chronic neuro problems

Question 1

Headaches

Answer 1

occur when pain-sensitive areas of the brain have been stimulated. Most common type of human pain. Only some parts of the brain are pain sensitive. (See Lewis, p 1527) Most people have functional HA. The rest have organic HA caused by intracranial or extracranial disease. One person can have more than one of the functional types described by the International HA Society (IHS).

Question 2

Tension-what are the 3 classifications? (you know this)

Answer 2

Most common type & most difficult to treat. Bilateral, dull, non-pulsitile. Called muscle-contraction, psychogenic, rheumatic. Have been classified as acute, episodic or chronic. No evidence that all these are the results of painful contractions of the neck and scalp muscles. May involve the same neurovascular factors as migraines.

Question 3

tension type -Etiology

Answer 3

May be related to pain sensitivity and muscle factors.

Question 4

tension type - Clinical Manifestations- what location?

Answer 4

no prodrome. IHS defines as 2 or more of the following: pressure or tightness, mild to moderate severity, bilateral, most often in the back of the neck, worsening with physical activity. May have photosensitivity or phonosensitivity. No N&V. Does not interfere with sleep. Pain is called tight, squeezing, band-like pressure, sustained, dull and persistent. May occur intermittently for weeks, months or years. Many have a combination of these and migraines, even simultaneously.

Question 5

tension type - Diagnosis

Answer 5

a good history. EMG may show sustained contraction of neck, scalp, facial muscles in those with migraines, but some don’t show this. If present during exam, there is increased resistance to passive movement of head and tenderness of the head and neck.

Question 6

tension type - treatment

Answer 6

Relaxation techniques, PT, massage and hot packs can help. Correction of faulty posture or injection of a local anesthetic. Drugs are given for symptoms and prophylaxis: NSAIDS, Analgesic combinations, Triclyclics, B-Adrenergic blockers.
(see Table 59-3)

Question 7

Migraines

Answer 7

( from the Greek: hemikronia meaning half-brain since most are on one side )
Episodic, familial (65 %); s/s unilateral (60 %) or bilateral, frontotemporal, throbbing often worse behind one ear or eye. Accompanied by sensitive scalp, anorexia, photophobia, nausea and sometimes vomiting. One client tends to have the same clinical manifestations q time, making them stop activities for days at a time. Goal is to try to relieve or stop in the early stage. May be preceded by prodrome (symptom indicative of an approaching condition or disease) or aura (sensation of light or warmth consisting of ocular sensory phenomena), spreading depression, diminished CBF starting in the occipital lobe and spreading forward. Often have no known precipitating events.

Question 8

migraines - Etiology- what neurotransmitter causes vasodilation?

Answer 8

Unknown; may have neurogenic, vascular & chemical involvement.
Neurogenic: stimulation of the trigeminovascular system with inflammation and vasodilation. (The neurotransmitter serotonin causes cerebrovascular vasodilation & stimulates pain fiber activation causing HA.)

Question 9

Migraines begin in early childhood or near puberty. - which ones increase during pregnancy?

Answer 9

Females 3:1 over males. Diminish in severity until middle age. “Classic” tend to increase in freq. during pregnancy.

Question 10

“Classic” or migraines with an aura - time?

Answer 10

(only 10%)– Have at least 3 of the following:
Reversible aura ( involves brain dysfunction )
Aura symptoms develop gradually over more than 4 minutes or 2 or more symptoms occur in succession.
No aura lasts more than 60 minutes.
HA follows aura within 60 minutes.

Question 11

1st Prodromal Phase

Answer 11

Aura lasts 10 minutes up to an hour, pain may be preceded by visual disturbances, flashing lights, lines or spots, shimmering or zig- zag lights. May also have paresthesias: numbness, tingling or burning,
confusion, aphasia, vertigo or dizziness, weakness, paralysis, drowsiness,
confusion, even loss of consciousness. Classic aura: scintillating scoto- mata or flashing lights in one quadrant of the visual field.

Question 12

Pain phase- 2nd Phase = migraines- when does it peak?

Answer 12

HA c N/V, Pain starts often at the temple, increases in intensity & becomes throbbing. Usually peaks within an hour; can last several hours.

Question 13

postdrome (migraine hangover) - 3rd Phase - migraines

Answer 13

Pain changes from throbbing to dull. HA, N/V last from 4 hrs to 3
days; (older clients may have a visual migraine: aura s pain)

Question 14

Migraines without an aura (common) - what time do they usually occur?

Answer 14

begins without aura before onset of HA. Early warning may be mood change (depression, lethargy, hyperactivity, craving for foods). Have at least 2 of the following:
Pain unilateral, pulsating, moderate to severe intensity, worsening with activity, N&V, photophobia, phonophobia. Lasts 4-72 hours.
Often in early morning hours, during periods of stress, premenstrual
tension or fluid retention.

Question 15

Clinical manifestations of migraines with and without auras might include

Answer 15

generalized edema, irritability, pallor, N&V. Prodrome can include psychic disturbances, GI upset, changes in fluid balance.

Question 16

Complicated migraines - and how long do they occur?

Answer 16

less common; include menstrual and cluster
menstrual – develop in early 20s and until menopause, during menstrual
cycle as estrogen levels decrease or at ovulation.
Cluster – occur in a series lasting 4-8 weeks with years or months of
remission in between clusters. (Cluster Migraine not Cluster HA)

Question 17

migraine triggers

Answer 17

are monosodium glutamate, aged cheese, caffeine, chocolate, nitrites, nitrates, ETOH, esp. red wine. Odors: cigarette or cigar smoke, paint, gasoline fumes, perfumes, aftershave lotion.
Lifestyle changes may help: regular meals, sleep patterns, exercise, reduce stress.

Question 18

migraines - Coping strategies

Answer 18

Tend to “hibernate” (common to most HAs) or seek shelter from noise, light, odors, people and problems. They will lie down in a darkened room, cover eyes and sleep until awakening. HA clinics: Biofeedback, exercise, relaxation techniques.
Herbs – feverfew, Bay, Willow, Ginger, Red Pepper (capsicum), lemon balm, purslane are some herbs that research confirms may help.
Can refer to a Migraine Mentor’s Program created by the National HA Foundation

Question 19

Cluster HA - during which decade do they occur?

Answer 19

8:1 men ages 20-50* compared to women. Usually in the 3rd or 4th decade of life.

Question 20

cluster HA - Diagnosis

Answer 20

History. CT or MRI only to R/O aneurysm, tumor or infection.c

Question 21

cluster HA - treatment

Answer 21

Drugs used are the some of the same as migraines, but not as effective as with other types of HA. See Table 59-3. Instruct the client to wear sunglasses and sit facing away from the window, 100% O2 may be ordered via mask at 7-9 LPM for 15-20 mins to reduce cerebral blood flow (vasoconstriction). May be repeated after a 5 minute rest.

Question 22

cluster HA - Precipitating factors

Answer 22

Angry outbursts, prolonged anticipation, excess physical activity, excitement. A consistent sleep/wake cycle may help.

Question 23

Epilepsy - which groups have the most seizures? you know this

Answer 23

may be inherited; recurrent, unprovoked seizure activity. Thought to be a result of brain or CNS irritation. A seizure is an abnormal, sudden, excessive discharge of electrical activity in the brain. Highest incidence in older adults and kids. Still prejudice towards those who have seizures.e

Question 24

epilepsy - types (just 2 - the same as always)

Answer 24

Epilepsy can be primary or idiopathic ( no identifiable brain lesion; ¾ of all seizure disorders are idiopathic ) and secondary which is the result of a brain lesion ( tumor, or trauma ). The word ictal means attack or stroke, as in a seizure.

Question 25

Seizures that are a result of a metabolic disorder are

Answer 25

not considered epilepsy because seizures will stop when the underlying problem is treated. Some metabolic causes are: ETOH & barbiturate withdrawal, electrolyte imbalances such as hyperkalemia, acidosis, hypoglycemia, dehydration and water intoxication. Extracranial disorders that can cause seizures are DM, HTN, septicemia, systemic lupis erythematosus (SLE), heart, lung, kidney or liver diseases.

Question 26

Kindling

(add kindling to the fire)

Answer 26

Kindling – Repetitive seizures can cause permanent changes to the neuron excitability. In humans, seizures can lead to more seizures and the longer a patient has poor control, the more likely his seizures will be uncontrollable. Treatment is aimed at controlling recurrent seizures.

Question 27

epilepsy - Triggers

Answer 27

Triggers may be increased physical activity, emotional stress, excessive fatigue, ETOH or caffeine and various foods and chemicals.

Question 28

epilepsy - Generalized

Answer 28

bilateral, loss of consciousness; involves the whole brain.

Question 29

Absence seizures

Answer 29

Absence – once called petit mal, rarely beyond teen years (either ceases or changes to another type of seizure); a brief loss of consciousness and blank staring. Returns to baseline immediately. You will not be tested typical and atypical absence.

Question 30

Myoclonic seizures

Answer 30

Myoclonic – brief jerking or stiffening of extremities, symmetric or not, lasts a few seconds, occurs singly or in groups. Could fall to the ground.

Question 31

Atonic seizures

Answer 31

Atonic (akinetic, astatic) – once called drop attack, sudden muscle loss of tone, lasting seconds followed by postictal confusion. Most times, client will fall, but consciousness returns by the time he hits the ground. Risk of head injury. Sometimes wear helmets.

Question 32

Partial seizures

Answer 32

Partial – also called focal seizures, further sub-divided into simple and complex. Involves a specific part of the brain (can progress to whole brain). May have a transient focal neurologic deficit: Todd’s paralysis. Resolves after a varying length of time.

Question 33

Complex seizures

Answer 33

Complex – some affecting of consciousness: clouding or confused state. Your book says rarely complete loss of consciousness but some black out or lose conscious-ness for 1-3 minutes. Involves behavioral, emotional, affective and cognitive functions: Automatisms or characteristic behavior of which the client is not aware, such as lip-smacking, patting, picking at clothes. May have postictal amnesia. Alterations in sexual functioning (usually hyposexuality, sometimes hypersexuality). Usually involves the temporal lobe.

Question 34

Simple seizures

Answer 34

Simple – remains conscious, fully aware, often a preictal aura (a déjà vu phenomenon, sensation of a bad smell or pain) Unilateral movement of an extremity, autonomic (changed HR, skin flush or upset stomach) or psychic symptoms. Rarely lasts > 1 min. Have also been termed Jacksonian, focal motor, focal sensory.

Question 35

Unclassified seizures

Answer 35

Unclassified – no known reason, about 50 % of seizure activity

Question 36

seizure management

Answer 36

Assess what happens preictal and if there is an aura. Ask pt, family and friends.
Watch what happens during the seizure (progression), time and record. Keep safe.

Question 37

seizure interventions

Answer 37

Secondary and non-epileptic seizures are treated by removing or treating the underlying cause.
Most seizures can be managed with AEDs (antiepilectic drugs) or anticonvulsants. Tried one at a time and if ineffective, may add one or increase the dose. Sometimes a combo is needed.

Question 38

seizure precautions

Answer 38

Have O2 and suctioning nearby; Pt should have a saline lock for IV drugs to stop seizure; padded side rails; bed in lowest position; NEVER use padded tongue blades, can obstruct airway and chip teeth. The chip can be aspirated.

Question 39

During the seizure,

Answer 39

During the seizure, observe, document and time. Safety: remove any items that might injure. If possible, turn head to one side to prevent aspiration. Clients often become cyanotic during a generalized tonic-clonic seizure. This is self-limiting and needs no Tx. Sometimes doctor will order O2 postictal especially for older more debilitated clients. May use a vest if they are in a chair

Question 40

Status epilepticus

Answer 40

Status epilepticus - Lasts longer than 30 minutes or a series of separate seizures in rapid succession., lasting more than 10 minutes or repeated over 30 minutes. Neurons become exhausted and stop functioning. This can cause respiratory problems, cardiac arrhythmias, hyperthermia, acidosis. THIS IS AN EMERGENCY: notify dr., intubation may be necessary, O2 given, IV NS; Meds include Valium (discussion), Ativan, Valproate to stop motor movement; follow with longer acting Dilantin (phenytoin) or phenobarbital. Last resort general anesthesia.

Question 41

Vagal nerve stimulation - seizures

Answer 41

Vagal nerve stimulation – a stimulating device or electrode is surgically implanted around the left vagus nerve in the neck. Client can activate it with a handheld magnet to abort the seizure. Does reduce the intensity and duration of seizures. May have a change in voice due to vagal stimulation. Used in a small number of patients with aura.

Question 42

seizures - surgery

Answer 42

Surgery if nothing else works. Crainiotomy after first identifying the important sites of language and memory (Wada test) and Intelligence, and other functions.
(neuropsychological testing) Goal is to excise the seizure area of the brain without losing vital functions. Electrodes are used to identify areas.
Options are; removal of 1 lobe (anterior temporal is safest), removal of cortex, or separation of the 2 hemispheres (corpus callostomy). Not all types of epilepsy benefit from surgery.

Question 43

Multiple Sclerosis

Answer 43

a chronic inflammatory disease of the CNS; autoimmune destruction of myelin in the CNS. Axonal injury occurs early in MS. Result is a periodic or chronic loss of neurological function and often progressive disability. Seems to have both environmental and genetic factors. African Americans and Asians have lower incidence, but among those with the disease, the most favorable prognostic indicators are early age of onset, female, optic neuritis or sensory symptoms as presenting episode, acute onset of symptoms, long inter-exacerbation period, little residual disability after each exacerbation. Unfavorable prognostic indicators in MS are later age of onset, progressive course from onset, male gender (especially African Americans), frequent exacerbations, involvement of cerebellar and/or motor functions.

Question 44

MS is the most common neuro disorder in young adults

Answer 44

MS is the most common neuro disorder in young adults, mostly women in their 20s and 30s. Onset is between 15-50. MS is 5X more common in temperate climates, especially northern USA, Canada, Europe, primarily in Caucasians. Age 15 a critical age: if a child moves to a climate before 15, he/she will take on the risk of that new area. Average life expectancy is 25 years from onset of symptoms. Death usually due to infection (pneumonia) or occasionally suicide.

Question 45

MS - Etiology

Answer 45

unknown. May be infectious (viral) immunologic as well as genetic and environmental. Susceptibility seems to be inherited. Relatives at slightly increased risk.
There is chronic inflammation, demyelinization with gliosis or scarring in the CNS. In a genetically susceptible individual, an environmental trigger, such as an infection, may activate T cells, disrupt the blood-brain barrier. Macrophages also cause damage. All this results in a characteristic plaque formation or sclerosis scattered throughout the CNS. Early in the disease, the myelin sheath is damaged, but the nerve fiber is unaffected and impulses still are transmitted. There may be weakness, but the myelin will regenerate (remission). As the disease continues, myelin is replaced with glial scar tissue (hard plaques). When myelin is gone, impulses slow down or are blocked.

Question 46

MS - Manifestations

Answer 46

insidious, gradual onset. Vague symptoms over months or years. Usually not diagnosed for a long time. Varies from person to person so hard to diagnose. Some have chronic progressive deterioration; some have remissions and exacerbations.
These are classified as: (You will not be tested on the following classifications.)
Relapsing-remitting – with clearly defined relapses with full recovery or sequelae and little residual deficit.
Primary-progressive - progression from onset with occasional plateaus and temporary minor improvements.
Secondary-progressive - relapsing-remitting initially, followed by progression with or without occasional lapses, minor remissions and plateaus.
Progressive-relapsing – progressive disease from onset, clear acute relapses with or without full recovery; continual progressive periods between.

Question 47

MS - s/sx

Answer 47

motor, sensory, cerebellar, emotional problems. Weakness and paralysis of limbs, trunk, head, diplopia, scanning speech, spasticity of muscles. Parathesias, blurred vision, patchy blindness, vertigo, tinnitus, decreased hearing. Nystagmus, ataxia, dysarthria, dysphagia. Bowel: usually constipation. Bladder: can be spastic or uninhibited bladder with small capacity for urine with urgency, frequency, dribbling or incontinence. Or can be flaccid or hypotonic bladder with no sensation or urge to void. Urinary retention. Large capacity for urine. More comfortable in a cool room.*
Sexual – Men have physiologic erectile dysfunction. Women have decreased libido, difficulty with orgasms, painful intercourse, decreased vaginal lubrication. Diminished sensation in both sexes. Loss of self-esteem contributes. No one client has all these.
Intellectual function intact (early), but emotional labile: anger, depression, euphoria.
Later: Cognitive dysfunction in 43%-65% of MS patients. Need for help with ADLs, unemployment in absence of physical disability, withdrawal from social activities.

Question 48

ms - diagonosis

Answer 48

no definitive test; primarily a clinical diagnosis, based mostly on Hx., clinical manifestations. CSF may show increased IgG (oligoclonal immunioglobulin G) and a high # of leukocytes and monocytes. MRI may show sclerotic plaques as small as 3-4 mm. Characteristic white matter lesions scattered through the brain and spinal cord.
Hallmark: multiple lesions at different locations in CNS at different times. Serial MRIs can show brain atrophy, increased size of ventricles, widening distance between sulci or convolutions. Very important to get an accurate diagnosis early for treatment

Question 49

review MS treatment and nursing care

Question 50

The many forms of parkinsonism include:

Answer 50

Parkinson’s Disease ( the most common type ), drug-induced parkinsonism, post-encephalitic parkinsonism, arteriosclerotic parkinsonism. It can also be caused by hydrocephalus, hypoxia, infections, stroke, tumor and trauma. Buck Institute: possible iron intake in 1st two years of life ( J. Andersen, researcher at the Buck )
Most commonly occurs after age 50 (likely a genetic defect if before age 50), with average age being 65.

Question 51

parkinson’s patho

Answer 51

damage or loss of dopamine-producing cells in the substantia nigra in the midbrain leads to depletion in the basal ganglia of dopamine that influences the initiation, modulation, and completion of movement and regulates unconscious movements. Pathophysiology of the drug-induced type is due to blocked dopamine receptors in the brain.

Question 52

parkinsons - manifestations

Answer 52

onset is gradual and insidious with progression and prolonged course. At first only a mild tremor, slight limp, or decreased arm swing. Later a shuffling, propulsive gait, with arms flexed and loss of postural reflexes. Sometimes a slight change in speech. None of these is enough to make a diagnosis.

Question 53

parkinsons - Diagnosis

Answer 53

is made when 2 of the 3 characteristic signs of the Classic Triad or characteristic signs (You will be tested on this):
Tremor
Rigidity
Bradykinesia – slow or retarded movement
Dementia occurs in up to 40 % of clients. Ultimate confirmation is a positive response to antiparkinsonian meds.

Question 54

parkinsons - tremor

Answer 54

Tremor may be the first sign, more prominent at rest and aggravated by emotional stress. Can affect handwriting. Described as “pill rolling”. Can involve the diaphragm, tongue, lips and jaw, but rarely shaking of the head.

Question 55

parkinsons - rigidity

Answer 55

Rigidity is increased resistance to passive motion. Cogwheel rigidity: a jerky quality, with intermittent cogwheel catches as a joint is moved. Slowness of movement.

Question 56

parkinsons - Bradykinesia

Answer 56

Bradykinesia is loss of involuntary movements such as blinking of eyelids, swinging of arms, swallowing saliva, self-expression with facial and hand movements and minor movement of postural adjustment. (This person unable to correct these.) Lack of spontaneous activity, stooped posture, “deadpan” expression (masked facies), shuffling gait or festination. Difficulty initiating movement. Has to consciously will movement.

Question 57

review parkinson’s treatment

Question 58

review Myasthenia Gravis

Question 59

Myasthenia Gravis - diagnosis

Answer 59

up to 90 % have elevated AChR, acetycholine receptor antibodies. Check thyroid function. Check thymus. Tensilon testing: within 30-60 secs, most MG pts show marked improvement in muscle tone lasting 4-5 mins. Simplest: have pt. look up for 2-3 mins. If MG, there will be increasing drooping of eyelids until pt. can hardly keep eyes open. After rest, can open again.

Question 60

Myasthenia Gravis- hallmark

Answer 60

Hallmark – muscle weakness increases when fatigued. Strongest at the beginning of day. As day progresses, becomes exhausted.

Question 61

on test - Myasthenic crisis

Answer 61

exacerbation of myasthenic symptoms caused by undermedication with anticholinesterase drugs. Often preceeded by some type of infection. Increased pulse and R, rise in BP, anoxia (skin color: ), Bowel & bladder incontinence, decreased urine output, absence of cough and swallow reflex. Adequate airway and artificial vent. needed; Caused by failure to take meds. Improves after IV anti-cholinesterase drugs, not with usual resuscitation. Need a Medic Alert bracelet or card.

Question 62

Cholinergic crisis: - on test

Answer 62

an acute exacerbation of muscle weakness caused by overmedication with anticlolinesterase drugs. Drugs are withheld while patient on ventilator. N&V, diarrhea, Abd. cramps, blurred vision, pallor (skin color: ), facial muscle twitching, papillary miosis, hypotension. Give Atropine.

Question 63

Nursing care: Cholinergic crisis and Myasthenic crisis

Answer 63

Assess gag reflex, give meds 30-60 minutes before eating. Soft diet, small frequent meals, small bites.

Question 64

cluster headache - peak and duration?

Answer 64

Abrupt onset with no prodromal. Peaks in 5-10 mins; Average duration 30-90 mins.

Question 65

cluster HA - pain type

Answer 65

Pain is unilateral orbital or supraorbital, oculotemporal, or oculofrontal, described as excrutiating, boring and non-throbbing. Felt deep in and around one eye, in upper face, and the forehead on one side of the face.

Question 66

cluster HA - how often do they occur?

Answer 66

Occur several times a day over several days with each cluster lasting about 2-3 months (time cluster) followed by a remission of 9 mos to a year.

Question 67

cluster HA = May have at least 1 of the following:

Answer 67

May have at least 1 of the following: ipsilateral tearing of the eye, ipsilateral rhinorrhea & nasal congestion, ptosis, eyelid edema, ipsilateral forehead sweating, miosis (constriction of pupils), bradycardia, flushing or pallor of the face, conjunctivitis, inc skin temp. and inc. Tend to pace, walk, cry out, sit or rock ( only HA where this is seen ) and resent being touched, ETOH induces during HA period, but not during remission. No genetic, dietary or personality link. No N&V.

Question 68

cluster HA - where is the pain?

Answer 68

Pain radiates to the forehead, temple or cheek and lesser to the ear, occiput and neck. intraocular pressure.

Question 69

epile