Basal Ganglia/Parkinson's Disease Flashcards
Another name for the basal ganglia
Basal nuclei
What does the basal ganglia consist of?
Caudate nucleus, putamen, globus pallidus (internus and externus)
What other 2 nuclei make up the basal ganglia?
Subthalamic nucleus, substantia nigra
What 2 nuclei make up the striatum?
Caudate nucleus, putamen
What 2 nuclei make up the lentiform nucelus?
Putamen, globus pallidus (internus and externus)
Where does the striatum get its name?
From its grey appearance which is due to white fibres of the corona radiata piercing through it
What kind of matter are the putamen and caudate nucleus made of?
Grey (unmyelinated) matter
What kind of matter is the corona radiata made of?
White (myelinated) matter
What is the function of the white fibres of the corona radiata?
They carry information from the cortex to the basal ganglia, internal capsule and thalamus and from the thalamus back to the cortex
What are the 2 key functions of the basal ganglia?
The basal ganglia regulates motor and psychological functions
What 3 aspects of psychological functions does the basal ganglia influence?
Decision-making - uses past information to inform decision-making
Social behaviour - it filters out unacceptable behaviour
Emotion - regulates reward-seeking behaviour e.g. gambling
What are the main functions of the basal ganglia?
Filters unnecessary information that arrives from the primary motor cortex such as inhibiting antagonistic movement
Has a role in starting, stopping and monitoring intensity of movements
What parts of the basal ganglia is responsible for filtering movement information before the information goes back to the cortex?
Globus pallidus and substansia nigra
Name 1 excitatory and 1 inhibitory neurotransmitter associated with the basal ganglia.
Excitatory: glutamate
Inhibitory: GABA (gamma-amino-buteric acid)
Is the neurotransmitter dopamine excitatory or inhibitory?
Both. It has 2 components: D1 which is excitatory and D2 with is inhibitory.
Where is dopamine released from in the brain?
The substantia nigra pars compacta
How many different types of dopamine receptor exist in the central nervous system?
5
What happens when D1 (dopamine) is released from the substantia nigra pars compacta?
D1 increases the inhibitory output from the striatum (via the direct pathway)
What happens when D2 (dopamine) is released from the substantia nigra pars compacta?
D2 decreases the inhibitory level of the striatum (via the indirect pathway)
What are the structures involved in the direct pathway?
cortex
- > striatum (caudate & putamen)
- > globus pallidus internus & substantia nigra & pars reticulata
- > thalamus
- > cortex
What are the structures involved in the indirect pathway?
cortex
- > striatum (caudate+putamen)
- > globus pallidus externus
- > subthalamic nucleus
- > globus pallidus internus, substantia nigra & pars reticulata
- > thalamus
- > cortex
What neurotransmitter does the cortex release when synapsing to the striatum?
Glutamate
What neurotransmitter does the striatum release when synapsing onto the output nuclei (globus pallidus internus & substantia nigra & pars reticulata)?
GABA
What neurotransmitter does the output nuclei (globus pallidus internus & substantia nigra & pars reticulata) release when synapsing onto the thalamus?
GABA
What neurotransmitter does the thalamus release when synapsing with the cortex?
Glutamate
What is the end result of the indirect pathway?
The production of movement
What neurotransmitter does the striatum emit when synapsing with globus pallidus externus?
GABA
What neurotransmitter does globus pallidus externus release when synapsing with the subthalamic nuclei?
GABA
What neurotransmitter does the subthalamic nuclei release when synapsing with the output nuclei (globus pallidus internus & substantia nigra & pars reticulata)?
Glutamate
What is the end result of the direct pathway?
The inhibition of movement
What is the difference between Parkinson’s and Huntington’s disease?
Parkinson’s - too little movement
Huntington’s - too much movement
Both a disease of the basal ganglia
What is the difference between Parkinson’s disease and Parkinsonism?
Parkinson’s disease is idiopathitic with genetic and environmental links
Parkinsonism occurs due to known damage to the basal ganglia e.g. professional boxing, ingesting a toxic drug
What is the pathology of Parkinson’s disease?
Cell death in the substantia nigra pars compacta causing a severe reduction in dopamine from it.
What are the 3 cardinal signs of Parkinson’s disease?
Bradykinesia
Rigidity
Tremor
What is bradykinesia?
Slowness/poverty of movement due to reduced dopamine and a decrease in level of functioning of the basal ganglia
Its a difficulty in selecting and initiating movement
What is festination? Give an example
A progressive reduction in speed and amplitude of repetitive actions
Reduction in step length during walking
What does bradykinesia cause?
Lack of automatic movements/responses such as;
- Saving reactions during loss of balance
- High risk of falls
- Swallowing, emotional expression on the face
What is rigidity in PD?
What are the two types?
Increased muscle activity causing resistance to passive movement felt throughout range of movement. Is present in opposing muscle groups
- Lead pipe rigidity - smooth resistance
- Cog wheel rigidity - intermittent catch and release of the muscle
What is the difference between resting and intension tremor?
Intention tremor - tremor gets worse as the movement progresses
Resting tremor - is slow, coarse and present at rest
Describe tremor in relation to PD.
More commonly seen in upper limbs
Tremor increases with anxiety and at the beginning of the movement
4 ways PD impacts the patient functionally.
Communication - limited non-verbal, slow & quiet voice
Swallow - reduced control of swallow, drooling and difficulty chewing, high risk of aspiration
ADL’s - gait, bed transfers
Posture - flexes trunk, hips and knees
Name 3 pharmaccologics that address hypokinesia in PD patients
L-Dopa
Dopamine agonists
Anticholinergics
How does L-Dopa work?
Synthetically increases dopamine levels
L-Dopa is the precursor to dopamine (which cannot cross the BBB) so it synthetically makes dopamine once it has crossed the BBB.
List the pros of L-Dopa.
Dramatic improvements in motor function
Improves physical functioning/independence
List the cons of L-Dopa. (4)
- End of dose decline in function
- On/off oscillations - drug reaches its optimal level 30min after ingestion
- Effectiveness diminishes with time as its neurotoxic to remaining dopaminergic cells
- Dyskinesia (hyperkinetic, uncontrolled movements)
How do dopamine agonists work?
Are an artificial form of dopamine mimicking the hormones endogenous action
Act on dopamine receptors.
They cross the BBB, bind to D1 and D2 receptors
Pros of dopamine agonists? (1)
Can be used to delay start of L-Dopa treatment
Cons of dopamine agonists?
Doesn’t bind to D1/D2 as well as L-Dopa
Many of the same side effects of L-Dopa (hallucinations, nausea, dizziness)
Long term effects not known
What is the mechanism of action of anticholinergic drugs for PD?
There is a balance between dopamine and acetylcholine in the brain
Anticholinergics block acetylcholine to readjust the balance between them
Pros of anticholinergic drugs for PD?
Effective for tremor as it doesn’t bind to D1/D2 receptors
Cons of anticholinergic drugs for PD?
Not effective for symptoms of bradykinesia (as it doesn’t bind to D1/D2)
Side effects can cause early onset dementia in the older population
What cues help reduce hypokinesia in PD patients?
Auditory - music with a strong beat so they can walk to the beat
Visual - markers on floor
What can cause falls in PD patients?
Physical problems - muscle tone becomes more rigid, change in posture, problems initiating movement/freezing
Effects of medication used to treat PD - side effect of med= they cause low blood pressure - increases dizziness
Hazards around the home - pets, rugs, loose carpet
