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Neurological Disorders

Terms in this set (84)

Patient will be on bedrest until the acute phase is over which is about 24-48 hours (some say up to 72 hours). With thrombolytic CVA, HOB is 0-30 to facilitate perfusion
1. maintain patent airway- may need artificial airway, may need to be intubated and on a ventilator; suctioning done only when necessary (suctioning leads to increased ICP)
2. Maintain adequate oxygen
- oxygen as ordered. remember decreased oxygen will lead to increased ischemia
- adequate hydration to decrease blood viscosity- IV 0.9% NaCl
- ABG's
-I&O
3. Assess for cardiac abnormalities
- of cardiac problem caused embolism, the cardiac problem must be corrected to prevent another clot i.e. dysrhythmia's and patients often get atrial fib after an intracranial hemorrhage
- if patient has high BP, needs to be controlled because high BP or low BP can both cause increased ischemia. Given beta blockers and vasodilators to slowly decrease BP and stabilize. Considered to have high BP if mean arterial pressure is >140 or sBP >200. Too quick of a drop in BP will also lead to ischemia. BP of 150/100 facilitates adequate cerebral perfusion (in acute phase)
- vital signs
4. Neuro Assessment
- level of responsiveness, includes response to pain, movement, resistance to changes of position, response to stimulation
- check if orientation X 3
- a slight decrease in LOC several hours after initial stroke --> probable ischemia (because of swelling)
- presence or absence or voluntary or involuntary movement of extremities, tone of muscles, body posture, position of head, grasp, neck stiffness or flaccidity of neck
- PERRLA, with eye opening
- color of face and extremities, temp and moisture of skin
- check ability to speak
5. positioning
- goal is to avoid extreme hip and neck flexion. Extreme hip flexion leads to possible increase in intrathoracic pressure. Extreme neck flexion prohibits venous drainage from the brain
- no foot board- increased the likelihood of isometric exercises which increases ICP
6. administration of drugs as ordered
7. avoid clustering of nursing interventions
- depends on the area of demyelination in brain
- early symptoms are due to a single or small number of lesions (plaques). Poses a problem in dx as the symptom may disappear with remission of 10 years
1. visual disturbance: common early sign that over 50% experience. Due to damage and inflammation of the optic nerve. Patient may c/o: diplopia (double vision), nystagmus (invol. jerky eye movement) which leads to blurred vision and oscillopsia (objects jump into the field of vision)
2. intentional tremors (when performing voluntary actions- opposite of resting tremors), weakness, paresthesia and pain around the trunk form spasm in spinal cord, and ataxia (uncoordinated movements)
3. sensitivity to heat occurs in 50% of cases. heat triggers symptoms and they may not realize how hot something is because of the numbness (environmental heat, being 90 outside)
4. 75% cases c/o fatigue. not related to muscle problem but due to effects of MS on CNS. comes on without a warning. Patients complain that they feel as though they have hit a brick wall after being normal all day. MS fatigue is called idiopathic lassitude
5. many patients will develop urinary retention from bladder spasticity and bowel spasticity
6. secondary symptoms
- UTI: from urinary retention
- Constipation: from bowel spasticity
- decubiti: from immobility
- contracture deformities: from immobility
- dependent peda; edema (swelling below knees)
- pneumonia (many die from)
- reactive depressions: patients who have MS often have social and psychological problems such as depression and mood swings. vocational problems such as job loss and job changes and redefining personal relationships. these must be addressed as they may contribute to marital difficulties and suicides. Suicide occurs 7.5 times more frequently among those with MS when compared to those of the same age
1. anti-inflammatory meds- corticosterioids such as Prednisone and methylprednisolone. Reduces edema and at the mylein sheath to prevent plaque formation. also decreases the length of each episode; teach side effects: take in morning or at noon to avoid insomnia. take with food, possible hyperglycemia, will be given IV for 1-5 days and then PO in tapered doses, oral prednisone reduces inflame and lesion formation, methylprednisolone IV is useful for eye disorders, teach about the need to taper and not dc abruptly. Possible weight gain, peripheral edema and moon face if taken long term. Also ACTH: acthar/corticotropin stimulates adrenal coretx to synthesize and secrete adrenocortical hormones and cortrosyn/ coyntripin used as anti-inflam agents that may improve nerve conduction (cushing syndrome)
2. anticholenergic ditropan/oxybutynin chloride, pro-banthine (propantheline bromide) used for bladder dysfunction
3. amantadine HCL (symmetrel) for fatigue. Pemoline (cylert) for patients with psychological fatigue
4. anti depressants- prozac/fluoxetine hydrochloride, zoloft/sertraline hydrochloride/ Remember that fatigue can be caused by depression and that some of the meds (prednisone) can cause depression
5. Other: inderal/propranolol hydrochloride- beta blocker for ataxia, diamox/acetazolamide- diuretic, and atarax/hyroxyzine- antihistamine used to treat tremors
6. pain: tegretol (carbamazepine), depakote (valproic acid), dilantin (phenytoin) for sharp lancing pain. Baclofen (lioresal), dantrium (dantrolene sodium), valium (diazepam), klonopin (clonazepam) to help reduce spasticity and fatigue. possible to have a baclofen pump surgically implanted to give minute doses directly to the spinal cord
7. immunoregulatory drugs: interferon beta-la/avonex or Rebif, interferon 1b/Betaseron) and copaxone/glatiramer acetate are known as the ABC's of immunotherapy and are given by IV, they decrease the occurrence of acute episodes by decreasing inflammation and inhibiting the autoimmune response
- side effects of these drugs are flu-like symptoms and can be treated with NSAIDS
8. sexual dysfunction:
- viagra/sildenafil citrate and lubricating gels. if patient experiences spastic pain during sexual activity then they should engage in sexual activity when the ant-spasmodic med is at peak effect
1. Patient education:
- triggers that cause exacerbations. patients must be be taught to handle stress. Family encouraged to help with household chores. want the patient to understand the need of remaining active but to avoid overdoing it. help the patient the need to avoid fatigue and to listen to signals the fatigue it presents. teach patients the effect of extreme fatigue- can trigger and exacerbation. golf is a better sport than tennis. remind the patients that too much exercise can bring on symptoms. patients need to find a balance. refer to physical therapist for stretching and other exercises
- adequate hydration (3000 cc/day) is necessary to relieve constipation. but should decrease fluids in the evening so sleep is not interfered with
- bladder training: to void within 30 mins of drinking fluids, to always respond to the urge to void, to establish a voiding schedule with a gradual increase in the time between voids to assist with frequency, urgency and incontinence. Kegal is not helpful as the problem is not the muscle. No diapers and retention catheters not used as the patient will be prone to UTIs. Pt. will be taught how to do self catheterization instead.
- bed rest during an acute spasm is advised. Warm baths may help to relieve symptoms but the temperature should be checked with a bath thermometer so that it is not too hot. a hot bath can bring on fatigue and then the patient may be too tired to get out of the tub
- frequent rest periods to avoid tiring
- AC is a must during the summer to prevent from overheating
- teach patients that a fever will exacerbate any exisiting symptoms and may bring on new ones. so tylenol should be available
- good nutrition: no "ms" diet exists but high fiber, low fat and lots of complex CHO are recommended
- refer patient to international MS support foundation, the MS association of america and national MS society
Cardinal or Classic Triad:
1) resting tremors: at first are slow and unilateral. hands may have tremors at rest causing micrographia (writing becomes smaller) and pill rolling (thumb and fingers rub back and forth). the forearm and hands have supination/pronation. the tongue has tremors that cause dysarthria (difficulty with speech). eventually the patient will have difficulty with fine motor movements For ex) holding a newspaper or using a touch phone. the resting tremors will disappear with slow purposeful movement. Anxiety, walking and when the patient is concentrating will cause an increase
2. rigidity: muscles become stiff and increasingly resistant to passive movement. classified as plastic-mildly restrictive movement where trying shoes and rising from an armed chair is difficult. cogwheel rigidity: rhythmic interruption of muscle movement when joint is moved inhibiting spontaneous movement (will have problems pivoting-lose balance)
- lead pipe rigidity: total resistance to movement leading to akenesia called freezing phenomena (joint locks and patient will be unable to move)
- truncal rigidity: causes the need to move the body as a unit when getting out of bed and chair. should sit in chair that has arms. rigidity of neck and back muscle-results in old man posture (stooped, flexed trunk, flexed elbows and abducted shoulders) stiffness of facial muscles also occurs. hypomimia- mask of P's (decreased facial expression)
- the rigidity may affect muscles of speech- resulting in slurring, stuttering, raspy voice and inability to speak. patient may also develop rigidity of voluntary muscles of the throat- dysphagia- leads to pooling of food which could cause choking- aspiration pneumonia
- also possible for chest wall and intercostals muscle rigidity leading to difficulty breathing
3. bradykenesia- reduced movement. related to rigidity, one leads to the other. a patient who has lead-pipe rigidity actually has an extreme form of bradykenesia. patient will develop arm swing and blinking and slowed speech and walking so patient has propulsive gait to keep them from falling (short accelerating steps with a shuffle) may speed up pace as leg muscles freeze. patient looks drunk and is at risk for falling
- the triad leads to other clinical manifestations
primary purpose is to control symotoms: focus is to prevent development of secondary symptoms (aspiration pneumonia from difficulty swallowing), becomes inactive, dependent and immobilized
1. meds: main objective to replace or supplement dopamine
- antiparkinsonian drugs: levodopa (larodopa), carbidopa-levodopa (sinemet), benztropine (congentin)
- levadopa therapy- sinemet. replaces dopamine in the form that the brain can use. is a combo of levodopa and carbidopa. levadopa is synthetic protein that closely resembles dopamine. converted to dopamine in brain. levadopa has been cornerstone of P treatment since 1960. problem 90% of it is converted to dopamine outside the brain. a large dose is needed to max the use of the 10% that gets to the brain. side effects of drug at high doses is a problem- nausea, vomiting, decreased appetite
- levadopa is combined with carbidopa (sinemet). Carbidipa allows more of drug to get inside of brain
- effects of levadopa wear off in about 5 years so the used of it postponed for as long as possible and other less potent drugs used first

- anticholinergics: benztropine (cogentin), trihexyphenidyl (artane)
- antispasmotiscs: procyclidine (kemadrin)
- antidepressants: amitriptyline (elavil) these drugs have anticholinergic properties as well as antidepressant effects
- antiviral- amantadine (symmetrol) used early to decrease rigidity, tremors, and bradykenesia
- monoamine oxidase-B inhibitor: selegiline (eldepryl) used to delay the use of levadopa and eldepryl as an adjunct to reduce dose of levadopa needed
- dopamine receptor agonists: bromocriptine (parlodel) mimics dopamine
2. activity as tolerated
3. PT/OT/Speech
4. high residue diet (fiber, at risk for constipation due to spasms)
5. surgery- when drug treatment has loss its effects. rapidly changing
- stereotactic- targets cells within the brain to quiet tremors and restore mobility. good for those with idiopathic form and max dose of anti P meds
- pallidotomy cells in internal globus pallidus are targeted
- thalamotomy- thalamus cells complications include ataxia and hemiparesis (weakness one side of body)
- deep brain stimulation- electrodes are placed in thalamus and electricity is delivered by a pacemaker
- neurotransplantation: from aborted fetuses- cells from CN transplanted into caudate nucleus
- tautologies tissue transplant- adrenalectomy with small pieces of the gland with dopamine producing cells implanted into the striatium where neurons are still active. palliative but results are encouraging
1. medications: cholinesterase inhibitors. first line of treatment increases of acetylcholine that is available at the neuromuscular junction. enhances the effects of acetylcholine on the muscle fibers which helps improve strength
- mestinon (pyridostigmine bromide)- least amount of side effects. dose started low and increased until s/s controlled. keep in mind that normal strength may not be possible
- prostigmin (neostigminembromide)- side effects: n/v, diarrhea, abd cramps, increased salivation and broncial secs
2. immunosuppressent drugs: given to reduce production of antireceptor antibody , may be given to patients who do not respond to cholinesterase inhibitors
- corticosterioids prednisone at the lowest possible dose, produces remission in about 70-80 % cases. side effects an issue
- cytotoxic meds: imuran and cytoxin are also used but are reserved wit more severe form of disease due to serious side effects

Also categorized in immunosupresssion are
1. plasmapheresis: removes circulating antibodies to acetylcholine receptors. this is used to help stabilize a patient in crisis and preop for a patient undergoing thymectomy
2. thymectomy: for most patients with MG the thymus does not recede as it is uspposed to (in infancy) and remains or may enlarge. the thymus plays an important role in development of immune system. in patients with MG the thymus goes awry and may be the reason why the patient developed MG. removal of thymus reduces symptoms of MG. A thymectomy is difficult surgery and patients with MG are at high risk for complications associated with anesthesia