Conditions and Case studies

• 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.

Cerebellar lesions cause disruption of precise movements, due to failure of motor error control – ataxia, intention tremor

• 2.23m tall, 240kg
• Massive size due to acromegaly
• Benign pituitary adenoma (tumor) led to continual excessive secretion of growth hormone

• 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)

• 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'

• 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

• 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