RT Book, Section
A1 Seeley, William W.
A1 Tanner, Caroline M.
A1 Miller, Bruce L.
A2 Jameson, J. Larry
A2 Fauci, Anthony S.
A2 Kasper, Dennis L.
A2 Hauser, Stephen L.
A2 Longo, Dan L.
A2 Loscalzo, Joseph
SR Print(0)
ID 1155958612
T1 Dementia with Lewy Bodies
T2 Harrison's Principles of Internal Medicine, 20e
YR 2018
FD 2018
PB McGraw-Hill Education
PP New York, NY
SN 9781259644016
LK accessmedicine.mhmedical.com/content.aspx?aid=1155958612
RD 2024/04/25
AB Although  Lewy  body  disease  (LBD)  was  once  conceptualized  as  a  disease  of  the  substantia  nigra,  modern  human  postmortem  studies  with  alpha-synuclein  immunohistochemistry  revealed  that  Lewy  body  and  Lewy  neurite  pathology  most  often  begins  in  the  enteric  and  autonomic  nervous  systems  before  ascending  through  the  brainstem  to  the  substantia  nigra,  limbic  system,  and  ultimately  the  cerebral  cortex.  In  other  individuals,  disease  may  begin  in  the  olfactory  bulb  and  spread  inward  through  olfactory  system  connections.  These  sites  of  onset,  positioned  as  they  are  at  neural  interfaces  with  the  environment,  have  suggested  to  some  that  a  toxic  environmental  exposure  may  trigger  the  disease.  Individual  patients  vary  in  their  adherence  to  these  general  patterns,  and  the  tempo  and  topology  of  progression  dictate  the  clinical  syndrome.  Some  patients  with  long-standing  Parkinson’s  disease  (PD)  (Chap.  427)  without  cognitive  impairment  slowly  develop  a  dementia  that  is  associated  with  visual  hallucinations  and  fluctuating  alertness.  In  this  scenario,  the  term  Parkinson’s  disease  dementia  (PDD)  is  often  used.  In  other  patients,  dementia  and  a  neuropsychiatric  syndrome  precede  or  co-emerge  with  the  parkinsonism,  and  the  patient  is  diagnosed  with  dementia  with  Lewy  bodies  (DLB).