1210 Week 23

1210 Week 23

1. Lecture 1

   • Motor Neurones
     • final effective pathway - brain to spinal cord to muscle
     • final effector pathway - basal ganglia to thalamus to 1st degree motor cortex and reticular formation to motor neurones
     • spinal motor output: alpha neurones - each is associated with specific muscle fibres forming a function entity called a motor unit
     • motor units cluster into motor pools in the ventral horn
     • motor units vary in size, tension produced, speed of contraction and degree of fatigability
     • motor pools - somatotropic organisation, axial structures medial and distal structures lateral
     • motor unit - motor unit and the innervated muscle fibre
     • the lateral premotor cortex, medial premotor cortex and primary motor cortex all help to control the associated effector muscles
     • muscle spindles - sensory apparatus, lie parallel to fibres, intrafusal fibres, detect changes in muscle length, contribute to proprioception and regulate contraction to match the need of the action
     • extrafusal fibres form the bulk of the muscle mass and generate tension, they receive their innervation from alpha motor neurones
     • intrafusal fibres have a sensory function and don't generate tension, they receive their innervation from gamma motor neurones
     • when the muscle is relaxed the spindle is sensitive to stretch
     • when the muscle is contracted the spindle isn't sensitive to stretch but when the gamma neurone is activated it becomes sensitive again
     • the golgi tendon organ is a mechanoceptor that lies in series with muscle fibres and detects tension in the muscle from the tendon
     • muscle spindle primary afferents, 1a, sense stretch and rate of change
     • muscle spindle secondary afferents, 2, sense stretch only
     • group 3 afferents are nociceptors in the muscle
     • muscle spindle tendon organs, 1b, sense force change in muscles
     • hierarchical organisation leads to stability
     • you can lose a few motor units without any major effects as you can compensate by using other local units more
     • however if you lose a section high up like the spine or the brain you will suffer serious losses
     • Brodmann's areas 4 and 6 - primary motor cortex, 4, and complementary motor area and premotor cortex, 6
     • Primary motor cortex is located in the precentral gyrus in the frontal lobe and is responsible for planning and initiating voluntary movement
     • pyramidal cells in the V cortical layer are upper motor neurones
     • axons descend in the coricobullar and corticospinal tracts to the spinal cord
   • Reflexes
     • 1a neurones form local circuit connections with motor neurones which are used in reflex reactions - they connect to the antagonist to counteract the action performed , they are poly/oligosynaptic
     • recurrent inhibition - you have to activate the agonist and deactivate the antagonist in order to avoid injury - done with renshaw cells
     • flexor withdrawal reflex - nociceptors react to danger by moving the at risk limb away from danger and stabilises the rest of the body to avoid instability and/or injury caused by moving away
     • monosynaptic reflex - sensory afferent - motor neurone - output
     • polysynaptic reflex - sensory afferent - interneurone - motor neurone - output
     • monosynaptic stretch reflex - muscle spindle 1a afferent - homonymous alpha motor neurone - output
     • polysynaptic reflex, crossed extensior reflex - sensory afferent - interneurone ( control system) - motor neurone - output

2. Lecture 2

   • Alzheimers
     • disease of aging, memory loss and dementia
     • symptoms - short term memory loss, disorientation, difficulty with words names and numbers, clumsiness, visuospatial orientation, loss of social skills, psychosis, bradykinesia, rigidity, mutism, incontinence and bedridden
     • from the first showing of symptoms it takes about 10 years to die
     • the language cortex and the hippocampus are significantly smaller in AD
     • pick's disease is alzheimers of the frontotemporal lobe
     • in AD there are lots of plaque build up on the brain
     • there is major neuronal shrinkage - cholinergic pathways mainly
     • treated with acetylcholinesterase inhibitors which increases acetylcholine levels and may slow the progression down
   • MS
     • symptoms - sensory changes, muscle weakness, coordination and balance, speech, swallowing, visual, fatigue, pain, incontinence, cognitive impairment
     • progressive relapsing MS - steady decline with superimposed attacks
     • primary progressive MS - steady decline without remission or attacks
     • secondary progressive MS - initial relapsing-remitting that turns into a steady decline
     • relapsing-remitting MS - unpredictable attacks with periods of remission
     • major loss of neuronal tissue surrounding ventricles
     • caused by autoimmune response that demyelinates axons by attacking oligodendrocytes
   • Parkinsons
     • extrapyramidal disorder, loss of movement, increased muscle tone
     • symtoms - tremor, rigidity, micrographia, akinesia, stooping and shuffling
     • pathology - diminished substantia nigra, loss of dopamine pathways >80%
   • Huntingtons
     • inherited, autosomal dominant, polyglutamine repeat on the Huntingtin gene - if there are more than 34 CAG repeats you are at risk
     • symptoms - irritability moodiness, antisocial behaviour, dementia, fidgeting and restlessness - gross choreiform movements
     • pathology - loss of GABAergic and cholinergic neurones in the cerebral cortex and corpus striatum