09. Motor Systems 2

• cerebellum and basal ganglia are both control loops within the brain - neither project beyond
• cerebellum has three functional components: spino-cerebellum, vestibulo-cerebellum and cerebro-cerebellum
• spino-cerebellum is medial region

  • output to reticular formation and red nucleus - control over musculature and posture

  damage -> decreased muscle tone, ataxia and intention tremor
• vestibulo-cerebellum is the caudal region

  • input and output from vestibular nucleus - control over posture and eye movement

  damage -> nystagmus and ataxia
• cerebro-cerebellum is the lateral hemispheres

  • instructs M1 about movement direction, timing and force

  damage -> ataxia, intention tremor and inarticulate speech
• inputs to cerebellum = climbing fibres and mossy fibres -> excite purkinje cells

  • purkinje cells go to deep cerebellar nuclei

  dcn compares input from mossy and climbing fibres - sends error signal and compensatory output to brainstem and thalamus
• basal ganglia normally inhibits the thalamus -> when cortex confirms this inhibition is removes
• the basal ganglia includes:

  • striatum - caudate nucleus, putamen and nucleus accumbens
  • globus pallidus - internal and external
  • substantia nigra - reticulata and pars compacta
  • subthalamic nucleus
• basal ganglia inhibits excitatory drive to motor cortex
• dopamine facilitates movement

  • acts on excitatory D1 receptors in direct pathway
  • acts on inhibitory D2 receptors in indirect pathway
• parkinsons is hypokinetic - resting tremor, bradykinesia, rigidity

  • loss of nigro-striatal dopaminergic pathway leads to overactive STN
  • dopamine replacing drugs like L-DOPA treat symptoms
  • surgical lesion of STN also treats
• huntingtons is hyperkinetics - uncontrollable rapid motor patterns

  • loss of striatal output neurones in indirect pathway -> predominance of direct pathway -> decreased basal ganglia output

  symptomatic treatments decrease dopamine activity to decrease movement