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:
http://umm.adam.com/pages/wc/articles/000002_1.htm
and
http://www.alzheimersonline.com
•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)