Chronic Neurologic Oct 23.pptx - Slide 1

Chronic Neurologic Problems
Fall 2009

Headache
The most common type of pain experienced by humans
Types
Tension type headache
Migraine headache
Cluster headache

Tension-Type Headache
Characterized by…
Neck and shoulder muscle pain; Bilateral pain at the base of the skull and in the forehead
Etiology and Pathophysiology
Exact cause is unknown
Sometimes difficult to distinguish
Precipitating factors may include: Stress; Hunger; Sleep deprivation; Eyestrain; Withdrawal from caffeine

Migraine Headache
…episodic familial disorder manifested by unilateral, frontotemporal, throbbing pain in the head which is often worse behind one eye or ear
Clinical manifestations
… often accompanied by sensitive scalp; Anorexia; Photophobia; Nausea with (or without) vomiting

Migraine Headache
Three classifications for migraine headache
Migraines with aura
Aura is a sensation that indicates the onset of a migraine or seizure (develops over several minutes; does not last more than an hour)
Aura may consist of flashing lights; buzzing noises; distorted vision (find out what triggers it)
Migraines without aura
Most are migraines without aura

Migraine Headache
Atypical migraine (more assoc w/ teens & 20 yr olds)
Less common
Associated with menstrual periods
Includes cluster headaches
Neuroimaging recommended for persons older than 50 years of age with new onset of headaches When and Why? (worrisome… MRI might be test of choice)
MRI is gold standard for migraine, but CT scan is much cheaper.

Stages of a Migraine Headache
Prodrome phase (specific symptoms including food cravings; mood changes)
Aura phase (visual changes; diplopia [double vision]; flashing lights)
Headache phase: few hours to a few days
Termination phase (intensity decreases)
Postprodrome phase (fatigue; muscle pain; irritable)

Cluster Headache
Less frequent than migraines
More common in men between 20 and 50 years of age
Definitive cause of headache is unknown
May be related to hypothalamic hyperactivity
Onset is associated with relaxation, napping, or rapid eye movement (REM) sleep
Pain is unilateral, oculotemporal or oculofrontal; Excruciating, boring and non-throbbing type

Cluster Headache
Intense pain felt deep in and around the eye (may radiate to the ear and neck)
Ipsilateral (same side) tearing of the eye; runny rhinorrhea (runny nose) or congestion; ptosis (drooping eyelid); miosis (abnormal constriction of pupils)
Headaches occur every 8 to 12 hours, up to 24 hours a day at the SAME TIME for 6 to 8 weeks
Remission follows for 9 months to 1 year
Duration of headache is usually 10 to 45 minutes
(tearing, runny nose might be the way to tell difference between cluster 7 migraine)

Headaches – Other Types
Can be first symptom of a more serious illness
Can be accompany subarachnoid hemorrhage; brain tumors; other intracranial masses; arteritis; vascular abnormalities; trigeminal neuroalgia (intense pain around the eyes, lips, nose, scalp, forehead and jaw); diseases of the eyes, nose, and teeth; and systemic illness

Headaches
Collaborative Care for Headaches
Drug therapy
Tension-type headache
Acetaminophen and NSAIDs
Migraine headache
Acetaminophen and NSAIDs (Naproxen) effective for mild migraine pain
Abortive therapy (aura phase) and Preventative therapy (with history of migraines 2 to 3 times/month)
Cluster headache
Drug therapy same as for migraine headache

Headaches:Nursing Management
Nursing assessment
Nursing diagnoses
Planning
Nursing Implementation
Evaluation

Headaches: Nursing Diagnoses
Acute pain related to lack of knowledge of pain control techniques or methods to prevent headaches
Disturbed energy field related to disharmony
Ineffective management of therapeutic regimen related to lack of knowledge, identification and elimination of aggravating factors

Chronic Neurologic Disorders
Other

Epilepsy
“To be seized from a force within”
Chronic condition characterized by recurrent paroxysmal (sudden attack)episodes of disturbance in
Skeletal muscle function
Sensation
Autonomic visceral function often lose bowel & bladder control
Behavior and consciousness: some have aura & may have behavioral change… don’t lose consciousness, but may become drowsy or stuporous
Amount of time between varies, usually there is repetition of activity
“pretty important”
Can be primary disease or a symptom of a disease… learn diff types of epilepsy & types of seizures
Don’t say grand mal any more… it is generalized or tonic clonic seizure.

Epilepsy
A symptom of CNS irritation, excessive and abnormal neuronal discharges
Present as a manifestation of disease in approximately 50 other diseases
Epilepsy in a nutshell: Epilepsy is a common neurological disorder characterized by recurrent seizures
Caused by a brief disruption of electrical activity in the brain

Epilepsy
Affects 2 – 4 million people*
Not accurate*
Not reportable
Individuals not likely to admit to condition
Why?

Epilepsy
Most common age groups:
Birth to 2 years
5-7 years
Early puberty (especially girls)
90% of all patients experience first seizure prior to age 20
Genetic tendency toward cerebral dysrrhythmias

Epilepsy
Cerebral epilepsy-cerebral lesions account for activity, usually due to…
Birth injuries (Example: Cerebral palsy)
Infectious disorders (Example: meningitis… once treated, the seizure disorder will go away… takes a long time to treat… on antiepileptic meds while treating for meningitis)
Circulation disorders (Example: stroke)
Cerebral trauma (Example: TBI)
Neoplasms (Recall prior slide!)

Epilepsy
Biochemical epilepsy – biochemical disorders that include epilepsy as a clinical feature
Alcohol ingestion/drug overdose (barbiturates, high doses, can be a cause of a seizure disorder)
Medications (Overdose or withdrawal. Examples: Antidepressants, Antipsychotics, PNC in high doses, Lithium)
Electrolyte imbalance (Example: Altered levels of sodium magnesium; calcium)
Vitamin deficiency
Diabetes mellitus (Example: Hypoglycemia; Hypercalcemia)
Pregnancy and/or menstruation

Epilepsy
Post traumatic epilepsy – from previously sustained cerebral injuries, few prior to 2 months or after 5 years
Head injuries
Birth injuries
Idiopathic epilepsy – no identifiable cause

Seizures: Terms to Remember
Prodromal (Early warning of impending attack)
Aura (Visual disturbances… can be any of the 5 senses…; buzzing sounds)
Ictus (The event; i.e., seizure)
Tonus (Maintained contraction r/t bombardment of motor impulses)
Clonus (Contraction/relaxation of muscles, wild muscle movement)
Postictal (Exhaustion): confusion common

Seizure Classification
Generalized – bilaterally symmetric and without local onset
Tonic-clonic seizures (Type most commonly associated with epilepsy; Generalized seizure)
Typical absence seizures (Stares into space without twitching; Lasts for seconds)
Atypical absence seizures (Stares but is somewhat responsive)
Other types of generalized seizures (Associated with AIDS; Acute infection; Alcohol or drug use)

Seizure Classification
Partial-focal in nature, may become generalized
Simple/partial: No loss of consciousness
Focal (or local) motor or sensory: can begin in one part of the cebrum & spread. Pt usually maintains level of consciousnesss… may report aura or feeling of déjà vu. Odd movement, twitching of hand or tapping of foot… may also have increase in heart rate (sypathetic response, become flush)
Complex partial seizure: loss of consciousness, 1 to 3 min. Aka psychomotor seizures or temporal lobe. Often a motor response.
Jacksonian
Pseudoseizure: don’t see them very often; no aura, don’t lose bladder function, won’t fall out of chair, don’t allow themselves to be harmed but will allow themselves to have the movement seen in a tonic clonic seizure. May be attention getting… could be the beginning of bad things that are going to happen.

Clinical Manifestations
Aura
Tonic-hypertonic-clonic phase
Loss of consciousness
Bowel and bladder incontinence
Tachycardia
Diaphoresis
Warm skin
Pallor, flushing, cyanosis
Post-ictal phase

Epilepsy
Complications
Status epilepticus (life threatening, need ER & immediate meds… valium/diazapem and ativan, can last 5 min or longer, w/ each event it increases in intensity
Psychosocial
Diagnostic Studies
Accurate description of seizures; EEG; CT; MRI
Rule out metabolic disorders

Epilepsy : Status epilepticus
Life threatening
Brain in a state of persistent seizure
Continuous seizure lasting more than 30 minutes or recurrent seizures w/o regaining consciousness between seizures for > 30 minutes
May be neuron damage at 5 minutes Why?
911for seizure lasting > 5 minutes

Epilepsy: Collaborative Care
75% can be managed successfully with anticonvulsant medications (great list in the book… tegretol, dilantin, phenobarbitol, kepra [newer w/ fewer side effects],
Medications will manage the symptoms, but will not cure the condition

Epilepsy: Medications
Generalized and Partial seizures
Phenytoin (Dilantin); Side effects: gingival hyperplasia; drug toxicity
Carbamazepine (Tegretol)
Phenobarbital
Divalproex (Depakote)
Gabapentin (Neurontin)

Epilepsy: Medications
Absent, Akinetic
Klonopin; Zarotin
Status Epilepticus
Ativan (benzodiazepine) and Valium

Epilepsy: Surgical Intervention
Remove focus: if alcohol w/drawal is causing seizure, then remove the problem
Prevent spread
Remove lobe, cortex
Separate hemispheres at corpus callosum
(similar to WPW ablation on heart, but done in brain)

Immediate Seizure Management
During Seizure
Provide privacy
Maintain airway (don’t put anything in mouth, maybe put them on side if able)
Ease to floor; protect from injury
After Seizure
Position on side
Allow time to sleep
Re-orient individual

When Observing a Seizure
Prodromal
Where there any warning signs?
Ictus
Where did it begin and how did it proceed?
Describe movements
How long?
Changes in pupil size?
Incontinence?
LOC?

When Observing a Seizure
Post-ictal
Behavior after the seizure (describe)
Any paralysis or weakness following the seizure?
Did the individual sleep?
After the seizure, document, do vitals, etc…

Multiple Sclerosis
Chronic, progressive, degenerative disorder of the CNS characterized by disseminated demyelination and inflammation of nerve fibers of the brain and spinal cord
MS in a nutshell: Results from progressive demyelination of the white matter of the brain and spinal cord; Hard yellow plaques of scar tissue form (gliosis); Damage to underlying axon fiber so nerve conduction is disrupted; irreversible as disease progresses

Multiple Sclerosis
Cause is unknown
Related to infectious, immunologic, and genetic predisposition
Multiple genes confer susceptibility to MS
Disease usually affects young to middle-aged adults,= with onset between 15 and 50 years of age
Women are affected more than men

Multiple Sclerosis
Possibility that the association between pathogenetic agents and MS is random and there is no cause-and-effect relationship

Multiple Sclerosis
Possible precipitating factors include:
Infection
Physical injury
Emotional stress
Excessive fatigue
Pregnancy
Poor state of health

Multiple Sclerosis
Primary neuropathologic condition is an autoimmune disease orchestrated by autoreactive T-cells
Remember “T” cells? Helper T cells and Killer T cells. Helper T cells stimulate B cells to make antibodies, and help killer cells develop. Killer T cells kill the body’s own cells that have been invaded by viruses or bacteria.
Characterized by chronic inflammation, demyelination (damage to myelin sheath of neurons) and gliosis (scar formation) in the CNS

Multiple Sclerosis
Initially triggered by a virus in a genetically susceptible individual
Subsequent antigen-antibody reaction leads to demyelination of axons

Multiple Sclerosis
Disease process consists of loss of myelin, disappearance of oligodendrocytes, and proliferation of astrocytes
Changes result from plaque formation with plaques scattered throughout the CNS

Multiple Sclerosis
Initially the myelin sheaths of the neurons in the brain and spinal cord are attacked, but the nerve fiber is not affected
Patient may complain of noticeable impairment of function
Myelin can regenerate, and symptoms disappear, resulting in a remission

Multiple Sclerosis
Myelin can be replaced by glial scar tissue
Without myelin, nerve impulses slow down
With destruction of axons, impulses are totally blocked
Results in permanent loss of nerve function

Multiple Sclerosis
Clinical Presentation
Vague symptoms occur intermittently over months and years
Disease may not be diagnosed until long after the onset of the first symptom
1st symptoms: sensory symptoms of the arms/legs; unilateral vision loss; slowly progressive motor deficit

Multiple Sclerosis
Clinical Presentation
Characterized by
Chronic, progressive deterioration in some
Remissions and exacerbations in others
Motor manifestations
Weakness or paralysis of limbs, trunk, and head
Foot drop; pressure ulcers
Scanning speech (slurred, stretching of words); dysarthria (motor speech disorder/poor articulation)
Spasticity of muscles
Tremor

Multiple Sclerosis
Clinical Presentation: Sensory
Numbness and tingling
Blurred vision;diplopia (double vision)
Vertigo and tinnitus
Decreased hearing
Chronic neuropathic pain

Multiple Sclerosis
Clinical Presentation: Cerebellar
Nystagmus(Involuntary movement of the eye)
Ataxia (Inability to coordinate muscle movement)
Dysarthria(motor speech disorder, i.e., slurred speech)
Dysphagia(Difficulty swallowing)

Multiple Sclerosis
Clinical Presentation: Emotional
Anger
Depression
Apathy
Inattentiveness
Euphoria

Multiple Sclerosis
Clinical Presentation: Other
Bowel and bladder functions may be impaired
Constipation
Spastic bladder; small capacity for urine results in incontinence
Inability of sphincter to open
Flaccid bladder; large capacity for urine and no sensation to urinate

Multiple Sclerosis
Clinical Presentation (Other)
Sexual dysfunction can occur in MS
- erectile dysfunction
- decreased libido
- painful intercourse
- decreased lubrication

Multiple Sclerosis: Diagnostic Studies
Based primarily on history, clinical presentation, and presence of multiple plaques over time measured by MRI
Certain laboratory tests are used as adjuncts to clinical exam
CSF analysis: high lymphocytes and monocytes (lumbar puncture, breakdown of meylin is breakdown of protein, should not be protein in CSF)

Multiple Sclerosis:Collaborative Care
Drug therapy
Corticosteroids (maintiain stability of cell wall so it doesn’t break down so fast & antiinflammatory effect… but you can’t stay on them forever)
Treat acute exacerbations by reducing edema and inflammation at the site of demyelination
Does not affect the ultimate outcome or degree of residual neurologic impairment from exacerbation of disease

Multiple Sclerosis: Collaborative Care
Immunosuppressive Therapy
Potential benefits are counterbalanced against potentially serious side-effects (even some chemo drugs can be used to slow down the progression of the disease, often can live a pretty normal life for a long time… 25 years)
Immunomodulators
Interferon ß-1b (Betaseron)
- Interferon ß-1a (Avonex, Rebif)

Antispasmotics (any muscle, bladder, etc…)
CNS stimulants
Anticholinergics and/or cholinergics
Tricyclic antidepressants and anti-seizure medications (unusual for anti-seizure meds)
These are symptom relief meds

Surgery (for patients with severe tremor)
Dorsal-column electrical stimulation (electrodes placed in the subdural extra arachnoid space over the center of the thoracic spinal cord – result is increased motor/sensory function)
Intrathecal baclofen pump (Baclofen is a muscle relaxant used to decrease spasticity in MS; SCI; Other neurologic problems)

Physical therapy helps…
Relieve spasticity
Increase coordination
Trains the client to substitute unaffected muscles for impaired ones

Multiple Sclerosis: Collaborative Care
Nutritional therapy includes…
Megavitamins and diets consisting of low-fat, gluten-free, food, and raw vegetables
High-protein diet with supplementary vitamins is often prescribed

Multiple Sclerosis:Nursing Assessment
Health history
Viral infections or vaccinations
Residence in cold or temperate climates
Physical and emotional stress
Medications
Elimination problems
Weight loss, dysphagia

Multiple Sclerosis:Nursing Diagnoses
Impaired physical mobility
Dressing/grooming self-care deficit
Risk for impaired skin integrity
Impaired urinary elimination pattern
Sexual dysfunction
Interrupted family processes

Multiple Sclerosis:Nursing Plan of Care
Maximize neuromuscular function
Maintain independence in activities of daily living for as long as possible
Optimize psychosocial well-being
Adjust to the illness
Reduce factors that precipitate exacerbation of symptoms

Multiple Sclerosis:Nursing Implementation
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 caused by diagnosis
Prevent major complications of immobility

Multiple Sclerosis: Nursing Implementation
Focus teaching on building general resistance to disease
Avoiding fatigue; extremes of hot and cold; exposure to infection
Teach good balance of exercise and rest, nutrition, avoidance of hazards of immobility

Multiple Sclerosis:Nursing Implementation
Teach self-catheterization if necessary
Teach adequate intake of fiber to aid in regular bowel habits

Parkinson’s Disease
Disease of basal ganglia characterized by…
Slowing down in the initiation and execution of movement
Increased muscle tone (no atrophy usually)
Tremor at rest
Impaired postural reflexes

Parkinson’s Disease:Etiology and Pathophysiology
Pathologic process involves degeneration of dopamine-producing neurons in substantianigra of the basal ganglia
Disrupts dopamine-acetylcholine balance in basal ganglia (decreased acetylcholine & dopamine)
Symptoms of the disease do not occur until 80% of neurons in the substantianigra (basal ganglia, lie near the lateral ventricles, when stimulated they release the dopamine) are lost

Diagnosis increases with age
Peak onset in the 6th decade of life
Onset before age 50 is likely related to genetic defect
More common in men: ratio is 3:1
Other causes include hydrocephalus; hypoxia; infections; stroke; tumor; and trauma (i.e., injury to the brain)

Clinical Presentations (goes from stage 1 to stage 5… book gives good description of stages)
Symptoms may involve only one side of the body initially
Beginning stages may involve only mild tremor, slight limp or decreased arm swing
Later stages may show shuffling, propulsive gait with arms flexed, loss of postural reflexes
Never progresses to complete paralysis

Classic triad of clinical symptoms include
Tremor
Rigidity
Bradykinesia (slow movement)
(proprioception, postural instability, loosing awareness of where their body is at all times)

Tremors
More prominent at rest and aggravated by emotional stress or increased concentration
Described as “pill rolling” because thumb and forefinger appear to move in rotary fashion
Tremor can involve diaphragm, tongue, lips and jaw
Benign essential tremor, which occurs during voluntary movement, has been misdiagnosed as Parkinson’s disease

Rigidity (2nd classic symptom)
Caused by sustained muscle contraction and consequently elicits:
Complaints of soreness
Feeling tired and achy
Pain in the head, upper body, spine, or legs
Rigidity is typified by a jerky-quality when the joint is moved
Rigidity is similar to intermittent catches in the movement of a cogwheel (“cogwheel rigidity”)
Inhibits the alternating contraction and relaxation in opposing muscle groups, thus slowing movement

Bradykinesia
Slowing down in initiation and execution of movement-lean forward to initiate ambulation
Evident in loss of automatic movements
Blinking
Swinging of arms while walking
Swallowing of saliva
Self-expression with facial movements (“masked facies”)

Parkinson’s Disease:Complications
Caused by progressive deterioration and loss of spontaneity of movement
Dysphagia can lead to malnutrition or aspiration
Debilitation may lead to pneumonia, UTI, and skin breakdown
30-40% have dementia
Orthostatic hypotension may occur along with loss of postural reflexes
Falls and other injuries can result

Parkinson’s Disease:Complications
Side effects from drugs, particularly levodopa, include…
Dyskinesia (involuntary movement)
Hallucinations
Orthostatic hypotension
Weakness
Akinesia (without movement or much movement)

Parkinson’s Disease:Diagnostic Tests
No specific tests
Diagnosis is based on history and clinical features
Firm diagnosis can be made when at least 2 of 3 characteristics of classic triad -tremor, rigidity and bradykinesia (slowness of movement)- are present
Ultimate confirmation of diagnosis is a positive response to antiparkinsonian drugs

Parkinson’s Disease:Collaborative Care
Drug therapy –
Aimed at correcting imbalances of neurotransmitters within the CNS
Enhance or release supply of dopamine
Antagonize or blocks the effect of over-active cholinergic neurons in the striatum

Levodopa with carbidopa (Sinemet) is often the first drug used
Precursor of dopamine and crosses the blood/brain barrier
Converted to dopamine in the basal ganglia
Carbidopa inhibits an enzyme that breaks down levodopa before it reaches the brain

Effectiveness of Sinemet can wear off after a few years of therapy
Initiation of therapy is with a dopamine receptor agonist (an agonist is site specific drug) instead (Parlodel)
Anticholinergics are also used in the management of Parkinson’s disease (Artane, Cogentin)
Decreases activity of acetylcholine

Parkinson’s Disease: Collaborative Care
Antihistamines with anticholinergic or beta-adrenergic blockers are used to manage tremors
Antiviral agent amantadine is effective though exact mechanism is unknown (Symmetryl)
As disease progresses, combination therapy is often required
Excessive amounts of dopaminergic drugs can lead to paradoxical intoxication (i.e., excessive drug load)

Surgical treatment
Procedures aimed at relieving symptoms in patients who are unusually unresponsive to drug therapy
Ablation surgery
Stereotactic ablation of areas in the thalamus, globus pallidus, and subthalmic nucleus (unilateral pallidotomy improves tremor and dyskinesia on one side of the body; deep brain stimulation preferable)

Deep brain stimulation
Involves placing an electrode in either the thalamus, globus pallidus, and subthalmic nucleus
Connected to a generator placed in the upper chest
Device is programmed to deliver specific current to target brain location
Is adjustable and reversible

Transplantation of fetal neural tissue into the basal ganglia provides dopamine producing cells in the brains of patients
Still experimental
Controversial

Nutritional therapy:
Malnutrition and constipation can be serious consequences
Patients with dysphagia and bradykinesia need food that is easily chewed and swallowed
Adequate roughage
Several small meals to prevent fatigue
Provide ample time to avoid frustration
Levodopa can be impaired by protein ingestion

Parkinson’s Disease:Nursing Assessment/Management
History
CNS trauma
Cerebrovascular disorders
Exposure to metals (23 types of heavy metals)
Encephalitis
Medications such as tranquilizers, amphetamines, methyldopa
Excessive salivation; dysphagia; weight loss

Parkinson’s Disease:Nursing Assessment / Management
History, continued
Difficulty initiating movements; falls; loss of dexterity
Constipation; incontinence
Diffuse pain in head, shoulders, neck, back, arms, legs, and hips
Depression; mood swings; hallucinations

Parkinson’s Disease: Nursing Diagnoses
Imbalanced nutrition: less than body requirements
Impaired verbal communication
Deficient diversion activity
Risk for falls

Parkinson’s Disease:Nursing Management/Planning
Maximize neurologic function (Pharm therapy as prescribed; Pilates, which teaches balance and control of body)
Maintain independence in ADLs for as long as possible
Optimize psychosocial well-being

Parkinson’s Disease:Nursing Management/Implementation
Teach maintenance of good health, independence, and avoidance of complications
Promotion of physical exercise and well-balanced diet
Specific exercises to strengthen muscles involved with speaking and swallowing
Healthy diet – fruits, vegetables, eggs, some cereal

Parkinson’s Disease: Nursing Management/Implementation
Problems secondary to bradykinesia can be alleviated by
Consciously thinking about stepping over a line on the floor
Lifting toes when stepping
One step back and…
Two steps forward

Parkinson’s Disease:Nursing Management/Implementation
Getting out of chair by using arms and placing the back legs on small blocks
Remove rugs and excess furniture
Simplify clothing from buttons and hooks
Elevated toilet seat

Myasthenia Gravis
A chronic, progressive disease of muscular weakness caused by a defect at the myoneural junction (The synaptic connection of the axon of a motor neuron with a muscle fiber)
Etiology - possibly autoimmune
Antibodies attack acetylcholine receptors->decreased acetylcholine->decreased muscle contraction
Gradual onset
Peak onset 20 – 30 years of age

Myasthenia Gravis:Hallmarks of the Disease
Weakness of certain voluntary muscles
Improvement of muscle strength at rest
Dramatic improvement of muscle strength with anticholinesterase drugs

Myasthenia Gravis:Symptoms
Muscles of the eye affected first
Facial, masticatory, speech and neck muscles are next
Muscles of fine hand movements
Intercostal muscles
Myasthenia crisis: acute exacerbation (breathing and throat muscle weakness)

Myasthenia Gravis:Diagnosis
Based on history of weakness in certain muscle groups which improve with rest
Tensilon test (Tensilon extends muscle stimulation, and briefly improves strength. Muscle strength increased as a result of Tensilon injection yields a probable diagnosis of MG)
Serum antibodies to acetycholine
Usually elevated in 80-90% of patients

Myasthenia Gravis:Medical Management
Anticholinesterase drugs facilitate impulse across neuromuscular junctions
Neostigmine; Pyridostigmine
Corticosteroids make symptoms worsen prior to improvement and remission
Plasmapheresis
Washes acetylcholine receptor antibodies from plasma (also done for guillianbarre… can be done over & over…)

Myasthenia Gravis:Nursing Management
Assess
Respiratory function
Degree of strength of all muscles involved
Observe for
Signs and symptoms of pneumothorax (as result to diaphragm & other intercostal muscles being affected)
Unpredictable responses to drugs
Patient teaching
Re exacerbations of the disease

Myasthenia Gravis:Nursing Diagnoses
Ineffective breathing pattern
Impaired gas exchange
Ineffective airway clearance
Activity intolerance
Imbalanced nutrition
Disturbed body image

Restless Leg Syndrome

Etiology and pathophysiology
Signs/Symptoms
Diagnostic studies
Collaborative care
Nursing management

Etiology and pathophysiology
Characterized by leg paresthesias (burning or prickling sensation, “crawing-like”) associated with a strong urge to move
20 million Americans affected
Signs/Symptoms
Worse in the evening when at rest

Diagnostic studies
Diagnosis based on history
Possible associated conditions
Vitamin and mineral deficiencies
Anemias
Polyneuropathies
Diabetes type II
Pregnancy
Peripheral nerve disease
Pinched nerves
Lumbar surgical procedures
Renal failure
Substances, i.e., caffeine, alcohol beta-blockers
Parkinson’s disease (Ignatavicius & Workman, 2006)

Collaborative Care
Treatment of contributing condition
Education on limiting caffeine, nicotine and alcohol
Routine bedtime
No strenuous exercise 2-3 hours before bedtime
Nursing Management
Education (Ignatavicius & Workman, 2006)

Trigeminal Neuralgia
Pathophysiology
Trigeminal neuralgia a/k/a tic douloreux
5th cranial nerve affected
Usually affects people > 50 years of age
Female to male ratio 2:1
Unilateral facial pain (intense spasms)
Provoked by minimal stimulation of a trigger zone
Pain described as…
Sharp; shooting; burning; jabbing; piercing; no motor or sensory deficits; usually life-long from onset; symptoms improve with aging
(Ignatavacius & Workman, 2006)

Trigeminal Nerve
(a/k/a 5th cranial nerve)
Trigeminal nerve sends sensations of pain, touch, pressure, temperature to the brain from the face, jaw, gums, forehead and around the eyes (Gama Knife Center, 2008)

Collaborative Management
Control pain
Dilantin or Tegretol
Neurontin
Local anesthesia
Microcirculation decompression

Trigeminal Neuralgia Nursing Management
Acute pain
Imbalanced nutrition
Anxiety
Impaired oral mucosa

Amyotrophic Lateral Sclerosis (ALS)(Lou Gehrig’s Disease)
Named after 1930s baseball player, Lou Gehrig
Rapidly progressive, degenerative, fatal disease (generally don’t live beyond 5 yrs past diagnosis).
Destruction of motor cells in the anterior grey horns of the spinal cord
Unknown etiology (no known cause, cure, treatment)

Lou Gehrig’s Disease:Classic Pattern
Weakness, atrophy, fasciculation (twitching) of muscles of the hands and arms
Converts to spastic paralysis of the limbs (contractures)
Sensory changes are not present (generally mentally they are completely fine)

Lou Gehrig’s Disease:Symptoms
Muscle weakness, wasting and atrophy
Muscle spasticity and hyperreflexia
Fasciculations
Fatigue
Dyspnea
Brain-stem signs (atrophy of tongue)

Lou Gehrig’s Disease: Symptoms
History and neuro exam
Electromyelogram (EMG) (a/k/a a nerve conduction study)
CPK (also called creatinine kinase) elevated
(CPK found in muscle and brain cells)
Myelogram (contrast x-ray) to rule out other conditions

Lou Gehrig’s Disease (Amyotrophic Lateral Sclerosis):Management
No known treatment or cure (symptomatic)
PT; OT
Gastrostomy tube
Ongoing counseling for patient and family (teaching)
Drug therapy – Rilutek(specific for ALS, will help slow the progression of the disease)

Lou Gehrig’s Disease (Amyotrophic Lateral Sclerosis):Management
Assist patient to remain independent
Limit complications
Prepare for discharge and crisis
Provide emotional and psychological support
Depression is common
Referral to community resources

Bell’s Palsy
CN VII (facial)
Cause is unknown, but reactivation of herpes simplex virus may be implicated
Clinical manifestation
Maximum paralysis evident within 48 hours for half of those affected; within 5 days for others

Bell’s Palsy
(Clinical manifestation, continued)
Drawing sensation and paralysis on affected side
Inability to close eyes, smile, grimace, wrinkle forehead
Face is mask-like and sags
Impaired taste

Bell’s Palsy
Diagnostic tests
No specific test
Exclusion diagnosis…
Collaborative care
Prednisone; Zovirax
Management of neurological deficits
Psychosocial support

Bell’s Palsy:Nursing Diagnoses
Acute pain related to inflammation of CN VII
Imbalanced nutrition related to inability to chew
Risk for injury – corneal abrasion related to inability to blink
Disturbed body image related to change in appearance related to facial muscle weakness

Bell’s Palsy:Nursing Planning
Warm-moist heat
Analgesics as prescribed
Dark glasses
Protect from cold
Artificial tears
Tape eyelids at night

Guillain-Barre Syndrome
Cell mediated immunologic reaction
Acute inflammatory polyneuropathy
Incidence of 1.7 per 100,000
Progressive disorder that affects the motor component of the peripheral nerves
Demyelination(myelin around axons is destroyed… pt has had some type of infection to set it off, auto-immune problem), edema and inflammation

Guillain-Barre Syndrome:Three Stages
Initial
Onset until no further deterioration (usually occurs about 3 wks after viral infection) (1-3 weeks)
Plateau
Little change (several days to 2 weeks) (if caught
Recovery
Coincides with myelination and axonal regeneration (4-6 months)

Guillain-Barre Syndrome:Types
Ascending
Descending
Pure Motor
Miller-Fisher variant

Guillain-Barre Syndrome:Ascending
Most common type
Weakness and numbess begin in legs
Paresthesia (numbness; tingling), hypotonia (abnormally low muscle tone), areflexia (absence of neurologic reflexes)
Respiratory function – insufficiency occurs in 50% of patients

Guillain-Barre Syndrome:Descending
Weakness progresses downward
Motor deficits – initial deficitis in the brainstem, cranial nerves, sternocleidomastoid muscle
Sensory deficits – numbness occurs distally, more often in the hands than in the feet
Paresthesia, hypotonia, and areflexia
Rapid respiratory involvement

Guillain-Barre Syndrome:Pure Motor
Identical to ascending GBS, except sensory signs and symptoms are absent (they have weakness & paralysis, but no numbness or tingling)
May be a mild form of ascending GBS
Muscle pain is generally not present

Guillain-Barre Syndrome:Miller-Fisher Variant
Opthalmoplegia (paralysis or weakness in muscle(s) that control the eye) (CN 3, 4 & 6 affected)
Areflexia
Severe ataxia
Normal motor strength
Intact sensory function

Guillain-Barre Syndrome:Clinical Presentation
Recent history of viral infection
80% to 90% will have little or no residual disability
GBS is characterized by muscle weakness and areflexia
Symptoms tend to be symmetrical and ascending from legs to trunk and arms

Guillain-Barre Syndrome:Clinical Presentation
Respiratory failure attributed to mechanical failure and fatigue of intercostals and diaphragm
If cranial nerves are involved the facial (VII) is most common
GBS does not affect level of consciousness, cognitive function, or pupillary signs
Diagnosis is based upon clinical picture

Guillain-Barre Syndrome:Collaborative Management
Immunotherapy
Plasmaphoresis
Respiratory support – frequently elective intubation
Supportive treatment

Guillain-Barre Syndrome:Nursing Diagnoses
Ineffective breathing pattern: Ineffective airway exchange; Impaired gas exchange
Self-care deficit
Anxiety; Anticipatory grieving

Spinal Cord Problems
Primary injury
Usually compression type injury; rarely dura is punctured
Secondary injury
Edema related to inflammatory response->cascade of events->tissue hypoxia

Spinal Cord Trauma
Mechanisms of injury
Flexion
Hyperextension
Flexion-rotation
Flexion/extension rotation
Compression

Spinal Cord Injury Classification

Incomplete Spinal Cord Injury
Anterior Cord Syndrome
May result in loss or impaired ability to sense pain, temperature or touch below the level of injury
Central Cord Syndrome
Usually results in loss of function in the arms, but some leg movement remains; May have some control over bladder and bowel. Some recovery is possible starting in the legs and moving up
(Apparelyzed, 2009)

Incomplete Spinal Cord Injury
Posterior Cord Syndrome
Muscle power; pain; temperature sensations are preserved.
May have difficulty coordinating movement of limbs
Brown Séquard Syndrome
Pain and temperature sensations may be preserved; has impaired or lost movement on the injured side. Opposite side of injury will have normal movement, but pain and temperature sensation will be impaired or lost.
(Apparelyzed, 2009)

Spinal Cord Trauma
Complete or incomplete
Mechanisms of Injury
Flexion
Hyperextension
Flexion/rotation
Flexion/extension/rotation
Compression

Spinal Cord Trauma
Clinical manifestations
Respiratory system
Cardiovascular system
Urinary system
GI system
Integumentary system
Thermoregulation
Metabolic needs
Peripheral vascular problems

Spinal Cord Trauma
Diagnostic tests
X-ray; CT; MRI (gold standard… CT scan is waste of time); neurologic exam; possibly angiogram
Collaborative care
Non-operative stabilization
ABCs! (always critical)
Stabilized; immobile; trach (+ halo); oxygen; maintain heart rate (atropine); blood pressure (dopamine)
UA catheter; NG
DVT Prevention; stress ulcer prevention;
Temperature control

Spinal Cord Trauma
Drug therapy: Large doses of prednisone
Side effects may include UGI bleeding (stress ulcer)
Surgical therapy
Cervical immobilization – halo
Decompression laminectomy

SCI: Nursing Management / Diagnoses
Impaired gas exchange R/T diaphragmatic fatigue; paralysis; retained secretions; as evidenced by (AEB) decreased PO2; adventitious breath sounds; decreased respiratory rate; respiratory fatigue or distress
Decreased cardiac output R/T venous pooling of blood; bradycardia; immobility; AEB hypotension, restlessness; pulmonary edema
Altered (spinal cord) tissue perfusion
Impaired skin integrity

Spinal Cord Injury: Nursing Diagnoses
Impaired urinary elimination
Constipation
Imbalanced nutrition: less than body requirements
Disturbed body image
Interrupted family processes
Risk for ineffective coping

Risk for autonomic dysreflexia R/T stimulated sympathetic nervous system after spinal shock resolves as evidenced by severe headache, hypertension, bradycardia, nasal stuffiness, flushing, sweating above the level of injury, feeling of apprehension related to noxious stimulation (i.e., distended bladder, fecal impaction, tactile stimulation)
Interventions: remove noxious stimulation
Antihypertensive meds, reverse Trendelenburg or sitting upright
Patient teaching on prevention, recognition, treating

Rehabilitation and Home Care
Respiratory rehabilitation
Neurogenic bladder
Neurogenic bowel
Neurogenic skin
Sexuality
Grief and depression
Long term adaption of patient and family

Affects of Spinal Cord Injury
Segmental Spinal Cord Level and Function
Cl-C6 Neck flexors
Cl-Tl Neck extensors
C3, C4, C5 Supply diaphragm (mostly C4)
C5, C6 Shoulder movement, raise arm (deltoid); flexion of elbow (biceps); C6 externally rotates the arm (supinates)
C6, C7 Extends elbow and wrist (triceps and wrist extensors); pronates wrist
C7, T1 Flexes wrist
C7, T1 Supply small muscles of the hand
T1 -T6 Intercostals and trunk above the waist
T7-L1 Abdominal muscles
L1, L2, L3, L4 Thigh flexion
L2, L3, L4 Thigh adduction
L4, L5, S1 Thigh abduction
L5, S1, S2 Extension of leg at the hip (gluteus maximus)
L2, L3, L4 Extension of leg at the knee (quadriceps femoris)
L4, L5, S1, S2 Flexion of leg at the knee (hamstrings)
L4, L5, S1 Dorsiflexion of foot (tibialis anterior)
L4, L5, S1 Extension of toes
L5, S1, S2 Plantar flexion of foot
L5, S1, S2 Flexion of toes
(Wikipedia, 2009)
(Won’t be tested on this)

Spinal Cord Injury: Functionality of C1, C2, C3 Quadriplegic
Mobility & Movement
Limited head and neck movement depending on muscle strength.
Complete paralysis of arms, body and legs.
Sympathetic nervous system will be compromised, possibility of Autonomic Dysreflexia.
Electric wheelchair may possibly be controlled by either a chin or "sip and puff" controller, this will vary depending on dexterity.
The person will require total assistance when transferring from a bed to a wheelchair and from a wheelchair into a car. A hoist will have to be used, possibly by two assistants for safety.
Complete assistance required during mealtimes.
Respiratory System
Inability to breathe using chest muscles or diaphragm, therefore the person will be dependant on a ventilator to breathe. A portable ventilator can be attached to the back of a wheelchair during transport.
Oxygen and humidification may be required.
Assistance required to clear secretions from trachea, and assistance in coughing will be required.
Personal Care
Complete personal assistance is required. The person will need assistance with washing, dressing, and assistance with bowel and bladder management.
Domestic Care
Complete domestic care is required, such as household cleaning, washing of clothes and kitchen duties, preparation of meals and general household duties.
Communication
A computer may be operated using iris recognition, mouth stick or voice recognition. Telephone can be used using voice recognition and headset.
(Apparelyzed, 2009)

Spinal Cord Injury:Functionality of C4 Spinal Cord Injury

Mobility & Movement
Full head and neck movement depending on muscle strength. Limited shoulder movement.
Complete paralysis of body and legs. No finger, wrist or elbow flexion or extension.
Electric wheelchair may be controlled by either a chin or "sip and puff" controller, this will vary depending on dexterity.
The person will require total assistance when transferring from a bed to a wheelchair and from a wheelchair into a car. A hoist will have to be used, possibly by two assistants for safety.
Complete assistance required during mealtimes.
Respiratory System
Able to breathe without a ventilator using diaphragm.
Assistance required to clear secretions and assistance in coughing will be required.
Personal Care
Domestic Care
Communication
A computer may be operated using iris recognition, mouth stick or voice recognition. Telephone can be used using voice recognition and headset. (Apparelyzed, 2009)

Spinal Cord Injury: Functionality of C5 Spinal Cord Injury
Mobility & Movement
Full head and neck movement with good muscle strength. Good shoulder movement.
Complete paralysis of body and legs. No finger or wrist movement. No elbow extension, good elbow flexion.
Electric wheelchair can be controlled with a hand control for uneven surfaces. A manual wheelchair may be used for short distances on flat surfaces.
The person will require total assistance when transferring from a bed to a wheelchair and from a wheelchair into a car. A hoist will have to be used, possibly by one to two assistants for safety.
Ability to feed self using feeding strap and fork or spoon during mealtimes. Food will need cutting.
Respiratory System
Able to breathe without a ventilator using diaphragm. Low stamina.
Assistance required to clear secretions and assistance in coughing will be required.
Personal Care
Ability to shave and brush hair may be possible with palm straps.
Domestic Care
Communication
A computer may be operated using a typing stick or voice recognition. Telephone can be used using voice recognition and headset. (Apparelyzed, 2009)

Spinal Cord Injury: Functionality of C6 Spinal Cord Injury
Mobility & Movement
Complete paralysis of body and legs. No finger movement, no elbow extension, no wrist flexion. Good wrist extension, good elbow flexion.
A passive key grip may be present by flexing the wrist backwards, but will be weak.
Electric wheelchair can be controlled with a hand control for uneven outdoor surfaces. A manual wheelchair may be used for short distances on flat surfaces.
The person will require total assistance when transferring from floor to chair. Assistance will vary for transfer from bed to wheelchair, and wheelchair to car. A sliding board may be used in assisting with the transfer
Ability to feed self using feeding strap and fork or spoon during mealtimes. Food will need cutting. Able to make hot drinks with adapted kettle using a "kettle tipper".
Respiratory System
Assistance required to clear secretions and assistance in coughing may be required. Additional coughing techniques can be applied to assist in coughing by leaning forward whilst exhaling.
Personal Care
Personal assistance is required. The person will need assistance with washing, dressing, and assistance with bowel and bladder management. Ability to empty own legbag will depend on dexterity and strength.
Ability to partially dress upper body, however, assistance may be required to dress lower body.
Ability to shave, brush hair and brush teeth is possible with palm straps.
Domestic Care
Complete domestic care is required, such as household cleaning, washing of clothes and kitchen duties.
Ability with adapted equipment to prepare simple meals and simple general household duties.
Communication
A computer may be operated using a typing stick or voice recognition. Telephone can be used using voice recognition and headset. (Apparelyzed, 2009)

Spinal Cord Injury: Functionality of C7 - C8 Spinal Cord Injury
Mobility & Movement
Complete paralysis of body and legs. Partial finger movement,full elbow extension and flexion, full wrist extension and flexion.
A C7 injured person will have movement in the thumb.
May use an electric wheelchair for long independent travel or uneven outdoor surfaces. A manual wheelchair may be used for short distances on flat surfaces.
Ability to transfer independently from bed to chair, and chair to car. Car transfers may need assistance depending on upper body strength.
Ability to drive a car adapted with hand controls. Assistance may be required to load wheelchair into car independently.
Ability to feed self independently during mealtimes. Food may need cutting. Able to make hot drinks , may require an adapted kettle using a "kettle tipper".
Respiratory System
Assistance required to clear secretions and assistance in coughing may be required. Additional coughing techniques can be applied to assist in coughing by leaning forward whilst exhaling.
Personal Care
Ability to manage bladder and bowel independently will vary depending on strength and dexterity.
Independent in upper body showering and dressing, lower body dressing and showering may need assistance.
Independent in grooming, usually without palm straps.
Domestic Care
Partial domestic assistance is required, such as heavy household cleaning, home maintenance, and complex preparation of meals.
Ability to prepare simple meals and simple general household duties independently.
Communication
A computer may be operated using a typing stick or voice recognition. Telephone can be used using voice recognition and headset.

Spinal Cord Injury: Functionality of T1 - T4 Paraplegic
Mobility & Movement
Full head and neck movement with normal muscle strength. Normal shoulder movement. Full use of arms, wrists and fingers.
Complete paralysis of lower body and legs. Upper body strength will vary depending on level of injury, but the lower the level, the stronger the upper body strength and balance.
A T4 injured person will have good strength in the chest muscles, however this will get progressively weaker the higher up the injury.
Sympathetic nervous system may be compromised, possibility of Autonomic Dysreflexia.
May use an electric wheelchair for long distance independent travel or uneven outdoor surfaces. A manual wheelchair may be used for everyday living, with the ability to go over uneven ground for short distances.
Ability to drive a car adapted with hand controls. Assistance may be required to load wheelchair into car.
Ability to feed self independently during mealtimes.
Respiratory System
Ability to breathe normal, although respiration capacity and endurance may be compromised.
Personal Care
Should be independent in personal care as long as no other factors are involved, ie, additional injuries, severe spasticity etc.
Domestic Care
Partial domestic assistance is required, such as heavy household cleaning and home maintenance.
Ability to prepare complex meals and general household duties independently.
Communication
Normal communication skills apply.

Spinal Cord Injury: Functionality of T5 - T9 Spinal Cord Injury
Mobility & Movement
Complete paralysis of lower body and legs. Upper body strength will vary depending on level of injury, but the lower the level, the stronger the upper body strength and balance.
A manual wheelchair may be used for everyday living, with the ability to go over uneven ground.
Ability to drive a car adapted with hand controls. Assistance may be required to load wheelchair into car.
Respiratory System
Ability to breathe normal, although respiration capacity and endurance may be compromised.
Personal Care
Domestic Care
Communication
Normal communication skills apply. (Apparelyzed, 2009)

Spinal Cord Injury: Functionality of T10 - L1 Spinal Cord Injury
Mobility & Movement
Partial paralysis of lower body and legs. Upper body strength and balance will vary depending on level of injury, but the lower the level, the stronger the upper body strength and balance.
Ability to transfer independently from bed to chair, and chair to car. It may be possible to transfer from floor to chair depending on upper body strength. It may also be possible to transfer from sitting position to standing frame independently.
Ability to drive a car adapted with hand controls. Ability to load wheelchair into car independently.
Respiratory System
Normal respiratory system.
Personal Care
Domestic Care
Communication

Spinal Cord Injury: Functionality of L2 - S5 Spinal Cord Injury
Mobility & Movement
Full upper body control and balance.
Some hip, knee and foot movement depending on the level of injury. The lower the injury, the more control over movement.
Ability to transfer independently from bed to chair, and chair to car. It may be possible to transfer from floor to chair depending on upper body strength.
Depending on the level of injury, walking may be possible with assistance or aids. Walking will be slow and difficult though.
Ability to drive a car adapted with hand controls. Ability to load wheelchair into car independently.
Respiratory System
Normal respiratory system.
Personal Care
Domestic Care
Partial domestic assistance is required, such as heavy household cleaning, home maintenance.
Communication

The End!

Chronic Neurologic Oct 23.pptx - Slide 1

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Chronic Neurologic Oct 23.pptx - Slide 1 Presentation Transcript