Neuro: Disorders of Motor Function Flashcards
Parkinson’s Disease About + Etiology
Idiopathic, chronic, progressive degenerative disorder of CNS
motor, neuropsychiatric manifestations
50+ in age
2nd most common neurodegenerative disorder
Parkinson’s s/s
tremors bradykinesia (chew, swallow, speak) muscle rigidity postural instability flat affect
Conditions Causing Secondary Parkinsonism
head trauma toxins metabolic disorders infections multiple strokes in basal ganglia atypical antipsychotics&antiemetics
Parkinson’s Causes
90% Idiopathic
10% Genetic
Increased RF for Parkinson’s
increased age (most significant) male exposure to pesticides, metals family history of PD genetic mutations
Decreased RF for Parkinson’s
cigarette smoking
caffeine intake
high blood urate levels
Parkinson’s Pathogenic Mechanisms
proteolytic stress (too many proteins, Lewy bodies) oxidative stress (too little gluutathione, increase in iron, reactiev oxygen species) mitochnodrial dysfunction (decreased mitochondrial activity by 30-40%) inflammation (overactive microglia, excess production of neurotoxic factors)
Parkinson’s Manifestations
insidious onset
Motor: tremor in resting hands/lips/chin/legs/mouth, regidity from increased muscle stiffness/tone, cogwheeling, bradykinesia, postural instability
Nonmotor: fatigue/sleep disturbances, olfactory dysfunction, pain, autonomic dysfunction
Neuropsychiatric: cognitive dysfunction, dementia, psychosis, hallucinations, mood disorders, depression, anxiety
Parkinson Disease Stages
Stage 1 (mild s/s on one side only, changes in posture/locomotion/facial expression) Stage 2 (bilateral symptoms/minimal disability, posture&gait effected) Stage 3 (significant slowing of body movements, early impairment of equilibrium on walking/standing, generalized dysfunction moderately severe) Stage 4 (severe symptoms, rigidity & bradykinesia, can still walk to a limited extent, unable to live alone, tremor may be less than in earlier stages) Stage 5 (cachectic stage, invalidism, cannot stand or walk, requires constant care)
Parkinson’s TX
pharmacologic replenishment w/ dopaminergic drugs dopamine agonists anticholinergic agents amantadine monoamine oxidase inhibitors catecol-o-methyltransferase inhibitors ablation surgery deep brain stimulation complementary & supportive therapies
Dopamine Agonists (ex/Moa/Se/Monitoring/Teaching/Preg)
levodopa/carbidopa
increases biosynthesis of dopamine in nerve terminals
uncontrolled/purposeless movements, involuntary movements, loss of appetite, n/v
monitor LFTs, contraindicated in narrow-angle glaucoma
discontinue gradually
C
Anticholinergic Agents (Moa/ex/Use/Se/monitoring/teaching/Preg)
block acetylcholine to inhibit overactivity
benztropine
tx early stages of Parkinson’s
dry mouth, blurred vision, photophobia, urinary retention, constipation, tachycardia, glaucoma
watch liver disease, severe constipation, blockage of urinary tract
monitor for hypotension/tachycardia
avoid alcohol
C
Multiple Sclerosis
chronic inflammatory demyelinating degenerative disorder of CNS inflammatory autoimmune diease lesions throughout CNS progressive disease unknown/no cure
MS RF
age gender ethnicity geography r/t latitude genetics
MS Pathogenesis
development of plaques
demyelination which causes conduction blocks and axonal degeneration
atrophy of gray matter (r/t cognition)
MS Development
initial: clinically isolated syndrome
Relapsing-remitting multiple sclerosis (RRMS) [stable for 10-20 years]
Secondary Progressive MS (SPMS) [gradual worsening may have occasional relapses, minor remissions, plateaus]
Primary Progressive MS (PPMS) [progressive deficits w/ occasional plateaus, temp improvements or acute relapses]
MS s/s
sensory symptoms in extremities/face visual loss double vision slurred speech weakness vertigo gait/balance disturbances bowl&bladder problems neuropathic pain spasticity bilateral internuclear opthalmoplegia fatigue cognitive dysfunction heat sensitivity sexual dysfunction
MS DX
CNS lesion disseminated in time & space
MRI (McDonald criteria/plaques present)
Blood tests to rule out other disorders
evoked potentials recording timing of CNS response to stimuli
EEG
lumbar puncture
MS TX
immunomodulatory therapy amantadine/modafinil for fatigue spasticity physical therapy routine stretching program medications intramuscular botulinum toxin nerve blocks intrathecal baclofen pump placement
Immune-modulating Drugs (Moa/use/SE/monitoring/teaching/preg)
uknonwn, interferes with cell-binding
reduces severity of MS symptoms, decreases lesions
flushing, chest pain, weakness, infection, pain, nausea, joint pain, anxiety, muscle stiffness
liver fx, depression, suicidal ideation
rotation of injection sites/use new needles
C
Amyotrophic Lateral Sclerosis
Lou Gehrig’s Disease
progressive neurodegenerative disease
causes weakness/disability/death w/in 3-5 years
Amyotrophic Lateral Sclerosis RF/Etiology
age/family history
no direct mechanism known
similar to prion disease/malignancy
motor axons die by wallerian degneration
Amyotrophic Lateral Sclerosis Pathways
oxidative stress mitochonodrial dysfunction defect of axonal transport abnormal growth factor expression excitotoxicity
Amyotrophic Lateral Sclerosis s/s
insidious onset slowly progressive, painless weakness in one or more body parts upper motor neuron s/s lower motor neuron s/s bulbar dysfunction (CN 9/10/11/12) frontotemporal executive dysfunction
