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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.
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Cerebellar Lesions
Cerebellar lesions cause disruption of precise movements, due to failure of motor error control – ataxia, intention tremor
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Andre the Giant
- 2.23m tall, 240kg
- Massive size due to acromegalyBenign pituitary adenoma (tumor) led to continual excessive secretion of growth hormone
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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)
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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'
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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
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Huntington's
- Lesioned basal ganglia = hyperkinesiaHyperkinesia 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
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