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NURS 319: C&D Disord
Chapter 34 Chronic and Degenerative Neurological Disorders
| Question | Answer |
|---|---|
| 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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