Question | Answer |
Multiple Sclerosis | Autoimmune disorder causing demyelination of the white matter anywhere in CNS - spares peripheral nerves
Life expectancy - 35 yrs post dx.
Patho:Optic nerves,Chiasm and tracts,Cerebrum,Brain stem,Cerebellum,Spinal cord. |
Multiple Sclerosis Clinical Manifestations | Diplopia
Nystagmus
Scanning speech
Muscle weakness
Muscle spasms
Paralysis
Gait/coordination problems
Paresthesias |
MS Diagnosis | CT- plaques
MRI - 2 lesions
Elevated immunoglobulin’s in CSF (IgG) |
MS Treatment | (No cure)
Immunosuppressive agents
Corticosteroids
Anti-spasmodics to decrease spasticity
Plasmapheresis |
Myasthenia Gravis | Deficit of acetylcholine at myoneural junction produces chronic progressive weakness of muscles
Autoimmune destruction likely cause
Thymus gland frequently enlarged
IgG antibody to acetylcholine
myoneural junction - diminished transmission |
Myasthenia Gravis | 2-3X more common in women
20-30 peak age of onset |
Myasthenia Gravis Etiology pathophysiology | Onset is slow
Precipitated by
Hormonal disturbances
Emotional stress
Infections
Trauma
Medications |
Myasthenia Gravis Common Symptoms | Speaking, Chewing, Swallowing Problems
Fatigue after exercise of muscle group
Eye muscle weakness
diplopia, ptosis
Facial muscle weakness
aspiration risk
Proximal limb weakness later
All muscle weakness is worse with effort and improves with rest. |
Myasthenia Gravis Diagnosis | Tensilon testing
PET scan
EEG
EMG
Blood work
History and clinical symptoms |
Myasthenia Gravis Treatment | Anticholinesterase medications
Prostigmin
Mestinon
Corticosteroids
Imuran
Cytoxan Thymectomy
Plasmapheresis
during crisis |
Plasmapheresis (plasma exchange) | Removal of patients plasma and plasma components
Produces a temporary reduction in the antibodies
Does not treat the underlying abnormality |
Myasthenia Gravis Life Threatening Complications
Myasthenia Crisis | Undiagnosed or under medicated
Stress or infection
Severe muscle weakness - respiratory insufficiency
Tensilon will improve symptoms |
Cholinergic Crisis | Too much medication
N&V, diarrhea, cramps
hypotension
Tensilon to distinguish from Myasthenia Crisis
Atropine to reverse
Respiratory support may be needed |
Myasthenia Gravis Patient Education | Avoid extreme temperatures
Avoid exposure to infections
Avoid emotional stress
Avoid medications that could precipitate an exacerbation
Signs and symptoms of crisis |
Myasthenia Gravis Adequate nutrition | Peak muscle strength while eating
Frequent small meals
Soft/semisolid
IV fluids
Enteral feedings |
Parkinson’s disease | Etiology pathophysiology
Basal ganglia disorder of dopamine deficiency is most common origin
May result from head trauma, medications, post encephalitis Dopamine decreases, acetylcholine no longer inhibited |
Parkinson’s disease Clinical Manifestations | Tremors
Rigidity
Bradykinesia
Gait disturbances
Postural disturbances
Heat intolerance
Urinary retention
Constipation
Dysphagia
Depression
Sleep disorders
Cognitive disorders
Memory deficits
Personality changes
Psychosis
Acute confusio |
Parkinson’s disease Complications | Respiratory tract infections
Urinary tract infections
Skin breakdown
Falls
Adverse affects of medications |
Parkinson’s Treatment | Levodopa is most common
Dopamine replacement
Antiparkinsons/antiviral agent
MAO inhibitor- inhibits dopamine metabolism
Anticholinergic medications for tremor
Stereotactic procedures |
Amyotrophic Lateral Sclerosis (ALS) | Loss of motor neurons in the spinal cord and brain stem
Death of nerve cells
Atrophic changes of muscle fibers
Autoimmune disease (theory)Free radical damage (theory)Cell injury and neuronal degeneration (theory) |
Amyotrophic Lateral Sclerosis (ALS) Disease progression | Peak onset 40-50; M/F ratio 3/2
Strong evidence to support genetic component
Progressive loss of motor function
Intelligence & sensation remain intact!
Total supportive care
No cure |
Amyotrophic Lateral Sclerosis (ALS) Supportive care | Treat symptoms
NG tubes
Mechanical ventilation
EOL counseling |
Spinal Cord Injury (SCI)
“Think first, SCI are forever.”
Mechanisms of injury | hyperextension - acceleration/deceleration
hyperflexion - neck propelled forward
Axial compression - force down from top
Flexion-rotation - shearing plus accel/decel |
Spinal Cord Injury (SCI) Fractures may or may not be present | Subluxation = atlas, axis dislocation (C1, C2) |
Degree of Injury | Complete cord involvement Results in total loss of sensory and motor function below level of lesion (injury)
Incomplete (partial) cord involvement
Results in a mixed loss of voluntary motor activity and sensation and leaves some tracts intact |
Terminology of SCI | Quadriplegia (4) and Paraplegia (2)
Cord concussion - temporary disruption
Cord contusion - bruising, temporary
Cord compression – pressure; need surgery
Laceration - tearing
Transection - severing |
Spinal Shock
Temporary neurologic syndrome | Reflexes
Loss of sensation
Flaccid paralysis below level of injury |
Neurogenic Shock | Loss of vasomotor tone caused by injury
Loss of sympathetic nervous system innervation causes
Peripheral vasodilation
Venous pooling
↓ Cardiac output |
Clinical Manifestations of SCI | Autonomic Hyperreflexia (Dysreflexia)
Sudden massive uncompensated CV response to stimulation of SNS: severe hypertension
Life threatening |
Diagnosis of SCI | X-ray
CT scan
MRI |
Treatment of SCI | Immobilization
Decompression and surgical fixation
Steroids
Nutrition
Respiratory support
Skin, bowel and bladder management
Life time rehabilitation program |
Clinical Manifestations
Immediate post injury problems include | Maintaining a patent airway
Adequate ventilation
Adequate circulating blood volume
Preventing extension of cord damage (secondary damage) |
Clinical Manifestations
Respiratory System | Respiratory complications closely correspond to level of injury |
Clinical Manifestations
Respiratory System | Cervical and thoracic injuries cause paralysis of
Abdominal muscles
Intercostal muscles
Patient cannot cough effectively
Leads to atelectasis or pneumonia |
Clinical Manifestations
Urinary System | Urinary retention common
Bladder is atonic and over distended |
Clinical Manifestations
Gastrointestinal System | njury level above T5, primary GI problems related to hypomotility
Injury level of T12 or below neurogenic bowel |
Clinical Manifestations
Integumentary System | Consequence of lack of movement is skin breakdown
Pressure ulcers can occur quickly
Can lead to major infection or sepsis |
Clinical Manifestations
Thermoregulation | Poikilothermism Adjustment of body temp to room temp.Occurs in spinal cord injuries bc sympathetic nervous system interruption prevents peripheral temp sensations from reaching hypothalamus. |
Clinical Manifestations
Thermoregulation | Don’t forget health promotion,disease prevention,&patient education! |
Cranial Nerve Disorders | Bell’s palsy (CN VII)
Unilateral paralysis of the facial muscles
Trigeminal neuralgia (CN V)
Chronic disease
Severe facial pain |
Etiology Pathophysiology Cranial Nerve Disorders | Inflammation
Infection
Viral |
Clinical Manifestations
Trigeminal neuralgia | Pain |
Clinical Manifestations Bell’s palsy | One-sided facial paralysis
Loss of corneal reflex
Loss or impairment of taste
Increased tearing from lacrimal gland |
Treatment
Trigeminal neuralgia | Anticonvulsants—Tegretol, Dilantin
Microvascular decompression
Rhizotomy |
Treatment Bell’s Palsy | Corticosteroids—prednisone
Antivirals
Eye patch/protective glasses |