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Chronic Neurologic Problems Fall 2009

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Page 1: Chronic Neurologic Oct 23.pptx - Slide 1

Chronic Neurologic Problems

Fall 2009

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Headache

• The most common type of pain experienced by humans

• Types– Tension type headache– Migraine headache– Cluster headache

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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

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Migraine Headache

• Etiology and Pathophysiology– …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

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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

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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.

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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)

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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

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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)

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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

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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

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Headaches:Nursing Management

• Nursing assessment• Nursing diagnoses• Planning• Nursing Implementation• Evaluation

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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

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Chronic Neurologic Disorders

Other

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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.

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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

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Epilepsy

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

Why?

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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

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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!)

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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

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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

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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

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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)

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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.

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Clinical Manifestations

• Aura• Tonic-hypertonic-clonic phase– Loss of consciousness – Bowel and bladder incontinence– Tachycardia – Diaphoresis– Warm skin– Pallor, flushing, cyanosis

• Post-ictal phase

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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

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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?• 911 for seizure lasting > 5 minutes

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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

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Epilepsy: Medications

• Generalized and Partial seizures– Phenytoin (Dilantin); Side effects: gingival

hyperplasia; drug toxicity– Carbamazepine (Tegretol)– Phenobarbital– Divalproex (Depakote)– Gabapentin (Neurontin)

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Epilepsy: Medications

• Absent, Akinetic– Klonopin; Zarotin

• Status Epilepticus – Ativan (benzodiazepine) and Valium

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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)

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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

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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?

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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…

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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

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Multiple Sclerosis Etiology and Pathophysiology• 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

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Multiple Sclerosis

Etiology and Pathophysiology

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

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Multiple Sclerosis

Etiology and Pathophysiology• Possible precipitating factors include:– Infection– Physical injury– Emotional stress– Excessive fatigue– Pregnancy– Poor state of health

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Multiple SclerosisEtiology and Pathophysiology• 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

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Multiple Sclerosis

Etiology and Pathophysiology

• Initially triggered by a virus in a genetically susceptible individual

• Subsequent antigen-antibody reaction leads to demyelination of axons

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Multiple Sclerosis

Etiology and Pathophysiology• 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

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Multiple Sclerosis Etiology and Pathophysiology• 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

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Multiple Sclerosis Etiology and Pathophysiology• 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

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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

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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

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Multiple Sclerosis

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

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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)

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Multiple Sclerosis Clinical Presentation: Emotional

• Anger• Depression• Apathy• Inattentiveness• Euphoria

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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

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Multiple Sclerosis

Clinical Presentation (Other)• Sexual dysfunction can occur in MS

- erectile dysfunction- decreased libido- painful intercourse- decreased lubrication

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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)

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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

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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)

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Multiple Sclerosis:Collaborative Care

• 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

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Multiple Sclerosis:Collaborative Care

• 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)

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Multiple Sclerosis:Collaborative Care

• Physical therapy helps…– Relieve spasticity– Increase coordination– Trains the client to substitute unaffected muscles

for impaired ones

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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

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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

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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

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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

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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

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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

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Multiple Sclerosis:Nursing Implementation

• Teach self-catheterization if necessary• Teach adequate intake of fiber to aid in regular

bowel habits

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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

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Parkinson’s Disease:Etiology and Pathophysiology

• Pathologic process involves degeneration of dopamine-producing neurons in substantia nigra 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 substantia nigra (basal ganglia, lie near the lateral ventricles, when stimulated they release the dopamine) are lost

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Parkinson’s Disease

• 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)

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Parkinson’s Disease

• 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

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Parkinson’s Disease

• Classic triad of clinical symptoms include– Tremor– Rigidity– Bradykinesia (slow movement)– (proprioception, postural instability, loosing

awareness of where their body is at all times)

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Parkinson’s Disease • 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

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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

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Parkinson’s Disease

• 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”)

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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

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Parkinson’s Disease:Complications

• Side effects from drugs, particularly levodopa, include…– Dyskinesia (involuntary movement)– Hallucinations– Orthostatic hypotension – Weakness– Akinesia (without movement or much movement)

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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

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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

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Parkinson’s Disease:Collaborative Care

• 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

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Parkinson’s Disease:Collaborative Care

• 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

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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)

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Parkinson’s Disease:Collaborative Care

• 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)

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Parkinson’s Disease: Collaborative Care

• 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

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Parkinson’s Disease: Collaborative Care

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

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Parkinson’s Disease: Collaborative Care

• 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

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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

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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

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Parkinson’s Disease: Nursing Diagnoses

• Impaired physical mobility• Imbalanced nutrition: less than body

requirements• Impaired verbal communication• Deficient diversion activity • Risk for falls

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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

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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

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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

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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

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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

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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

Page 92: Chronic Neurologic Oct 23.pptx - Slide 1

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)

Page 93: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 94: Chronic Neurologic Oct 23.pptx - Slide 1

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 guillian barre… can be done over & over…)

Page 95: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 96: Chronic Neurologic Oct 23.pptx - Slide 1

Myasthenia Gravis:Nursing Diagnoses

• Ineffective breathing pattern• Impaired gas exchange• Ineffective airway clearance• Activity intolerance• Impaired verbal communication• Imbalanced nutrition • Disturbed body image

Page 97: Chronic Neurologic Oct 23.pptx - Slide 1

Restless Leg Syndrome

Page 98: Chronic Neurologic Oct 23.pptx - Slide 1

Restless Leg Syndrome

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

Page 99: Chronic Neurologic Oct 23.pptx - Slide 1

Restless Leg Syndrome

• 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

Page 100: Chronic Neurologic Oct 23.pptx - Slide 1

Restless Leg Syndrome• 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)

Page 101: Chronic Neurologic Oct 23.pptx - Slide 1

Restless Leg Syndrome

• 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)

Page 102: Chronic Neurologic Oct 23.pptx - Slide 1

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)

Page 103: Chronic Neurologic Oct 23.pptx - Slide 1

Trigeminal Neuralgia

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)

Page 104: Chronic Neurologic Oct 23.pptx - Slide 1

Trigeminal Neuralgia

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

Page 105: Chronic Neurologic Oct 23.pptx - Slide 1

Trigeminal Neuralgia Nursing Management

• Acute pain• Imbalanced nutrition• Anxiety• Impaired oral mucosa

Page 106: Chronic Neurologic Oct 23.pptx - Slide 1

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)

Page 107: Chronic Neurologic Oct 23.pptx - Slide 1

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)

Page 108: Chronic Neurologic Oct 23.pptx - Slide 1

Lou Gehrig’s Disease:Symptoms

• Muscle weakness, wasting and atrophy• Muscle spasticity and hyperreflexia• Fasciculations• Fatigue• Dyspnea• Brain-stem signs (atrophy of tongue)

Page 109: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 110: Chronic Neurologic Oct 23.pptx - Slide 1

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)

Page 111: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 112: Chronic Neurologic Oct 23.pptx - Slide 1

Bell’s Palsy

• Etiology and Pathophysiology– 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

Page 113: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 114: Chronic Neurologic Oct 23.pptx - Slide 1

Bell’s Palsy

• Diagnostic tests– No specific test– Exclusion diagnosis…

• Collaborative care– Prednisone; Zovirax – Management of neurological deficits– Psychosocial support

Page 115: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 116: Chronic Neurologic Oct 23.pptx - Slide 1

Bell’s Palsy:Nursing Planning

• Warm-moist heat• Analgesics as prescribed • Dark glasses• Protect from cold• Artificial tears• Tape eyelids at night

Page 117: Chronic Neurologic Oct 23.pptx - Slide 1

Guillain-Barre Syndrome

• Etiology and Pathophysiology– 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

Page 118: Chronic Neurologic Oct 23.pptx - Slide 1

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)

Page 119: Chronic Neurologic Oct 23.pptx - Slide 1

Guillain-Barre Syndrome:Types

• Ascending• Descending• Pure Motor• Miller-Fisher variant

Page 120: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 121: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 122: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 123: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 124: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 125: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 126: Chronic Neurologic Oct 23.pptx - Slide 1

Guillain-Barre Syndrome:Collaborative Management

• Immunotherapy• Plasmaphoresis• Respiratory support – frequently elective

intubation • Supportive treatment

Page 127: Chronic Neurologic Oct 23.pptx - Slide 1

Guillain-Barre Syndrome:Nursing Diagnoses

• Ineffective breathing pattern: Ineffective airway exchange; Impaired gas exchange

• Impaired physical mobility• Self-care deficit• Impaired verbal communication• Anxiety; Anticipatory grieving

Page 128: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Problems

• Etiology and Pathophysiology– Primary injury• Usually compression type injury; rarely dura is

punctured

– Secondary injury• Edema related to inflammatory response→cascade of

events→tissue hypoxia

Page 129: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Trauma

• Mechanisms of injury– Flexion– Hyperextension– Flexion-rotation– Flexion/extension rotation– Compression

Page 130: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Injury Classification

Page 131: Chronic Neurologic Oct 23.pptx - Slide 1

Incomplete Spinal Cord InjuryAnterior Cord Syndrome

May result in loss or impaired ability to sense pain,

temperature or touch below the level of injury

Central Cord SyndromeUsually 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)

Page 132: Chronic Neurologic Oct 23.pptx - Slide 1

Incomplete Spinal Cord Injury

Posterior Cord SyndromeMuscle power; pain; temperature

sensations are preserved.May have difficulty coordinating

movement of limbs

Brown Séquard SyndromePain 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)

Page 133: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Trauma

• Complete or incomplete • Mechanisms of Injury– Flexion– Hyperextension– Flexion/rotation– Flexion/extension/rotation– Compression

Page 134: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Trauma

• Clinical manifestations – Respiratory system– Cardiovascular system– Urinary system– GI system– Integumentary system– Thermoregulation – Metabolic needs– Peripheral vascular problems

Page 135: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 136: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Trauma

• Drug therapy: Large doses of prednisone – Side effects may include UGI bleeding (stress

ulcer)• Surgical therapy– Cervical immobilization – halo– Decompression laminectomy

Page 137: Chronic Neurologic Oct 23.pptx - Slide 1

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

Page 138: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Injury: Nursing Diagnoses

• Impaired urinary elimination • Impaired physical mobility• Constipation• Imbalanced nutrition: less than body

requirements• Disturbed body image• Interrupted family processes• Risk for ineffective coping

Page 139: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Injury: Nursing Diagnoses

• 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

Page 140: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Injury: Nursing Diagnoses

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

Page 141: Chronic Neurologic Oct 23.pptx - Slide 1

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)

Page 142: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Injury: Functionality of C1, C2, C3 Quadriplegic

Mobility & MovementLimited 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 SystemInability 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 CareComplete personal assistance is required. The person will need assistance with washing, dressing, and assistance with bowel and bladder management.Domestic CareComplete domestic care is required, such as household cleaning, washing of clothes and kitchen duties, preparation of meals and general household duties.CommunicationA computer may be operated using iris recognition, mouth stick or voice recognition. Telephone can be used using voice recognition and headset.

(Apparelyzed, 2009)

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Spinal Cord Injury:Functionality of C4 Spinal Cord Injury

 Mobility & MovementFull 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.Sympathetic nervous system will be compromised, possibility of Autonomic Dysreflexia.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 SystemAble to breathe without a ventilator using diaphragm.Assistance required to clear secretions and assistance in coughing will be required.Personal CareComplete personal assistance is required. The person will need assistance with washing, dressing, and assistance with bowel and bladder management.Domestic CareComplete domestic care is required, such as household cleaning, washing of clothes and kitchen duties, preparation of meals and general household duties.CommunicationA computer may be operated using iris recognition, mouth stick or voice recognition. Telephone can be used using voice recognition and headset. (Apparelyzed, 2009) 

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Spinal Cord Injury: Functionality of C5 Spinal Cord Injury

Mobility & MovementFull 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.Sympathetic nervous system will be compromised, possibility of Autonomic Dysreflexia.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 SystemAble to breathe without a ventilator using diaphragm. Low stamina.Assistance required to clear secretions and assistance in coughing will be required.Personal CareComplete personal assistance is required. The person will need assistance with washing, dressing, and assistance with bowel and bladder management.Ability to shave and brush hair may be possible with palm straps.Domestic CareComplete domestic care is required, such as household cleaning, washing of clothes and kitchen duties, preparation of meals and general household duties.CommunicationA computer may be operated using a typing stick or voice recognition. Telephone can be used using voice recognition and headset. (Apparelyzed, 2009)

Page 145: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Injury: Functionality of C6 Spinal Cord Injury

Mobility & MovementFull head and neck movement with good muscle strength. Good shoulder 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.Sympathetic nervous system will be compromised, possibility of Autonomic Dysreflexia.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 transferAbility 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 SystemAble to breathe without a ventilator using diaphragm. Low stamina.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 CarePersonal 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 CareComplete 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.CommunicationA computer may be operated using a typing stick or voice recognition. Telephone can be used using voice recognition and headset. (Apparelyzed, 2009) 

Page 146: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Injury: Functionality of C7 - C8 Spinal Cord Injury

Mobility & MovementFull head and neck movement with good muscle strength. Good shoulder 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. Sympathetic nervous system will be compromised, possibility of Autonomic Dysreflexia.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 SystemAble to breathe without a ventilator using diaphragm. Low stamina.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 CareAbility 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 CarePartial 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.CommunicationA computer may be operated using a typing stick or voice recognition. Telephone can be used using voice recognition and headset.  

Page 147: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Injury: Functionality of T1 - T4 ParaplegicMobility & MovementFull 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 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.Ability to feed self independently during mealtimes.Respiratory SystemAbility to breathe normal, although respiration capacity and endurance may be compromised.Personal CareShould be independent in personal care as long as no other factors are involved, ie, additional injuries, severe spasticity etc.Domestic CarePartial domestic assistance is required, such as heavy household cleaning and home maintenance.Ability to prepare complex meals and general household duties independently.CommunicationNormal communication skills apply. 

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Spinal Cord Injury: Functionality of T5 - T9 Spinal Cord Injury

Mobility & MovementFull 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 manual wheelchair may be used for everyday living, with the ability to go over uneven ground.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.Respiratory SystemAbility to breathe normal, although respiration capacity and endurance may be compromised.Personal CareShould be independent in personal care as long as no other factors are involved, ie, additional injuries, severe spasticity etc.Domestic CarePartial domestic assistance is required, such as heavy household cleaning and home maintenance.Ability to prepare complex meals and general household duties independently.CommunicationNormal communication skills apply. (Apparelyzed, 2009)

Page 149: Chronic Neurologic Oct 23.pptx - Slide 1

Spinal Cord Injury: Functionality of T10 - L1 Spinal Cord Injury

Mobility & MovementFull head and neck movement with normal muscle strength. Normal shoulder movement. Full use of arms, wrists and fingers.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.A manual wheelchair may be used for everyday living, with the ability to go over uneven ground.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 SystemNormal respiratory system.Personal CareShould be independent in personal care as long as no other factors are involved, ie, additional injuries, severe spasticity etc.Domestic CarePartial domestic assistance is required, such as heavy household cleaning and home maintenance.Ability to prepare complex meals and general household duties independently.CommunicationNormal communication skills apply. (Apparelyzed, 2009)

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Spinal Cord Injury: Functionality of L2 - S5 Spinal Cord Injury

Mobility & MovementFull head and neck movement with normal muscle strength. Normal shoulder movement. Full use of arms, wrists and fingers.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.A manual wheelchair may be used for everyday living, with the ability to go over uneven ground.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 SystemNormal respiratory system.Personal CareShould be independent in personal care as long as no other factors are involved, ie, additional injuries, severe spasticity etc.Domestic CarePartial domestic assistance is required, such as heavy household cleaning, home maintenance.Ability to prepare complex meals and general household duties independently.CommunicationNormal communication skills apply. (Apparelyzed, 2009)

Page 151: Chronic Neurologic Oct 23.pptx - Slide 1

The End!