PNS & CVA Exam Flashcards
What are the two types of PNS disorders
Neuromuscular
Cranial nerve disorders
Define Neuromuscular disorder
are chronic and degenerative.
They disrupt the transmission of impulses b/w neurons and the muscles they stimulate.
Define Multiple Sclerosis or MS
MS Involves the degeneration of myelin sheath
Myelin covers the axons and is responsible for the smooth transmission of nerve impulses.
It can be damaged due to inflammation, detachment, or if it becomes swollen.
Onset 20s to 40s
etiology of MS
Unknown
Possible autoimmune response
Possible viral infection
Heredity
What are the two types of MS
Relapsing remitting (most common): worsening signs and symptoms followed with improvement Progressive MS: gets worse without improvement
What are problems associated with MS
Weakness/paralysis of limbs Double /blurred vision Slurred speech Spasticity of muscles Numbness Tinnitus and vertigo Dysphagia Spastic or flaccid bladder Mood swings
What can trigger onset of symptoms in MS
extreme heat extreme cold fatigue infection emotional stress
S/S of MS
tinnitus decreased hearing urinary retention spastic bladder constipation nystagmus blurred vision dysarthia dysphagia weakness or paralysis ataxia vertigo
Dx of MS
H&P: symptoms that the patient reports
MRI: will detect sclerotic plaques and will rule out other disease processes.
Lab tests: aides in diagnosing and ruling out other diseases.
Therapeutic interventions for MS
Steroids: Decrease inflammation of the neurons. They are given oral or IV.
Immunosuppressant’s: given to depress the immune system
Anticonvulsants: Relieve neuro pain
Muscle relaxants: Control muscle spasms
PT/OT: Help adapt to home environment
There is no cure: Treat symptomatically
Rehab after an acute episode includes PT, Speech therapy, and OT.
Patient teaching includes: to teach the patient to avoid factors that can exacerbate symptoms.
What is needed for muscle contraction
Acetylcholine
What is Myasthenia Gravis
When there is none or the receptors for Acetylcholine are destroyed. The contraction doesn’t take place
The muscle weakness occurs during activity and improves with rest.
It effects the facial muscles, neck, and limb movement.
S/S of Myasthenia Gravis
Progressive muscle weakness Fatigue with activity Ptosis (droopy eyelids) Difficulty chewing and swallowing Difficulty breathing An early sign can be double vision or slurred speech
Complications of Myasthenia Gravis or MG
Aspiration
Respiratory infection and failure
What is Mysathenic crisis
Sudden onset of symptoms due to not enough medication or triggered by infection
What is a Cholinergic crisis
due to overmedication
What is anti cholinesterase
drugs help improve nerve-muscle communications and increase your muscle strength
Medications given of MG
anticholinesterase
corticosteroids
What is a Tensilon test
Anticholinergic med is given and there is temporary improvement of droopy eyelids. It is an injection of tensilon and muscle strength improves for 1-3 minutes.
pt education for MG
Methods to conserve energy Avoidance of infection Signs and symptoms of crisis Support group Encourage timing of meds so peak of drug will be used when most needed
therapeutic interventions for MG
Can be controlled with meds: they improve neuromuscular transmission and increase muscle strength. They also slow down the time of acetylcholine breakdown.
Immunosuppressive drugs: decrease the production of antibodies.
Surgery: to remove the Thymus. This will work on the immune system so it doesn’t work against the body.
pathophysiology of Amyotrophic Lateral Sclerosis aka Lou Gehrig’s Disease
Motor neurons degenerate: they stop sending messages and nerve impulse transmission are then blocked.
This results in muscle weakness and atrophy
As it progresses, it effects the muscles that control breathing and swallowing.
Etiology of ALS aka Lou Gehrig’s Disease
Unknown
Possible genetic predisposition
Possible Auto-immune disorder
REMEMBER: this doesn’t effect the brain!! Only motor neurons!
Description of ALS or Lou Gehrig’s Disease
Amyotrophic lateral sclerosis causes both the upper and the lower motor neurons that control voluntary movement to die off.
This leads to weakness, muscle death and then paralysis.
The disease begins with the lesser needed muscles, moves to the arms and legs and eventually the muscles that control swallowing and breathing.
Patients inevitably end up on feeding tubes and ventilators.
S/S of ALS
Progressive muscle weakness (gradual): The muscles weaken, and waste away.
Decreased coordination
May effect 1 leg = stumbling
or hands = can’t button shirt
Muscle spasms occur
Difficulty chewing and swallowing
Speech difficulty
Pulmonary compromise: this is when the muscles of the diaphragm are effected. They eventually end up on a vent.
Eventual loss of voluntary movement and can not move
Death in 3–5 years due to complications.
Dx of ALS
assessment of symptoms
nerve biopsy
Therapeutic Interventions for ALS
Muscle relaxants: to control muscle spasticity and cramps PT/OT/Speech therapy Pain control Infection precautions (URI’s and UTI’s) Good skin care Communication support Tube feedings due to decreased nutritional status and easily chokes. Prevention of infection
Pathophysiology of Guillain-Barre Syndrome
Myelin sheath of the spinal cord and cranial nerves is destroyed d/t an inflammatory reaction which cause a slowed or blocked nerve conduction.
Immune system begins attacking the nerves that cary signals to your brain
Commonly follows a respiratory infection
What are the 2 main categories of Guillain-Barre Syndrome
Ascending: characterized by progressive weakness beginning in the legs and works it’s way up the body
Descending (less common) affects the cranial nerves of the brain stem first, making difficulty in swallowing and speaking and progresses downward to the legs.
S/S of Guillan-Barre Syndrome
Starts with the onset of symptoms and lasts until the progression of symptoms stop.
Abrupt onset weakness and paralysis
May affect respiration
Pain ranges from numbness to intense pain
Progression of symptoms stops
Some recover completely and others have debilitations
Complications of Guillan-Barre Sndryome
Respiratory failure
Infection
Depression
Therapeutic Interventions for Guillan-Barre Syndrome
The goal of therapy is to support body systems until the patient recovers. Monitor respiratory status Manage pain Tube feedings if indicated Communication board
Dx of Guillan-Barre Syndrome
LP
EMG
Nerve conduction velocity
Pathophysiology of Trigeminal Neuralgia (aka Tic douloureux)
Involves the fifth cranial nerve (trigeminal)
The 5th cranial nerve has three branches so it effects different parts of the face.
Effected are the forehead, nose, cheek and jaw
May be from irritation or chronic compression of the cranial nerve.
S/S of Trigeminal Neuralgia
Intense pain on one side of face
The periods of pain last from seconds to minutes and can last several days.
Triggered by items such as touching the face or talking.
Sleep provides a period of relief
As time progresses, the episodes become more frequent.
Treatment for Trigeminal Neuralgia
Anticonvulsants: Reduce transmission of nerve impulses
Nerve blocks: Provides a longer period of relief than meds.
Surgery: To remove the nerve or pad it
Pathophysiology of Bell’s Palsy
Cranial nerve VII is effected
The 7th cranial nerve controls most facial muscles, ears, and salivation/tearing
Patient looses motor control on one side of face.
Contracture may develop
Palsy = paralysis
