Neurological Disorders - Valencia



Neurological Disorders

Developed by:

Cathie Hansen RN, MSN.

MULTIPLE SCLEROSIS (MS)

DEFINITION

Remission

Exacerbation

PATHOPHYSIOLOGY

Brain of MS Client

Major types of Multiple Sclerosis

Relapsing-remitting

Progressive-relapsing

Primary progressive

Secondary progressive

DIANGOSTIC PROCEDURES &

LAB ASSESSMENT

CSF Analysis

CT Scan

MRI

EMG

Early - ASSESSMENT FINDINGS

Fatigue

Weakness &/or paresthesia

Total or partial loss of vision in 1 eye

Unsteady gait

Muscle spasticity

Diplopia

Dizziness

Early - ASSESSMENT FINDINGS (cont.)

Blurred vision

Nystagmus

Nausea / vomiting

Signs of facial & trigeminal nerve involvement

Bowel &/or Bladder dysfunction

Retention &/or incontinence

( or absence of touch sensation

ASSESSMENT FINDINGS (cont.)

After Several Years

Signs / symptoms probably more severe

Most patients develop Charcot’s Triad

Nystagmus

Intention tremors

Scanning speech

Late - ASSESSMENT FINDINGS (con’t)

Partial or total paralysis of lower extremities

Use of upper extremities may be severely limited

Small percent have gross loss of memory

Crippling joint contractures

Muscle atrophy

Lhermitte’s Sign

Electric sensation down the spine upon passive flexion of the neck.

“Zipper Effect”

NURSING INTERVENTIONS

Assess

Assist

Monitor

Administer

Encourage

Maintain

Establish

Protect

Provide

Home Care Instructions

Identify

Recognize

Avoid Exposure

Alternate

Maintain

Use of assistive devices

Reinforce

Avoid Temperatures

Complications

Urinary Tract Infection

Respiratory Tract Infection

Contractures

Depression

Paraplegia

Quadriplegia

MEDICATIONS

Meds – Please see MEDS in Neuro Section on Website

BMR’s (biologic response modifiers

Avonex (interferon beta-1a)

Betaseron (interferon beta-1b)

Copaxone (glatiramer acetate)

Steroids

Examples:

Solu-Medrol (methylprednisolone)

ACTH (adrenocorticotrophic hormone

Decadron (dexamethasone)

MEDICATIONS (cont.)

Immunosuppressive Therapy

A combination of Cytoxan (cyclophosphamide) and SoluMedrol (methylprednisolone) may be used to stabilize the disease process.

Adjunctive Drug Therapy

Muscle relaxants to decrease spasticity

Symmetrel (amantadine hydrochloride) for fatigue

Inderal (propranolol hydrochloride for ataxia

Klonopin (clonazepam) for ataxia

Ditropan (oxybutynin chloride) for bladder problems

Urispas (flavoxate HCl) for bladder problems

Guillain – Barré Syndrome (GBS)

PATHOPHYSIOLOGY

THREE STAGES OF ACUTE GBS

The Initial Period

Plateau Period

Recovery Period

ASSESSMENT FINDING

Paresthesia and Pain

Generalized Weakness

Paralysis starting in Legs *

Ascending Paralysis *

Respiratory Paralysis *

Tachycardia, HTN, increase Temp.

Ptosis

Dysphasia

Difficulty speaking

DIAGNOSTIC TEST FINDINGS

Cerebrospinal Fluid (CSF)

EMG

NURSING INTERVENTION

Assess Respiratory & Neuro status

Assess Muscle strength *

Assess gag and swallowing reflex *

Maintain the Pt. Diet

Position & Administer

Suction

Maintain the position

Semi-fowlers position

Establish alternate communication

NURSING INTERVENTIONS con’t

Protect

Prevent

Provide bowel & bladder

Assess for Homan’s sign

Establish

Apply Ted hose

HOME CARE INTERVENTIONS

Identify ways to reduce stress

Maintain a safe, quiet environment

Minimize environment stress

Exercise hands, arms, legs and regularly

Complications with GBS

Respiratory Failure

Contractures

Aspiration

Pneumonia

PARKINSON’S DISEASE (PD)

INTRODUCTION / PATHO

INTRODUCTION / PATHO

(4) CARDINAL SYMPTOMS

Tremors

Rigidity

Akinesia

Postural Instability

CLINICAL MANIFESTATIONS

Postural / mobility abnormalities*

Head bent forward

Kyphosis

Gait: shuffling; short steps; toe-heel; hesitancy then propulsion

( arm swinging

Inability to pivot

Bradykinesia / Akinesia *

CLINICAL MANIFESTATIONS

Mask-like expression

( blinking

Staring expression

CLINICAL MANIFESTATIONS cont.

Speech changes

Soft, low monotone

Handwriting changes

Micrographia

Depression

Bone demineralization

Mental changes

Cognitive, perceptual & memory deficit

MANAGEMENT of PD CLIENTS:

MEDICATIONS

Meds – Please see MEDS in Neuro Section on Website

Dopaminergics

To treat rigidity and bradykinesia

Examples:

Levodopa

Sinemet (carbidopa and levodopa)

- Eldepryl or Deprenyl (selegiline)

. - Requip (ropinirole)

Medications cont

Meds – In Neuro Section on Website

Anticholinergics (example: Cogentin)

Tasmar (tolcapone)

Mirapex (pramipexote)

Symmetrel (amantadine hydrochloride)

Antidepressants

NURSING INTERVENTIONS

MAINTAIN A PATENT AIRWAY

Assess Respiratory & Neuro Status

Maintain Patient diet

Position Patient prevent contractures

Administer Meds

Promote daily ambulation

Promote measures to prevent falls

Change patients position slowly

Provide active and passive ROM

Provide ADL’s

Reinforce independence

HOME CARE INSTRUCTIONS

Recognize signs & Symptoms

Alternate rest periods

Promote a safe environment

Take measures to prevent choking

Offer intake of roughage and fluids

Monitor weights

COMPLICATIONS

Depression

Corneal Ulceration

Injury

Aspiration

Constipation

STROKE

INTRODUCTION / DEFINITION

Other terms:

Cerebral Vascular Accident (CVA)

Now it’s called: Brain Attack

Definition:

Condition in which neurological deficits result from decreased blood flow to the brain

TYPES of STROKE

Two basic categories

Occlusive (Ischemic Stroke)

Thrombotic Stroke

Embolic Stroke

Transient Ischemic Attack and

Reversible Ischemic Neurological Deficit

Hemorrhagic

CLASSIFICATIONS / CATEGORIES

Ischemic

Blood supply to part of the brain is suddenly interrupted by:

Thrombus

Embolus

TIA’s (transient ischemic attack)

Hemorrhagic

Blood vessel breaks and spills blood into the brain

TANSIENT ISCHEMIC STROKES

& REVERSIBLE ISCHMIC NEUROLOGICAL DEFICIT TIA’s

Localized cerebral ischemia which causes temporary neurological deficits

Considered to be a warning signal for ischemic Brain Attacks

Difference between the two is the length of time

TIA’s (cont.)

Causes:

Inflammatory artery disorders

Sickle cell anemia

Atherosclerotic changes in cerebral vessels

Thrombosis

Emboli

TIA’s (cont.)

Manifestations

Depend upon location and size of cerebral vessel involve

Sudden onset with disappearance within minutes, hours or a couple of days

Contra-lateral numbness or weakness of hand, forearm, corner of mouth (middle cerebral artery)

Aphasia

Visual disturbances such as blurring (posterior cerebral artery)

THROMBOTIC STROKES

Definition

Occlusion of a large cerebral vessel by a thrombus

Target Population

Often seen in older people who are resting or sleeping

THROMBOTIC STROKE (cont.)

Pathophysiology

Clots tend to form in:

Large arteries that bifurcate and . . .

Narrowed lumens as a result of atherosclerotic plaque

Common locations:

Internal carotid artery

Vertebral arteries

THROMBOTIC STROKE (cont.)

Lacunar strokes

Thrombotic strokes which affect smaller cerebral vessels.

Manifestations

Occur rapidly but usually progress slowly

May start as TIA and worsen (“stroke-in-evolution”)

Maximum neurological damage usually reached in 3 days (“completed stroke”)

Affected area is edematous & may become necrotic

EMBOLIC STROKE

Definition

Pathophysiology

Most frequent site: bifurcation of vessels (carotid and middle cerebral arteries)

Most embolic stroke originates from thrombi in the left chamber of the heart during atrial fibrillation.

Other sources of emboli

Target Population

HEMORRHAGIC STROKE

Defined as “intracranial hemorrhage

Pathophysiology

HEMORRHAGIC STROKE (cont.)

CAUSES

Sustained increase in BP *

Intracranial aneurysms

Trauma

Erosion of blood vessels by tumors

Arterio-venous malformations

Anticoagulant therapy

Blood disorders

HEMORRHAGIC STROKE (cont.)

Prognosis

Manifestations

Onset of S/Sx is rapid unless bleed is a slow leak.

Depend upon location of hemorrhage

Vomiting

Headache

Seizures

Hemiplegia

S/Sx of increased intracranial pressure

LOC (loss of consciousness)

ETIOLOGY / GENETIC RISK FACTORS

TIA’s

Hypertension

Diabetes mellitus

Substance abuse

Atherosclerosis (Heart Disease)

Obesity

Illicit Drug Use (Cocaine)

Hyperlipidemia

Oral contraceptives

Cigarette smoking

TYPICAL SIGNS/SYMPTOMS OF A

BRAIN ATTACK

Focal Assessment

Weakness

Paralysis

Sensory loss

Language disorders

Broca’s

Wernicke’s

Reflex changes

Visual changes

TYPICAL SIGNS/SYMPTOMS OF BRAIN ATTACK

Generalized Assessment

Headache

Vomiting

Confusion / Disorientation

Seizures

Coma

( BP

Memory impairment & other mental changes

Fever

Cardiac abnormalities

Nuchal rigidity

Sclerosis of peripheral vessels & retinal vessels

TYPICAL SIGNS/SYMPTOMS (cont.)

Left Brain Injury

Right hemiplegia

Dysphasia / aphasia / agraphia

Frequently understand more than they can speak or write.

Behavioral style

Slow

Cautious

Disorganized

Anxious

TYPICAL SIGNS/SYMPTOMS (cont.)

Right Brain Injury

Left hemiplegia

Difficulty with spatial-perceptual tasks:

Distance

Size

Position

Rate of movement

Form

Relationship of parts to the whole

Impaired time perception

TYPICAL SIGNS/SYMPTOMS (cont.)

Right Brain Injury (cont.)

Errors are inconsistent

Behavioral style

Quick

Impulsive

Often unaware of deficits

Perform unsafe activities

DIAGNOSTIC TEST FINDINGS

Lumbar Puncture

CT

MRI

EEG

Brain Scan

Digital Subtraction Angiography

ONE-SIDED NEGLECT

Deficit of:

Looking

Listening

Touching

Searching

May have visual field cuts

ONE-SIDED NEGLECT (cont.)

Clinical Manifestations

Eat food only on one side of the plate.

Ignore person who approaches impaired side.

Fail to attend to one side of the body.

MEDICAL MANAGEMENT - BRAIN ATTACKS

Diet low-sodium, increased K+

Position – Semi-Fowlers

Oxygen Therapy

N/G tube - decompression

Physical therapy - Active /Passive ROM

Seizure precautions

Nutritional Support -TPN

Lab= Na+, K+, glucose, ABG’s, PT, PTT

Medications (next slide)

MEDICATIONS

Please see additional material in the Neuro section on my website.

NURSING INTERVENTIONS

Maintain airway

Frequent neuro-checks, vital signs and general assessment (resp. assess)

Observe for signs of progression of thrombosis or hemorrhage

LOC changes

Increased loss of motor or sensory function

Progressive aphasia

Increased respiratory difficulty

NURSING INTERVENTIONS

Ensure F&E balance

Maintain proper positioning & alignment

Maintain adequate elimination

Prevent constipation / impaction

Involve significant others in plan of care

Provide restful, quiet environment

Administer meds

NURSING INTERVENTIONS

If eyelids remain open protect the eye:

Sterile saline (no preservatives)

Artificial tears

Patch

Mouth care

Prevent intellectual regression *

Reorient

Talk with client

Post the date, Nurse’s name

Place clock where client can easily see it

MANAGEMENT (cont.)

SURGERY

Carotid Endarterectomy

(Most common)

HOME CARE INSTRUCTIONS

Identify ways to reduce stress

Recognize S & Sx of seizures

Minimize environmental stress

Reinforce established methods of communication (aphasic pt.)

Monitor B/P

Use of assistive devices with ADL’s

COMPLICATIONS

Cerebral Edema

Pneumonia

Increased ICP Problems of immobility

Thrombophlebitis

Pulmonary Embolism

Osteoporosis

Urinary Stasis

THE END

DOUBLE check your

CRANIAL NERVES!

ALZHEIMER’S DISEASE (AD)

Internet sites used in the development of this material:



and



INTRODUCTION / DEFINITION

Form of dementia

A syndrome of intellectual deterioration severe enough to interfere with occupational or social performance

Involves progressive ( in at least 2 areas of cognition

Usually memory + …

Most common cause of dementia in older adults

WHAT CAUSES ALZHEIMER’S DISEASE?

Cause unknown

Causal Theories

Biologic Factors in the Brain

Neurofibrillary tangles

Beta-Amyloid

Neuritic Plaques

Senile Plaques

RISK FACTORS

Age

Family history

Race/cultural background

Some studies show higher risk in African Americans and Hispanics than in Caucasian Americans and . . .

Lower risk in Native Cherokees and in Asians

Cardiovascular disease

Hypertension

High cholesterol

High homocysteine levels

RISK FACTORS (cont)

Down’s Syndrome

Lower education and economic groups

Small head size

Depression

Head injury

PATHOPHYSIOLOGY

Neurofibrillary tangles and neuritic plaques are located in areas of brain cell loss.

Areas of cell loss are in the cerebral cortex which controls intellectual functioning

such as:

Learning and reasoning

Memory storage

Language abilities

Consciousness

DIAGNOSIS

No definitive test until autopsy

R/O other causes of dementia

History and assessment

are important in determining if the following conditions are met:

2 or more areas of cognition involved

Onset insidious

Steady downward progression

Exhibit normal level of alertness in early stages

DIAGNOSIS (cont)

MRI / CAT / PET

EEG

EKG

Lab tests

Beta-amyloid protein (CSF)

Other lab tests to R/O reversible causes of dementia (ex: Vit 12 deficiency, thyroid dysfunction, electrolyte imbalances)

CLINICAL MANIFESTATIONS

Progressive but rate varies

Most patients have long periods with little change

Numerous factors can worsen S/Sx

CVA

Meds

Hypoglycemia

Brain lesion

CLINICAL MANIFESTATIONS (cont)

-

CLINICAL MANIFESTATIONS

STAGE ONE (MILD) EARLY

Memory loss

Difficulty performing familiar tasks

Problems with language

Poor or decreased judgment

Problems with abstract thinking

Misplacing things

Changes in mood or behavior

Changes in personality

Loss of initiative

CLINICAL MANIFESTATIONS (cont)

STAGE TWO (MODERATE) MIDDLE

( memory loss

( attention span

Difficulty recognizing friends & family

Problems with language

Difficulty organizing thoughts

Trouble learning new things or coping with the unexpected

Restlessness, agitation, anxiety, tearfulness and wandering especially after sundown

CLINICAL MANIFESTATIONS (cont)

STAGE TWO (cont)

Repetitive statements or movements

Hallucinations, delusions, suspiciousness or paranoia

Reduced impulse control

CLINICAL MANIFESTATIONS (cont)

STAGE THREE (SEVERE) LATE

Completely Incapacitated

loss of language & memory

Weight loss

Seizures, skin infections and dysphasia

Making noises & muttering

Increased sleeping

Incontinence (bowel &/or bladder)

Loss of physical coordination

Totally dependent with ADL’s

TREATMENT

Please see Meds in the Neuro Section on Website

Selective acetylcholinesterase inhibitors

Aricept( (donepezil)

Exelon( (rivastigmine)

Reminyl( (galantamine)

Cognex( (tacrine)

NSAIDS

Nicotine replacement

PRN meds for symptomatic treatment

HOME CARE TREATMENT

Early stage

Telling the patient

Mood and emotional behavior

Appearance and cleanliness

Driving

Wandering – Safe *

Speech problems

Sexuality

HOME CARE TREATMENT

Late stage

24 hour-a-day care

Incontinence

Immobility

Pain

Dehydration

Eating problems

COMPLICATIONS

Malnutrition or dehydration

Pressure ulcers

Muscle contractions

Physical injuries

Abuse

Infection

Death

AMYOTROPHIC LATERAL SCLEROSIS

PATHOPHYSIOLOGY

Degenerative disease involving the motor system

Atrophy

Ending result

SIGNS & SYMPTOMS

Fatigue

Atrophy of the tongue

Dysphagia

Weakness

Fasciculation

Dysarthria

DIAGNOSTIC TESTING

No specific test to diagnosis

Abnormal pulmonary Function Test

Decrease in vital capacity

Usage of Oxygen 2L

Increase in Creatine Kinase

EMG = fibrillations, twitching of muscles

Monitor liver enzymes ALT and AST

MEDICATIONS

No cure , it extends survival time

Medications are also prescribed for pain, fatigue, spasticity, secretions, and sleep

Disturbances.

Medication Riluzole (Rilutek)

COLLABORATES

Respiratory Therapy

Physical Therapy

Occupational Therapy

Speech Therapy

Dietary

NURSES RESPONSIBILITY

Airway

Safety

HOSPICE PROGRAM

Medication

Support

Counseling

Advance Directives/Living Wills

ALS Association

The End

Study material for Neuro

Read the chapters in book

Read over notes

Medications (Website under Neuro.)

Take quizzes

Print and read hyperlinks (Alzheimer's)

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