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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