Conditions and Case studies

  1. Phineas Gage
    • 1848: foreman impaled in the frontal lobe of cortex with steel rod and survived.
    • BUT major changes to aspects of personality ->
    • Contemporary Dr.s understood that there were different parts of the brain but it wasn't yet known that each part had specific, defined functions.
    • Landmark patient in development of functional specialisation of the brain
    • -> frontal lobe of cerebral cortex not essential for life but clearly involved in certain higher functions.
  2. Cerebellar Lesions
    Cerebellar lesions cause disruption of precise movements, due to failure of motor error control – ataxia, intention tremor
  3. Andre the Giant
    • 2.23m tall, 240kg
    • Massive size due to acromegaly
    • Benign pituitary adenoma (tumor) led to continual excessive secretion of growth hormone
  4. Henry Molaison
    • Developed epilepsy (seizures, convulsions etc.) that increased in severity with age.
    • Experimental surgery removed medial temporal lobe, including most of the hippocampus.
    • -> severe anterograde amnesia = couldn't form new memories
    • E.g. Researchers would introduce themselves everyday and he'd greet them as unfamiliar strangers.
    • -> limited retrograde amnesia = some loss of existing memories from years immediately prior to surgery.
    • Affected only declarative memory (facts)
    • Working memory (short-term store) & procedural memory (unconscious memory) unaffected (E.g. he learned to mirror write (procedural memory) but had no recollection)
    • Previously thought learning and memory was a general function of the whole cortex BUT HM showed that memory is modular
    • -> Hippocampus essential for formation (but not storage) of declarative memories (not procedural)
  5. Clive Wearing
    • Prominent classical musician in 1980's
    • Hippocampus destroyed by a viral infection in 1985.
    • -> procedural memories unaffected (piano playing skills)
    • -> working memory limited to 30 seconds
    • Describes like as a constant sensation of 'waking up'
  6. Parkinson's
    • Overactive basal ganglia = hypokinesia
    • Parkinson’s disease (1% of >60’s) involves dopamine depletion in striatum
    • – Bradykinesia (slow movement)
    • – Akinesia (difficulty initiating movement)
    • – Rigidity (increased muscle tone)
    • – Resting tremor
    • Progressive, no cure, but symptoms can be alleviated by increasing dopamine release from remaining neurons
  7. Huntington's
    • Lesioned basal ganglia = hyperkinesia
    • Hyperkinesia seen in hemiballismus – movement disorder affecting only one side
    • Spontaneous, uncontrollable, jerky movements (chorea)
    • Due to damage/loss of function in subthalamic nucleus
    • Normally: subthalamic nucleus excites globus pallidus, which then inhibits thalamus = normal movement control
    • Damage to subthalamic nucleus reduces excitatory input to globus pallidus, leading to reduced inhibition of thalamus
    • Thalamus is involved in control of movement initiation, loss of inhibition = spontaneous movement
    • Chorea also part of symptoms of Huntington’s disease – also involves loss of basal ganglia neurons
Card Set
Conditions and Case studies
Neurological conditions and case studies