Brain lesions and chemical control of behaviours

Question 1

Astereognosis

Answer 1

Can’t identify objects by touch

Question 2

Ideomotor apraxia

Answer 2

can’t carry out actions to command but may perform action spontaneously - occipital area

Question 3

Conduction aphasia

Answer 3

Inability to repeat sentences/phrases and a defective ability to identify/name objects and people

Question 4

Sx frontal lobe disorders

Answer 4

• Contralateral spastic paraplegia if big enough to press on motor cortex
• Mood elevation
• Anosmia (if anterior and inferior)
• Entirely prefrontal: no hemiplegia, grasp reflex regained
• Frontal dysexecutive function: talkative, loss of initiative, difficulty adapting, tendency to joke, gregarious

Question 5

Cholinergic system

Answer 5

• Cholinergic nerve cell bodies and projections contain ACh
• Initial projections from nucleus basalis
• ACh from nerve ending - travels to post-synaptic neurone and causes signal transduction
• Can be broken down by AChE or recycled
• Binds to nicotinic receptors
• Pyridostigmine
• NMJ disorders: Myasthenia gravis, lambert eaton, botulism,

Question 6

Dopaminergic pathways

Answer 6

• Produced in substantia nigra → basal ganglia
• Substantia nigra die back = cardinal Parkinson sx
• Decreased dopamine production
• Rigidity, tremor, postural instability, bradykinesia
• Dopamine enters cleft and binds to downstream receptors (d1 and d2)
• When bound, G protein signalling causes downstream transduction
• Some reabsorbed via dopamine transporter to be recycled
• MAO breaks down dopamine
• Dopamine transporter studied using DAT scan
• Bright colour = basal ganglia

Question 7

Parkinson’s treatment

Answer 7

Sinemet replaces dopamine

Dopamine agonists allow for re-constitution of dopaminergic pathways - ropinerol etc