Parkinsons Disease Flashcards
(16 cards)
Definition
Chronic, progressive, neurodegenerative disorder resulting from the degeneration of dopamine producing neurones in the substantia nigra of the basal ganglia
Risk factors
Environmental factors
Genetic factors
Pesticides
Genetic mutations
4 Cardinal signs
Bradykinesia - slow movement
Rigidity
Resting tremor
Postural instability
Function of the basal ganglia
Well-learned motor skills and movement sequences
Preparation and planning
Initiation and termination
Sequencing and timing
Regulating muscle tone and inhibition of antagonistic muscles
What are the 5 nuclei of the basal ganglia
Globus pallidus
- internus and external
Caudate
Putamen
Subthalamic nuclei
Substantia nigra
- pars compacta
- pars reticulata
Secondary clinical symptoms
Difficulty initiating and terminating movement
Fatigue
Freezing
Sleep disorders
Dysphagia
Anxiety and depression
Festinating gait pattern - shuffling
What are the 2 basal ganglia pathways
Direct - promotes movement - go pathway
Indirect - inhibits movement - stop pathway
Explain the direct pathway
Cortex sends excitatory signals to the striatum
Striatum sends inhibitory signals to the globus pallidus internus and substantia nigra pars reticulum
Meaning no signals are sent to the thalamus
Meaning the thalamus is not sending signals resulting in more excitation to context so more movement
Describe the indirect pathway
Cortex sends excitatory to striatum
Striatum sends inhibitory to globus pallidus externus
- meaning inhibition isnt sent to the sub thalamic
Cortex sends excitation to subthalamic as not getting inhibition from GPE
Excitation sent to globus pallidus internus and substantia nigra pars reticulum
They send inhibitory to thalamus
Meaning less excitation to cortex and less movement
What is dopamines role
Dopamine excites direct (go)
Dopamine inhibits indirect (stop)
- dopamine promotes movement
Parkinson’s effect on dopamine
Parkinson’s is a lack of dopamine
Less excitation of direct
Less inhibition of indirect
- less movement
Medications
Dopamine replacements
- replace lost dopamine but dopamine cannot cross the blood/brain barrier
- these medications contain drugs that facilitate the crossing to the brain
- e.g madopar, sinemet
Dopamine copycats
- aka dopamine agonists
- e.g apomorphine, perdolide
Dopamine protectors
- protect current levels of dopamine by blocking enzymes that break it down
- e.g MAO-B inhibitors
Secondary effects of medication
Various and wide ranging
Especially when considering variety of meds people end up taking
Treatment:
- deep brain stimulation
Postural instability
Develops later in the disease
Characterised flexed posture
flexed hips and knees
Unable to access balance reactions
Appearance of PD
Stooped posture
Masked facial expression
Rigidity
Forward tilt of trunk
Flexed elbows and wrists
Reduced arm swing
Slightly flexed hips and knees Unable to
Trembling of extremities
Shuffling, short-stepped gait
Principles for enhancing function
Cueing
Duel tasking
Balance training
Gait re-education
Symptom specific exercise