Parkinson's Flashcards
Definition
Result of problems occurring with the basal ganglia of the brain
Epidemiology
Most common disorder affecting 1-2% of the general population over the age of 65
70-79 most common age range
Prevalence rates in men are slightly higher
Risk factors
Age- most important factor
Positive family history
Male
Race
Life experiences (trauma, emotional stress)
Clinical presentations
Resting tremor:
– most common first symptom, usually asymmetric and most evident in one hand with the arm at rest
Bradykinesia:
– difficulty with daily activities such as writing, shaving, using a knife and fork, and opening buttons, decreased blinking, masked facies, slowed chewing and swallowing
Rigidity:
– muscle tone increase in both flexor and extensor muscles providing a constant resistance to passive movements of the joints; stooped posture, anteroflexed head, and flexed knee and elbows
Postural instability:
– due to loss of postural reflexes
Dysfunction of the autonomic nervous system:
– imparted gastrointestinal motility, bladder dysfunction, sialorrhea, excessive head and neck sweating, and orthostatic hypotension
Depression:
– mild to moderate depression in 50% of patients
Cognitive impairments:
– mild cognitive decline including impaired visual-spatial perception and attention, slowness in execution of motor tasks, and impaired concentration in most patients; at least 1/3 become demented during the course of the disease
Craniofacial features:
– hypomimia (decrease in facial expression), dysphagia, hypophonia
Visual:
– blurred vision
– slower blinking
Investigations
Case history and clinical examination
No disease-specific biological marker available
PET or SCPECT with dopaminergic radioligands
Exclusion of several causes of secondary Parkinsonism
Neuropathology
Normal movement pattern:
– cortex (initiation of volunteer movement)–> basal ganglia –> cortex –> spinal cord to muscle
In parkinsons, there is a problem with the message being sent back to the cortex from the basal ganglia
Interconnections:
input- cortex–> striatum
output- globus pallidus interna–>thalamus
thalamus–>cortex
cortex–>spinal cord etc
Role of substantia nigra
Dopaminergic neurone release dopamine into the striatum
In Parkinson’s the dopaminergic neurone die meaning there is no dopamine
Dopaminergic death usually apoptosis or necrosis because of:
– protein misfolding
– defective proteolysis
– mitochondrial dysfunction
– oxidative stress
– all of these are only theories though
Dopamine affects
D1 or D2 receptors
D1- excitatory (will stimulate neuron)
D2- inhibitory
Pathophysiology
No dopamine, so cant bind to the D2 receptor to inhibit the gabaergic neuron.
this means that the gabaergic neuron coming out of the striatum is now overactive and will release gaba, inhibiting the gabaergic neuron in the globus pallidus externa
Due to this being inhibited, it cant inhibit the glutaminergic neuron in the sub thalamic nucleus, so the neuron will release glutamate into the globus pallidus interna and externa
This will stimulate the gabaergic neuron in the globus pallidus interna, and because of no dopamine cant be inhibited by neuron above.
Leading to excessive inhibitory input to the thalamus
leading further to thalamus suppression, which means the thalamo-cortico pathway is suppressed, meaning signals dont get back to the cortex.
leading to Parkinson’s
Pathology
Demyelination, neuronal loss, gliosis occur in the substantia nigra of a person with parkinsons
Also presence of Lewy bodies:
– round occlusions in the nuclei of neurone
– made up of alpha-synuclein
Treatment
No cure, but are trt to help improve and maintain QOL
Supportive therapies:
– physiotherapy- make moving easier, relieve muscle stiffness through manipulation and exercise, try and improve fitness levels
– speech and language therapy- help with speaking and swallowing, as parkinsons causes dysphagia
Medication:
– levodopa- absorbed by nerve cells in the brain and turned into the chemical dopamine
Surgery (for some people):
– deep brain stimulation- inserting a pulse generator similar to a heart pacemaker into chest wall.
the electrical impulse will stimulate the part of the brain affected by parkinsons (basal ganglia)
