. The gait disturbance had progressively worsend in about four months. Neurological exami-nation revealed ataxic gait, hyperreflexia of the lower extremities, and bilateral Babinski's signs. Laboratory examination revealed slight liver dysfunction with minimal GPT and moderate γ-GTP elevation. Examination of serum B12 was normal. Cranial CT scan and MRI revealed atrophy of the cerebellar vermis. Though bilateral Babinski's signs disappeared after the abstinence from heavy drinking, ataxic gait and hyperreflexia of the lower extremities have continued. Alcoholic myelopathy without hepatic cirrhosis was rarely reported. In the relation of alcoholic cerebellar degeneration to alcoholic myelopathy, our cases are interesting and important.