Neurocognitive 2 - Parkinsons + Flashcards
Parkinson’s disease
syndrome of resting tremor, rigidity, bradykinesia, postural instability
degeneration of dopaminergic neurons in basal ganglia
basal ganglia components
“middle manager”
composed of substantial migrant, striatum, gobs pallid us, subthalamic nucleus, thalamus
basal ganglia function
control and regulate activity of motor and premotor cortical ares so that voluntary movements are smooth
INHIBIT number of motor systems
Parkinson’s patho
loss of dopaminergic neurons in substantia nigra
loss of excitatory input from thalamus to cerebral cortex
increased inhibition to cerebral cortex form other nuclei in basal ganglia
etiologies of Parkinson’s
genetic (10%) - suspect if <50 @ diagnosis
environmental risk factors (rural environment, exposure to pesticides, well water)
Parkinson’s disease epidemiology
more common in older individuals, men > women
mc in white boys
Parkinson’s disease presentation
MC INITIAL IS RESTING asymmetric TREMOR of finger/thumb
rigidity, bradykinesia, postural instability, dystonia
general decreased dexterity
rigidity in PD
stiff limbs, poor mobilization of face
bradykinesia in PD
slowed movement BUT muscle strength is NOT weak on exam
facial (decreased blinking, drooling)
truncal (difficulty turning in bed, worse in small areas)
UE (micrographia)
LE (scuffing/dragging of feet)
dystonia
foot inversion or dorsiflexion
adduction of arm and Hand causing it to rest
other presenting symptoms of PD
decreased arm swing
soft voice, monotone, less distinct
decreased sense of smell
sleep disturbances
symptoms of autonomic dysfunction
weakness/malaise
depression or anhedonia
slowness in thinking/major neurocognitive dysfunction
cardinal signs of PD
- resting tremor (goes away with movement!!!)
- rigidity (resistance to moving wrist)
- Bradykinesia
- postural instability
dementia of PD
executive functioning, short term memory and visuospatial ability impaired
typically doesn’t occur right away (>1 yr following diagnosis)
making PD diagnosis
if pt presents with tremor = no workup
lack of tremor = imaging and lab work (will be normal)
MUST asses for depression (@ diagnosis and periodically)
meds used in PD tx
levodopa
MAO-B inhibitors
dopamina agonists
typically good for 4-6 yrs
drug class that will WORSEN PD symptoms
deplete central dopamine
antipsychotics, prochlorperazine, Reglan
levodopa/carbidopa
L = metabolic precursor of dopamine, but if given alone causes n/v
c= inhibits systemic breakdown of levodopa so more effective in CNS, can’t cross BBB
levodopa/carbidopa ADRs + brand
orthostatic HoTN, syncope, dizziness, anorexia, n/v, confusion, dark urine
Sinemet
why do we delay levodopa/carbidopa
delay use = delay onset of motor fluctuations
these are when pts wear off the med and have to continually increase dose to sustain normal function
MAOIs used in PD
Selegiline (Eldepryl/Zelapar)
Rasagiline (Azilect)
MAOIs use and Moa
initial or add on tx (can delay motor fluctuations)
block degradation of dopamine, extend action of L-Dopa
MAOIs drug facts (ADRs_
excellent profiles, improved long term outcomes
nausea, confusion, hallucinations, HA, bitterness, orthostasis
what meds are not good mixed w/ MAOIs
antidepressants, pain meds, cold and weight loss meds
esp. dextromethorphan, tramadol, methadone
dopamine agonists used inPD
Ropinirole (Requip)
Pramipexole (Mirapex)
dopamine agonists MOA
stimulate dopamine receptors in striatum
mono therapy in early dz or add on therapy in later PD
why aren’t dopamine agonists mainstay of tx
cause increased ADRS such as somnolence, sudden onset sleep, halucinations, edema, impure control disorder
amantadine
symmetrel
antiviral drug that has beneficial effects on PD thru mechanisms unknown
improves symptoms in mildly affected pts reduces motor fluctuations and dyskinesias in pts with advanced dz
ADRs of amantadine and symmetrel
confusion hallucinations nausea HA dizziness insomnia lived reticulars peripheral edema anticholinergics
anticholinergics in PD
Benztropine mesylate (cognentin)
Trigexyphenidyl (artane)
benefit for tremor in 50% of pts, don’t improve bradykinesia or rigidity
avoid in pts > 70
anti cholinergic side effects
dry mouth blurred vision constipation cognitive impairment hallucinations urinary retention
Later stages of PD
over time, levodopa stops working (have to add on other medications or increase does)
will get peak dose dyskinesia
COMT inhibitors
Catechol o methy transferase inhibitor
inhibits metabolism of dopamine so longer effects
may cause liver failure, removed from markets
COMT inhibitors used in PD
entacapone (Comtan)
Carbidopa/levodopa.entacapone (Stalevo)
tolcapone (tasmar)
surgical PD tx
create lesions in overactive part of brain to improve symptoms
can also implant DBS into a patient
parkinsonian plus syndrome is suspected when
poor response to therapy with L dopa in patient who displays Parkinson’s syndrome
Normal Pressure hydrocephalus
buildup of too much CSF in cranium when patient does not reabsorb CSF adequately or overproduce CSF
NPH results in
transiently high pressure ad compression of brain and spinal cord
causing edema of brain
NPH pathophys
enlarging ventricles to relieve pressure = shrinkage of brain parenchyma
may be 2/2 SAH, tumor, meningitis, head injury
classic NPH symptoms
- abnormal gait (earliest, responds to tx)
- urinary incontinence
- dementia
diagnosis of NPH
labs are normal
CT/MRI will show ventricular enlargement out of proportion to sulcus atrophy
NPH tx
VP shunt to drain CSF from ventricle into the abdomen to be absorbed
risk of pump dysfunction and infection
