Chapter 59: Chronic Neurological Problems Flashcards

1
Q

Probably the most common type of pain. Primary are not caused by a disease or another medical condition. Secondary are caused by another condition or disorder, such as sinus infection, neck injury, and stroke.

A

Headache

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2
Q

Also called a stress headache. Most common type. Bilateral location and pressing or tightening quality. Usually of mild or moderate intensity and can last from minutes to days. Believed to be associated with neuromuscular factors similar to those involved in migraine headaches. Bilateral frontal-occipital headache- constant, dull pressure, or sandlike headache associated with neck pain and increased tone in the cervical and neck muscles. May involve sensitivity to light (photophobia), but does not involve n/v. No prodrome (early manifestation of impending disease), and physical activity does not aggravate sx. Careful hx taking for dx. May have increased resistance to passive movement of the head and tenderness of the head and neck. EMG may reveal sustained contraction of the neck, scalp, or facial muscles.

A

Tension-type headache

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3
Q
Recurring headache characterized by unilateral (sometimes bilateral) throbbing pain, a triggering event or factor, and manifestations associated with neurologic and autonomic NS dysfunction. Most common age for onset is 20-30 years. More common in women than men. Risk factors include family hx, low level of education, low socio-economic status, high workload, and frequent tension-type headaches. Complex series of neuromuscular events may initiate it. May have specific factors that trigger it (foods, menstruation, head trauma, physical exaggeration, fatigue, stress, missed meals, weather, and drugs. Chocolate, cheese, oranges, tomatoes, onions, MSG, aspartame, and alcohol- particularly red wine). 
A prodrome (may include neurologic [eg photophobia], psychologic [eg hyperactivity, irritability] and other [eg food craving] manifestation) and an aura (complex of neurologic sx characterized by visual [eg bright lights, scotomas-patchy blindness, visual distortions, sensory, and/or motor phenomena) may precede the headache phase.  Presentation varies in severity. Dx usually based on hx. No specific lab or radiologic tests.
A

Migrane headache

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4
Q

Rare form of headache. Involve repeated headaches that can occur for weeks to months at a time, followed by periods of remission. Trigeminal nerve has a role in the production of pain, but they also involve dysfunction of intracranial blood vessels, the SNS, and pain modulation systems. Alcohol is a dietary trigger, along with strong odors, weather changes, and napping. One of the most severe forms of headache, with intense pain lasting from a few minutes to 3 hours. The pain is sharp and stabbing, which is in contrast to the pulsing pain of the migraine headache. The pain is generally located around the ye, radiating to the temple, forehead, cheek, or gums. Other manifestations include swelling around the eye, lacrimation, facial flushing or pallor, nasal congestion, and constriction of the pupil. The pt is often agitated and restless, unable to sit still or relax. They can occur every other day and as often as 8 times/day. The attacks occur in clusters. The clusters occur with regularity, usually at the same time each day, during the same seasons of the year. A cluster typically lasts 2 weeks to 3 months, and then the pt goes into remission for months to years.
Dx based on hx. CT, MRI, MRA may rule out an aneurysm, tumor, or infection.

A

Cluster headaches

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5
Q

Other types of headaches

A

Although tension, migraine, and cluster headaches are by far the most common types of headaches, other types can occur. These headaches may be the first sx of a more serious illness. HA can accompany subarachnoid hemorrhage; brain tumors; other intracranial masses; vascular abnormalities; trigeminal neuralgia; disease of the eyes, nose and teeth; and systemic illness (e.g. bacteremia, CO poisoning, mountain sickness, polycythemia vera). The sx vary greatly. B/c of the variety of causes, clinical evaluation must be thorough. It should include an evaluation of personality, life adjustment, environment, and family situation, as well as a comprehensive eval of neuro and physical status

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6
Q

Tx for tension-type headache

A

ASA, Tylenol, or NSAIDs. Nonopioid analgesics.

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7
Q

Tx for migrane headache

A

The aim of drug tx of an acute migraine attack is terminating or decreasing the sx. Many people with mild to moderate sx can obtain relief with NSAIDs, ASA, or caffeine-containing combination of analgesics. For moderate to severe headaches, the triptans have become the first line of therapy (e.g. sumatriptan [Imitrex]. affect selected serotonin receptors, thus reducing neurogenic inflammation of the cerebral blood vessels and producing vasoconstriction. most effective when taken at the onset or during the aura. Pts with heart disease or stroke should avoid).
Prevention is important. Topiramate [Topamax], an anti seizure drug, taken daily, is effective in prevention (S/Es- hypoglycemia, paresthesia, weight loss, cognitive changes. Must be used for 2-3 months to determine effectiveness).
Dark, quiet area. Sleep.
Botox- prophylactic. Additional anti seizure drugs (divalproex [Depakote], gabapentin [Neurontin]), tricyclic antidepressants (e.g. amitriptyline [Elavil]), SSRIs (eg fluoxetine [Prozac]).

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8
Q

Tx for cluster headaches

A

Because cluster headaches occur suddenly, often at night, and do not last long, drug therapy is not as useful as it is for other types of headaches. Acute tx is inhalation of 100% O2 delivers at a rate of 6-8 L/min for 10 min, which may relieve HA by causing vasoconstriction and increasing synthesis of serotonin in the CNS. This can be repeated after a 5 minute rest. A drawback to this tx is that the pt must have continuous access to the O2 supply.
Triptans (e.g. sumatriptan [Imitrex]) are also effective.
Prophylactic drugs- verapamil, lithium, ergotamine, divalproex, melatonin, anti seizure meds.

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9
Q

Other headache interventions

A

Thorough assessment; daily exercise; relaxation techniques; quiet, dimly lit environment; massage; moist hot packs; dietary counseling (wine can trigger migraines); medications)

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10
Q

Paroxysmal, uncontrolled electrical discharge of neurons in the brain that interrupts normal function. May accompany a variety of disorders, or may occur spontaneously without any apparent cause.

A

Seizures

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11
Q

Metabolic disturbances that cause seizures:

A

acidosis, electrolyte imbalances, hypoglycemia, hypoxia, alcohol and barbiturate withdrawal, water intoxication or dehydration. Not considered epilepsy if cease when underlying condition is treated.

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12
Q

Extra cranial disorders associated with seizures

A

Heart, lung, liver or kidney disease; systemic lupus erythematosus; DM; HTN; and septicemia.

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13
Q

A condition in which a person has spontaneous recurring seizures c/b a chronic underlying condition. Incidence is increasing in older adults. Males are more likely to develop it than females. People at high risk: those with Alzheimer’s disease or those who have had a stroke.

A

Epilepsy

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14
Q

Etiology and pathophys of seizures

A

Have many possible causes, with the most common causes varying by age.
First 6 months of lief: severe birth injury, congenital defects involving the CNS, infections, and inborn errors of metabolism
2-20 y/o: birth injury, infection, trauma, and genetic factors
20-30 y/o: usually occurs as the result of structural lesions, such as trauma, brain tumors, or vascular disease
50+ y/o: stroke and metastatic brain tumors.
Nearly 30% (70% according to Bonnie’s lecture) are idiopathic (idiopathic generalized epilepsy [IGE]), meaning they are not attributable to a specific cause.
Abnormal neurons undergo spontaneous firing. This firing spreads by physiologic pathways to involve adjacent or distant areas of the brain. If it speaks to involve the whole brain, a generalized seizure occurs. Factor that causes this is unclear. Any stim that causes the cell membrane of the neuron to depolarize induces a tendency for spontaneous firing.

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15
Q

Genetic link of IGE

A

Genetic abnormalities may be the most important factor contributing to IGE. The role of genetics has been difficult to determine because of the problem of separating genetic from environmental or acquired influences.

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16
Q

Clinical manifestations of seizures

A

Determined by the site of the electrical disturbance. Divided into two major classes: generalized and focal. Depending on the type, a seizure may progress through several phases: 1) prodromal phase (signs or activity that precede seizure); 2) aural phase (sensory warning); 3) ictal phase (full seizure); 4) postictal phase (period of recovery after).

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17
Q

Involve both sides of the brain and are characterized by bilateral synchronous epileptic discharges in the brain from the onset of the seizure. In most cases pt loses consciousness for a few seconds to several minutes

A

generalized seizures

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18
Q

Most common generalized seizure. Formerly known as gran mal. Characterized by losing consciousness and falling to the ground if the pt is upright, followed by stiffening of the body (tonic phase) for 10 to 20 seconds and subsequent jerking of the extremities (clonic phase) for another 30 to 40 seconds. Cyanosis, excessive salivation, tongue or cheek biting, and incontinence may accompany the seizure. The postictal phase- pt usually has muscle soreness, is tired, and may sleep for several hours. Some pts may not feel normal for several hours or days after. Pt has no memory of the seizure.

A

Tonic-clonic seizure

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19
Q

Usually occurs only in children and rarely continues beyond adolescence. May cease altogether as the child matures, or it may evolve into another type of seizure. Brief staring spell resembling “day dreaming” that lasts only a few seconds, so it goes unnoticed. When left untreated, the seizures may occur up to 100X/day. EEG demonstrates a spike-and-wave pattern that is unique to this type of seizure. Hyperventilation and flashing lights can precipitate these seizures.

A

Absence seizures

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20
Q

Characterized by a staring spell accompanied by other s/s, including brief warning signs, peculiar behavior during the seizure, or confusion after the seizure. It is longer lasting than a typical absence seizure and may be associated with loss of postural tone. EEG demonstrates atypical spike-and-wave patterns.

A

Atypical absence seizures

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21
Q

Characterized by a sudden, excessive jerk of the body or extremities. Jerk may be forceful enough to hurl the person to the ground. These seizures are brief and may occur in clusters.

A

Myoclonic seizure

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22
Q

“Drop attack.” Involves either a tonic episode or a paroxysmal loss of muscle tone and begins suddenly with the person falling to the ground. Consciousness returns by the time the person hits the ground, and normal activity can be resumed immediately. Pts with this type of seizure are at a great risk of head injury and often have to wear protective helmets.

A

Atonic seizure

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23
Q

Involves a sudden onset of maintained increased tone in the extensor muscles. These pts often fall.

A

Tonic seizures

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24
Q

Beings with loss of consciousness and sudden loss of muscle tone, followed by limb jerking that may or may not be symmetric.

A

Clonic seizures

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25
Q

Also called partial or partial ____ seizures. Are the other major class of seizures. Being in one hemisphere of the brain in a specific region of the cortex. Produce s/s r/t the function of the area of the brain involved. Divided according to their clinical expressions.

A

Focal seizures

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26
Q

Pts remain conscious but experience unusual feelings or sensations that can take many forms. They may experience sudden and unexplainable feelings of joy, anger, sadness, or nausea. They also may hear, smell, taste, see, or feel things that are not real.

A

Simple focal seizure

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27
Q

Pts have loss of consciousness or an alteration in their consciousness, producing a dream-like experience. They display strange behavior such as lip smacking and automatisms (repetitive movements that may not be appropriate). Pts may continue an activity started before the seizure, but after the seizure they do not remember the activity performed during the seizure. Other automatisms are less organized, such as picking at clothing, fumbling with objects (real or imaginary), or simply walking away. These seizures usually last just a few seconds.

A

Complex focal seizure

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28
Q

May be confined to one side of the brain and remain focal (partial) in nature, or they may spread to involve the entire brain, culminating in a generalized tonic-clonic seizure. Any tonic-clonic seizure that is preceded by an aura or warning sign is a ____ seizure that generalizes secondarily. Many tonic-clonic seizures appear to be generalized from the outset but may actually be 2* generalized seizures, but the preceding partial component may be so brief that is is undetected by the pt. Unlike the 1* generalized tonic-clonic seizure, the 2* generalized seizure may result in a transient residual neurologic deficit postictally. This is called Todd’s paralysis (focal weakness), which resolves after varying lengths of time.

A

Focal seizures.

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29
Q

Also called pseudo seizures. Psychiatric in origin. Closely resemble epileptic seizures (often misdiagnosed as epilepsy). Proper dx requires video-EEG monitoring to capture a typical episode. Pts frequently have a hx of emotional abuse, physical neglect, or a specific traumatic episode

A

Psychogenic seizure

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30
Q

A state of continuous seizure activity in which seizures recur in rapid succession without return to consciousness between seizures. The most serious cx of epilepsy and is a neurologic emergency. Can occur with any type of seizure. During repeated seizures, the brain uses more energy than can be supplied. Neurons become exhausted and cease to function. Permanent brain damage may result. Tonic-clonic ____ ____ is the most dangerous because it can cause ventilatory insufficiency, hypoxemia, cardiac dysrhythmias, hyperthermia, and systemic acidosis, all of which can be fatal.

A

Status epilepticus

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31
Q

Cx of seizures

A

Severe injury and even death from trauma suffered during a seizure. Pts who lose consciousness during a seizure are at greatest risk. Persons with epilepsy have a mortality rate 2-3x the rate of the general population.
Most common cx of seizure disorder is the effect it has on a pt’s lifestyle. The pt may develop ineffective coping methods b/c of the psychosocial problems r/t having a seizure disorder. Pt with epilepsy may experience discrimination in employment and educational opportunity. Transportation may be difficult because of legal sanctions against driving.

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32
Q

Diagnosis of seizure disorders

A

Has many socioeconomic, physical, and psychologic consequences for the pt. Most useful diagnostic tools are an accurate and comprehensive description of the seizures and the pt’s health hx. EEG is helpful but only if it shows abnormalities. Abnormal findings help determine the type of seizure and help pinpoint the seizure focus. Not a definitive test b/c some pts who do not have seizure disorders have abnormal patterns on their EEGs, whereas many pts with seizure disorders have normal EEGs bw seizures. CBC, serum chemistries, studies of liver and kidney function, and a urinalysis should be done to rule out metabolic disorders. A CT scan or MRI should be done in any new-onset seizure to rule out a structural lesion. Cerebral angiography, SPECT, MRS, MRA, and PET may be used in select clinical situations.

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33
Q

Collaborative care

A

Most seizures do not rewire professional emergency medical care b/c they are self-limiting and rarely cause bodily injury. However, if status epilepticus occurs, if significant bodily harm occurs, or if the event is a first-time seizure, medical care should be sought immediately.

34
Q

Drug therapy for seizure disorders

A

1* tx is anti seizure drugs. The goal of therapy is to prevent seizures with a minimum of toxic s/e’s from drug therapy. Act by stabilizing nerve cell membranes and preventing spread of the epileptic discharge. The principle of drug therapy is to begin with a single drug based on the pt’s age and weight; type, frequency, and cause of seizure; and then increase the dosage until seizures are controlled or toxic s/e’s occur. If seizure control is not achieved with a single drug, the drug dosage or timing of administration may be changed or a second drug may be added. About 1/3 of pts require a combination regimen for adequate control. The therapeutic range for each drug indicated the serum level above which most pts experience toxic s/e’s and below which most continue to have seizures. Drugs for seizure disorder must be taken regularly and continuously, often for a lifetime. Teach pts the importance of following the specific drug regimen and what to do if a dose is missed

35
Q

Primary drugs for tx of generalized tonic-clonic and focal seizures

A
Phenytoin (Dilantin) 
Carbamazepine (Tegretol) 
Phenobarbital (Luminal) 
Divalproex (Depakote) 
Primidone (Mysoline)
36
Q

Primary drugs used to treat absence and myoclonic seizures

A

Ethosuzimide (Zarontin)
Divalproex (Depakote)
Clonazapam (Klonopin)

37
Q

Broad spectrum drugs that can be effective for multiple seizure types

A
Gabapentin (Neurontin) 
Lamotrigine (Lamictal) 
Topiramate (Topamax) 
Tiagabine (Gabitril) 
Levetiracetam (Keppra) 
Zonisamide (Zonegran)
38
Q

Used as “add-on” for control of focal seizures that are not successfully managed with a single medication

A

Pregabalin (Lyrica)

39
Q

Tx of status epilepticus

A

Initiation of a rapid-acting IV anti seizure drug. The drugs most commonly used are lorazepam (Ativan) and diazepam (Valium). B/c these are short-acting drugs, their administration is followed with long-acting drugs such as phenytoin or phenobarbital.

40
Q

Long-acting anti seizure meds

A

ie Phenytoin, phenobarbital, ethosuximide, lamotrigine, topiramate. Have long half-life so can be given in once- or twice-daily doses. This increases the pt’s adherence to the drug regimen by simplifying it and avoiding the need to take the drug at work or school.

41
Q

Anti seizure drug education

A

Anti seizure drugs should not be discontinued abruptly as this can precipitate seizures. Common s/e’s include diplopia, drowsiness, ataxia, and mental slowing.

42
Q

Neurologic assessment for seizure care

A

Involves testing for toxicity (nystagmus, hand and gait coordination, cognitive functioning, general alertness). Noncompliance is a concern.

43
Q

Gerontologic considerations for seizures

A

The incidence of new-onset seizure disorders is high among older adults. Carefully consider the action of anti seizure drugs and normal changes that occur with aging. Phenytoin may be problematic for older adults with compromised liver function. Phenobarbital, Tegretol, Mysoline negatively affect cognitive function. Drug interactions with carbamazepine, phenytoin, phenobarbital.
Newer anti seizure drugs may be safer for older adults (fewer effects on cognitive function and less drug interactions. Gabapentin, Lamotrigine, Oxcarbazepine, Levetiractam).

44
Q

Surgical intervention for epilepsy

A

Remove the epileptic focus or prevent spread of epileptic activity in brain. Benefits: cessation of seizures; reduction in frequency of seizures.
Anterior temporal lobe resection is the most common surgical intervention (about 70% of pts are essentially seizure free after this procedure). Not all types of epilepsy benefit from surgery.

45
Q

Nursing dx for seizures and planning

A

Ineffective breathing pattern. Ineffective self-health management. Risk for injury.
Overall goals are that pt will: be free from injury during seizure; have optimal mental and physical functioning while taking anti seizure meds; have satisfactory psychosocial functioning

46
Q

Nursing implementation: health promotion for seizures

A

Promote safety measures: wear helmet if risk for head injury; general health habits (diet, exercise); assist to identify events or situations precipitating seizures and avoid if possible; instruct pt to avoid excessive alcohol, fatigue, and loss of sleep.

47
Q

Nursing implementation: acute intervention for seizures. Ambulatory and home care

A

Acute: Observe, treat, and document seizure. Maintain patent airway, support head, turn to side, loosen constrictive clothing, ease to floor. Do not restrain pt or place any objects in mouth. May require positioning, suctioning, or oxygen after seizure.
Home: Prevention of recurring seizures is the major goal in tx. Instruct on importance of adherence to meds, not to adjust dose w/o physician. Keep regular appointments. Teach family members emergency management. Emotional support and identification of coping mechanisms to adjust to personal limitations imposed by the disease (medical alert bracelets; referrals to agencies and organizations).

48
Q

Chronic, progressive, degenerative disorder of the CNS characterized by disseminated demyelination of nerve fibers of the brain and spinal cord. Onset is usually b/w 20 and 50 years of age, although can occur earlier and later. Women are affected 2-3x more often than men. 5x more prevalent in temperate climates (b/w 45-65* latitude).
Cause is unknown. R/t infectious (viral), immunologic, and genetic factors. Demyelination of nerve fibers of the brain and spine in random patchy areas. Myelin damaged but nerve impulses are still transmitted (will show weakness). The myelin can regenerate and the pt goes into remission. Progresses to damage and plaque formation and no nerve transmission. Course can be very variable with clear relapses and remissions or with constant progression.
Onset of the disease is often insidious and gradual, with vague sx occurring intermittently over months to years.

A

Multiple sclerosis (MS)

49
Q

S/S: vary with each pt according to the areas of the CNS involved. Motor (weakness or paralysis of the limbs, the trunk, or the head; diplopia; scanning speech; and spasticity of the muscles that are chronically affected), sensory (numbness and tingling and other paresthesias, patch blindness [scotomas], blurred vision, vertigo, tinnitus, decreased hearing, and chronic neuropathic pain), cerebellar (nystagmus, ataxia, dysarthria, dysphagia), and emotional problems (anger, depression, or euphoria). Vague sx occur intermittently over months and years. Disease may not be dx until long after onset of the first sx.

A

MS

50
Q

Looks a lot like lyme disease, but it will not respond to ABX. Average life expectancy after the onset of sx is more than 25 years. Death usually occurs as the result of infectious cx (i.e. pneumonia) or immobility or because of an unrelated disease.

A

MS

51
Q

Dx of MS

A

No definitive diagnostic test for MS. Factors considered: hx, clinical manifestations, and results of certain tests. MRI of the brain and spinal cord may show plaques, inflammation, atrophy, and tissue breakdown and destruction.
For a dx: evidence of at least 2 inflammatory demyelinating lesions in at least 2 different locations within the CNS. Damage or an attack occurring at different times (usually >1mo apart), all other possible diagnoses must have been ruled out.

52
Q

Tx of MS

A

Currently there is no cure for MS. Collaborative care is aimed at treating the disease process and providing symptomatic relief. Therapy is tailored specifically to the disease pattern and manifestations that the pt is experiencing.

53
Q

Used in the initial tx of MS. Modify the disease progression and prevent relapses.

A

Immunosuppressants. Immunomodulators (take at bedtime; interferon: flu-like sx; sun sensitivity).

54
Q

Helpful to treat acute exacerbations of MS. Work by reducing edema and acute inflammation at the site of demyelination. Do not affect the ultimate outcome or the degree of residual neurologic impairment from the exacerbation.

A

Corticosteroids (ie methylprednisolone, prednisone)

55
Q

Other drug therapy for MS

A

Muscle relaxants for spasticity. CNS stimulants to treat fatigue (pemoline [Cylert], methylphenidate [Ritalin], and modafinil [Provigil]). Anticholinergics for bladder sx. Tricyclic antidepressants and anti seizure drugs for chronic pain.

56
Q

Other interventions for the tx of spasticity in MS

A

Surgery. Doral column electrical stimulation. Intrathecal baclofen pump. Physical therapy (also improves coordination, trains pt to substitute unaffected muscles for impaired muscles). Water therapy.

57
Q

Nursing dx and planning for MS

A

Impaired physcial mobility. Impaired urinary elimination. Ineffective self-health management.
Maximize neuromuscular function. Maintain independence in activities of daily living for as long as possible. Manage disabling fatigue. Optimize psychosocial well-being. Adjust to the illness. Decrease factors that precipitate exacerbations.

58
Q

Nursing implementation for MS

A

Help to identify triggers and develop ways to avoid them or minimize their effects. Reassure pt during diagnostic phase. Assist pt in dealing with anxiety and grief c/b diagnosis. During acute exacerbation, prevent major cx of immobility. Focus teaching on building general resistance to illness (avoiding fatigue, extremes of hot and cold, exposure to infection). Teach pt (good balance of exercise and rest. Minimize caffeine intake. Nutritious, well-balanced meals [increase roughage if constipated]. Treatment regimen [Management of meds]. Self-catheterization if necessary. Adequate intake of fiber to aid in regular bowel habits. Emotional adjustments. Lifestyle changes).

59
Q

Expected outcomes with MS

A

Maintain or improve muscle strength and mobility. Use assistive devices appropriately for ambulation and mobility. Maintain urinary continence. Make decisions about lifestyle modifications to manage MS

60
Q

Chronic, progressive neurodegenerative disorder characterized by slowness in the initiation and execution of movement (bradykinesia), increased muscle tone (rigidity), tremor at rest, and gait disturbance. Dx increases with age. More common in men.
Exact cause unknown. Familial component. Suspected causes: encephalitis, chemical intoxication, drug-induced, illicit drug use, hydrocephalus, MS, hypoxia, infection, stroke, tumor, trauma, Huntington’s.
Lack of dopamine in the brain (pathologic process involves degeneration of dopamine-producing neurons in substantia nigra of the midbrain. Disrupts dopamine-acetylcholine balance in basal ganglia)

A

Parkinson’s disease (PD)

61
Q

Onset is gradual and insidious with ongoing progression. Triad: tremor, rigidity, and bradykinesia. Beginning stages may involve only a mild tremor, slight limp, or a decreased arm swing. Later stages may have shuffling, propulsive gait with arms flexed, and loss of postural reflexes. Some have slight speech changes.
Tremor: so minimal initially that only pt may notice it. More prominent at rest and is aggravated by emotional stress or increased concentration. Described as pill rolling b/c thumb and forefinger appear to move in rotary fashion.
Rigidity: increased resistance to passive motion when limbs are moved through ROM. Typified by a jerky quality when the joint is moved. Similar to intermittent catches in the movement of a cogwheel. C/b sustained muscle contraction and consequently elicits- complaint of soreness, feeling tired and achy; pain in the hear, upper body, spine, or legs.
Bradykinesia: Slowing down in initiation and execution of movement. Evident in loss of autonomic movements (blinking, swinging of arms while walking, swallowing of saliva, self-expression with facial movements).

A

PD

62
Q

Nonmotor sx of PD

A

Depression, anxiety, fatigue, pain, constipation, sleep problems, short-term memory loss

63
Q

Cx of PD

A

Increase as disease progresses. Motor sx (e.g. dyskinesias [spontaneous, involuntary movements], weakness, akinesia [total immobility]), neurologic problems (e.g. dementia), and neuropsychiatric problems (e.g. depression, hallucinations, psychosis). Dementia occurs in 70% of pts as disease progresses.
Dysphagia may result in malnutrition and aspiration. General debilitation may lead to pneumonia, UTIs, and skin breakdown. Orthostatic hypotension may occur (can result in falls and injury)

64
Q

Dx tests for PD

A

No specific tests. Dx based on hx and clinical sx. Firm dx can be made when at least two or three characteristics of the classic triad (tremor, rigidity, and bradykinesia) are present.

65
Q

Drug therapy for PD

A

No cure. Aimed at relieving sx. Aimed at correcting imbalances of NTs within the CNS. Antiparkinsonian drugs either enhance or release supply of DA or antagonize or block the effects of overactive cholinergic neurons in the striatum.

66
Q

Often first drug used in tx of PD. Precursor of DA and crosses blood-brain married. Converted to DA in the basal ganglia. ___ inhibits an enzyme that breaks down ____ before it reaches the brain. Effectiveness could wear off after a few years of therapy. Therefore, some initiate therapy with a DA receptor agonist instead. ___ is added when moderate to severe sx develop.

A

Carbidopa; levadopa. Sinemet.

67
Q

Trihexyphenidyl (artane) and benztropine (Cogentin). Decrease the activity of ACh, thus providing balance between cholinergic and dopaminergic actions. Diphenhydramine (Benadryl) with _____ properties may be used to manage tremors.

A

Anticholinergic drugs.

68
Q

Antiviral agent. Promote the effect of DA>

A

amantadine

69
Q

Drug therapy for PD

A

Use of only one drug is preferred (fewer s/e’s, dosages are easier to adjust). Combination therapy is often required as disease progresses. Excessive dopaminergic drugs can lead to paradoxic intoxication. Within 3-5 years of tx, pts experience episodes of hypo mobility (treated with apomorphine [Apokyn]. needs to be taken with antiemetic drug).

70
Q

Surgical therapy for PD

A

Procedures aimed at relieving sx: ablation (destruction), deep brain stimulation (DBS), transplantation of fetal neural tissue (still in experimental stages).

71
Q

Nutritional therapy for PD

A

Malnutrition and constipation can be serious consequences. Pts with dysphagia and bradykinesia need food that is easily chewed and swallowed. Adequate roughage. Food should deb cut into bite-sized pieces. Several small meals should be taken to prevent fatigue. Provide ample time to avoid frustration. Levodopa can be impaired by protein and vitamin B6 ingestion.

72
Q

Nursing Dx and care for PD

A

Impaired physical mobility. Imbalanced nutrition: less than body requirements. Impaired swallowing. Impaired verbal communication.
Maintain independence in ADLs for as long as possible (independent but safe). Optimize psychosocial well-being (emphasize abilities, not disabilities). Simplify clothing. Fall prevention (remove rugs and excess furniture). Well-balanced diet. Elevated toilet seat. Exercise with assistance of PT (improve gait, strengthen muscles involved in speaking and swallowing). Caregiver strain

73
Q

Improving gait in PD

A

Have them consciously think about stepping over an imaginary line. Drop rice kernels and step over them. Lift the toes when stepping. Rock from back to front. Take one step backward and two steps forward. Slow-stretch-hold movements. Wide base of support.

74
Q

Autoimmune disease of the neuromuscular junction characterized by the fluctuating weakness of certain skeletal muscle groups. Occurs in either gender and in persons of any ethnicity. C/b an autoimmune process in which antibodies attack ACh receptors, resulting in a decreased number of ACh receptor sites at the NMJ. This prevents ACh molecules from attaching and stimulating muscle contraction.
1* feature of MG is fluctuating weakness of skeletal muscle. The muscles most often involved are those used for moving the eyes and eyelids, chewing, swallowing, speaking, and breathing. These muscles are generally the strongest in the most and become exhausted with continued activity. A period of rest usually restores strength. By the end of the day, muscle weakness is prominent.
S/S: Progressive muscle weakness w/o atrophy. No change in sensation or relfexes. Fatigue. Speech difficulties. Ocular palsies (1st sign). Ptosis. Diplopia. Respiratory distress. Cough, gag reflexes.

A

Myasthenia gravis (MG)

75
Q

Cx of MG

A

Myasthenia crisis: acute exacerbation of muscle weakness triggered by infection, surgery, emotional distress, drug overdose, or inadequate drugs. Major cs result from muscle weakness in areas that affect swallowing and breathing. This results in aspiration, resp. insufficiency, and respiratory tract infection.

76
Q

Dx of MG

A

EMG and Tension test: used to dx MG or to distinguish b/w myasthenic or cholinergic crisis. Administer a small dose of IV Tension. Fatigue the muscles. Give the rest of the IV Tension. Fatigue the muscles again. If they develop twitching, they don’t have MG. If their strength improves, they have MG or myasthenia crisis. If they get increased weakness, they have cholinergic crisis.

77
Q

Tx of MG

A

Anti cholinesterase drugs (Mestinon or pyridostigmine [Neostigmine] to enhance function of the NMJ. Alternate-date corticosteroids (prednisone) to suppress immune response (also immunosuppressants [Cyclosporin, Imuran]). Avoid many classes of drugs (anesthetics, antidysrhythmics, ABX, quinine, antipsychotics, barbiturates and sedative-hypnotics, cathartics, diuretics, opioids, muscle relaxants, thyroid preparations, tranquilizers). Thymectomy. Plasmapheresis weekly and Immunoglobulin G (can yield a short-term improvement in sx and are indicated for pts in myasthenia crisis or in preparation for surgery when corticosteroids must be avoided).

78
Q

Nursing care for MG

A

Distinguish between myasthenic crisis and cholinergic crisis. Watch for s/s of respiratory insufficiency. Semisolid foods. Schedule drugs so peak action is at mealtimes. Perform physically demanding activity early in the AM.

79
Q

Rare progressive neurologic disorder characterized by loss of motor neurons. Usually leads to death (by resp. failure) 2-6 years after dx, but a few pts may survive for more than 10 years. Lou Gehrig’s disease. S/S: weakness of upper extremities, dysarthria, dysphagia
Tx: none
Remains cognitively intact while wasting away

A

Amyotropic lateral sclerosis (ALS)

80
Q

Genetic disease with deficiency of ACh and GABA. S/S: chorea, worsening gait, risk for aspiration/malnutrition, cognitive deterioration, loss of speech. Need 4000-5000 calories/day. Death with 10-20 years, no cure. Xenaxine for chorea, halloo, valium, dopamine-depleting agents.

A

Huntington’s disease (HD).