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PSYC370 Ch 10.pdf

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PSYC 370
Janet L Menard

PSYC  370   Chapter  10   Brain  Damage  &  Neuroplasticity  (Can  the  Brain  Recover  from  Damage?)     Causes  of  Brain  Damage     -­‐ Brain  tumors   -­‐ Cerebrovascular  disorders   -­‐ Closed-­‐head  injuries   -­‐ Infections  of  the  brain   -­‐ Neurotoxins   -­‐ Genetic  factors   -­‐ Programmed  cell  death     Brain  tumors.     Tumor:  mass  of  cells  that  grows  independently  of  the  rest  of  the  body.     -­‐ Also  called  a  neoplasm,  or  a  cancer.     Meningiomas:  tumors  that  grow  between  the  meninges  (membranes  that  cover  the  CNS).     -­‐ Account  for  20%  of  human  brain  tumors   -­‐ All  are  encapsulated  tumors  (see  next)     Encapsulated  tumors:  grown  within  their  own  membrane.   -­‐ Easy  to  find  on  a  CT  scan   -­‐ Usually  benign   - Only  influence  function  of  the  brain  by  exerting  force     Most  tumors  are  not  encapsulated  but  infiltrating.     Infiltrating  tumors:  grow  diffusely  throughout  surrounding  tissue.   -­‐ Usually  malignant   - Difficult  to  destroy  –  tissue  often  remains  after  they  are  removed     Metastatic  tumors:  infiltrating  cells  originate  in  the  body  but  are  transferred  to  the  brain  via  the   bloodstream;  about  10%  of  tumors  are  metastatic.   -­‐ Many  begin  in  the  lungs     Cerebrovasular  Disorders:  Strokes.     Stokes:  sudden-­‐onset  cardiovascular  disorders  that  cause  brain  damage.       The  symptoms  of  a  stroke  vary  based  on  the  area  of  the  brain  that  is  affected,  but  some  common   symptoms  are  amnesia,  aphasia,  paralysis,  and  coma.       Infarct:  dead  or  dying  tissue  caused  by  a  stroke.   (10  :  1)   PSYC  370   Penumbra:  dysfunctional  area  surrounding  an  infarct;  this  tissue  may  be  saved  or  could  die.     Major  types  of  stoke   -­‐ Caused  by  cerebral  hemorrhage   -­‐ Caused  by  cerebral  ischemia     Cerebral  Hemorrhage.     Cerebral  hemorrhage:  occurs  when  a  cerebral  blood  vessel  ruptures  and  blood  seeps  into  the   surrounding  tissue,  damaging  it.       Aneurysm:  balloon-­‐like  dilation  that  forms  in  the  wall  of  an  artery  at  a  point  where  the  elasticity   of  the  artery  wall  is  defective.     Aneurysms  that  burst  are  one  of  the  main  causes  of  cerebral  hemorrhages.       Causes  of  aneurysms   -­‐ Congenital  (present  at  birth)   -­‐ Exposure  to  vascular  poisons   -­‐ Infection     Cerebral  Ischemia.     Cerebral  ischemia:  disruption  of  the  blood  supply  to  an  area  of  the  brain.       Causes  of  cerebral  ischemia   -­‐ Thrombosis   -­‐ Embolism   -­‐ Arteriosclerosis     Thrombosis:  a  plug  (thrombus)  blocks  blood  flow  at  the  site  of  its  formation.         A  thrombus  can  be  composed  of  a  blood  clot,  fat,  oil,  an  air  bubble,  tumor  cells,  or  a     combination.     Embolism:  a  plug  (embolus)  is  carried  by  the  blood  from  a  larger  vessel,  where  it  was  formed,  to  a   smaller  vessel,  where  it  becomes  clogged.       “An  embolus  is  just  a  thrombus  that  has  taken  a  trip.”     Arteriosclerosis:  blood  vessels  become  blocked  as  their  walls  thicken  and  their  channels  narrow.   This  usually  occurs  due  to  fat  deposits.       The  damage  of  an  ischemia  takes  1-­‐2  days  to  fully  develop.  During  this  time,  the  body’s  own   neurotransmitters  play  a  role  –  much  of  the  damage  comes  from  excessive  glutamate  release;  see   next  page.   (10  :  2)   PSYC  370       i. Blood  vessel  becomes  blocked   ii. Blood-­‐deprive  neurons  become  overactive  and   release  excessive  amounts  of  glutamate.     iii. Glutamate  overactivates  NMDA  receptors,  which   trigger  a  release  of  sodium  and  calcium  ions.     iv. Sodium  and  calcium  ions  are  harmful  in  two   ways:   - Kill  the  postsynaptic  neuron   - Triggers  an  excessive  release  of  glutamate,   thus  spreading  the  toxic  cascade.     Properties  of  ischemia-­‐induced  brain  damage:   i. Takes  time  to  develop   ii. Does  not  occur  equally  in  different  parts  of  the   brain  –  hippocampal  areas  are  particularly  sensitive   iii. Mechanisms  of  damage  are  different  in  various   brain  regions.     Research  into  treatment  focuses  on  glutamate  antagonists.     Closed-­‐head  injuries.     Closed-­‐head  injuries:  brain  injuries  that  involve  a  blow  to  the  head  that  does  not  penetrate  the   skull.       All  head  injuries  should  be  treated  seriously,  but  particular  caution  should  be  taken  if  any  of  these   symptoms  are  present...   - Loss  of  consciousness   - Sensorimotor  Disturbances   - Confusion     Hematoma:  Localized  collection  of  collected  blood  in  an  organ  or  tissue.       Contusions:  closed-­‐head  injuries  that  involve  damage  to  the  cerebral  circulatory  system.   - Causes  internal  hemorrhaging,  and  a  hematoma  as  a  result   - Occur  when  the  brain  is  hit  against  the  side  of  the  skull.       Blood  collects  in  the  subdural  space  and  damages  the  surrounding  tissue.     Contrecoup  injuries:  occurs  when  the  brain  damage  occurs  on  the  opposite  side  as  the  blow  to   the  head.       Concussion:  occurs  when  a  blow  to  the  head  causes  loss  of  consciousness  but  not  a  contusion.   Punch-­‐drunk  syndrome:  dementia  and  cerebral  scarring  that  occur  with  repeated  concussions.   (10  :  3)   PSYC  370     Infections  of  the  brain.     Brain  infection:  invasion  of  the  brain  by  microorganisms,  resulting  in  inflammation.   - Bacterial  infections   - Viral  infections     Encephalitis:  inflammation  caused  by  a  brain  infection.     Bacterial  infections.     Cerebral  abscess:  pocket  of  puss  in  the  brain.       When  bacteria  invade  the  brain  they  often  lead  to  the  formation  of  cerebral  abscesses.     Meningitis:  inflammation  of  the  meninges;  the  leading  cause  is  bacterial  infection.     - Fatal  in  about  25%  of  adults   - Can  be  treated  with  antibiotics,  but  these  cannot  restore  damaged  brain  tissue     Common  bacterial  infection  that  attacks  the  brain:  syphilis.   - Bacteria  contracted  from  genital  warts   - Bacteria  lay  dormant  for  several  years,  until  they  attack  many  parts  on  the  body  including   the  brain.     General  paresis:  syndrome  of  insanity  and  dementia  resulting  from  a  syphilitic  infection.     Viral  infections.     Types   - Those  that  have  an  affinity  for  neural  tissue  (e.g.,  rabies)   - Those  that  attack  the  neural  tissue  (but  do  not  have  a  particular  affinity  for  it)   - e.g.,  mumps  and  herpes     Neurotoxins.     Neurotoxins  can  inter  the  nervous  system  via...   - GI  tract   - Lungs   - Skin     Toxic  psychosis:  chronic  insanity  caused  by  a  neurotoxin  (e.g.,  the  mad  hatter).     Tardive  dyskinesia:  motor  disorder  caused  by  chronic  use  of  certain  antipsychotic  drugs.     Some  neurotoxins  are  endogenous  (made  by  the  body  –  such  as  glutamate  during  a  stroke).   Genetic  factors.     (10  :  4)   PSYC  370     Most  genetic  neurological  diseases  are  carried  on  the  recessive  gene  (e.g.,  PKU)  but  others  involve   mistakes  in  cell  duplication  during  development  (“genetic  accidents,”  such  as  Down  Syndrome).       Programmed  cell  death.     Apoptosis:  programmed  cell  death.     Necrosis:  passive  cell  death  resulting  from  injury.       Apoptosis  has  important  implication  in  brain  damage.  All  of  the  mechanisms  of  brain  damage   discussed  previously  produce  damage,  in  some  part,  by  activating  apoptosis.     - If  a  cell  is  damaged  by  necrosis  it  summons  energy  to  commit  suicide     Apoptosis  is  more  desirable  than  necrosis  because  necrosis  involves  the  cell’s  contents  entering   the  cerebral  system.  This  can  cause  inflammation  and  can  spread  the  damage  to  other  cells.       Neuropsychological  Diseases     - Epilepsy   - Huntington’s  disease   - Parkinson’s  disease   - Multiple  sclerosis   - Alzheimer’s     Disorders  that  are  associated  with  brain  damage.     Epilepsy.     Epilepsy:  neurological  disorder  characterized  by  spontaneously  recurring  seizures.   - 1%  of  the  population     Convulsions:  motor  seizures.   - Tremors  (clonus)   - Rigidity  (tonus)   - Loss  of  balance  and  loss  of  consciousness     It  can  be  hard  to  diagnose  epilepsy  because  seizures  can  take  many  different  forms.  Diagnosis  can   require  EEG.     Epileptic  auras:  psychological  symptoms  that  precede  the  onset  of  a  seizure.  Important:   - Warn  patient  that  a  seizure  is  coming   - Give  clues  as  to  where  the  epileptic  focus  is  (i.e.,  the  place  where  the  synchronized  firing   originates  from)   Partial  seizures.   (10  :  5)   PSYC  370     Partial  seizure:  does  not  involve  the  entire  brain.  Neuronal  firing  may  spread,  but  it  is  only  a   partial  seizure  if  it  does  not  involve  the  entire  brain.       Because  partial  seizures  involve  only  part  of  the  brain,  they  do  not  usually  have  total  loss  of   consciousness  or  equilibrium  as  symptoms.     Major  categories  of  partial  seizures   i. Simple  partial  seizures:  symptoms  are  primarily  sensory  or  motor  (or  both).   ii. Complex  partial  seizures:  symptoms  are  compulsive,  repetitive,  simple  behaviours   (called  automatisms);  abnormal  firing  usually  restricted  to  the  temporal  lobes.   - Makes  up  50%  of  the  seizures  experienced  by  all  epileptic  patients     It  appears  that  the  person  is  conscious  but  they  may  have  no  memory  of  the  seizure.       Generalized  seizures.     Generalized  seizures:  involve  the  entire  brain.  This  can  occur  either  by  firing  spreading  from  an   epileptic  focus  or  can  involve  simultaneous  firing  in  various  places  of  the  brain  at  once.       Types  of  generalized  seizures   i. Grand  mal:  loss  of  consciousness,  loss  of  equilibrium,  and  violent  tonic-­‐clonic  convulsion   (see  later).  Can  also  involve  tongue  biting,  loss  of  bladder  control,  hypoxia  (shortage  of   blood  supply)  and  cyanosis  (turning  blue).     ii. Petit  mal:  disruption  of  consciousness,  ceasing  current  activity,  while  maintaining  a  vacant   look.  This  can  involve  fluttering  eyelids.  Recall  the  young  boy  from  the  video.   - Most  common  in  young  children,  often  stop  after  puberty     Hypoxia:  shortage  of  oxygen  supply  to  the  tissues,  including  the  tissues  of  the  brain.     Tonic-­‐clonic  convulsion:  involves  loss  of  balance  (i.e.,  falling  over),  and  muscle  rigidity  (“tonic”)   accompanied  by  convulsions  (“clonic”).   - Associated  with  a  grand  mal  seizure     The  EEG  of  a  petit  mal  seizure  is  unique  (3-­‐per-­‐second  spike-­‐and-­‐wave  discharge).  Know  this,   because  the  name  of  its  pattern  is  bolded  as  a  key  term  (see  next).     3-­‐per-­‐second  spike-­‐and-­‐wave  discharge:  characteristic  EEG   pattern  of  a  petit  mal  seizure.     Regarding  epilepsy  in  general:  The  cause  is  not  entirely  known.   Over  70  faulty  genes  have  been  implicated.  It  could  also  be  faults   at  inhibitory  synapses  (i.e.,  GABA),  causing  groups  of  neurons  to   fire  in  synchronized  bursts.     Huntington’s  disease.   (10  :  6)   PSYC  370     Huntington’s  disease:  progressive  terminal  disorder  of  motor  and  intellectual  function  that  is   produced  in  adulthood  by  a  dominant  gene.     - Associated  with  severe  dementia     - Strong  genetic  basis   - 1  in  10,  000     Signs  of  Huntington’s  disease  (numbers  represent  progression):   1. Fidgetiness   2. Rapid,  complex,  jerky  movements   3. Motor  and  intellectual  deterioration   4. Death  (about  15  years  after  the  first  symptoms  appear)     Huntingtin:  dominant  gene  that  causes  Huntington’s  disease  and  codes  for  the  huntingtin  protein.     Parkinson’s  disease.       Parkinson’s  disease:  movement  disorder  associated  with  degeneration  of  dopaminergic  neurons   in  the  nirgostriatal  pathway.     First  sign  is  slight  stiffness  or  tremor.       The  most  common  symptom  is  a  tremor  that  is  produced  only  during  inactivity  (but  not  sleep).  It   involves:  muscular  rigidity,  difficulty  initiating  movement,  slowness  of  movement,  and  a  mask-­‐like   face.       Pain  and  depression  often  appear  before  the  motor  symptoms  become  severe.       - No  obvious  cause   - 10  different  gene  mutations  implicated   - All  disrupt  the  function  of  mitochondria     Degeneration  is  pronounced  in  the  substantia  nigra.     Substantia  nigra:  midbrain  nucleus  whose  neurons  project  via  the  nigrostriatal  pathway  to  the   striatum  of  the  basal  ganglia;  major  source  of  dopamine  in  the  body.   - There  is  little  dopamine  found  here  in  Parkinson’s  patients     Lewy  bodies:  clumps  of  proteins  observed  in  the  surviving  dopaminergic  neurons  of  Parkinson’s   patients.       L-­‐dopa  can  be  used  to  alleviate  symptoms  but  is  not  a  permanent  solution.       Deep  brain  stimulation  is  a  controversial  method  of  treating  Parkinson’s.     (10  :  7)   PSYC  370   - Low-­‐intensity  electrical  stimulation  to  the  subthalamic  nucleus  is  applied  constantly  via   an  electrode     Multiple  sclerosis.     Multiple  sclerosis:  progressive  disease  that  attacks  the  myelin  of  axons  in  the  CNS.       - Manifests  in  young  adults     Damage  to  the  myelin  sheaths  becomes  progressively  worse  until  the  associated  axons  become   dysfunctional  and  degenerate.       - Areas  of  the  CNS  develop  scar  tissue     Autoimmune  disorder:  body’s  immune  system  attacks  part  of  the  body  as  if  it  were  a  foreign   substance.       Multiple  sclerosis  is  an  autoimmune  disorder,  in  which  the  body  attacks  the  myelin  sheath.       Diagnosis  can  be  tricky  because:   - There  is  variance  in  the  number  of  lesions  patients  have   - Patients  can  go  into  a  state  of  remission     Major  symptoms:   - Visual  disturbances   - Muscular  weakness   - Numbness   - Tremor   - Ataxia  (loss  of  motor  coordination)   - Cognitive  deficits  and  emotional  changes  (some  patients)     Epidemiology:  study  of  multiple  factors  on  the  development  of  disease.     - Environmental  and  genetic  factors  implicated  in  MS  (see  next)     Genetic  factors   Environmental  factors   -­‐  MS  has  a  higher  discordance  between   -­‐  Incidence  is  higher  in  populations  in  colder   monozygotic  twins  (25%)  than  diygotic  twins   climates  as  opposed  to  those  living  near  the   (5%)   equator       -­‐  Incidence  is  3x  higher  in  females  than  in  males   -­‐  People  who  migrate  from  a  high-­‐risk  region  to     a  low-­‐risk  region  reduce  their  susceptibility     (and  vice  versa)       -­‐  Substantially  higher  incidence  in  Caucasians   -­‐  Cigarette  smokers  at  greater  risk   Alzheimer’s  disease.   (10  :  8)   PSYC  370     Alzheimer’s  disease:  characterized  by  neurofibrillary  tangles,  amyloid  plaques,  and  neuron  loss.   - Major  cause  of  dementia  in  old  age     Early  stages   - Selective  decline  in  memory   - Attentional  deficits   - Personality  changes     Intermediate  stages   - Confusion   - Irritability   - Anxiety   - Deterioration  of  speech     Advanced  stages   - Cannot  control  simple  responses  (e.g.,  swallowing)     Neurofibrillary  tangles:  thread-­‐like   tangles  of  protein  in  the  neural  
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