Quiz 4: Basal ganglia disorders Flashcards
Basal ganglia disorders (think PD)
* Hallmark sign - movement disorder
* Movement activation and loss of relexive or automatic movement - think walking, transfering, speaking is all impacted
* Movement becomes reliant on cortical control (think motor cortex). The ability to perform known tasks, such as walking, changing direction, writing, and basic activities of daily living, is diminished
comes w/
* Tremor
* Rigidity - velocity independent
* The kinesias
* Gait
* posture
most common inital manifestation of basal ganglia disorder (PD)
* unilateral or bilateral
Tremor - helps w/ deep brain stimulation
Unilateral
KNOW: The tremors usually start in one upper limb (UE) for months or years –> spread to all 4 limbs as well as neck and facial muscles
First seen as a rhythmic, back and forth motion of the thumb and finger, referred to as the pill-rolling tremor
* so this is how tremor starts (so I guess it starts distal)
When are tremors most obvisous?
Stresfful periods
What happens to tremors w/ sleep?
Tension / exertion will cause the tremor to increase, and it will disappear during sleep
Rigidity is common w/ BG disorder (PD) as well
* what limbs does it start in?
* Is it bilateral or unilateral?
* Is it distal or prox
Appears unilaterally and prximally then spreads distally in an upper limb and then spreads to the other extemities and trunk
** one of the earlist signs of rigidity is the loss of assocaited movements of the arms when walking** - super common w/ PD
KNOW: Rigidity is velocity indpendent resistance to passive stretch
Lead pipe = slow and sustained resistance
Cogwheel = jerky response
The kinesias come w/ BG disorders (PD)
Know: substantia nigra degenerates in PD
What is bradykinesia?
Slowness of movement
What is hypokinesia?
Decreasing range and size of movement
What is akinesia?
Disorder of movement initiation, smallness of natural and automatic movements
* difficulty initaiting movement
Freezing of gait (akinesia of gait) - sudden cessation of movement in the middle of an action sequence
* commone w/ PD
* typically triggered by something - think stepping over something, turning around, walking through a door
The abnormal kinesias w/ BG disorder may lead to:
* eye movements affected
* Mask like face - leaving not a lot of expression (joe)
* Garbled speech pattern (joe)
* Loss of fine motor skills
* Difficulty w/ dual tasks (joe)
Clinical manifestations - gait (PD/BG disorder)
Highly sterotypes and characerized by impoverished movement, with distinctive feastures of stooped posture, narrow-based, short shuffling steps, foot drags or “catch” reduced arm swing, difficulty inititaling walking or turning and slowness
typically they speed up cardince because steps are smaller (not safe cant control it) but when they become more rigid they actaully really slow down and that cadience drops
Clinical manifestations - posture
Characterized by flexion of the neck, trunk, hips, and knees, with elbows bent and arms adducted
Postural instability
MSK constrains
Weakness/fatigue
Clinical manigestations - Non motor symptoms
* autonomic dysfunction
* Excessive sweating, excessive salivation, incontinece, and disabling orthostatic hypotension
* Olfactory dysfunction is an early sign of PD in most individuals
* Visual acuity, alterations in the blink pattern, contrast senstivity, color discrimination, vergence eye movements/ocular motilties and visual field sensitivity, and visual processing speeds
* Rapid eye movement sleep behavior disorders
* Fatigue, depression, excessive daytime sleepiness
* Sensory integration issues - how are they processing their environment
* Pain
* deression
* deconditioning
Clinical manigestations - non motor symptoms cont’d
* Cognitive impairment, 80% progression to dementia in pts w/ PD longer than 20 years - because its just a long time to have such a harsh progressive disease
* Cognitive deficits in PD typically affect executive functions, attention, visuospastial function, and processing speed
* Bradyphrenia, a slowing of thought processes, with lack of concentration and attention, may also occur
* REM sleep behavior disorder is closely releated to PD cognitive impairment, and greater daytime sleepiness has been associated w/ worse cognition in PD - greater daytime sleepiness = worse daytime cognition
What is stage 1 PD like (Hoehn and Yahr)
Minimal or absent; unilateral if present - think small tremor in one hand
What is stage 2 PD like (Hoehn and Yahr)
Minimal bilateral or midline involvement; balance not impaired
What is stage 3 PD like (Hoehn and Yahr)
Impaired righting reflexes; unsteadiness when turning or rising from chair; some activities restricted but pt can live indepcently and continue some forms of employment
* so i guess balance is impaired here
What is stage 4 PD like (Hoehn and Yahr)
All symptoms present and severe; standing and walking possible only w/ assistance
* need help to move (some kind of assistive device)
What is stage 5 PD like (Hoehn and Yahr)
Confined to bed or wheelchair
Scale above is important for tx outcomes
What is used to detect level of dopamine transporters in the brains of people w/ suspected parkinsonian synromes?
DATSCAN
Most helpful in differentiating between PD and essential tremor, drug-induced parkinsonism, and psychogenic parkinsonism. It is not able to differentiate betweebn PD, progressive supranuclear palsy, multiple systems atrophy, and other neurodegenerative diseases affecting the dopamine neurons in the brain
For classic motor symptoms of PD to be present, typically 50% or more of these neurons must be list. DaTSCAN is able to detect this decreased activity early in the course of PD, when the diagnosis may still be uncertain
* so to get motor you need a lot of loss
* datscan can tell us way earlier if its suspected
Only an autopsy can conclusivel determine whether a person brain exhibits PD pathology
* because you need to look at the substaintia nigra in the mid brain
so cant dilinate between other dopamine issues in brain, but can dilinate it from non dopamine pathologies
A Note on ICF
* Body structure and fucntion (directly releated to PD: tremor, bradykinesia, rigidty, akinesia, postural instability; indirectly releated to PD: decreased flexibility decreased endurance)
* Activity (gait, transfers, bed mobility)
* PArticipation (ability to work and interact socialy, self-care, recreational sports, quality of life)
* Environmental factors (home and community settings) and personal factors (resources, personal attitudes, self-efficacy, emotions and feelings) all need to be considered
Levodopa = used for PD
GI symptoms
Cardiovascular symptoms
Dyskinesias
Beahvioral changes
GI = nausa / vomitting
cardio = arrhyhmias, orthostatic hypotension
Dyskinesias
* EX: choreoathetoid movements, ballismus, dystonia, myoclonus and various tics and tremors
Behavior changes
Problems and adverse effects of levodopa therapy for PD
Diminished repsonse and/or fluctiations in response to the medication
End of dose akinesia
* when the drugs effectiveness seems to wear off prior to the next dose
On/Off phenomenon
* Effectiveness of levodopa may suddently and spontaenously decrease, resulting in the abript worsening of parkinsonsian symptoms (the off period)
* Remession of symptoms may then occur spontaneously or after taking a dose of levodopa (the on period)
* so on = less ysmptoms - when symptoms are contorlled
* off periods = medication wearing off and you’ll see their symptoms
* shouldnt be a distinct off period w/ good treatment - hopefully the disease is just contorlled
* change dosage / timing of medications if this isnt working
Drug holiday - done if they arent getting benefits of medication
* Patient who has become refractory to the beneficial effects of levodopa or who has had a sudden increase in the adverse side effects
* Removed from meds for 3 days to 3 weeks under close medical supervision
* Purpose is to allow body to recover from toxicity of tolerance tissue
* goal is to be able to return to the same drug with better results
* Not used routinely due to potential risks
