Angelite Nurses

THURSDAY, Oct. 23 (HealthDay News) -- Two medications may prove to be advances in the treatment of multiple sclerosis, researchers say.

In one study, an experimental drug called oral fumarate (BG00012) substantially reduced symptoms in patients with relapsing-remitting multiple sclerosis, according to a phase II clinical trial by European and North American researchers.

And in a second trial, researchers found that the leukemia drug alemtuzumab (Campath) was about 70 percent more effective than another drug already widely used to treat MS. However, alemtuzumab also had significant side effects, including bleeding disorders, a greater risk of thyroid disease, and infections. This prompted experts to say that much more research is needed before alemtuzumab can be prescribed to treat multiple sclerosis.

Multiple sclerosis is a nervous system disease that affects the brain and spinal cord. It damages the myelin sheath, the material that surrounds and protects nerve cells. This damage slows or blocks messages between the brain and the body, according to the U.S. National Library of Medicine.

Symptoms of the disease can include visual disturbances; muscle weakness; trouble with coordination and balance; sensations such as numbness, prickling, or "pins and needles;" and thinking and memory problems.

It's not known what causes multiple sclerosis. It may be an autoimmune disease, which happens when the body attacks itself. MS affects women more than men, and it often begins between the ages of 20 and 40. An estimated 400,000 Americans have the disease. Usually, the disease is mild, but some people lose the ability to write, speak or walk. There's no cure for MS, but medicines may slow it down and help control symptoms, according to the National Library of Medicine.

The 24-week study of BG00012 included 257 patients, ages 18 to 55, who were randomly assigned to receive either 120 milligrams of BG00012 once a day (64 patients), 120 milligrams three times a day (64 patients), 240 milligrams three times a day (64 patients), or a placebo (65 patients). The patients were assessed at weeks 12, 16, 20 and 24.

MRI brain scans showed that patients treated with 240 milligrams of BG00012 three times a day had 69 percent fewer new gadolinium enhancing (GdE) lesions -- a marker of MS-related inflammatory activity -- from week 12 to 24 than those who received the placebo. They also had fewer new or enlarging T2-hyperintense and T1-hypointense lesions at week 24.

The study also found that BG00012 reduced the annual relapse rate by 32 percent, but this finding wasn't statistically significant. Patients who received the drug were more likely than those in the placebo group to suffer adverse events such as abdominal pain and hot flush. Dose-related adverse events in patients taking the drug included headache, fatigue and feeling hot, the researchers said.

"Longer-term (phase III) studies of BG00012 in larger patient populations are underway to define its place in the future of relapsing-remitting multiple sclerosis treatment. If these studies show similar relapse rate reductions with BG00012, interferon beta, and glatiramer acetate, BG00012 could be a suitable initial treatment for relapsing-remitting multiple sclerosis," wrote Professor Ludwig Kappos, of University Hospital Basel, in Switzerland, and colleagues.

The study was published in the Oct. 24 issue of the The Lancet.

In an accompanying comment in the journal, Professor Per Soelberg Sorensen and Dr. Finn Sellebjerg of the Danish Multiple Sclerosis Research Center, noted that "BG00012 might have a favorable benefit-to-risk ratio profile compared with its oral competitors and the currently available first-line injectable drugs. However, we will have to await the results from the ongoing large phase III trials to establish the place of BG00012 and of other oral drugs in the treatment of relapsing-remitting multiple sclerosis."

The study of the leukemia drug alemtuzumab, which temporarily depletes white blood cells and is part of a class of drugs called monoclonal antibodies, included 334 patients. Patients were randomly assigned to get either alemtuzumab or interferon beta, a standard MS therapy, for three years.

Alemtuzumab reduced by 74 percent the risk of MS relapse, the researchers reported in the Oct. 23 issue of the New England Journal of Medicine.

"The ability of an MS drug to promote brain repair is unprecedented," Alasdair Coles, of Cambridge University in England, and one of the study's leaders, told the AFP news service. "We are witnessing a drug which, if given early enough, might effectively stop the advancement of the disease and also restore lost function by promoting repair of the damaged brain tissue."

However, in an accompanying journal editorial, Dr. Stephen L. Hauser, a neurologist at the University of California, San Francisco, said the "toxic effects associated with alemtuzumab considerably dampen any enthusiasm for its routine use in patients with multiple sclerosis until more is known about its long-term safety and sustained efficacy."

• Headache
• 
  
• Meningitis
• 
  
• Encephalitis
• 
  
• Brain Abscess
• 
  
• Brain Tumors
• 
  
• Cerebrovascular Accident (CVA)
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• Cerebral Aneurysm
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• Parkinson's Disease
• 
  
• Multiple Sclerosis (MS)
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• Myasthenia Gravis
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• Hydrocephalus
• 
  
• Shunts
• 
  
• Spina Bifida (Myelodysplasia)
• 
  
• Reye's Syndrome
• 
  
• Seizure Disorders
• 
  
• Cerebral Palsy (CP)
• 
  
• Tay-Sachs Disease
• 
  
• Blindness
• 
  
• Conjunctivitis
• 
  
• Deafness
• 
  
• Otitis Media
• 
  
• Head Injury
• 
  
• Intracranial Surgery
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• Spinal Cord Injuries
• 
  
• Trigeminal Neuralgia (Tic Douloureux)
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• Bell's Palsy
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• Guillain-Barre Syndrome
• 
  
• Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease)

1. General information
1. Progressive motor neuron disease, which usually leads to death in 2-6 years
2. Onset usually between ages 40-70; affects men more than women
3. Cause unknown
4. There is no cure or specific treatment; death usually occurs as a result of respiratory infection secondary to respiratory insufficiency.
2. Assessment findings
1. Progressive weakness and atrophy of the muscles of the arms, trunk, or legs
2. Dysarthria, dysphagia
3. Fasciculations
4. Respiratory insufficiency
5. Diagnostic tests: EMG and muscle biopsy can rule out other diseases.
3. Nursing interventions
1. Provide nursing measures for muscle weakness and dysphagia.
2. Promote adequate ventilatory function.
3. Prevent complications of immobility.
4. Encourage diversional activities; spend time with the client.
5. Provide compassion and intensive support to client/significant others.
6. Provide or refer for physical therapy as indicated.
7. Promote independence for as long as possible.

1. General information
1. Symmetrical, bilateral, peripheral polyneuritis characterized by ascending paralysis
2. Can occur at any age; affects women and men equally
3. Cause unknown; may be an autoimmune process
4. Precipitating factors: antecedent viral infection, immunization
5. Progression of disease is highly individual; 90% of clients stop progression in 4 weeks; recovery is usually from 3-6 months; may have residual deficits
2. Medical Management
1. Mechanical ventilation if respiratory problems present
2. Plasmapheresis to reduce circulating antibodies
3. Continuous ECG monitoring to detect alteration in heart rate and rhythm
4. Propranolol to prevent tachycardia
5. Atropine may be given to prevent episodes of bradycardia during endotracheal suctioning and physical therapy.
3. Assessment findings
1. Mild sensory changes; in some clients severe misinterpretation of sensory stimuli resulting in extreme discomfort
2. Clumsiness: usually first symptom
3. Progressive motor weakness in more than one limb (classically is ascending and symmetrical)
4. Cranial nerve involvement (dysphagia)
5. Ventilatory insufficiency if paralysis ascends to respiratory muscles
6. Absence of deep tendon reflexes
7. Autonomic dysfunction
8. Diagnostic tests
1. CSF studies: increased protein
2. EMG: slowed nerve conduction
4. Nursing interventions
1. Maintain adequate ventilation.
1. Monitor rate and depth of respirations; serial vital capacities.
2. Observe for ventilatory insufficiency.
3. Maintain mechanical ventilation as needed; keep airway free of secretions and prevent pneumonia.
2. Check individual muscle groups every 2 hours in acute phase to check for progression of muscle weakness.
3. Assess cranial nerve function: check gag reflex and swallowing ability; ability to handle secretions; voice.
4. Monitor vital signs and observe for signs of autonomic dysfunction such as acute periods of hypertension fluctuating with hypotension, tachycardia, arrhythmias.
5. Administer corticosteroids to suppress immune reaction as ordered.
6. Administer antiarrhythmic agents as ordered.
7. Prevent complications of immobility.
8. Promote comfort (especially in clients with sensory changes): foot cradle, sheepskin, guided imagery, relaxation techniques.
9. Promote optimum nutrition.
1. Check gag reflex before feeding.
2. Start with pureed foods.
3. Assess need for nasogastric tube feedings if unable to swallow.
10. Provide psychologic support and encouragement to client/significant others.
11. Refer for rehabilitation to regain strength and to treat any residual deficits.

1. General information
1. Disorder of cranial nerve VII resulting in the loss of ability to move the muscles on one side of the face
2. Cause unknown; may be viral or autoimmune
3. Complete recovery in 3-5 weeks in majority of clients
2. Assessment findings
1. Loss of taste over anterior two-thirds of tongue on affected side
2. Complete paralysis of one side of face
3. Loss of expression, displacement of mouth toward unaffected side, and inability to close eyelid (all on affected side)
4. Pain behind the ear
3. Nursing interventions
1. Assess facial nerve function regularly (see Table 4.15).
2. Administer medications as ordered.
1. Corticosteroids: to decrease edema and pain
2. Mild analgesics as necessary
3. Provide soft diet with supplementary feedings as indicated.
4. Instruct to chew on unaffected side, avoid hot fluids/foods, and perform mouth care after each meal.
5. Provide special eye care to protect the cornea.
1. Dark glasses (cosmetic and protective reasons) or eyeshield
2. Artificial tears to prevent drying of the cornea
3. Ointment and eye patch at night to keep eyelid closed
6. Provide support and reassurance.

1. General information
1. Disorder of cranial nerve V causing disabling and recurring attacks of severe pain along the sensory distribution of one or more branches of the trigeminal nerve
2. Incidence increased in elderly women
3. Cause unknown
2. Medical management
1. Anticonvulsant drugs: carbamazepine (Tegretol), phenytoin (Dilantin)
2. Nerve block: injection of alcohol or phenol into one or more branches of the trigeminal nerve; temporary effect, lasts 6-18 months
3. Surgery
1. Peripheral: avulsion of peripheral branches of trigeminal nerve
2. Intracranial
1. retrogasserian rhizotomy: total severance of the sensory root of the trigeminal nerve intracranially; results in permanent anesthesia, numbness, heaviness, and stiffness in affected part; loss of corneal reflex
2. microsurgery: uses more precise cutting and may preserve facial sensation and corneal reflex
3. percutaneous radio-frequency trigeminal gangliolysis: current surgical procedure of choice; thermally destroys the trigeminal nerve in the area of the ganglion; provides permanent pain relief with preservation of sense of touch, proprioception, and corneal reflex; done under local anesthesia
4. microvascular decompression of trigeminal nerve: decompresses the trigeminal nerve; craniotomy necessary; provides permanent pain relief while preserving facial sensation
3. Assessment findings
1. Sudden paroxysms of extremely severe shooting pain in one side of the face
2. Attacks may be triggered by a cold breeze, foods/fluids of extreme temperature, toothbrushing, chewing, talking, or touching the face
3. During attack: twitching, grimacing, and frequent blinking/tearing of the eye
4. Poor eating and hygiene habits
5. Withdrawal from interactions with others
6. Diagnostic tests: x-rays of the skull, teeth, and sinuses may identify dental or sinus infection as an aggravating factor.
4. Nursing interventions
1. Assess characteristics of the pain including triggering factors, trigger points, and pain management techniques.
2. Administer medications as ordered; monitor response.
3. Maintain room at an even, moderate temperature, free from drafts.
4. Provide small, frequent feedings of lukewarm, semiliquid, or soft foods that are easily chewed.
5. Provide the client with a soft washcloth and lukewarm water and perform hygiene during periods when pain is decreased.
6. Prepare the client for surgery if indicated.
7. Provide client teaching and discharge planning concerning
1. Need to avoid outdoor activities during cold, windy, or rainy weather
2. Importance of good nutrition and hygiene
3. Use of medications, side effects, and signs of toxicity
4. Specific instructions following surgery for residual effects of anesthesia and loss of corneal reflex
1. protective eye care
2. chew on unaffected side only
3. avoid hot fluids/foods
4. mouth care after meals to remove particles
5. good oral hygiene; visit dentist every 6 months
6. protect the face during extremes of temperature.

1. General information
1. Occurs most commonly in young adult males between ages 15 and 25
2. Common traumatic causes: motor vehicle accidents, diving in shallow water, falls, industrial accidents, sports injuries, gunshot or stab wounds
3. Nontraumatic causes: tumors, hematomas, aneurysms, congenital defects (spina bifida)
4. Classified by extent, level, and mechanism of injury
1. Extent of injury
1. may affect the vertebral column: fracture, fracture/dislocation
2. may affect anterior or posterior ligaments, causing compression of spinal cord
3. may be to the spinal cord and its roots: concussion, contusion, compression or laceration by fracture/dislocation or penetrating missiles
2. Level of injury: cervical, thoracic, lumbar
3. Mechanisms of injury
1. hyperflexion
2. hyperextension
3. axial loading (force exerted straight up or down spinal column as in a diving accident)
4. penetrating wounds
5. Pathophysiology: hemorrhage and edema cause ischemia, leading to necrosis and destruction of the cord
2. Medical management: immobilization and maintenance of normal spinal alignment to promote fracture healing
1. Horizontal turning frames (Stryker frame)
2. Skeletal traction: to immobilize the fracture and maintain alignment of the cervical spine
1. Cervical tongs (Crutchfield, Gardner- Wells, Vinke): inserted through burr holes; traction is provided by a rope extended from the center of tongs over a pulley with weights attached at the end.
2. Halo traction
1. stainless steel halo ring fits around the head and is attached to the skull with four pins; halo is attached to plastic body cast or plastic vest
2. permits early mobilization, decreased period of hospitalization and reduces complications of immobility
3. Surgery: decompression laminectomy, spinal fusion
1. Depends on type of injury and the preference of the surgeon
2. Indications: unstable fracture, cord compression, progression of neurologic deficits
3. Assessment findings
1. Spinal shock
1. Occurs immediately after the injury as a result of the insult to the CNS
2. Temporary condition lasting from several days to three months
3. Characterized by absence of reflexes below the level of the lesion, flaccid paralysis, lack of temperature control in affected parts, hypotension with bradycardia, retention of urine and feces
2. Symptoms depend on the level and the extent of the injury.
1. Level of injury
1. quadriplegia: cervical injuries (C₁-C₈) cause paralysis of all four extremities; respiratory paralysis occurs in lesions above C₆ due to lack of innervation to the diaphragm; (phrenic nerves at the C₄-C₅ level).
2. paraplegia: thoraco/lumbar injuries (T_1-L₄) cause paralysis of the lower half of the body involving both legs
2. Extent of injury
1. complete cord transection
1. loss of all voluntary movement and sensation below the level of the injury; reflex activity below the level of the lesion may return after spinal shock resolves.
2. lesions in the conus medullaris or cauda equina result in permanent flaccid paralysis and areflexia.
2. incomplete lesions: varying degrees of motor or sensory loss below the level of the lesion depending on which neurologic tracts are damaged and which are spared.
3. Diagnostic test: spinal x-rays may reveal fracture.
4. Nursing interventions: emergency care
1. Assess airway, breathing, circulation
1. Do not move the client during assessment.
2. If airway obstruction or inadequate ventilation exists: do not hyperextend neck to open airway, use jaw thrust instead.
2. Perform a quick head-to-toe assessment: check for LOC, signs of trauma to the head or neck, leakage of clear fluid from ears or nose, signs of motor or sensory impairment.
3. Immobilize the client in the position found until help arrives.
4. Once emergency help arrives, assist in immobilizing the head and neck with a cervical collar and place the client on a spinal board; avoid any movement during transfer, especially flexion of the spinal column.
5. Have suction available to clear the airway and prevent aspiration if the client vomits; client may be turned slightly to the side if secured to a board.
6. Evaluate respiration and observe for weak or labored respirations.
5. Nursing interventions: acute care
1. Maintain optimum respiratory function.
1. Observe for weak or labored respirations; monitor arterial blood gases.
2. Prevent pneumonia and atelectasis: turn every 2 hours; cough and deep breathe every hour; use incentive spirometry every 2 hours.
3. Tracheostomy and mechanical ventilation may be necessary if respiratory insufficiency occurs.
2. Maintain optimal cardiovascular function.
1. Monitor vital signs; observe for bradycarida, arrhythmias, hypotension.
2. Apply thigh-high elastic stockings or Ace bandages.
3. Change position slowly and gradually elevate the head of the bed to prevent postural hypotension.
4. Observe for signs of deep-vein thrombosis.
3. Maintain fluid and electrolyte balance and nutrition.
1. Nasogastric tube may be inserted until bowel sounds return.
2. Maintain IV therapy as ordered; avoid overhydration (can aggravate cord edema).
3. Check bowel sounds before feeding client (paralytic ileus is common).
4. Progress slowly from clear liquid to regular diet.
5. Provide diet high in protein, carbohydrates, calories.
4. Maintain immobilization and spinal alignment always.
1. Turn every hour on turning frame.
2. Maintain cervical traction at all times if indicated.
5. Prevent complications of immobility; use footboard/high-topped sneakers to prevent foot drop; provide splint for quadriplegic client to prevent wrist drop.
6. Maintain urinary elimination.
1. Provide intermittent catheterization or maintain indwelling catheter as ordered.
2. Increase fluids to 3000 ml/day.
3. Provide acid-ash foods/fluids to acidify urine and prevent infection (see Bladder Surgery).
7. Maintain bowel elimination: administer stool softeners and suppositories to prevent impaction as ordered.
8. Monitor temperature control.
1. Check temperature every 4 hours.
2. Regulate environment closely.
3. Avoid excessive covering or exposure.
9. Observe for and prevent infection.
1. Observe tongs or pin site for redness, drainage.
2. Provide tong- or pin-site care. Cleanse with antiseptic solution according to agency policy.
3. Observe for signs of respiratory or urinary infection.
10. Observe for and prevent stress ulcers.
1. Assess for epigastic or shoulder pain.
2. If corticosteroids are ordered, give with food or antacids; administer cimetadine (Tagamet) as ordered.
3. Check nasogastric tube contents and stools for blood.
6. Nursing interventions: chronic care
1. Neurogenic bladder
1. Reflex or upper motor neuron bladder; reflex activity of the bladder may occur after spinal shock resolves; the bladder is unable to store urine very long and empties involuntarily
2. Nonreflexive or lower motor neuron bladder: reflex arc is disrupted and no reflex activity of the bladder occurs, resulting in urine retention with overflow
3. Management of reflex bladder
1. intermittent catheterization every 4 hours and gradually progress to every 6 hours.
2. regulate fluid intake to 1800-2000 ml/day.
3. bladder taps or stimulating trigger points to cause reflex emptying of the bladder.
4. Management of nonreflexive bladder
1. intermittent catheterization every 6 hours.
2. Credé maneuver or rectal stretch.
3. regulate intake to 1800-2000 ml/day to prevent overdistention of bladder.
5. Management depends on life-style, age, sex, home care, and availability of care giver.
2. Spasticity
1. Return of reflex activity may occur after spinal shock resolves; severe spasticity may be detrimental
2. Drug therapy: baclofen (Lioresal), dantrolene (Dantrium), diazepam (Valium)
3. Physical therapy: stretching exercises, warm tub baths, whirlpool
4. Surgery: chordotomy
3. Autonomic dysreflexia
1. Rise in blood pressure, sometimes to fatal levels
2. Occurs in clients with cord lesions above T₆ and most commonly in clients with cervical injuries
3. Reflex response to stimulation of the sympathetic nervous system
4. Stimulus may be overdistended bladder or bowel, decubitus ulcer, chilling, pressure from bedclothes
5. Symptoms: severe headache, hypertension, bradycardia, sweating, goose bumps, nasal congestion, blurred vision, convulsions
6. Interventions
1. raise client to sitting position to decrease BP.
2. check for source of stimulus (bladder, bowel, skin).
3. remove offending stimulus (e.g., catheterize client, digitally remove impacted feces, reposition client).
4. monitor blood pressure.
5. administer antihypertensives (e.g., hydralazine HCl [Apresoline]) as ordered.
7. Nursing interventions: general rehabilitative care
1. Provide psychologic support to client/significant others.
1. Support during grieving process.
2. Assist client to adjust to effects of injury.
3. Encourage independence.
4. Involve the client in decision making.
2. Provide sexual counseling.
1. Work with the client and partner.
2. Explore alternative methods of sexual gratification.
3. Initiate rehabilitation program.
1. Physical therapy.
2. Vocational rehabilitation
3. Psychologic counseling
4. Use of braces, electronic wheelchair, and other assistance devices to maximize independence.

1. Types
1. Craniotomy: surgical opening of skull to gain access to intracranial structures; used to remove a tumor, evacuate blood clot, control hemorrhage, relieve increased ICP
2. Craniectomy: excision of a portion of the skull; sometimes used for decompression
3. Cranioplasty: repair of a cranial defect with a metal or plastic plate
2. Nursing interventions: preoperative
1. Routine pre-op care (see Perioperative Nursing).
2. Provide emotional support; explain post-op procedures and that client's head will be shaved, there will be a large bandage on head, possibly temporary swelling and discoloration around the eye on the affected side, and possible headache.
3. Shampoo the scalp and check for signs of infection.
4. Shave hair.
5. Evaluate and record baseline vital signs and neuro checks.
6. Avoid enemas unless directed (straining increases ICP).
7. Give pre-op steroids as ordered to decrease brain swelling.
8. Insert Foley catheter as ordered.
3. Nursing interventions: postoperative
1. Provide nursing care for the unconscious client (see Care of the Unconscious Client).
2. Maintain a patent airway and adequate ventilation.
1. Supratentorial incision: elevate head of bed 15°-45° as ordered; position on back (if intubated or conscious) or on unaffected side; turn every 2 hours to facilitate breathing and venous return.
2. Infratentorial incision: keep head of bed flat or elevate 20°-30° as ordered; do not flex head on chest; turn side to side every 2 hours using a turning sheet; check respirations closely and report any signs of respiratory distress.
3. Instruct the conscious client to breathe deeply but not to cough; avoid vigorous suctioning.
3. Check vital signs and neuro checks frequently; observe for decreasing LOC, increased ICP, seizures, hyperthermia.
4. Monitor fluid and electrolyte status.
1. Maintain accurate I&O.
2. Restrict fluids to 1500 ml/day or as ordered to decrease cerebral edema.
3. Avoid overly rapid infusions.
4. Watch for signs of diabetes insipidus (severe thirst, polyuria, dehydration) and inappropriate ADH secretion (decreased urine output, hunger, thirst, irritability, decreased LOC, muscle weakness).
5. For infratentorial surgery: may be NPO for 24 hours due to possible impaired swallowing and gag reflexes.
5. Assess dressings frequently and report any abnormalities.
1. Reinforce as needed with sterile dressings.
2. Check dressings for excessive drainage, CSF, infection, displacement and report to physician.
3. If surgical drain is in place, note color, amount, and odor of drainage.
6. Administer medications as ordered.
1. Corticosteroids: to decrease cerebral edema
2. Anticonvulsants: to prevent seizures
3. Stool softeners: to prevent straining
4. Mild analgesics
7. Apply ice to swollen eyelids; lubricate lids and areas around eyes with petrolatum jelly.
8. Refer client for rehabilitation for residual deficits.

1. General information
1. Usually caused by car accidents, falls, assaults
2. Types
1. Concussion: severe blow to the head jostles brain, causing it to strike the skull; results in temporary neural dysfunction
2. Contusion: results from more severe blow that bruises the brain and disrupts neural function
3. Hemorrhage
1. epidural hematoma: accumulation of blood between the dura mater and skull; commonly results from laceration of middle meningeal artery during skull fracture; blood accumulates rapidly
2. subdural hematoma: accumulation of blood between the dura and arachnoid; venous bleeding that forms slowly; may be acute, subacute, or chronic
3. subarachnoid hematoma: bleeding in subarachnoid space
4. intracerebral hematoma: accumulation of blood within the cerebrum
4. Fractures: linear, depressed, comminuted, compound
2. Assessment findings (depend on type of injury)
1. Concussion: headache, transient loss of consciousness, retrograde or posttraumatic amnesia, nausea, dizziness, irritability
2. Contusion: neurologic deficits depend on the site and extent of damage; include decreased LOC, aphasia, hemiplegia, sensory deficits
3. Hemorrhages
1. Epidural hematoma: brief loss of consciousness followed by lucid interval; progresses to severe headache, vomiting, rapidly deteriorating LOC, possible seizures, ipsilateral pupillary dilation
2. Subdural hematoma: alterations in LOC, headache, focal neurologic deficits, personality changes, ipsilateral pupillary dilation
3. Intracerebral hematoma: headache, decreased LOC, hemiplegia, ipsilateral pupillary dilation
4. Fractures
1. Headache, pain over fracture site
2. Compound fractures: rhinorrhea (leakage of CSF from nose); otorrhea (leakage of CSF from ear)
5. Diagnostic tests
1. Skull x-ray: reveals skull fracture or intracranial shift
2. CT scan: reveals hemorrhage
3. Nursing interventions (see also Care of the Unconscious Client and Care of the Client with Increased ICP)
1. Maintain a patent airway and adequate ventilation.
2. Monitor vital signs and neuro checks; observe for changes in neurologic status, signs of increased ICP, shock, seizures, and hyperthermia.
3. Observe for CSF leakage.
1. Check discharge for positive Testape or Dextrostix reaction for glucose; bloody spot encircled by watery, pale ring on pillowcase or sheet.
2. Never attempt to clean the ears or nose of a head-injured client or use nasal suction unless cleared by physician
4. If a CSF leak is present
1. Instruct client not to blow nose.
2. Elevate head of bed 30° as ordered.
3. Observe for signs of meningitis and administer antibiotics to prevent meningitis as ordered.
4. Place a cotton ball in the ear to absorb otorrhea; replace frequently.
5. Gently place a sterile gauze pad at the bottom of the nose for rhinorrhea; replace frequently.
5. Prevent complications of immobility.
6. Prepare the client for surgery if indicated.
1. Depressed skull fracture: surgical removal or elevation of splintered bone; debridement and cleansing of area; repair of dural tear if present; cranioplasty (if necessitated for large cranial defect)
2. Epidural or subdural hematoma: evacuation of the hematoma
7. Provide psychologic support to client/significant others.
8. Observe for hemiplegia, aphasia, and sensory problems, and plan care accordingly (see Cerebrovascular Accident)
9. Provide client teaching and discharge planning concerning rehabilitation for neurologic deficits; note availability of community agencies.

1. General information: infection of membrane covering anterior surface of eye globe and inner surface of eyelid due to multiple causes (bacterial, viral, allergic)
2. Medical management: ophthalmic antibiotics, steroids, anesthetics
3. Assessment findings: weeping eye, reddened conjunctiva, sensitivity to light, eyelid stuck shut with exudate
4. Nursing interventions
1. Administer medications as ordered: apply ophthalmic antibiotic ointments from inner to outer canthus (do not let container touch eye).
2. Provide client teaching and discharge planning concerning measures to prevent spread of infection
1. Very contagious if bacterial or viral; no school until antibiotics have been taken for 24-48 hours
2. Should not share pillows, tissues, toys
3. Good hand-washing technique
4. Medication regimen: schedule, dosage, desired and side effects

1. General information
1. Degenerative brain disease, caused by absence of hexosaminidase A from all body tissues
2. Autosomal recessive inheritance
3. Occurs predominantly in children of Eastern European Jewish ancestry
4. A fatal disease; death usually occurs before age 4
2. Assessment findings
1. Progressive lethargy in a previously healthy 2- to 6-month-old infant
2. Loss of developmental accomplishments
3. Loss of visual acuity
4. Hyperreflexia, decerebrate posturing, dysphagia, malnutrition, seizures
5. Diagnosis confirmed by classic cherry-red spot on the macula and by enzyme measurements in serum, amniotic fluid, or white cells
3. Nursing interventions
1. Support parents at time of diagnosis; help them cope with feelings of anger and guilt.
2. Assist parents in planning long-term care for the child.
3. Provide genetic counseling and psychologic follow-up as needed.

1. General information
1. Neuromuscular disorder resulting from damage to or altered structure of the part of the brain responsible for controlling motor function
2. Incidence: 1.5-5 in 1,000 live births
3. May be caused by a variety of factors resulting in damage to the CNS; possible causes include
1. Prenatally: genetic, altered neurologic development, or trauma or anoxia to mother (toxemia, rubella, accidents)
2. Perinatally: during the birth process (drugs at delivery, precipitate delivery, fetal distress, breech deliveries with delay)
3. Postnatally: kernicterus or head trauma (child falls out of crib or is hit by a car)
2. Medical management
1. Drug therapy
1. Antianxiety agents
2. Skeletal muscle relaxants
3. Local nerve blocks
2. Physical/occupational therapy
3. Speech/audiology therapy
4. Surgery: muscle- and tendon-releasing procedures
3. Assessment findings: disease itself does not progress once established; progressive complications, however, cause changes in signs and symptoms
1. Spasticity: exaggerated hyperactive reflexes (increased muscle tone, increase in stretch reflex, scissoring of legs, poorly coordinated body movements for voluntary activities)
1. Occurs with pyramidal tract lesion
2. Found in 40% of all CP
3. Results in contractures
4. Also affects ability to speak: altered quality and articulation
5. Loud noise or sudden movement causes reaction with increased spasm
6. No parachute reflex to protect self when falling
2. Athetosis: constant involuntary, purposeless, slow, writhing motions
1. Occurs with extrapyramidal tract (basal ganglia) lesion
2. Found in 40% of all CP
3. Athetosis disappears during sleep, therefore contractures do not develop
4. Movements increase with increase in physical or emotional stress
5. Also affects facial muscles
3. Ataxia: disturbance in equilibrium; diminished righting reflex (lack of balance, poor coordination, dizziness, hypotonia)
1. Occurs with extrapyramidal tract (cerebellar) lesion
2. Found in 10% of all CP
3. Muscles and reflexes are normal
4. Tremor: repetitive rhythmic involuntary contractions of flexor and extensor muscles
1. Occurs with extrapyramidal tract (basal ganglia) lesion
2. Found in 5% of all CP
3. Interferes with performance of precise movements
4. Often a mild disability
5. Rigidity: resistance to flexion and extension resulting from simultaneous contraction of both agonist and antagonist muscle groups
1. Occurs with extrapyramidal tract (basal ganglia) lesion
2. Found in 5% of all CP
3. Diminished or absent reflexes
4. Potential for severe contractures
6. Associated problems
1. Mental retardation: the majority of CP clients are of normal or higher than average intelligence, but are unable to demonstrate it on standardized tests; 18%-50% have some form of mental retardation
2. Hearing loss in 13% of CP clients
3. Defective speech in 75% of CP clients
4. Dental anomalies (from muscle contractures)
5. Orthopedic problems from contractures or inability to mobilize
6. Visual disabilities in 28% due to poor muscle control
7. Disturbances of body image, touch, perception
8. Feelings of worthlessness
4. Nursing interventions
1. Obtain a careful pregnancy, birth, and childhood history.
2. Observe the child's behavior in various situations.
3. Assist with activities of daily living (ADL), help child to learn as many self-care activities as possible; CP clients cannot do any task unless they are consciously aware of each step in the task; careful teaching and demonstration is essential.
4. Provide a safe environment (safety helmet, padded crib).
5. Provide physical therapy to prevent contractures and assist in mobility (braces if necessary).
6. Provide client teaching and discharge planning concerning
1. Nature of disease: CP is a nonfatal, noncurable disorder
2. Need for continued physical, occupational, and speech therapy
3. Care of orthopedic devices
4. Provision for child's return to school
5. Availability of support groups/community agencies.

1. General information
1. Seizures: recurrent sudden changes in consciousness, behavior, sensations, and/or muscular activities beyond voluntary control that are produced by excess neuronal discharge
2. Epilepsy: chronic recurrent seizures
3. Incidence higher in those with family history of idiopathic seizures
4. Cause unknown in 75% of epilepsy cases
5. Seizures may be symptomatic or acquired, caused by
1. Structural or space-occupying lesion (tumors, subdural hematomas)
2. Metabolic abnormalities (hypoglycemia, hypocalcemia, hyponatremia)
3. Infection (meningitis, encephalitis)
4. Encephalopathy (lead poisoning, pertussis, Reye's syndrome)
5. Degenerative diseases (Tay-Sachs)
6. Congenital CNS defects (hydrocephalus)
7. Vascular problems (intracranial hemorrhage)
6. Pathophysiology
1. Normally neurons send out messages in electrical impulses periodically, and the firing of individual neurons is regulated by an inhibitory feedback loop mechanism
2. With seizures, many more neurons than normal fire in a synchronous fashion in a particular area of the brain; the energy generated overcomes the inhibitory feedback mechanism
7. Classification (see Table 5.3 below)
1. Generalized: initial onset in both hemispheres, usually involves loss of consciousness and bilateral motor activity
2. Partial: begins in focal area of brain and symptoms are appropriate to a dysfunction of that area; may progress into a generalized seizure, further subdivided into simple partial or complex partial
2. Medical management
1. Drug therapy (refer to Anticonvulsants, in Unit 2)
1. Phenytoin (Dilantin)
1. often used with phenobarbital for its potentiating effect
2. inhibits spread of electrical discharge
3. side effects include gum hyperplasia, hirsutism, ataxia, gastric distress, nystagmus, anemia, sedation
2. Phenobarbital: elevates the seizure threshold and inhibits the spread of electrical discharge
2. Surgery: to remove the tumor, hematoma, or epileptic focus
3. Assessment findings
1. Clinical picture varies with type of seizure (see Table 5.3 below)
2. Diagnostic tests
1. Blood studies to rule out lead poisoning, hypoglycemia, infection, or electrolyte imbalances
2. Lumbar puncture to rule out infection or trauma
3. Skull x-rays, CT scan, or ultrasound of the head, brain scan, arteriogram, or pneumoencephalogram to detect any pathologic defects
4. EEG may detect abnormal wave patterns characteristic of different types of seizures
1. child may be awake or asleep; sedation is ordered and child may be sleep deprived the night before the test
2. evocative stimulation: flashing strobe light, clicking sounds, hyperventilation
4. Nursing interventions
1. During seizure activity
1. Protect from injury.
1. prevent falling, gently support head.
2. decrease external stimuli; do not restrain.
3. do not use tongue blades (they add additional stimuli).
4. loosen tight clothing.
2. Keep airway open.
1. place in side-lying position.
2. suction excess mucous.
3. Observe and record seizure.
1. note any preictal aura.
1. affective signs: fear, anxiety
2. psychosensory signs: hallucinations
3. cognitive signs: "déjà-vu" symptoms
2. note nature of the ictal phase.
1. symmetry of movement
2. response to stimuli; LOC
3. respiratory pattern
3. note postictal response: amount of time it takes child to orient to time and place; sleepiness.
2. Provide client teaching and discharge planning concerning
1. Care during a seizure
2. Need to continue drug therapy
3. Safety precautions/activity limitations
4. Need to wear Medic-Alert identification bracelet or carry identification card
5. Potential behavioral changes and school problems
6. Availability of support groups/community agencies
7. How to assist the child in explaining disorder to peers

TABLE 5.3 Types of Seizures

Type of Seizure	Clinical Findings
Generalized seizures
Major motor seizure (grand mal)	May be preceded by aura; tonic and clonic phases. Tonic phase: limbs contract or stiffen; pupils dilate and eyes roll up and to one side; glottis closes, causing noise on exhalation; may be incontinent; occurs at same time as loss of consciousness; lasts 20–40 seconds. Clonic phase: repetitive movements, increased mucus production; slowly tapers. Seizure ends with postictal period of confusion, drowsiness.
Absence seizure (petit mal)	Usually nonorganic brain damage present; must be differentiated from daydreaming. Sudden onset, with twitching or rolling of eyes; lasts a few seconds.
Myoclonic seizure	Associated with brain damage, may be precipitated by tactile or visual sensations. May be generalized or local. Brief flexor muscle spasm; may have arm extension, trunk flexion. Single group of muscles affected; involuntary muscle contractions; myoclonic jerks.
Akinetic seizure (tonic)	Related to organic brain damage. Sudden brief loss of postural tone, and temporary loss of consciousness.
Febrile seizure	Common in 5% of population under 5, familial, nonprogressive; does not generally result in brain damage. Seizure occurs only when fever is rising. EEG is normal 2 weeks after seizure.
Partial seizures
Psychomotor seizure	May follow trauma, hypoxia, drug use. Purposeful but inappropriate, repetitive motor acts. Aura present; dreamlike state.
Simple partial seizure	Seizure confined to one hemisphere of brain. No loss of consciousness. May be motor, sensory, or autonomic symptoms.
Complex partial seizure	Begins in focal area but spreads to both hemispheres. Impares consciousness. May be preceded by aura.
Status epilepticus	Usually refers to generalized grand mal seizures. Seizure is prolonged (or there are repeated seizures without regaining consciousness) and unresponsive to treatment. Can result in decreased oxygen supply and possible cardiac arrest.

1. General information
1. An acute encephalopathy with fatty degeneration of the liver
2. Reye's syndrome is a true pediatric emergency: cerebral complication may reach an irreversible state
3. Increased ICP secondary to cerebral edema is major factor contributing to morbidity and mortality
4. Early recognition and prompt management reducing mortality
5. Etiology unknown
2. Medical management
1. Proper initial staging essential.
2. Treatment is supportive, based on stage of coma and level of blood ammonia.
3. Treatment should take place in a pediatric intensive care unit.
3. Assessment findings
1. Child appears to be recovering from a viral illness, such as influenza or chickenpox, during which salicylates have been administered; symptoms then appear that follow a definite pattern, which has led to clinical staging.
1. Stage I: sudden onset of persistent vomiting, fatigue, listlessness
2. Stage II: personality and behavior changes, disorientation, confusion, hyperreflexia
3. Stage III: coma, decorticate posturing
4. Stage IV: deeper coma, decerebrate rigidity
5. Stage V: seizures, absent deep tendon reflexes, respiratory reflexes, flaccid paralysis
2. Pathophysiologic changes include
1. Increased free fatty acid level
2. Hyperammonemia due to reduction of enzyme that converts ammonia to urea
3. Impaired liver function
4. Structural changes of mitochondria in muscle and brain tissue
5. Significant swelling of the brain
4. Nursing interventions (depend on stage)
1. Stage I: assess hydration status: monitor skin turgor, mucous membranes, I&O, urine specific gravity; maintain IV therapy.
2. Stages I-V: assess neurologic status: monitor LOC, pupils, motor coordination, extremity movement, orientation, posturing, seizure activity.
3. Stages II-V
1. Assess respiratory status: note changing rate and pattern, presence of circumoral cyanosis, restlessness, agitation.
2. Assess circulatory status: frequent vital signs, note neck vein distension, skin color and temperature, abnormal heart sounds.
3. Support child/family.
1. explain all treatments and procedures.
2. incorporate family members in treatment as applicable.
3. organize regular family and client-care conferences.
4. use support services as needed.
4. Provide additional parental and community education to ensure early recognition and treatment.

1. General information
1. Failure of posterior vertebral arches to fuse during embryologic development
2. Incidence: 2 in 1,000 infants in the U.S.
3. Although actual cause is unknown, frequency of the defect is increased if a sibling has had a neural tube defect; radiation, viral, and environmental factors have been suggested as causative.
4. Site of the defect varies
1. Approximately 85% of the defects in the spine involve the lower thoracic lumbar or sacral area.
2. Defects in the upper thoracic and cervical regions make up the remaining 15%.
2. Types
1. Spina bifida occulta
1. Spinal cord and meninges remain in the normal anatomic position.
2. Defect may not be visible, or may be identified by a dimple or a tuft of hair on the spine.
3. Child is asymptomatic or may have slight neuromuscular deficit.
4. No treatment needed if asymptomatic; otherwise treatment aimed at specific symptoms.
2. Spina bifida cystica
1. Meningocele
1. sac (meninges) filled with spinal fluid protrudes through opening in spinal canal; sac is covered with thin skin
2. no nerves in sac
3. no motor or sensory loss
4. good prognosis after surgery
2. Myelomeningocele/meningomyelocele
1. same as meningocele except there are spinal nerves in the sac (herniation of dura and meninges).
2. child will have sensory/motor deficit below site of the lesion.
3. 80% of these children have multiple handicaps.
3. Medical management
1. Surgery
1. Closure of the sac within 48 hours of birth to prevent infection and preserve neural tissue
2. Shunt procedure if accompanying hydrocephalus
3. Orthopedic procedures to correct defects of hips, knees, or feet
2. Drug therapy
1. Antibiotics for prevention of infections.
2. Anticholinergic drugs to increase bladder capacity and lower intravesicular pressure.
3. Immobilization (casts, braces, traction) for defects of the hips, knees, or feet
4. Assessment findings
1. Examine the defect for size, level, tissue covering, and CSF leakage.
2. Motor/sensory involvement may include
1. Voluntary movement of lower extremities
2. Withdrawal of lower extremities or crying after pinprick
3. Paralysis of lower extremities
4. Joint deformities
5. Hydrocephalus
6. Evaluate bowel and bladder function. Neurogenic bowel and bladder occur in up to 90% of the children.
3. Diagnostic tests
1. Prenatal
1. ultrasound image of the pregnant uterus shows fetal spinal defect and sac
2. amniocentesis: increased alphafetoprotein (AFP) level prior to 18th week of gestation
2. Postpartal
1. x-ray of spine shows vertebral defect; CT scan of skull may show hydrocephalus
2. myelogram shows extent of neural defect
3. encephalogram may show hydrocephalus
4. urinalysis, culture and sensitivity (C&S) may identify organism and indicate appropriate antibacterial therapy
5. BUN may be increased
6. creatinine clearance rate may be decreased
5. Nursing interventions
1. Prevent trauma to the sac.
1. Cover with sterile dressing soaked with normal saline.
2. Position infant prone or side-lying.
3. Keep the area free from contamination by urine or feces. A protective barrier drape may be necessary.
4. Inspect the sac for intactness or signs of infection.
5. Administer antibiotics as ordered.
2. Prevent complications.
1. Observe for signs of hydrocephalus, meningitis, joint deformities.
2. Clean intermittent urinary catheterization to manage neurogenic bladder.
3. Administer medications to prevent urinary complications as ordered.
4. Perform passive ROM exercises to lower extremities.
3. Provide adequate nutrition: adapt diet and feeding techniques according to the child's position.
4. Provide sensory stimulation.
1. Adjust objects for visual stimulation according to child's position.
2. Provide stimulation for other senses.
5. Provide emotional support to parents/family.
6. Provide client teaching and discharge planning to parents concerning
1. Wound care
2. Physical therapy, range of motion exercises
3. Signs of complications
4. Medication regimen: schedule, dosage, effects, and side effects
5. Feeding, diapering, positioning
6. Availability of appropriate support groups/community agencies/genetic counseling

1. General information
1. Insertion of a flexible tube into the lateral ventricle of the brain
2. Catheter is then threaded under the skin and the distal end positioned in the peritoneum (most common type) or the right atrium; a subcutaneous pump may be attached to ensure patency
3. Shunt drains excess CSF from the lateral ventricles of the brain in communicating or noncommunicating hydrocephalus; fluid is then absorbed by the peritoneum or enters the general circulation via the right atrium
2. Nursing interventions
1. Provide routine pre-op care with special attention to monitoring neurologic status.
2. Provide post-op care.
1. Maintain patency of the shunt.
1. position child off the operative site.
2. pump the shunt as ordered.
3. observe for signs of infection of the incision.
4. observe for signs of increased ICP.
5. position the child with head slightly elevated or as ordered.
3. Instruct parents regarding
1. Wound care, positioning of infant, and how to pump the shunt
2. Signs of infection
3. Signs of increased ICP
4. Need for repeated shunt revisions as child grows or if shunt becomes blocked or infected
5. Expected level of developmental functioning
6. Availability of support groups and community agencies

1. General information
1. Increased amount of CSF within the ventricles of the brain
2. May be caused by obstruction of CSF flow or by overproduction or inadequate reabsorption of CSF
3. May result from congenital malformation or be secondary to injury, infection, or tumor
4. Classification
1. Noncommunicating: flow of CSF from ventricles to subarachnoid space is obstructed.
2. Communicating: flow is not obstructed, but CSF is inadequately reabsorbed in subarachnoid space.
2. Assessment findings: depend on age at onset, amount of CSF in brain
1. Infant to 2 years: enlarging head size; bulging, nonpulsating fontanels; downward rotation of eyes; separation of cranial sutures; poor feeding, vomiting, lethargy, irritability; high-pitched cry and abnormal muscle tone
2. Older children: changes in head size less common; signs of increased ICP (vomiting, ataxia, headache) common; alteration in consciousness and papilledema late signs
3. Diagnostic tests
1. Serial transilluminations detect increases in light areas
2. CT scan shows dilated ventricles as well as presence of mass; with dye injection shows course of CSF flow
3. Nursing interventions: provide care for the child with increased ICP and for the child undergoing shunt procedures.

1. General information
1. A neuromuscular disorder in which there is a disturbance in the transmission of impulses from nerve to muscle cells at the neuromuscular junction, causing extreme muscle weakness
2. Incidence
1. Highest between ages 15-35 for women, over 40 for men.
2. Affects women more than men
3. Cause: thought to be autoimmune disorder whereby antibodies destroy acetylcholine receptor sites on the postsynaptic membrane of the neuromuscular junction.
4. Voluntary muscles are affected, especially those muscles innervated by the cranial nerves.
2. Medical management
1. Drug therapy
1. Anticholinesterase drugs: ambenonium (Mytelase), neostigmine (Prostigmin), pyridostigmine (Mestinon)
1. block action of cholinesterase and increase levels of acetylcholine at the neuromuscular junction
2. side effects: excessive salivation and sweating, abdominal cramps, nausea and vomiting, diarrhea, fasciculations (muscle twitching)
2. Corticosteroids: prednisone
1. used if other drugs are not effective
2. suppress autoimmune response
2. Surgery (thymectomy)
1. Surgical removal of the thymus gland (thought to be involved in the production of acetylcholine receptor antibodies)
2. May cause remission in some clients especially if performed early in the disease
3. Plasma exchange
1. Removes circulating acetylcholine receptor antibodies
2. Use in clients who do not respond to other types of therapy
3. Assessment findings
1. Diplopia, dysphagia
2. Extreme muscle weakness, increased with activity and reduced with rest
3. Ptosis, masklike facial expression
4. Weak voice, hoarseness
5. Diagnostic tests
1. Tensilon test: IV injection of Tensilon provides spontaneous relief of symptoms (lasts 5-10 minutes)
2. Electromyography (EMG): amplitude of evoked potentials decreases rapidly
3. Presence of antiacetylcholine receptor antibodies in the serum
4. Nursing interventions
1. Administer anticholinesterase drugs as ordered.
1. Give medication exactly on time.
2. Give with milk and crackers to decrease GI upset.
3. Monitor effectiveness of drugs: assess muscle strength and vital capacity before and after medication.
4. Avoid use of the following drugs: morphine and strong sedatives (respiratory depressant effect), quinine, curare, procainamide, neomycin, streptomycin, kanamycin and other aminoglycosides (skeletal muscle blocking effects).
5. Observe for side effects.
2. Promote optimal nutrition.
1. Mealtimes should coincide with the peak effects of the drugs: give medications 30 minutes before meals.
2. Check gag reflex and swallowing ability before feeding.
3. Provide a mechanical soft diet.
4. If the client has difficulty chewing and swallowing, do not leave alone at mealtimes; keep emergency airway and suction equipment nearby.
3. Monitor respiratory status frequently: rate, depth; vital capacity; ability to deep breathe and cough
4. Assess muscle strength frequently; plan activity to take advantage of energy peaks and provide frequent rest periods.
5. Observe for signs of myasthenic or cholinergic crisis.
1. Myasthenic crisis
1. abrupt onset of severe, generalized muscle weakness with inability to swallow, speak, or maintain respirations
2. caused by undermedication, physical or emotional stress, infection
3. symptoms will improve temporarily with Tensilon test.
2. Cholinergic crisis
1. symptoms similar to myasthenic crisis and, in addition, the side effects of anticholinesterase drugs (e.g., excessive salivation and sweating, abdominal cramps, nausea and vomiting, diarrhea, fasciculations)
2. caused by overmedication with the cholinergic (anticholinesterase) drugs
3. symptoms worsen with Tensilon test; keep atropine sulfate and emergency equipment on hand.
3. Nursing care in crisis
1. maintain tracheostomy or endotracheal tube with mechanical ventilation as indicated (see Mechanical Ventilation).
2. monitor arterial blood gases and vital capacities.
3. administer medications as ordered.
1. myasthenic crisis: increase doses of anticholinesterase drugs as ordered.
2. cholinergic crisis: discontinue anticholinesterase drugs as ordered until the client recovers.
4. establish a method of communication.
5. provide support and reassurance.
6. Provide nursing care for the client with a thymectomy.
7. Provide client teaching and discharge planning concerning
1. Nature of the disease
2. Use of prescribed medications, their side effects and signs of toxicity
3. Importance of checking with physician before taking any new medications including OTC drugs
4. Importance of planning activities to take advantage of energy peaks and of scheduling frequent rest periods
5. Need to avoid fatigue, stress, people with upper-respiratory infections
6. Use of eye patch for diplopia (alternate eyes)
7. Need to wear Medic-Alert bracelet
8. Myasthenia Gravis Foundation and other community agencies

1. General information
1. Chronic, intermittently progressive disease of the CNS, characterized by scattered patches of demyelination within the brain and spinal cord
2. Incidence
1. Affects women more than men
2. Usually occurs from 20-40 years of age
3. More frequent in cool or temperate climates
3. Cause unknown; may be a slow-growing virus or possibly of autoimmune origin
4. Signs and symptoms are varied and multiple, reflecting the location of demyelination within the CNS
5. Characterized by remissions and exacerbations
2. Assessment findings
1. Visual disturbances: blurred vision, scotomas (blind spots), diplopia
2. Impaired sensation: touch, pain, temperature, or position sense; paresthesias such as numbness, tingling
3. Euphoria or mood swings
4. Impaired motor function: weakness, paralysis, spasticity
5. Impaired cerebellar function: scanning speech, ataxic gait, nystagmus, dysarthria, intention tremor
6. Bladder: retention or incontinence
7. Constipation
8. Sexual impotence in the male
9. Diagnostic tests:
1. CSF studies: increased protein and IgG (immunoglobulin)
2. Visual evoked response (VER) determined by EEG: may be delayed
3. CT scan: increased density of white matter
4. MRI: shows areas of demyelination
3. Nursing interventions
1. Assess the client for specific deficits related to location of demyelinization.
2. Promote optimum mobility.
1. Muscle-stretching and strengthening exercises
2. Walking exercises to improve gait: use wide-based gait
3. Assistive devices: canes, walker, rails, wheelchair as necessary
3. Administer medications as ordered.
1. For acute exacerbations: corticosteroids (ACTH [IV], prednisone) to reduce edema at sites of demyelinization
2. For spasticity: baclofen (Lioresal), dantrolene (Dantrium), diazepam (Valium)
3. Beta interferon (Betaseron) to alter immune response
4. Encourage independence in self-care activities.
5. Prevent complications of immobility.
6. Institute bowel program.
7. Maintain urinary elimination.
1. Urinary retention
1. administer bethanecol chloride (Urecholine) as ordered.
2. perform intermittent catheterization as ordered.
2. Urinary incontinence
1. establish voiding schedule.
2. administer propantheline bromide (Pro-Banthine) if ordered.
3. Force fluids to 3000 ml/day.
4. Promote use of acid-ash foods like cranberry or grape juice (see Bladder Surgery).
8. Prevent injury related to sensory problems.
1. Test bath water with thermometer.
2. Avoid heating pads, hot-water bottles.
3. Inspect body parts frequently for injury.
4. Make frequent position changes.
9. Prepare client for plasma exchange (to remove antibodies) if indicated.
10. Provide psychologic support to client/significant others.
1. Encourage positive attitude and assist client in setting realistic goals.
2. Provide compassion in helping client adapt to changes in body image and self-concept.
3. Do not encourage false hopes during remission.
4. Refer to multiple sclerosis societies and community agencies.
11. Provide client teaching and discharge planning concerning
1. General measures to ensure optimum health
1. balance between activity and rest
2. regular exercise such as walking, swimming, biking in mild cases
3. use of energy conservation techniques
4. well-balanced diet
5. fresh air and sunshine
6. avoiding fatigue, overheating or chilling, stress, infection
2. Use of medications and side effects
3. Alternative methods for sexual gratification; refer for sexual counseling if indicated.