TOPIC 11 - neuro part 1 Flashcards
bells palsy
acute peripheral facial paresis of unknown cause. as the most common facial nerve disorder
characterized by inflammation of the facial nerve (cn vii) on one side of the face in the absence of any other disease such as a stroke
theories of causes of bells palsy
acute demyelination similar to guillain barre disease
reactivated herpes
other infection
hallmark signs of bell palsy
inability to close the eyelid, with an upward movement of the eyeball when closure is attempted, is a inability to smile, frown, or whistle
unilateral loss of taste is common
decreased muscle movement may alter chewing ability.
pain behind the ear
onset of bells palsy
onset is sudden with a rapid onset of unilateral facial weakness that can occur in a few hours.
complications of bells palsy
psychologic withdrawal - changes in appearance
malnutrition
dehydration
mucous membrane trauma
corneal abrasions
muscle stretching
facial spasms
contractures
interventions for pain related to bells palsy
analgesics
hot packs for herpetic lesions
interventions for hypersensitivity to heat and cold related to bells palsy
protect face
interventions for risk for aspiration related to bells palsy
Teach to chew on the unaffected side
Avoid trapping food
Good oral hygiene
interventions for risk for cornea damage related to bells palsy
Teach to cover the eye with a protective shield at night.
Apply eye ointment to keep eyelids closed duringsleep.
interventions for muscle tone change related to bells palsy
Show patient how to perform facial massage with gentle
upward motion several times daily when the patient can tolerate the massage.
Demonstrate facialexercises, such as wrinkling the forehead,
blowing out the cheeks, and whistling, in an effort to prevent muscle atrophy.
interventions for diet and nutrition related to bells palsy
Instruct patient to chew on the unaffected side of hismouth.
Eliminate hot fluids and foods.
Give frequent mouth care, being particularly careful to remove residues of food that collects between the cheeks and gums.
what is myasthenia gravis and how is is causes
autoimmune disease of the neuromuscular junction characterized by the fluctuating weakness of certain skeletal muscle groups.
antibodies attack acetylcholine (ach) receptors, resulting in a decreased number of ach receptor (achr) sites at the neuromuscular junction. this prevents ach molecules from attaching and stimulating muscle contraction.
which neurotransmitter is related to myasthenia gravis
ACH
assessment of myasthenia gravis
fluctuating weakness of skeletal muscle
the muscles most often involved are those used for moving the eyes and eyelids, chewing, swallowing, speaking, and breathing
eyelid muscles or extraocular muscles are involved. facial mobility and expression can be impaired
the patient may have difficulty chewing and swallowing food. speech is affected, and the voice often fades after a long conversation.
acute exacerbation of muscle weakness related to myasthenic crisis is triggered by
infection
surgery
emotional distress
drug overdose
inadequate drugs
major complications with myasthenic crisis
muscle weakness in areas that affect swallowing and breathing = aspiration, resp insufficiency, resp tract infection
drug therapy for MG
anticholinesterase agents
corticosteroids
immunosuppressive agents
what is removed in surgery for MG
thymus gland
other therapies for MG
plasmapheresis
iv immunoglobulin g
interventions for MG
balanced diet that is easily chewed and shallowed (semi-solid foods)
scheduling doses of drugs so that peak action is reached at mealtime may make eating less difficult.
arrange diversional activities that require little physical effort and match the patient’s interests.
help the patient plan activities of daily living to avoid fatigue.
multiple sclerosis
chronic, progressive, degenerative disorder of the CNS characterized by disseminated demyelination of nerve fibers of the brain and spinal cord.
possible precipitating factors of multiple sclerosis
infection, smoking, physical injury, emotional stress, excessive fatigue, pregnancy, and a poor state of health, type 1 diabetes, thyroid problems, IBS
what is the patho of multiple sclerosis
The activated t cells in the systemic circulation migrate to the cns, disrupting the blood-brain barrier. this is likely the initial event in the development of ms. subsequent antigen-antibody reaction within the cns activates the inflammatory response and leads to the demyelination of axons.
manifestations of multiple sclerosis
Onset of the disease is often insidious and gradual
Chronic, progressive deterioration in some patients
Remissions and exacerbations in others
Overall trend is progressive deterioration in neurologic function
assessment of multiple sclerosis
severe fatigue
tremors
bladder and bowel dysfunction
c/o pain in low thoracic area or abdominal region.
decrease peripheral sensation (pain, temperature, touch)
emotional instability
speech impediments
cognitive functions
spasticity of muscles
visual disturbances
dizziness
hearing loss
dysphagia
interprofessional management of multipole sclerosis
no cure - supportive therapy
energy conservation
maintain adequate fluid intake 2000 ml/day
provide bowel and bladder training
encourage activity independence
regulate temperatures on water heaters, baths, and heating pads
home safety (rugs, cords, etc.)
drug therapy
disease modifying drugs immunomodulators for multiple sclerosis
glatiramer acetate (copaxone)
education for glatiramer acetate
inj-site: hives, rash, irritation, severe pain, flushing, chest pain
allergic reaction: itching, trouble breathing, chest pain, dizziness, sweating
do not change dosing or stop taking product without hcp advice
interventions for multiple sclerosis
Help patient identify triggers and develop ways to avoid them or minimize their effects
Reassure patient during diagnostic phase
Assist patient in dealing with anxiety and grief caused by diagnosis
During acute exacerbation, prevent major complications of immobility
Focus teaching on building general resistance to illness
interventions for multiple sclerosis
Help patient identify triggers and develop ways to avoid them or minimize their effects
Reassure patient during diagnostic phase
Assist patient in dealing with anxiety and grief caused by diagnosis
During acute exacerbation, prevent major complications of immobility
Focus teaching on building general resistance to illness
parkinsons disease
chronic, progressive neurodegenerative disorder characterized by slowness in the initiation and execution of movement
symptoms of parkinsons disease
increased muscle tone (rigidity), tremor at rest, and gait disturbance.
manifestations of parkinsons
tremor
rigidity
bradykinesia, hypokinesia or akinesia
postural instability
depression
dementia
sleep disturbances
difficulty smelling
complications related to parkinsons
Dysphagia may result in malnutrition or aspiration
General debilitation may lead to pneumonia, UTIs, and skin breakdown
Orthostatic hypotension
TRAP parkinsons mnemonic
T – tremors at rest
R – cogwheel rigidity of limbs and movement
A – akinesia or bradykinesia, slowing of movements
P – postural instability, clumsy, shuffling gait
surgical therapy for parkinsons
dbs – deep brain stimulation
ablation – destruction
transplantation
antiparkinsonian drug therapy effects
aimed at correcting imbalances of neurotransmitters within the cns
enhance or release supply of da
antagonize or block the effects of overactive cholinergic neurons in the striatum
primary treatment of parkinsons
levodopa carbidopa
signs of dyskinesia
report any uncontrolled movement of face, eyelids, mouth, tongue, arms, hands, or legs
mental changes
Palpitations
severe nausea and vomiting
difficulty urinating
ablation surgery
locating, targeting, and destroying an area of the brain affected by PD.
The goal is to destroy tissue that produces abnormal chemical or electrical impulses leading to tremors or other symptoms.
what is targeted in ablation surgery
Typical targets of ablation are the thalamus (thalamotomy), globus pallidus (pallidotomy), and subthalamic nucleus (subthalamic nucleotomy).
nutritional therapy for parkinsons
malnutrition and constipation can be serious consequences
patients with dysphagia and bradykinesia need food that is easily chewed and swallowed
adequate fiber
eating more numerous small meals is less exhausting than eating fewer large meals each day
provide ample time to avoid frustration
levodopa can be impaired by protein and vitamin b6 ingestion
