Neuro: Control of Movement (incl. basal ganglia) Flashcards
What are the basal ganglia?
- They’re a group of interconnected nuclei within the brain
- They take in massive input from cortical and branstem areas and then output to those same areas
The basal ganglia are associated with many different functions and have different loops based on those functions. What are some of the loops of the basal ganglia?
- Motor loop
- Limbic loop
- Associative loop
How are the basal ganglia segregated within their different circuits/loops?
- They are seperated anatomically within the different circuits/loops
- E.g. There would be an area within each of the nuclei of the basal ganglia of the motor loop that deal with motor function of the leg
Describe the main features of the basal ganglia loops
- There’s a main ouput from one of the nuclei of the basal ganglia which is Inhibitory (decreases movement)
- This main output projects onto the thalamus and then the mortex cortex
- There are 2 pathways that affect this main output:
- One of these pathways decreases output activity (Direct “go” pathway)
- The other pathway increases output activity (Indirect “stop” pathway)
What does the rate (Alexander and Delong model) state?
States that changes in firing rate of the output nuclei determine the degree of inhibition in the thalamus and therefore the degree of movement
What changes occur in the motor loop pathway of the basal ganglia as a result of Parkinson’s disease?
- During parkinson’s disease the Substantia nigra degenerates
- This means Substania nigra can’t release dopamine
- This means dopamine isn’t able to bind to the Putamen and activate the Direct “go” pathway so instead you get constant activation of the Indirect “stop” pathway
- This means the inhibitory output nucleus is activated and so inhibits the thalamus and therefore inhibits motor cortex
- This leads to loss of movement
What is Hemiballismus (Hyperkinesia)?
A flinging movement of one side of the body caused by a stroke in the subthalamic nucleus
What changes occur in the motor loop pathway of the basal ganaglia as a result of hemiballismus?
- Subthalamic nucleus is a major part of the indirect “stop” pathway that activates the main output nucleus of the motor loop pathway
- During hemiballismus subthalamic nucelus isn’t present due to stroke
- Without the subthalamic nucleus the main output nucleus is constantly inhibited
- This means that the thalamus and then the motor cortex are activated leading to excessive movement
What are some of the problems with the rate (Alexander and Delong) model of the motor loop pathway of the basal ganglia?
- Anatomically the model is incorrect as there are many other outputs within the regions of the basal ganglia that make up the motor loop pathway apart from the dopamine outputs
- The model also doesn’t make sense clinically
- This is because lesioning the main output nuclei doesn’t cause dyskinesia (Involuntary movement)
- Also, lesioning thalamus doesn’t cause Akinesia (loss of movement)
Explain the differences in the firing rate of the nerve cells of the basal ganglia in a normal situation and in somebody with Parkinson’s disease. What does this difference in firing rate mean?
- In the basal ganaglia of a normal person the different nerve cells populations are firing at diffrerent rates/frequencies
- This allows those nerves cells to transmit and process lots of information
- During parkinson’s disease however, the nerve cell populations of the basal ganglia all start to fire at similar a similar frequency (β-frequency)
- This means that nerve cells of someone with Parkinson’s disease are less able to process and transmit information which may lead to symptoms of disease
What evidence is there that the Beta frequency of firing of the nerve cells of the basal ganglia is related to Parkinson’s disease?
- When you give people with Parkinson’s disease L-dopa (replacement dopamine) there is suppresion of the Beta activity of these nerve cells in the basal ganglia
- This suppresion of Beta activity correlates with the improvement in movement control seen in people with Parkinson’s disease who take their replacement dopamine medication
What happens to patients with Parkinson’s disease during deep brain stimulation surgery if you stimulate nerve cells of basal ganaglia? Why is this?
- During deep brain stimulation surgery if you turn on deep brain stimulation electrode it causes their symptoms to improve
- This is because deep brain stimulation causes inhibition of the Beta frequencies of firing of the nerve cells in the basal ganglia
What happens to patients with Parkinson’s disease during deep brain stimulation surgery if you un-stimulate nerve cells of basal ganaglia? Why is this?
- During deep brain stimulation surgery of you turn of deep brain stimulation electrode Parkinson’s symptoms return to normal
- This is because electrode is no longer supressing Beta frequency of firing in nerve cells of basal ganglia
Describe the characteristics of dopamine release in a normal person that results in movement
- In a normal person dopamine release happens at the beginning of movement (phasic dopamine release)
- In a normal person there’s a particular threshold that needs to be met in order for the phasic dopamine release to induce movement
Describe the characteristics of dopamine release in a person with Parkinson’s disease and how it affects their movement
- In a person with Parkinson’s disease there’s a reduction in doapmine levels in basal ganaglia
- This means that although person with Parkinson’s can still go through Phasic dopamine release because their dopamine levels are low the release doesn’t allow for the threshold level of dopamine to be reached in order to produce movement
How does giving a person with Parkinson’s disease L-dopa (replacement dopamine) improve their movement?
- L-dopa increases levels of doapmine within substantia nigra
- This means that when there is phasic dopamine release at the beginning of movement the release is big enough to get dopamine levels above threshold needed to induce movement
- This allows for greater control of movement in person with Parkison’s disease
What are the different stages that need to occur in order for you to move?
- Turn down current sensory state (lower beta power/frequency)
- Have an accurate prediction of the new sensory state
- Stabilise the new sensory state (higher beta power/frequeny)
