TY  - CHAP
M1  - Book, Section
TI  - Cranial Nerve Motor Nuclei and Brain Stem Motor Functions
A1  - Martin, John H.
PY  - 2016
T2  - Neuroanatomy Text and Atlas, 4e
AB  - CLINICAL  CASE  |  Hemiparesis  and  Lower  Facial  DroopA  69-year-old  man,  with  a  history  of  hypertension  and  cigarette  smoking,  suddenly  developed  difficulty  walking  as  he  was  returning  home  from  shopping.  Upon  reaching  his  apartment,  he  was  unable  to  raise  a  cup  of  coffee  with  his  right  hand.  He  called  his  daughter  for  assistance,  who  later  noted  that  his  speech  was  slurred.  She  brought  him  to  the  emergency  room.On  neurological  examination,  somatic  sensations  on  his  limbs  and  trunk  were  normal.  His  cranial  nerve  functions  were  also  found  to  be  normal  except  for  a  flattening  of  the  right  nasolabial  fold.  The  patient  understood  verbal  commands,  and  speech  was  intact  but  slurred  (disarthric).  He  was  able  to  extend  his  tongue  fully  at  the  midline.  On  further  testing,  the  patient's  right  arm  and  leg  strength  were  found  to  be  3  out  of  5.  (Note,  strength  is  qualitatively  assessed  according  to  a  0  to  5  scale,  where  0  is  complete  paralysis  and  5  is  normal.  In  between,  1  is  the  presence  of  a  small  muscle  contraction  but  no  movement;  2,  movement,  but  not  against  gravity;  and  3,  movement  against  gravity  but  not  against  resistance.)  Left  arm  and  leg  strength  were  normal  (ie,  5/5).  His  gait  required  support.  Reflex  testing  revealed  a  stronger  knee  jerk  and  other  tendon  reflexes  on  the  right  side  compared  with  the  left.Figure  11–1A  is  a  MRI  that  shows  brain  structure  well.  The  image  in  part  B,  at  the  same  level  as  A,  shows  more  clearly  an  intense  signal  in  the  ventral  pons,  on  the  patient's  left  side.  This  corresponds  to  the  site  of  an  infarction.  Note  that  the  bright  signals  in  the  temporal  poles  are  artifacts.  Part  C  shows  the  level  of  the  MRIs  in  relation  to  brain  stem  vasculature.  The  site  of  infarction  is  represented  on  the  ventral  pontine  surface.Unfortunately,  the  patient  died  several  years  later,  due  to  complications  related  to  the  stroke  he  suffered.  Figure  11–1D  shows  a  myelin-stained  cervical  spinal  section  after  supraspinal  stroke.  Two  prominent  regions  of  demyelination,  and  accompanying  axon  degeneration,  are  noted  (arrows);  one  on  the  right  side  (contralateral  to  infarction)  in  the  dorsolateral  white  matter  and  the  other  in  the  left  (ipsilateral)  ventromedial  white  matter.Answer  the  following  questions  based  on  your  reading  of  this  and  the  previous  chapter.1.  Occlusion  of  what  artery  likely  produced  the  infarction?2.  Why  are  the  only  somatic  motor  signs  a  flattening  of  the  contralateral  nasolabial  fold  and  contralateral  limb  muscle  weakness?3.  Why  is  the  knee  jerk  reflex  stronger  (hyperreflexia)  on  the  paretic  (weakened)  side?Key  neurological  signs  and  corresponding  damaged  brain  structuresSelective  flattening  of  nasolabial  foldThe  nasolabial  fold  is  produced  by  tone  in  facial  musculature;  flattening  signifies  a  loss  of  tone,  and  associated  weakness  or  paralysis  of  facial  musculature.  There  is  no  loss  of  capacity  to  contract  upper  facial  muscles.  In  this  patient's  case,  where  the  lesion  is  in  the  descending  cortical  fibers  in  the  pons,  sparing  of  upper  facial  control  is  likely  due  to  control  by  both  the  contralateral  and  ipsilateral  cortical  motor  areas.  Since  the  lesion  is  limited  to  the  contralateral  pathway,  ...
SN  - 
PB  - McGraw-Hill Medical
CY  - New York, NY
Y2  - 2024/04/19
UR  - neurology.mhmedical.com/content.aspx?aid=1129849645
ER  -