Bulbar Palsy

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M. Nakazato - One of the best experts on this subject based on the ideXlab platform.

  • Bulbar Palsy in senile onset familial amyloid polyneuropathy 30val met transthyretin amyloid deposits in the hypoglossal nerve root
    European Journal of Neurology, 1998
    Co-Authors: K. Ikeda, M. Kinoshita, K. Takamiya, Y. Iwasaki, Y. Tomita, I. Nakano, M. Nakazato
    Abstract:

    Japanese familial amyloid polyneuropathy (FAP type I) is characterized clinically by autonomic and sensorimotor polyneuropathy. Bulbar Palsy or lower cranial amyloid neuropathy has not been reported in this disease. We report a 72-year-old man with senile onset FAP type I, who developed Bulbar Palsy and sensorimotor polyneuropathy without autonomic failures. He noticed dysesthesia and muscle weakness in the feet at the age of 67 years. Neurological examination showed Bulbar signs and sensorimotor polyneuropathy, but not autonomic neuropathy. Electromyography showed denervation in the tongue and extremities. Sural nerve biopsy revealed a profound reduction of myelinated fibers. Neuropathological studies indicated axonal degeneration and transthyretin-amyloid deposits in the peripheral nerves and hypoglossal nerves or roots. DNA analysis demonstrated transthyretinMet30 mutation. We provide the novel possibility that Bulbar Palsy, due to amyloid neuropathy, can occur in FAP type I. Copyright Rapid Science Ltd

  • Bulbar Palsy in senile onset familial amyloid polyneuropathy (30Val-->Met): transthyretin-amyloid deposits in the hypoglossal nerve root.
    European journal of neurology, 1998
    Co-Authors: K. Ikeda, M. Kinoshita, K. Takamiya, Y. Iwasaki, Y. Tomita, I. Nakano, M. Nakazato
    Abstract:

    Japanese familial amyloid polyneuropathy (FAP type I) is characterized clinically by autonomic and sensorimotor polyneuropathy. Bulbar Palsy or lower cranial amyloid neuropathy has not been reported in this disease. We report a 72-year-old man with senile onset FAP type I, who developed Bulbar Palsy and sensorimotor polyneuropathy without autonomic failures. He noticed dysesthesia and muscle weakness in the feet at the age of 67 years. Neurological examination showed Bulbar signs and sensorimotor polyneuropathy, but not autonomic neuropathy. Electromyography showed denervation in the tongue and extremities. Sural nerve biopsy revealed a profound reduction of myelinated fibers. Neuropathological studies indicated axonal degeneration and transthyretin-amyloid deposits in the peripheral nerves and hypoglossal nerves or roots. DNA analysis demonstrated transthyretinMet30 mutation. We provide the novel possibility that Bulbar Palsy, due to amyloid neuropathy, can occur in FAP type I. Copyright Rapid Science Ltd

K. Ikeda - One of the best experts on this subject based on the ideXlab platform.

  • Bulbar Palsy in senile onset familial amyloid polyneuropathy 30val met transthyretin amyloid deposits in the hypoglossal nerve root
    European Journal of Neurology, 1998
    Co-Authors: K. Ikeda, M. Kinoshita, K. Takamiya, Y. Iwasaki, Y. Tomita, I. Nakano, M. Nakazato
    Abstract:

    Japanese familial amyloid polyneuropathy (FAP type I) is characterized clinically by autonomic and sensorimotor polyneuropathy. Bulbar Palsy or lower cranial amyloid neuropathy has not been reported in this disease. We report a 72-year-old man with senile onset FAP type I, who developed Bulbar Palsy and sensorimotor polyneuropathy without autonomic failures. He noticed dysesthesia and muscle weakness in the feet at the age of 67 years. Neurological examination showed Bulbar signs and sensorimotor polyneuropathy, but not autonomic neuropathy. Electromyography showed denervation in the tongue and extremities. Sural nerve biopsy revealed a profound reduction of myelinated fibers. Neuropathological studies indicated axonal degeneration and transthyretin-amyloid deposits in the peripheral nerves and hypoglossal nerves or roots. DNA analysis demonstrated transthyretinMet30 mutation. We provide the novel possibility that Bulbar Palsy, due to amyloid neuropathy, can occur in FAP type I. Copyright Rapid Science Ltd

  • Bulbar Palsy in senile onset familial amyloid polyneuropathy (30Val-->Met): transthyretin-amyloid deposits in the hypoglossal nerve root.
    European journal of neurology, 1998
    Co-Authors: K. Ikeda, M. Kinoshita, K. Takamiya, Y. Iwasaki, Y. Tomita, I. Nakano, M. Nakazato
    Abstract:

    Japanese familial amyloid polyneuropathy (FAP type I) is characterized clinically by autonomic and sensorimotor polyneuropathy. Bulbar Palsy or lower cranial amyloid neuropathy has not been reported in this disease. We report a 72-year-old man with senile onset FAP type I, who developed Bulbar Palsy and sensorimotor polyneuropathy without autonomic failures. He noticed dysesthesia and muscle weakness in the feet at the age of 67 years. Neurological examination showed Bulbar signs and sensorimotor polyneuropathy, but not autonomic neuropathy. Electromyography showed denervation in the tongue and extremities. Sural nerve biopsy revealed a profound reduction of myelinated fibers. Neuropathological studies indicated axonal degeneration and transthyretin-amyloid deposits in the peripheral nerves and hypoglossal nerves or roots. DNA analysis demonstrated transthyretinMet30 mutation. We provide the novel possibility that Bulbar Palsy, due to amyloid neuropathy, can occur in FAP type I. Copyright Rapid Science Ltd

Y. Tomita - One of the best experts on this subject based on the ideXlab platform.

  • Bulbar Palsy in senile onset familial amyloid polyneuropathy 30val met transthyretin amyloid deposits in the hypoglossal nerve root
    European Journal of Neurology, 1998
    Co-Authors: K. Ikeda, M. Kinoshita, K. Takamiya, Y. Iwasaki, Y. Tomita, I. Nakano, M. Nakazato
    Abstract:

    Japanese familial amyloid polyneuropathy (FAP type I) is characterized clinically by autonomic and sensorimotor polyneuropathy. Bulbar Palsy or lower cranial amyloid neuropathy has not been reported in this disease. We report a 72-year-old man with senile onset FAP type I, who developed Bulbar Palsy and sensorimotor polyneuropathy without autonomic failures. He noticed dysesthesia and muscle weakness in the feet at the age of 67 years. Neurological examination showed Bulbar signs and sensorimotor polyneuropathy, but not autonomic neuropathy. Electromyography showed denervation in the tongue and extremities. Sural nerve biopsy revealed a profound reduction of myelinated fibers. Neuropathological studies indicated axonal degeneration and transthyretin-amyloid deposits in the peripheral nerves and hypoglossal nerves or roots. DNA analysis demonstrated transthyretinMet30 mutation. We provide the novel possibility that Bulbar Palsy, due to amyloid neuropathy, can occur in FAP type I. Copyright Rapid Science Ltd

  • Bulbar Palsy in senile onset familial amyloid polyneuropathy (30Val-->Met): transthyretin-amyloid deposits in the hypoglossal nerve root.
    European journal of neurology, 1998
    Co-Authors: K. Ikeda, M. Kinoshita, K. Takamiya, Y. Iwasaki, Y. Tomita, I. Nakano, M. Nakazato
    Abstract:

    Japanese familial amyloid polyneuropathy (FAP type I) is characterized clinically by autonomic and sensorimotor polyneuropathy. Bulbar Palsy or lower cranial amyloid neuropathy has not been reported in this disease. We report a 72-year-old man with senile onset FAP type I, who developed Bulbar Palsy and sensorimotor polyneuropathy without autonomic failures. He noticed dysesthesia and muscle weakness in the feet at the age of 67 years. Neurological examination showed Bulbar signs and sensorimotor polyneuropathy, but not autonomic neuropathy. Electromyography showed denervation in the tongue and extremities. Sural nerve biopsy revealed a profound reduction of myelinated fibers. Neuropathological studies indicated axonal degeneration and transthyretin-amyloid deposits in the peripheral nerves and hypoglossal nerves or roots. DNA analysis demonstrated transthyretinMet30 mutation. We provide the novel possibility that Bulbar Palsy, due to amyloid neuropathy, can occur in FAP type I. Copyright Rapid Science Ltd

I. Nakano - One of the best experts on this subject based on the ideXlab platform.

  • Bulbar Palsy in senile onset familial amyloid polyneuropathy 30val met transthyretin amyloid deposits in the hypoglossal nerve root
    European Journal of Neurology, 1998
    Co-Authors: K. Ikeda, M. Kinoshita, K. Takamiya, Y. Iwasaki, Y. Tomita, I. Nakano, M. Nakazato
    Abstract:

    Japanese familial amyloid polyneuropathy (FAP type I) is characterized clinically by autonomic and sensorimotor polyneuropathy. Bulbar Palsy or lower cranial amyloid neuropathy has not been reported in this disease. We report a 72-year-old man with senile onset FAP type I, who developed Bulbar Palsy and sensorimotor polyneuropathy without autonomic failures. He noticed dysesthesia and muscle weakness in the feet at the age of 67 years. Neurological examination showed Bulbar signs and sensorimotor polyneuropathy, but not autonomic neuropathy. Electromyography showed denervation in the tongue and extremities. Sural nerve biopsy revealed a profound reduction of myelinated fibers. Neuropathological studies indicated axonal degeneration and transthyretin-amyloid deposits in the peripheral nerves and hypoglossal nerves or roots. DNA analysis demonstrated transthyretinMet30 mutation. We provide the novel possibility that Bulbar Palsy, due to amyloid neuropathy, can occur in FAP type I. Copyright Rapid Science Ltd

  • Bulbar Palsy in senile onset familial amyloid polyneuropathy (30Val-->Met): transthyretin-amyloid deposits in the hypoglossal nerve root.
    European journal of neurology, 1998
    Co-Authors: K. Ikeda, M. Kinoshita, K. Takamiya, Y. Iwasaki, Y. Tomita, I. Nakano, M. Nakazato
    Abstract:

    Japanese familial amyloid polyneuropathy (FAP type I) is characterized clinically by autonomic and sensorimotor polyneuropathy. Bulbar Palsy or lower cranial amyloid neuropathy has not been reported in this disease. We report a 72-year-old man with senile onset FAP type I, who developed Bulbar Palsy and sensorimotor polyneuropathy without autonomic failures. He noticed dysesthesia and muscle weakness in the feet at the age of 67 years. Neurological examination showed Bulbar signs and sensorimotor polyneuropathy, but not autonomic neuropathy. Electromyography showed denervation in the tongue and extremities. Sural nerve biopsy revealed a profound reduction of myelinated fibers. Neuropathological studies indicated axonal degeneration and transthyretin-amyloid deposits in the peripheral nerves and hypoglossal nerves or roots. DNA analysis demonstrated transthyretinMet30 mutation. We provide the novel possibility that Bulbar Palsy, due to amyloid neuropathy, can occur in FAP type I. Copyright Rapid Science Ltd

K. Takamiya - One of the best experts on this subject based on the ideXlab platform.

  • Bulbar Palsy in senile onset familial amyloid polyneuropathy 30val met transthyretin amyloid deposits in the hypoglossal nerve root
    European Journal of Neurology, 1998
    Co-Authors: K. Ikeda, M. Kinoshita, K. Takamiya, Y. Iwasaki, Y. Tomita, I. Nakano, M. Nakazato
    Abstract:

    Japanese familial amyloid polyneuropathy (FAP type I) is characterized clinically by autonomic and sensorimotor polyneuropathy. Bulbar Palsy or lower cranial amyloid neuropathy has not been reported in this disease. We report a 72-year-old man with senile onset FAP type I, who developed Bulbar Palsy and sensorimotor polyneuropathy without autonomic failures. He noticed dysesthesia and muscle weakness in the feet at the age of 67 years. Neurological examination showed Bulbar signs and sensorimotor polyneuropathy, but not autonomic neuropathy. Electromyography showed denervation in the tongue and extremities. Sural nerve biopsy revealed a profound reduction of myelinated fibers. Neuropathological studies indicated axonal degeneration and transthyretin-amyloid deposits in the peripheral nerves and hypoglossal nerves or roots. DNA analysis demonstrated transthyretinMet30 mutation. We provide the novel possibility that Bulbar Palsy, due to amyloid neuropathy, can occur in FAP type I. Copyright Rapid Science Ltd

  • Bulbar Palsy in senile onset familial amyloid polyneuropathy (30Val-->Met): transthyretin-amyloid deposits in the hypoglossal nerve root.
    European journal of neurology, 1998
    Co-Authors: K. Ikeda, M. Kinoshita, K. Takamiya, Y. Iwasaki, Y. Tomita, I. Nakano, M. Nakazato
    Abstract:

    Japanese familial amyloid polyneuropathy (FAP type I) is characterized clinically by autonomic and sensorimotor polyneuropathy. Bulbar Palsy or lower cranial amyloid neuropathy has not been reported in this disease. We report a 72-year-old man with senile onset FAP type I, who developed Bulbar Palsy and sensorimotor polyneuropathy without autonomic failures. He noticed dysesthesia and muscle weakness in the feet at the age of 67 years. Neurological examination showed Bulbar signs and sensorimotor polyneuropathy, but not autonomic neuropathy. Electromyography showed denervation in the tongue and extremities. Sural nerve biopsy revealed a profound reduction of myelinated fibers. Neuropathological studies indicated axonal degeneration and transthyretin-amyloid deposits in the peripheral nerves and hypoglossal nerves or roots. DNA analysis demonstrated transthyretinMet30 mutation. We provide the novel possibility that Bulbar Palsy, due to amyloid neuropathy, can occur in FAP type I. Copyright Rapid Science Ltd