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1 Jerry Carley RN, MSN, MA, CNE Spring, 2009

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Page 1: 1 Jerry Carley RN, MSN, MA, CNE Spring, 2009.  2

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Jerry Carley RN, MSN, MA, CNESpring, 2009

Page 2: 1 Jerry Carley RN, MSN, MA, CNE Spring, 2009.  2

http://www.youtube.com/watch?v=tzFNTtHyTzo&feature=related

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Page 3: 1 Jerry Carley RN, MSN, MA, CNE Spring, 2009.  2

Concept Map: Selected Topics in Neurological Nursing

PATHOPHYSIOLOGY

Traumatic Brain InjurySpinal Cord Injury

Specific Disease Entities: Amyotropic Lateral Sclerosis Multiple Sclerosis Huntington’s Disease Alzheimer’s Disease Myasthenia Gravis Guillian-Barre’ Syndrome Meningitis Parkinson’s Disease

PHARMACOLOGY

--Decrease ICP--Disease Specific Meds

ASSESSMENTPhysical Assessment Inspection Palpation Percussion Auscultation

ICP Monitoring“Neuro Checks” Lab Monitoring

Care PlanningPlan for client adl’s, Monitoring, med admin.,Patient education, more…basedOn Nursing Process: A_D_P_I_E

Nursing Interventions & EvaluationExecute the care plan, evaluate for Efficacy, revise as necessary

Page 4: 1 Jerry Carley RN, MSN, MA, CNE Spring, 2009.  2

Alzheimer's Disease Non - reversible dementia that

progressively develops through 3 stages over many years

Alzheimer's disease is the most common cause of dementia, or loss of intellectual function, among people aged 65 and older

Alzheimer's disease is NOT a normal part of aging

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Page 5: 1 Jerry Carley RN, MSN, MA, CNE Spring, 2009.  2

Characteristics

Memory loss Impaired Judgment Personality changes Severe physical decline

with cognitive changes

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Pathophysiology Neurons, which produce acetylcholine

(neurotransmitter) break connections with other nerve cells and ultimately die

Two types of abnormal lesions clog

the brains of individuals with Alzheimer's disease:

Beta-amyloid plaques—sticky clumps of protein fragments and cellular material that form outside and around neurons

Neurofibrillary tangles—insoluble twisted fibers composed largely of the protein that build up inside nerve cells

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Stage 1First 1-3 years:

-Short-term memory loss-Subtle personality changes-Shorter attention span-Mild cognitive deficits-Difficulty with money, numbers and bills-Difficulty with depth perception

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Stage 2From 2 – 10 years:

-Obvious memory loss-Wandering-Confabulation-“Sundowning”-Irritability / Agitation-Impaired motor skills,

judgment-Self-care deficits

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Page 9: 1 Jerry Carley RN, MSN, MA, CNE Spring, 2009.  2

Stage 3From 8 – 10 years:

-Severe impairment of all cognitive abilities

-Disoriented-B & B incontinence

-Inability to recognize family & friends

-Loss of speech

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The 4 A’s of Alzheimer'sAmnesia

(inability to remember facts or events). Short-term memory is programmed in temporal lobe, while long-term memory is stored throughout extensive nerve cell networks in the temporal and parietal lobes. In Alzheimer's disease, short-term memory storage is damaged first

Aphasia (inability to communicate effectively). The loss of ability to speak and write is called

expressive aphasia. With receptive aphasia, an individual may be unable to understand spoken or written words. Sometimes an individual pretends to understand and even nods in agreement; this is to cover-up aphasia. Although individuals may not understand words and grammar, they may still understand non-verbal behavior, i.e. smiling

Apraxia (inability) to do pre-programmed motor tasks, or to perform activities of daily living such

as brushing teeth and dressing. Sophisticated motor skills that require extensive learning, such as job-related skills, are first functions that become impaired. More instinctive functions like chewing, swallowing and walking are lost in the last stages of the disease

Agnosia (inability to correctly interpret signals from their five senses). May not recognize familiar

people and objects. A common yet often unrecognized agnosia is the inability to appropriately perceive visceral, or internal, information such as a full bladder or chest pain.

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Diagnosis Clinicians can now diagnose with up to 90 % accuracy.

But it can only be confirmed by an autopsy, pathologists look for the disease's characteristic plaques and tangles in brain tissue

Clinicians diagnose "probable" Alzheimer's disease by

medical history, lab tests, physical exam, brain scans and neuropsychological tests that gauge memory, attention, language skills and problem-solving abilities

Proper diagnosis of Alzheimer's disease is critical since

there are dozens of other reversible causes for Sx’s

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Page 12: 1 Jerry Carley RN, MSN, MA, CNE Spring, 2009.  2

Treatment U.S. Food and Drug Administration (FDA) has

so far approved four drugs for the treatment of mild to moderate Alzheimer's disease:

- Cognex®), introduced in 1993- Donepezil hydrochloride (Aricept®), marketed since 1996- Rivastigmine (Exelon®), available since the spring 2000 -Galantamine hydrobromide (RazadyneTM-formerly called

Reminyl®) approved in Feb/01

These drugs inhibit the enzyme that breaks down the brain chemical acetylcholine, and thereby may help slow the worsening of symptoms

The FDA in October 2003 approved memantine HCI (NamendaTM) for the treatment of moderate to severe Alzheimer's disease, which can slow the decline in mental function

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Page 13: 1 Jerry Carley RN, MSN, MA, CNE Spring, 2009.  2

Risk Factors

People with a family history of Alzheimer's have a greater risk, implying that a genetic factor is involved. Some involve a mutation of the gene for the protein APP, found on chromosome 21

Adults who have had head injuries are three times more likely to develop Alzheimer's disease

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Page 14: 1 Jerry Carley RN, MSN, MA, CNE Spring, 2009.  2

Nursing Care

CONSISTENCY - Introduce change gradually

Use repetition Therapeutic touch if able Avoid overstimulation and

clutter Don’t argue / Don’t reinforce –

Acknowledge feelings / Distract Regular toileting Reality orientation, memory

training Meds as needed

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Safety Precautions Identification (on back of

gown, etc) Alarm systems / Lock exit

doors Keep up to date Picture Frequent supervision No throw rugs Fall Program Etc

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