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Yasuo Suzuki - One of the best experts on this subject based on the ideXlab platform.

  • Ataxia and middle cerebellar peduncle lesions in hepatic encephalopathy.
    Neuroradiology, 2009
    Co-Authors: Ryuichi Furukawa, Ryuji Sakakibara, Nobuo Hosoe, Masahiko Kishi, Emina Ogawa, Yasuo Suzuki
    Abstract:

    Sir,Brain MRI in patients with hepatic encephalopathy (HE)shows hyperintensity in the globus pallidus on T1-weightedimages, which is thought to reflect manganese andammonia accumulation in situ [1, 2]. Those patientscommonly have asterexis, disturbed consciousness, andextrapyramidal features [1, 2]. In contrast, ataxia in HE israre [3], and MRI correlates for ataxia have not beenentirely clear [4, 5]. We recently had a woman who, duringa course of HE, presented with bilateral, middle cerebellarpeduncle lesions and ataxia, both of which ameliorated afterbranched amino acid treatment.A 57-year-old woman suffered from primary biliarycirrhosis and hepatocellular carcinoma for the past 7 years.One year after the onset of diseases, she developedasterexis and disorientation to time and place. An intrave-nous administration of branched amino acid ameliorated hersymptoms. She was then started on kanamycin andlaxatives. However, 1 month before admission to ourhospital, an abdominal MRI revealed a recurrence ofhepatocellular carcinoma; in addition, she developedunsteadiness of the gait but without Flapping Tremor. Onadmission, she had slight disorientation to place. She hadcerebellar ataxia on finger to nose test, diadochokinesis,and heel-to-knee test. She had no extrapyramidal features orFlapping Tremor. Blood tests showed increased serum levelsof ammonia 183μg/dl (30–80) and total bilirubin 1.5 mg/dl(0.2–1.0). Brain MRI revealed high signal intensity in theglobus pallidus on T1-weighted image, and markedly highsignal intensity in the middle cerebellar peduncle bilaterally(Fig. 1a) and slightly high signal intensity in the cerebralwhite matter on T2-weighted image. We started her on anintravenous administration of 500 ml/day (valine 0.84%,leucine 1.10%, isoleucine 0.90%) intravenous branchedamino acid and low protein diet. Three weeks later, herataxia ameliorated significantly, and serum ammonia levelsdecreased to 113μg/dl. A post-treatment MRI scan, whichwas performed 1 month later, showed reduction inhyperintense signal (Fig. 1b).Previously, four reports of brain MRI imaging for ataxiain HE are available [4–7]. Park and Heo [4] reported a46-year-old man with acquired hepatocerebral degenerationwho developed ataxia and bilateral, middle cerebellarpeduncle lesions. In a review article, Uchino and colleagues[5] showed similar MRI findings. Nagura and colleagues[6] reported a 66-year-old man with portal-systemic shunt,with irreversible middle cerebellar peduncle involvement,attributed to hyperammonemia. Deguchi and colleagues [7]reported a 58-year-old woman with similar MRI findings,which improved by intravenous branched amino acids. Todate, no pathology studies are available accounting for theMRI abnormalities in the middle cerebellar peduncle.However, in cases of HE, demyelination has been demon-strated in the cerebral white matter [8], pontine base [9],and corticospinal tract [10]. Since myelinated axon is themain histological constituent in the cerebellar peduncle, theMRI findings in the middle cerebellar peduncle mightreflect demyelination. Since intravenous branched aminoacid soon ameliorated ataxia and the MRI lesions, togetherwith reversal of serum ammonia levels, cytotoxic edema

Rasoul Fatima - One of the best experts on this subject based on the ideXlab platform.

  • Rifampicin-isoniazid induced fatal fulminant hepatitis during treatment of latent tuberculosis: A case report and literature review
    Medknow Publications on behalf of the Indian Society of Critical Care Medicine, 2010
    Co-Authors: Khan, Fahmi Yousef, Rasoul Fatima
    Abstract:

    A 42-year-old Indian man received 450 mg rifampicin (RIF) and 150 mg isoniazid (INH) daily after being diagnosed of a latent tuberculosis infection. Baseline serum aminotransferase and total bilirubin levels were within normal limits. On day 31 of treatment, the patient experienced epigastric discomfort and general malaise and one week later he developed nausea and episodic vomiting. The patient missed his first scheduled clinic appointment and he continued taking RIF-INH despite his symptoms. He visited the tuberculosis clinic on day 47 of treatment where he was found to be jaundiced and his liver enzymes were elevated. RIF-INH was stopped and the patient was admitted to our hospital as a case of RIF-INH induced hepatitis. On the 7th day of hospitalization, the patient developed consciousness disturbance with Flapping Tremor and high ammonia level. The patient was diagnosed with fulminant hepatic failure and transferred immediately to the medical intensive care unit, where he died 4 days later

  • Rifampicin-isoniazid induced fatal fulminant hepatitis during treatment of latent tuberculosis: A case report and literature review
    Medknow Publications, 2010
    Co-Authors: Khan Fahmi, Rasoul Fatima
    Abstract:

    A 42-year-old Indian man received 450 mg rifampicin (RIF) and 150 mg isoniazid (INH) daily after being diagnosed of a latent tuberculosis infection. Baseline serum aminotransferase and total bilirubin levels were within normal limits. On day 31 of treatment, the patient experienced epigastric discomfort and general malaise and one week later he developed nausea and episodic vomiting. The patient missed his first scheduled clinic appointment and he continued taking RIF-INH despite his symptoms. He visited the tuberculosis clinic on day 47 of treatment where he was found to be jaundiced and his liver enzymes were elevated. RIF-INH was stopped and the patient was admitted to our hospital as a case of RIF-INH induced hepatitis. On the 7th day of hospitalization, the patient developed consciousness disturbance with Flapping Tremor and high ammonia level. The patient was diagnosed with fulminant hepatic failure and transferred immediately to the medical intensive care unit, where he died 4 days later

Takeyori Saheki - One of the best experts on this subject based on the ideXlab platform.

  • complete neurological recovery of an adult patient with type ii citrullinemia after living related partial liver transplantation
    Transplantation, 1996
    Co-Authors: Masahide Yazaki, Shuichi Ikeda, Yoichi Takei, Nobuo Yanagisawa, Hidetoshi Matsunami, Yasuhiko Hashikura, Seiji Kawasaki, Masatoshi Makuuchi, Keiko Kobayashi, Takeyori Saheki
    Abstract:

    Type II citrullinemia is an adult-onset hepatocerebral disease caused by a deficiency of argininosuccinate synthetase in liver. A 25-year-old Japanese man suddenly developed encephalopathy, showing disorientation and Flapping Tremor. Plasma concentrations of ammonia and citrulline were extremely high, and hepatic argininosuccinate synthetase activity was deficient. The patient's condition deteriorated rapidly in spite of intensive medications. Therefore, we performed a partial liver transplantation using a graft obtained from his healthy 61-year-old father. After surgery, his neurological symptoms soon disappeared and plasma levels of ammonia and citrulline were normalized within 3 months after operation. Type II citrullinemia is one fulminant form of various liver-based metabolic diseases, and immediate liver transplantation is necessary to rescue patients with this disease. As liver transplantation from cadaveric donor is still not possible in Japan, it seems justifiable to use living related partial liver transplantation for our patient.

Hans Rittmannsberger - One of the best experts on this subject based on the ideXlab platform.

  • medikamentos ausgeloste asterixis
    Deutsche Medizinische Wochenschrift, 2008
    Co-Authors: Hans Rittmannsberger, F Leblhuber
    Abstract:

    : A 54-year-old woman with acute schizoaffective psychosis was treated with lithium carbonate (1,350 mg daily) and zuclopenthixol. On admission, clozapine was added (250 mg daily). Because extrapyramidal symptoms (rigor, akinesia) developed, she was additionally given biperiden retard (4 mg daily) from the fourth hospital day onwards. Eleven days after admission she began to complain of "unsteadiness" and "Tremors" in her arms and she had asterixis (Flapping Tremor) on holding up her arms. The electromyogram showed electrical pauses of 60-120 ms, typical for asterixis. There were no significant metabolic or organic cerebral changes that could have accounted for the symptoms which presumably had been induced by the drugs even though their dosage was not unusual. The symptoms in fact regressed completely after the clozapine dose had been reduced, at first to 125 mg then to 50 mg. Previous experience has suggested that the risk of asterixis is particularly high when lithium and clozapine are taken together.

  • asterixis induced by psychotropic drug treatment
    Clinical Neuropharmacology, 1996
    Co-Authors: Hans Rittmannsberger
    Abstract:

    Summary:Asterixis (Flapping Tremor) can be induced by treatment with psychopharmacologic agents. We observed 10 cases of asterixis in psychiatric inpatients, most with affective spectrum disorders being treated with combination therapy. The drugs most often used were clozapine (eight cases), lithium

Ryuichi Furukawa - One of the best experts on this subject based on the ideXlab platform.

  • Ataxia and middle cerebellar peduncle lesions in hepatic encephalopathy.
    Neuroradiology, 2009
    Co-Authors: Ryuichi Furukawa, Ryuji Sakakibara, Nobuo Hosoe, Masahiko Kishi, Emina Ogawa, Yasuo Suzuki
    Abstract:

    Sir,Brain MRI in patients with hepatic encephalopathy (HE)shows hyperintensity in the globus pallidus on T1-weightedimages, which is thought to reflect manganese andammonia accumulation in situ [1, 2]. Those patientscommonly have asterexis, disturbed consciousness, andextrapyramidal features [1, 2]. In contrast, ataxia in HE israre [3], and MRI correlates for ataxia have not beenentirely clear [4, 5]. We recently had a woman who, duringa course of HE, presented with bilateral, middle cerebellarpeduncle lesions and ataxia, both of which ameliorated afterbranched amino acid treatment.A 57-year-old woman suffered from primary biliarycirrhosis and hepatocellular carcinoma for the past 7 years.One year after the onset of diseases, she developedasterexis and disorientation to time and place. An intrave-nous administration of branched amino acid ameliorated hersymptoms. She was then started on kanamycin andlaxatives. However, 1 month before admission to ourhospital, an abdominal MRI revealed a recurrence ofhepatocellular carcinoma; in addition, she developedunsteadiness of the gait but without Flapping Tremor. Onadmission, she had slight disorientation to place. She hadcerebellar ataxia on finger to nose test, diadochokinesis,and heel-to-knee test. She had no extrapyramidal features orFlapping Tremor. Blood tests showed increased serum levelsof ammonia 183μg/dl (30–80) and total bilirubin 1.5 mg/dl(0.2–1.0). Brain MRI revealed high signal intensity in theglobus pallidus on T1-weighted image, and markedly highsignal intensity in the middle cerebellar peduncle bilaterally(Fig. 1a) and slightly high signal intensity in the cerebralwhite matter on T2-weighted image. We started her on anintravenous administration of 500 ml/day (valine 0.84%,leucine 1.10%, isoleucine 0.90%) intravenous branchedamino acid and low protein diet. Three weeks later, herataxia ameliorated significantly, and serum ammonia levelsdecreased to 113μg/dl. A post-treatment MRI scan, whichwas performed 1 month later, showed reduction inhyperintense signal (Fig. 1b).Previously, four reports of brain MRI imaging for ataxiain HE are available [4–7]. Park and Heo [4] reported a46-year-old man with acquired hepatocerebral degenerationwho developed ataxia and bilateral, middle cerebellarpeduncle lesions. In a review article, Uchino and colleagues[5] showed similar MRI findings. Nagura and colleagues[6] reported a 66-year-old man with portal-systemic shunt,with irreversible middle cerebellar peduncle involvement,attributed to hyperammonemia. Deguchi and colleagues [7]reported a 58-year-old woman with similar MRI findings,which improved by intravenous branched amino acids. Todate, no pathology studies are available accounting for theMRI abnormalities in the middle cerebellar peduncle.However, in cases of HE, demyelination has been demon-strated in the cerebral white matter [8], pontine base [9],and corticospinal tract [10]. Since myelinated axon is themain histological constituent in the cerebellar peduncle, theMRI findings in the middle cerebellar peduncle mightreflect demyelination. Since intravenous branched aminoacid soon ameliorated ataxia and the MRI lesions, togetherwith reversal of serum ammonia levels, cytotoxic edema