Session 6 Flashcards
(20 cards)
What are the pyramidal and extra-pyramidal tracts?
Pyramidal - corticospinal and corticonuclear (or corticobulbar). Voluntary control.
Extra-pyramidal tracts - vestibulospinal, reticulospinal, rubrospinal and tectospinal tracts. Involuntary control.
Where is the cerebellum found and what separates it from other structures?
Posterior cranial fossa
Separated from occipital and parietal lobes by the tentorium cerebelli. Separated from the pons by the 4th ventricle.
Briefly describe the structure of the cerebellum
Consists of a middle vermis (trunk musculature) and two lateral hemispheres (limb musculature). Ipsilateral tracts.
How does the cerebellum communicate with the brainstem?
Via the CEREBELLAR peduncles:
Superior - cerebellum to midbrain
Middle - cerebellum to pons
Inferior - cerebellum to medulla
What are the signs of cerebellar dysfunction?
DANISH
Dysdiadochokinesia, ataxia, nystagmus, intention tremor, scanning speech and hypotonia
Name some structures of the basal ganglia
Caudate nucleus Lentiform nucleus (made up of putamen and globus pallidus) Substantia nigra (made up of pars compacta and pars reticularis)
What is the gross function of the basla ganglia?
Stimulates motor activity in the cerebral cortex via the thalamus
What can result from basal ganglia disorders?
Abnormal motor control
Altered posture
Abnormal muscle tone
Dyskinesia
What is the characteristic triad of Parkinson’s disease?
Bradykinesia, tremor (disappears during movement) and rigidity
What causes Parkinson’s disease?
Degeneration of the substantia nigra pars compacta causes deficiency of dopamine
What are symptoms of Parkinson’s disease (other than 3 core)?
Hypophonia, reduced facial expression, shuffling gait, micrographia (small handwriting), dementia and depression
What is the age of onset and symptoms of Huntington’s disease?
30-50 years
Chorea (jerky movements), dystonia, incoordination, cognitive decline and behavioural difficulties
What is the main drug treatment for Parkinson’s?
Levodopa (not dopamine as cannot cross blood-brain barrier). Given in combination with a peripheral DOPA decarboxylase inhibitor to reduce nausea and vomiting and to increase the L-DOPA reaching the brain
Why may the efficacy of L-DOPA be reduced with long term use?
Only effective in the presence of dopaminergic neurones. Results in a shorter lived response - on/off phenonomen. Requires increased dose
Name 2 common dopamine receptor agonists and give their advantages and disadvantages
Ropinirole, pramipexole.
Advantages - less dyskinesias or motor complications than L-DOPA, delays need for L-DOPA
Disadvantages - less efficacy, more psychiactric effects, expensive
Side effects - sedation, hallucinations, confusion, nausea, hypotension, compulsive behaviour
Describe the mechanism of action and pros of monoamine oxidase B and COMT inhibitors
Slow enzymatic breakdown of dopamine
May be used alone, prolongs action of L-DOPA
MAOB - Selegiline and rasagiline
COMT - Entacapone. Doesn’t cross BBB
Describe the effect of acetylcholine on dopamine
Probably antagonist
Anticholinergics for mild parkinsons. Treats tremor but lots of side effects
What surgical options are available for Parkinsons?
Ablation of overactive ganglia circuits e.g. subthalamic nuclei
Deep brain stimulation
What is the pathophysiology and presentation of myasthenia gravis?
Reduced number of postsynaptic ACh receptors at the neuromuscular junction due to anti-AChR antibodies
Painless muscle weakness after repetitive/sustained contraction - worse at end of day or after exercise. Most marked in face and eyes (extra ocular or bulbar muscles). Normal tendon reflexes
Outline the treatment of myasthenia gravis
Acetylcholinesterase inhibitors - pyridostigmine. Cholinergic side effects. Excess dose can cause depolarising block (cholinergic crisis)
Immunosuppression with prednisolone or azathioprine
