Neuro Stressors 3 Student

7/27/2019 Neuro Stressors 3 Student

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Neurological Stressors III

Chronic Neurological DisordersJoy Borrero, RN, MSN

AndNUR240 Nursing Students

12/11


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Topics

Multiple Sclerosis Amyotropic Lateral Sclerosis (ALS)

Parkinsons Disease Myasthenia Gravis Guillain-Barre Syndrome

Huntingtons Disease


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Chronic Neuromuscular Dysfunction

Some commonalities in adaptations are: Altered motor activity Altered coordination Altered sensory function Altered urinary/bowel patterns Altered role/self perception Altered speech/swallowing

Impaired physical mobility Risk for injury Nutrition less than body requirements Risk for aspiration


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Multiple Sclerosis (MS)

Etiology:Types:S&S:

Dx:Triggers:Tx:
http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/


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Multiple Sclerosis

Chronic autoimmune disease affecting the myelinsheath and conduction pathway of the CNS

Characterized by periods of remission and

exacerbation Inflammatory response resulting in random or patchy areas of plaque in the white matter of theCNS

Demyelination of brain and spinal cord, affectsconduction pathway of CNS Two major courses: relapsing and remitting, and

chronic and progressive


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Multiple Sclerosis (MS)

Exact cause unknown, may be defective immuneresponse, early viral infection.

More common in people living in northern

temperate climate. Affects twice as many women than men. Typically occurs between ages 20-40 Family hx of MS in 15% of cases No cure for the disease Dx- McDonald criteria http://www.nmss.org/
http://www.nmss.org/http://www.nmss.org/


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MSPrimary Symptoms: Fatigue, weakness, numbness Difficulty in coordination, loss of balance Visual disturbances: blurring, diplopia, patchy or total

blindness, change in peripheral vision, nystagmus Speech defects Dysarthria, dysphagia Spastic weakness, ataxia, tremors, dysmetria Emotional lability, depression/euphoria. Bladder/bowel dysfunction Tinnitus, vertigo, decreasing hearing acuity Cognitive changes-memory loss, impaired judgement


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MS

Secondary symptoms-Problems/complications that occur a/r/oprimary symptoms

Repeated UTIs Loss of muscle tone and disuse weakness Poor posture and control of torso

Decreased bone density Shallow inefficient breathing Pressure ulcers from immobility


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PharmacologyBiological response modifiers- InteferonMonoclonal antibody- NatalizumabSynthetic protein-Glatiramer acetate

Immunosuppressives-CyclosporineCorticosteroids-PrednisoneAntispasmodic drugs-Dantrolene, BaclofenAnticonvulsants-Dilantin

Stool softeners-ColaceAnticholinergics-ProbanthineBeta-blockers- Inderal (tremors)CAM Therapy


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Biological Response Modifiers

Interferon Betaseron- blocks replicationof viruses and stimulates hostimmunoregulatory activities.

Reduce frequency of exacerbations Dose 0.25 mg sc every other day. Adverse effects: Dizziness, confusion,

anorexia, hypotension, leukopenia, flu likesymptoms, depression,suicidal ideation Thrombocytopenia


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Amytropic Lateral Sclerosis ALS

Etiology:Types:S&S:

Dx:Triggers:Tx:


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Amyotrophic Lateral Sclerosis(ALS)

Deteriorating disease of motor neurons inanterior horn of spinal cord and motor nuclei of lower brain stem

AKA Lou Gehrigs disease Etiology unknown. More common men 50-60. Manifestations: Depends on location of affected

motor neurons, atrophy and twitching. Death occurs within 2-5 years after onset of

symptoms.


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Diagnostic Procedures

Creatine kinase (CK)- increased Electromyography (EMG)- Muscle

fasciculations

http://www.youtube.com/watch?v=k0uSpYd_Ics

Muscle biopsy- Muscle atrophy

Serial muscle testing- Loss of musclestrength Pulmonary function tests
http://www.youtube.com/watch?v=k0uSpYd_Icshttp://www.youtube.com/watch?v=k0uSpYd_Icshttp://www.youtube.com/watch?v=k0uSpYd_Icshttp://www.youtube.com/watch?v=k0uSpYd_Ics


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Assessments & Interventions

Assess airway, resp status Assess speech patterns, skin integrity

No known cure, no treatment, nopreventive measures Riluzole, only drug approved by FDA to

extend survival time Exercise and mobility program Management of swallowing difficulties


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Interventions

Teach swallowing technique Maintain resp. function- assess lung

sounds,suction prn, C&DB Administer Quinine for muscle cramps Antispasmotics: baclofen, dantrolene, diazepam

www.als.org for pt/family support and education
http://www.als.org/http://www.als.org/


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Parkinsons Disease

Etiology:Types:S&S:

Dx:Triggers:Tx:


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Parkinsons disease Cause unknown-progressively debilitating disease

that affects gross motor function.Degeneration of the nerves that control voluntary

movement.Occurs in the part of the brain called the substantia

nigraNeurons here communicate with other neurons in the

brain using a neurotransmitter called dopamine.

When these neurons that make dopamine die,signaling between neurons is severely hampered,causing a loss of controlled movement

Risk factors

Dx Procedures


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Manifestations

Manifestations: Stooped posture, postural instability , head

bent forward Tremors of head and hand, pill rolling Akinesia , Bradykinesia Rigid stance, shuffling and propulsive gait

Mask like facial expression


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Parkinsons disease

Impaired physical mobility r/t musclerigidity and weakness.

Self care deficit r/t to tremor and motor disturbance.

Risk for falls Risk for imbalanced nutrition: Less than

body requirements, r/t tremor, slowness ineating, difficulty in chewing andswallowing.


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Drug Therapy for Parkinsons Goal: Increase patients functional abilities

PDMeds

Levodopa

COMTInhibitors

MAOI:

Eledepryl

Amantadine:Symmetrel

Dopamine Agonists:

Mirapex

Anticholinergics:

Cogentin


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Parkinsons disease

levodopa (Dopar, Laradopa)- antiparkinsonagent, precursor of dopamine that cancross the blood brain barrier, then istransformed to dopamine.

levodopa and carbidopa ( Sinemet )- GOLDSTANDARD, antiparkinsonian combo med-dosage is adjusted to patients symptoms

Adverse effects involuntary movements,ataxia, increased tremor, anorexia


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Parkinsons disease

Amantadine hydrochloride (Symmetrel) Antiviral and Antiparkinsonian Therapeutic actions thought to increase

dopamine release, helpful in treatingbradykinesia, rigidity and tremor.

Dose 100 mg po bid (up to 400 mg)

Adverse- dizziness, insomnia, dry mouth,confusion, constipation, urinary retention,orthostatic hypotension.


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Parkinsons Disease

Complications: Aspiration pneumonia Altered cognition, dementia

Additional therapeutic options:ThalamotomyStereotactic PallidotomyDeep Brain Stimulation

http://www.parkinsons.org
http://www.parkinsons.org/http://www.parkinsons.org/http://www.parkinsons.org/


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Myasthenia Gravis

Etiology:Types:S&S:

Dx:Triggers:Tx:


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Myasthenia Gravis

Progressive autoimmune disease resulting insevere muscle weakness.Women 15-35 or men over 40.

Exacerbations and remissionsManifestations:Extreme muscle weakness and fatiguability.Diplopia and ptosis are early signsSleepy, mask like expression, dysphonia.Problems chewing and swallowing aspirationProgressive weakness of diaphragm- resp. distress.


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Myasthenia Gravis

Diagnostic tests pt. history and exam,Tensilon testing

IV tensilon relieves symptoms within 30seconds. Positive result.

AChR-Acetylcholine receptor antibodiesfound serum of 90%.

EMG- shows neuromuscular transmissioncharacteristics.


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Therapeutic Procedures

Plasmapheresis Thymectomy

http://www.myasthenia.org
http://www.myasthenia.org/http://www.myasthenia.org/


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Medications

Anticholinesterase meds- pyridostigmine(Mestinon) and ambenonium (Mytelase)

Administer with small amount of food toavoid GI upset and eat within 45 minutes.

Must be administerd on time and sametime each day.

Potential SE is cholinergic crisisCotricosteroidsImmunosuppressants


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ComplicationsMyasthenic Crisis

Undermedication

Cholinergic Crisis

OvermedicationResp muscle weakness-mechanical ventilation

Muscle twitching results inresp muscle weakness, mechventilation

Myasthenic symptoms-weakness,incontinence,fatigue

Cholinergic symptoms-hypersecretions,hypermotility

Hypertension Hypotension

Temp improvement of symptoms with Tensilon

Tensilon has no positive effecton symptomsSymptoms improve with

anticholinergic meds


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Guillain-Barre Syndrome

Etiology:Types:S&S:

Dx:Tx:
http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/


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Guillian Barre Syndrome

Acute inflammatory disease of unknownorigin

Usually preceeded by a viral infection (URIor GI) 1-4 weeks

Degeneration of the myelin sheath of peripheral nerves

Manifestations: paresthesias, ascendingweakness in legs progresses toparalysis,autonomic dysfunction

Diagnosis by H&P, CSF exam.


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Facts

Most people reach the stage of greatestweakness within 2 weeks after symptomsappear, and by the 3 rd week 90% of all

patients are at their weakest. Recovery may be from a few weeks to a

few years

30% will have residual weakness after 3yrs 3% may suffer a relapse


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Huntingtons Disease

Etiology:S&S:Dx:

Tx:
http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/


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MANAGEMENT

Dx: made on basis of symptoms and familyhx

Genetic counseling and testingTx: Haldol and Navane

Riluzole Antidepressants

Documents

Neuro Stressors 3 Student