Article info
Image of the moment
Familial progressive bilateral facial paralysis in Finnish type hereditary amyloidosis
- Correspondence to Dr Paulo Victor Sgobbi de Souza, Department of Neurology and Neurosurgery, Universidade Federal de São Paulo (UNIFESP), São Paulo, Brazil. Rua Estado de Israel, 899; ZIP CODE: 04022-002. Vila Clementino, São Paulo SP, Brazil; pvsgobbi{at}gmail.com
Citation
Familial progressive bilateral facial paralysis in Finnish type hereditary amyloidosis
Publication history
- Revised May 18, 2017
- Accepted May 20, 2017
- First published June 3, 2017.
Online issue publication
September 19, 2017
Article Versions
- Previous version (19 September 2017).
- You are viewing the most recent version of this article.
Request permissions
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.
Copyright information
© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.
Other content recommended for you
- Danish type gelsolin related amyloidosis: 654G-T mutation is associated with a disease pathogenetically and clinically similar to that caused by the 654G-A mutation (familial amyloidosis of the Finnish type)
- Ocular manifestations of familial amyloidotic polyneuropathy type I: long term follow up
- Familial amyloidosis of the Finnish type: clinical and neurophysiological features of two index cases
- Late onset lattice corneal dystrophy with systemic familial amyloidosis, amyloidosis V, in an English family
- Amyloid diseases of the heart: assessment, diagnosis, and referral
- Pathological changes long after liver transplantation in a familial amyloidotic polyneuropathy patient
- Bilateral optic neuropathy in a patient with familial amyloidotic polyneuropathy
- Amyloidosis
- Amyloid heart disease: a brief review of treatment options
- Common origin of the Val30Met mutation responsible for the amyloidogenic transthyretin type of familial amyloidotic polyneuropathy