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NURS 319: C&D Disord

Chapter 34 Chronic and Degenerative Neurological Disorders

QuestionAnswer
acetylcholine neurotransmitter
aura smell/lights
dopamine neurotransmitter
interictal period period between attacks
myoclonus type of muscle tetany
ataxia unusual uncoordination
chorea symptom that causes involuntary, irregular or unpredictable muscle movements
glutamate neurotransmitter
midbrain middle of brain
postictal period following seizure
athetosis snake like movements
basal ganglia motor control/ executive function in brain
ictal period time from first symptom until end of seizure attack
myelin muscle/ nerve conduction
serotonin neurotransmitter
substantia nigra tonic tone of muscle
how common are headaches 1%-4% of all emergency department visits
who has headaches? 75% women
what is the difference between a seizure and epilepsy? seizure: temporary absence of attention, uncontrolled muscle movements epilepsy: chronic, unprovoked seizures that are unpredictable
how many people will have a seizure in their lifetime? 9%
how many people will be diagnosed with epilepsy? 3%
degenerative neurological diseases diminish neurological impulse transmission
at what age does parkinson disease become more likely to develop? 60 years
Multiple sclerosis immune mediated and involves the destruction of myelin sheaths
cns central nervous system
pns peripheral nervous system
function of neurons transmit signals, process information, and connect with other neurons
what travels between gaps (synapses) between neurons? neurotransmitters
what are glial cells and what do they do? Glial cells are a type of cell that provides physical and chemical support to neurons and maintain their environment
acetylcholine (function) brain function, memory and learning, muscle contractions (myasthenia gravis)
dopamine (function) behavior and cognition, voluntary movement, motivation, reward center (addiction) produced in a region of the brain (substantia nigra)
substantia nigra (and loss of dopamine) are responsible for parkinson disease
too much dopamine causes the "positive" symptoms of schizophrenia
GABA calm, sleep, pleasure, contentment; helps decrease muscle tone and spasm, involved with seizure activity
glutamate (function) brain's primary excitatory neurotransmitter; involved in cognition, memory, learning, can be toxic to brain cells in accumulation;
nerve conduction impulses action potentials
how do action potentials work? begin at the cell body and travel down the axon
action potentials activate sodium ions
what do sodium ions do? increases the concentration of positively charged cations in the cell and causes depolarization
what is depolarization? inside ion is more positive
depolarization at the peak threshold is called peak phase
why is a refractory period so important? allows for everything to return back to normal
if these impulses are not orderly, what kinds of things can happen? rapid firing of neurons and chaos; lost conduction
myelin (definition) protective sheath around ions
myelin can be compared to insulation
what happens to nerve impulses when myelin is impaired? disrupted and nerves can wither away
can myelin grow back? sometimes but not always
location of upper motor neuron cell bodies cortex- brain's motor control region
location of lower motor neurons spinal cord
what is involved in a good neurological exam motor, sensory, reflexes, balance, visual fields, speech
what is the clinician looking for in a neurological exam? tremors, fasciculations, motor rigidity, spasm
what diagnostic test would you perform on a patient with a new onset seizure? EEG
what diagnostic tests would you run on a patient being evaluated for multiple sclerosis? EMG & NCV
What tests would you run on patient who was in a coma to see if they could see or hear? evoked potentials
epilepsy chronic disease characterized by recurrent seizures
seizure sudden, abnormal, disorderly discharge of neurons within the brain that is characterized by a sudden transient alteration in brain function
who is most commonly affected by seizures and why? infants less than 1 year old and adults older than 60; most susceptible to brain damage
what are some known causes of epilepsy? stroke, tumor, trauma, genetics
generalized seizures impaired awareness
focal seizures aware or impaired awareness
stages of seizure prodome, aura, ictal, postictal
focal seizure: motor yes or no
focal seizure: absence no
generalized seizure: motor yes
generalized seizure: absence yes
other seizure: motor yes
other seizure: absence yes
are EEGs a reliable source of diagnosis for seizures? no, it cannot show abnormalities; seizure activity would have to occur during EEG
how are headaches categorized? primary or secondary disorder
causes of secondary headaches other primary disorders
most common types of primary headaches are migraine, tension-type headaches (TTH), and trigeminal autonomic cephalgia
three subtypes of TTH? infrequent episode, frequent episode, chronic TTH
infrequent episode less than a day a month
frequent episode 10 headache episodes per month for 3 months
chronic TTH 15 or more days per month for at least 3 months
presenting symptoms of TTH neck/shoulder pain, stable pain throughout head
how is TTH different from a migraine? no nausea/ vomit or photophobia and exercise does not impact them
triggers of TTH hormonal cycle, food, sunlight, odors
who gets the most migraines? women
four stages of migraine headache prodome, aura, pain, postdrome
prodome neural hhyperexcitability in the brain
aura cortical spreading depression (CSD) occurs (similar to seizures)
pain trigeminovascular complex activation accounting for the pain
postdrome sensitization of the trigeminal vascular process complex
serotonin and calcitonin involvement with migraines gene related peptides are thought to be released and it is known to be potent vasodilators (cause "pounding")
what is the prodromal stage of a migraine like? constipation, mood changes from depression to euphoria, food cravings, neck stiffness, increased thirst and urination or frequent yawning
what does the typical migraine patient report? unilateral pain, nausea/ vomit, worsens with movements
what are common migraine triggers smells, light, stress, medications
how is migraine diagnosed? clinical findings of physical exam
who gets parkinson's disease men and women equally
when does parkinson's disease usually get diagnosed 50-60 years old
what is the age below which a parkinson's diagnosis is considered young onset younger than 40
what produces dopamine cells of substantia nigra
what causes the symptoms of parkinson;'s disease? imbalance of dopamine and acetylcholine
dopamine function give you feelings of pleasure, satisfaction and motivation
acetylcholine function regulating cardiac contractions and blood pressure, intestinal peristalsis, glandular secretion
ANS symptoms can include orthostatic hypertension, constipation, impaired thermoregulation, insomnia, night waking, night terrors
TRAP tremor, rigidity (bradykinesia), postural instability
tremor at rest; thumb moving across the hand; unintentional "pillrolling" tremor
rigidity tightness or stiffness in arms; one side of body, can progress to other side
bradykinesia state of slowed movement; bent forward, shuffling gait
postural instability later manifestation; lose balance easily, increase risks for falls
what are some neuropsychiatric concerns with parkinson's disease? depression (40%), cognitive dysfunction (80%), dementia, anxiety, lack of joy/ interest in life
how is parkinson's diagnosed? TRAP; newer PET CT scans, positive response to medications (low dopamine areas)
how does medicating patients help confirm diagnosis if they positively respond, the body is experiencing the necessary symptoms/ deficits for diagnosis
ALS amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis progressive neurodegenerative disease; eventually results in loss of upper and lower motor neurons, eventually leading to respiratory failure- accompanied by progressive muscle weakness and atrophy
prevalence of ALS 6 in 100,000 individuals per year
what ages is ALS typically diagnosed? 40-60
what ethnic groups typically get ALS? caucausian
ALS risk factors men more than women, heavy metal toxic effects, environmental/ occupational exposure, smoking, physical trauma, heavy physical activity
two types of ALS inherited (familial) or sporadic
which type of ALS is more common? sporadic (90%)
pathophysiology of ALS upper and motor neurons become sclerotic and die (autoimmune response)
whats symptoms of ALS require a ventilator to assist breathing? muscles no longer receive messages from neurons, muscles reach paralysis, unable to breathe
is there cognitive impairment with ALS? no
presenting symptoms of ALS pain in upper/lower extremities, head droop, problems speaking and swallowing, muscle spasms, hyperreflexia, positive reflex, weakness, atrophy
how is ALS diagnosed? clinical criteria, no lab tests/ biomarkers, rule out competing conditions, symptoms based on physical exam
huntington's disease involuntary motor symptoms and cognitive decline; inherited progressive neurodegenerative disease (autosomal dominant)
if you have HD, what are the chances your child will inherit HD? 50% chance of inheritance
how many people in the US currently have HD? 30,000 people
how many years on average does a person live with HD? live from 10-20 years after diagnosis
where does the Huntingtons protein accumulate? collects within cytoplasm of brain cells causing cellular deterioration
HD: involuntary motor symptoms dyskinesia, loss of voluntary movement (chorea), thrashing movements
HD: emotional and behavioral symptoms major depressive episodes, mania episodes, irritability/ anger/ agitation
HD: cognitive symptoms apathy, impaired mental flexibility, slowing of thought process
how is HD diagnosed? genetic test- blood test for genetic mutation
guillain barre syndrome acute peripheral neuropathy leading to weakness over weeks
what is meant by GBS being a post-infectious disease? immune response to antigen also accidentally starts attacking myelin sheaths
common antecedent infections for GBS epstein-barr virus, cytomegalovirus, mycoplasma pneumonia
who is mostly affected by GBS men slightly more than women
why would an older patient become susceptible to GBS? more susceptible to infections (lowered immune system)
what part of the nerves does the immune system attack in GBS? why do we think the immune system turns on itself? myelin sheath; adverse response to antigen
cardinal presentation of GBS progressive, symmetric, ascending muscle weakness that progresses for days and usually stops at about 4 weeks
GBS patho starts with paresthesia and travels up limbs or torso; range of severity is possible with GBS from mild to weakness to respiratory arrest from paralysis requiring ventilation
is GBS recovery possible? to some extent, after 2 years extent of recovery has been realized
myasthenia gravis descending; loss of functioning acetylcholine receptors
why are we diagnosing myasthenia gravis more? better recognition of the disease
MG is caused by loss of functioning acetylcholine receptors in the neuromuscular junction; 80% reduction in receptor sites
MG common presentation extraocular muscle weakness and atosis (drooping of eyelid)
where do T cells mature thymus
why do researchers think the thymus and T-cells may be involved with MG? T-cell mediated immunity in thymus, thymus issues found with this disease (70% patients)
who is at risk for MG? genetics, other autoimmune diseases
how does a patient with MG present? muscle weakness and ocular symptoms
what is meant by ocular presentation versus generalized presentation? ocular: drooping eyes; generalized: trouble swallowing, speaking, fluctuating muscle weakness
if an MG patient only presents with ocular symptoms, how many of them will go on to have generalized disease? in what time period? the majority of cases within 2 years
why are muscular MG symptoms worse in the afternoon? weaker as they lose energy
two major causes of death in MG aspiration and respiratory failure
what would happen if an MG patient got a dose of edrophonium significant improvements within 30 to 45 seconds
what other tests can help diagnose MG serum acetylcholine receptor antibodies and EMG (measures muscle response)
multiple sclerosis chronic neurological condition that affects both the brain and spinal cord; demyelinating disorder resulting in inflammation and damage to the myelin sheaths
how is MS characterized? remissions and exacerbations
what does MS result in? CNS damage and neurological disability
prevalence of MS european women twice as much as men; cooler climates, farther from equator
MS etiology unknown cause provokes T-cells to attack myelin sheath- trauma, exposure to heavy metals and viruses have also been implicated
why is there a predilection for optic nerves presumed? they are so heavily resolved
during MS remission, what can happen myelin sheath repairs, but sometimes damage is so severe it is irreversible
MS presentations numbness and tingling, painful motor movements (ADLs, sensory loss), blurred vision, fatigue
what percentage of patients have remitting and relapsing form of MS? 85%
how long do MS episodes last? several weeks to 3 months
how long between MS episodes? 1-3 years
what is PPMS? primary progressive multiple sclerosis
what percentage of people with MS have PPMS form? 10-15%
when does severe motor impairment occur in the course of MS? within 10-15 years
what disabilities can spinal cord involvement lead to? urinary/fetal incontinence, sexual dysfunction, paralysis
lifetime risk of major depression for patients with MS is? high as 50%
how many MS patients have cognitive impairments? 45-65%; memory and executive functioning
how many patients with relapsing-remitting MS go on to develop PPMS? 50%
what imaging can be done to diagnose MS MRI
what do blood tests show for MS normal, CSF may be elevated
what is an evoked potential for MS what is the brain doing during symptoms
can any single symptomatic episode be used to diagnose MS? no, need several checkboxes to rule out other diseases
Created by: lcorlew1
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