TY  - CHAP
M1  - Book, Section
TI  - Guillain–Barré Syndrome and Related Disorders
A1  - Amato, Anthony A.
A1  - Russell, James A.
Y1  - 2015
N1  - 
T2  - Neuromuscular Disorders, 2e
AB  - Landry  described  a  condition  characterized  by  acute  ascending  paralysis  in  1859.  Later,  Guillain,  Barré,  and  Strohl  noted  the  areflexia  and  the  albuminocytologic  dissociation  in  the  cerebral  spinal  fluid  (CSF)  associated  with  this  neuropathy.1  The  contributions  of  Landry  and  Strohl  have  been  neglected,  and  the  neuropathy  has  been  most  commonly  referred  to  as  Guillain–Barré  syndrome  (GBS).  In  1949,  Haymaker  and  Kernohan  detailed  the  histopathologic  features  seen  in  50  fatal  cases  of  GBS.  The  earliest  features  noted  were  edema  of  the  proximal  nerves  and  the  subsequent  degeneration  of  the  myelin  sheaths  within  the  first  week  of  the  illness.  They  did  not  appreciate  inflammatory  cell  infiltrate  until  later  in  the  course  of  the  illness.2  However,  another  group  reported  prominent  perivascular  inflammation  in  the  spinal  roots,  dorsal  root  ganglia,  cranial  nerves,  and  randomly  along  the  whole  length  of  peripheral  nerves,  along  with  segmental  demyelination  adjacent  to  the  areas  of  inflammation,  in  19  autopsy  cases  of  GBS.3  Thus,  the  term  acute  inflammatory  demyelinating  polyradiculoneuropathy  (AIDP),  which  is  quite  descriptive  of  the  disease  process,  has  been  historically  used  synonymously  with  GBS.4–7  It  is  now  appreciated  that  GBS  is  not  a  single  disorder  but  again  a  syndrome  of  several  types  of  acute  immune-mediated  polyneuropathies  (Table  13-1).8–11  In  addition  to  AIDP,  there  are  two  axonal  forms  of  GBS:  acute  motor–sensory  axonal  neuropathy  (AMSAN)  and  acute  motor  axonal  neuropathy  (AMAN).  Further,  some  disorders  that  appear  clinically  different  from  AIDP  (e.g.,  the  Miller  Fisher  syndrome  [MFS]  and  acute  autonomic  neuropathy)  may  share  similar  pathogenesis  and  can  be  considered  variants  of  GBS.  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/23
UR  - neurology.mhmedical.com/content.aspx?aid=1115658281
ER  -