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Nursing Management CHRONIC NEUROLOGIC PROBLEMS

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Title: Nursing Management CHRONIC NEUROLOGIC PROBLEMS


1
Nursing ManagementCHRONIC NEUROLOGIC PROBLEMS
2
Compare and contrast tension-type, migraine, and
cluster headaches in terms of etiology, clinical
manifestations, and collaborative care and
nursing management
  • Tension-type
  • Etiology
  • ? pain sensitivity
  • Muscle factors
  • Clinical manifestations
  • No prodrome
  • Pain bilateral---tight squeezing head band
  • Does not interfere with sleep
  • Management
  • Non-narcotic analgesic, muscle relaxant,
    tricyclic antidepressant
  • Patient education

3
  • Migraine
  • Etiology
  • ? Inflammation and dilation of intracranial blood
    vessels
  • Clinical manifestations
  • Two types
  • Migraine without aura
  • Migraine with aura
  • Pain
  • Steady, throbbing and synchronous with pulse
  • Unilateral
  • Accompanied by N V, irritability, pallor,
    desire to hibernate
  • Management
  • Prevention
  • Beta-blockers, (propranolol Inderal)
  • Abortive
  • Aspirin-like drugs
  • Metoclopromide (Reglan)

4
  • ergotamine
  • Promotes vasoconstriction and ? amplitude of
    pulsations
  • Adm.---sublingual, inhalation, PO, rectal
  • Side effects---NV, weakness in legs, numbness
    and tingling, can cause physical dependance
  • Contraindications---concurrent use of selective
    serotonin receptor agonists, hepatic or renal
    impairment, sepsis, CAD, PVD ---Preg X
  • dihydroergotamine
  • Similar to above with SQ, IM, IV or nasal adm.
  • Selective Serotonin Receptor Agonists
    (Triptans)
  • somatriptan(Imitrex)
  • Adm.---PO, inhalation, SQ
  • Selectively binds to intracranial blood
    vessels to cause vasoconstriction and to the
    trigeminal nerve to ? inflammatory peptides
  • Side effects---well tolerated, avoid with
    pregnancy and CAD, client may experience heavy
    arms and chest pressure

5
  • Cluster
  • Etiology
  • Trigeminal nerve activation causes vasodilation,
    stimulation of pain fibers and neurogenic
    inflammatory reaction
  • May be triggered by alcohol ingestion
  • Clinical Manifestations
  • A cluster of attacks lasting from 15min to 2
    hours over a period of 4-12 weeks --- may have
    remission of weeks to years
  • Nonthrobbing, unilateral, usually in or around
    the eye
  • Conjunctival injection, lacrimation, nasal
    congestion, rhinorrhea, miosis, ptosis
  • Associated with pacing and crying out
  • Deep steady, penetrating but not throbbing
  • Management
  • Prophylaxis
  • Verapamil
  • Abortive
  • Sumatriptan or ergot preparation
  • 100 O2
  • Analgesic rebound HA
  • 15 days/month

6
  • Collaborative Care
  • R/O organic HA caused by significant intracranial
    or extracranial disease
  • HX
  • Ominous signs of HA
  • Abnormal physical signs
  • Papilledema, widening pulse pressure, nuchal
    rigidity, fever
  • New-onset, unilateral, particularly in pts. gt 35
    yoa
  • Severe HA or different from previous ones
  • worst HA of my life
  • Is becoming more continuous or intense
  • HA accompanied by vomiting but not nausea
  • PE
  • Diagnostic Studies
  • CT or MRI to rule out aneurysm, tumor or infection

7
  • Nursing Management Nursing Care Plan 57-1
  • Pain
  • Anxiety
  • Hopelessness
  • Sleep pattern disturbance

8
Describe the etiology, clinical manifestations,
diagnostic studies, and collaborative management
of epilepsy, multiple sclerosis, Parkinsons
disease, and myasthenia gravis
  • Epilepsy
  • EtiologySpontaneous firing of abnormal neurons
    that may spread throughout the brain (idiopathic)
  • Clinical manifestations
  • Generalized Seizures
  • Tonic-clonic---loss of consciousness, stiffening
    (tonic) and jerking(clonic) movements, cyanosis,
    salivation, tongue biting, incontinence,
    postictal phase with no memory of seizure
  • Typical absence---(petit mal) only in children,
    brief staring spell
  • Atypical absence---staring spell accompanied by
    other signs, peculiar behavior and confusion
    afterwards
  • Partial Seizures
  • Simple --- no LOC
  • Complex --- complex symptoms and postictal
    confusion

9
  • Diagnostic studies
  • EEG (often not definitive)
  • R/O organic pathology
  • Blood work, UA, MRI or CT (new onset), LP
  • Collaborative Care (Table 57-7)
  • Acute intervention
  • Emergency management (Table 57-8)
  • Observation
  • Complications
  • Status epilepticus
  • Injury from trauma

10
  • Psychosocial
  • Patient and Family Teaching
  • Drug therapy
  • Phenytoin (Dilantin)
  • Carbamazepine (Tegretol)
  • Phenobarbitol
  • Divalproex (Depakote)
  • Table 57-12

11
  • Multiple Sclerosis
  • Etiology
  • Loss of myelin and proliferation of astrocytes ?
    plaque formation (sclerosis) throughout the CNS
  • Early in the process myelin is damaged but
    replaces itself ? remission
  • Progression ? total myelin disruption with axon
    involvement and permanent loss of nerve function

12
  • Clinical Manifestations
  • Insidious onset/vague symptoms between 15 and 50
    YOA
  • More prevalent in temperate climated
  • Chronic, progressive / remissions and
    exacerbations Table 57-13
  • Relapsing-remitting MS
  • Primary-progressive MS
  • Secondary-progressive MS
  • Progressive-relapsing MS
  • Signs/symptoms
  • Weakness or paralysis of limbs, trunk, head,
    diplopia, muscle spasticity, numbness tingling,
    patchey blindness (scotomas), blurred vision,
    vertigo, tinnitus, nystagmus, dysarthria
  • Bowel and bladder symptoms vary
  • Sexual dysfunction

13
  • Collaborative Management
  • Diagnosis
  • No definitive test for MS
  • HX and clinical manifestations
  • MRI
  • Sclerotic plaques 3-4 mm
  • Characteristic white-matter lesions scattered
    throughout the brain and spinal cord
  • Drug therapy
  • ACTH and prednisone
  • Antiinflammatory during acute exacerbations
  • Immunosuppressive drugs

14
  • Immunomodulators --- control disease, decrease
    new lesions and remissions
  • Beta-interferon (Betaseron)
  • Interferon-B1a (Avonex)
  • Anticholinergics may help with urinary
    urgency/frequency
  • Muscle Relaxants
  • Baclofen(Lioresal)
  • Nursing management 57-3 NCP
  • Impaired physical mobility
  • Self-care deficits
  • Risk for impaired skin integrity
  • Sensory-perceptual alterations
  • Altered urinary elimination
  • Constipation
  • Sexual dysfunction
  • Self-esteem disturbance
  • Altered family processes

15
  • Parkinsons Disease
  • A syndrome characterized by slowing in initiation
    and execution of movement (bradykinesia),
    increased muscle tone (rigidity), tremor, and
    impaired postural reflexes
  • Etiology
  • Unknown
  • Pathophysiology
  • Degeneration of dopamine-producing neurons in the
    substantia nigra of the midbrain causing an
    imbalance between the neurotransmitters
    acetylcholine and dopamine
  • Clinical manifestations
  • Gradual and insidious
  • Tremor at rest, limp, ? arm movement
  • Shuffling-propulsive gait, flexed arms and loss
    of postural reflexes, speech changes

16
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17
  • Complications
  • Loss of spontaneous movement
  • Swallowing (dysphagia) ? malnutrition, aspiration
  • General lack of movement ? pneumonia, UTIs, skin
    breakdown
  • Orthostatic hypotension
  • Seborrhea
  • Collaborative Care
  • Drug therapy (Table 57-18)
  • Dopaminergic
  • Levodopa with carbidopa (Sinemet) (converted to
    dopamine in the basal ganglia)
  • Dopamine agonists
  • Bromocriptine (Parlodel), pergolide (Permax)

18
  • Anticholinergic drugs
  • Trihexiphenidyl (Artane), benztropin (Cogentin),)
  • Antihistamines with anticholinergic properties
  • Dephenhydramine (Benadryl)
  • Antiviral
  • Amantadine (Symmetrel)
  • MAO inhibitor
  • selegiline (Eldepryl)
  • Surgical Therapy
  • Nutritional Therapy

19
  • Nursing Management (NCP 57-4)
  • Impaired physical mobility
  • Self Care deficits
  • Impaired verbal communication
  • Constipation
  • Altered nutrition
  • Diversional activity deficit
  • Sleep pattern disturbance

20
  • Myasthenia Gravis
  • Disease of the neuromuscular junction
    characterized by fluctuating weakness of certain
    skeletal muscle groups
  • Etiology
  • Autoimmune process that results in production of
    antibodies directed against ACh receptors and a
    reduction in the number of ACh receptor sites at
    the neuromuscular junction ? ACh molecules are
    unable to affect muscle contraction (loss of
    muscle strength)
  • Thymic tumors are found in 15 of patients

21
  • Clinical manifestations
  • Easy fatigability of skeletal muscles during
    activity
  • Muscles most often involved
  • Eyelids, chewing, swallowing, speaking, breathing
  • Complications
  • Aspiration and difficulty breathing (myasthenic
    crisis)
  • Collaborative Management
  • Diagnostic Studies
  • Have the person look upward for 2-3 minutes
  • Tensilon Test
  • Improved muscle strength after IV
    anticholinesterase agent Tensilon
    (diagnostic)---Atropine should be readily
    available to counteract the effects of Tensilon
    if needed

22
  • Drug therapy
  • Anticholinesterase drugs
  • Neostigmine (Prostigmin)
  • Pyridostigmine (Mestinon)
  • Corticosteroids
  • Prednisone
  • Many drugs must be used with caution in patients
    with MG
  • Surgical therapy
  • Removal of thymus gland
  • Others
  • plasmapheresis

23
  • Nursing Management
  • Ineffective breathing pattern related to
    intercostal weakness
  • Ineffective airway clearance
  • Impaired verbal communication
  • Altered nutrition
  • Sensory/perceptual alterations related to ptosis,
  • ? eye movements,
  • Activity intolerance
  • Body image disturbance

24
Describe the clinical manifestations and
collaborative care of amyotrophic lateral
sclerosis and Huntingtons chorea
  • Amyotrophic lateral sclerosis
  • Progressive loss of motor neurons with weakness
    of upper extremities, dysartheria, dysphagia,
    muscle wasting and death from respiratory
    infection 2-5 years after diagnosis
  • Care is to support the pts cognitive and
    emotional functions by facilitating
    communication, providing diversional therapies,
    and helping the family with planning and
    anticipatory grieving
  • Huntingtons disease
  • Genetically transmitted autosomal dominant
    disorder that affects both men and women with off
    spring having a 50 risk of inheriting the
    disease
  • Excess dopamine that leads to symptoms opposite
    from Parkinsons Disease
  • Onset around 35-45 years --- excessive
    involuntary movements (chorea)
  • Death occurs 10-20 years after onset of symptoms
  • Care is palliative
  • Drug therapy
  • Safety
  • Nutrition

25
Explain the potential impact of chronic
neurologic disease on physical and psychologic
well-being
26
Outline the major goals of treatment for the
patient with a chronic, progressive neurologic
disease
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