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Terms in this set (93)

Increased intracranial pressure is a life-threatening situation that results from an increase in any or all of the three components of the skull: brain tissue, blood, and cerebrospinal fluid (CSF).

Factors that influence ICP
-Arterial pressure
-Venous pressure
-Intraabdominal and intrathoracic pressure
-Blood gases (CO2 levels)

Degree to which the above factors increase ICP depends on the ability of the brain to accommodate to the changes

-Intracranial pressure valsalva movement
-Coughing increase ICP
-Posture: squatting cause pressure, best posture=10-30 degrees in the bed

Regulation and Maintenance:
Normal intracranial pressure
-Pressure exerted by the total volume from the brain tissue, blood, and CSF
-Modified Monro-Kellie doctrine: Describes relatively constant volume within skull structure
--If volume in any one of the components increases within cranial vault and volume from another component is displaced, the total intracranial volume will not change

Normal compensatory adaptations
-Alteration of CSF absorption or production
-Displacement of CSF into spinal subarachnoid space
-Dispensability of the dura

Ability to compensate is limited
-If volume increase continues, ICP rises

Measuring ICP
Can be measured in
-Subarachnoid space
-Epidural space
-Brain parenchymal tissue

Pressure transducer

Normal ICP: 5 to 15 mm Hg

Mechanisms of Increased ICP:
-Mass lesion
-Cerebral edema
-Head injury
-Brain inflammation
-Metabolic insult

Potential causes results in:
-Hypercapnia , cerebral acidosis, impaired autoregulation, and systemic hypertension
-Promote the formation and spread of cerebral edema
-Edema distorts brain tissue, further increasing ICP
-Leads to more tissue hypoxia and acidosis

-Sustained increases in ICP result in brainstem compression and herniation of brain from one compartment to another
-With brain displacement and herniation, ischemia and edema are further increased.
-Herniations force the cerebellum and brainstem downward through the foramen magnum.
-If compression of the brainstem is unrelieved, respiratory arrest may occur.

Part of the brain moves to another part where it's not supposed to be

Clinical manifestations:
Manifestations of increased ICP depend on
-Cause, location, and rate at which the pressure occurs.
-The earlier the conditon is recognized and treated, the better the prognosis.

Change in level of consciousness
-LOC—sensitive and important indicator of the patient's neurologic status
-May be dramatic as in coma
-May be subtle, such as a change in orientation or a in level of attention

Most important indicator of ICP is level of consciousness

Pulling on restraints increases ICP, don't want to restrain them

Don't want to sedate them: can't check the level of consciousness

Change in vital signs :
Cushing's triad
-increased systolic pressure (widening pulse pressure)
-Bradycardia with a full and bounding pulse
-Irregular respiratory pattern
--Often does not appear till ICP has been increased for some time or markedly increased suddenly (e.g. head trauma)

Effect of ICP on hypothamus can cause a change in body temperature

Compression of the oculomotor nerve (CN III) results in:
-dilation of the pupil ipsilateral to the mass
-Sluggish or no response to light
-an inability to move the eye upward
-ptosis of the eyelid

Other cranial nerves may also be affected with signs of:
-blurred visions
-changes in extra ocular eye movement
-doll's eyes

Papilledema, a nonspecific sign, associated with persistent increased ICP

Fixed, unilaterally, dilated pupil is a neurologic emergency that indicates brain herniation.

decreased In motor function

Contralateral hemiparesis or hemiplegia may be seen

Painful stimuli may elicit a motor response of localization or withdrawal from stimuli

Noxious stimuli may precipate posturing
-Decorticate posturing (flexor): arms are like C's, move in toward the cord
(problems with cervical spinal tract or cerebral hemisphere)
-Decerebrate posturing (extensor): arms are like e's
(problems within midbrain or pons)
--Indicates more serious damage

-Brain itself is insensitive to pain, compression of other intracranial structures, such as the walls of arteries and veins and the cranial nerves produce headache
-Often continuous and worse in the morning
-Straining or movement may accentuate the pain

-Nonspecific sign of ICP
-Not preceded by nausea

-Mental status
-Breathing pattern
-Blood pressure

Two major complications of uncontrolled increased ICP
-Inadequate cerebral perfusion
-Cerebral herniation
--Tentorial herniation
--Uncal herniation
--Cingulate herniation

Diagnostic Studies:
Aimed at identifying underlying cause
-Magnetic resonance imaging (MRI)
-Computed tomography (CT)
-Skull, chest, and spinal x-rays
-Cerebral angiography
-Electroencephalogram (EEG)
-Brain tissue oxygenation measurement
-ICP measurement
-Transcranial Doppler studies
-Evoked potential studies
-Positron emission tomography (PET)
-Laboratory studies: complete blood count (CBC), coagulation profile, electrolytes, creatinine, arterial blood gases (ABGs), ammonia level, general drug and toxicology screen, and CSF protein

Collaborative Care:
Adequate oxygenation:
-PaO2 maintenance at 100 mm Hg or greater
-ABG analysis guides the oxygen therapy
-May require mechanical ventilator

Drug Therapy:
-Antiseizure drugs
-Histamine (H2)—receptor antagonist or proton pump inhibitor

-Was the mainstay treatment, but now found that aggressive hyperventilation increases risk of focal cerebral ischemia and adversely affects outcome
-Brief periods may be useful for refractory intracranial hypertension

Nutritional Therapy:
-Patient is in hypermetabolic and hypercatabolic state
-↑ Need for glucose
Keep patient normovolemic
-IV 0.9% NaCl

increased ICP causes hypermetabolic and hypercatabolic state
-increased ed glucose need to provide the necessary fuel for metabolism of the injured brain
-malnutrition promotes continued cerebral edema, maintenance of optimal nutrition is imperative
-patient cannot maintain an adequate oral intake, other means of meeting the nutritional requirements, such as enteral or parenteral nutrition, should be started
-fluid therapy is directed at keeping patients normovolemic.

Nursing Assessment
-Subjective data from patient or family members
-Glasgow Coma Scale
-Neurologic assessment

Motor strength and response

Vital signs
-Respiratory rate

Nursing Diagnoses
-Ineffective tissue perfusion (cerebral)
-Decreased intracranial adaptive capacity
-Risk for disuse syndrome
-Altered family process

-Maintain a patent airway
-ICP within normal limits
-Normal fluid and electrolyte balance
-No complications secondary to immobility and decreased LOC

Nursing Implementation
-Respiratory function
-Fluid and electrolyte balance
-Monitoring of intracranial pressure
-Body position maintained in head-up position
-Protection from injury
-Psychologic considerations
Any trauma to the

Head trauma includes an alteration in consciousness, no matter how brief

-Firearm-related injuries
-Motor vehicle accidents
-Sports-related injuries
-Recreational accidents

High potential for poor outcome:
Deaths occur at three points in time after injury
-Immediately after the injury
-Within 2 hours after injury
-3 Weeks after injury

Types of Head Injuries:
Scalp lacerations
-The most minor type of head trauma
-Scalp is highly vascular → profuse bleeding
-Major complication is infection

Skull fractures
-Linear or depressed
-Simple, comminuted, or compound
-Closed or open
-Location of fracture alters the presentation of the manifestations
-Facial paralysis
-Raccoon Eyes
-Battle's sign
-Conjugate deviation of gaze
-Rhinorrhea or otorrhea indicate that a fracture has traversed the dura
--Leaking fluid should be tested to determine if fluid is CSF

Minor head trauma:
-A sudden transient mechanical head injury with disruption of neural activity and a change in LOC
-Brief disruption in LOC
-Short duration

Postconcussion syndrome
-2 weeks to 2 months
-Persistent headache
-Personality and behavior changes
-Shortened attention span, decreased short-term memory
-Changes in intellectual ability

Major head trauma
-Includes cerebral contusions and lacerations
-Both injuries represent severe trauma to the brain

-Bruising of brain tissue within a focal area that maintains the integrity of the pia mater and arachnoid layers
-Usually associated with closed head injury
-Coup-contrecoup injury
-Prognosis is dependent on amount of bleeding around the contusion site

-Involve actual tearing of the brain tissue
-Often occur in association with depressed and open fractures and penetrating injuries
-Intracerebral hemorrhage is generally associated with cerebral laceration
-Surgical repair of laceration is impossible
-Prognosis is poor with large intracerebral lacerations

Coup and Contrecoup Head Injury After Blunt Trauma.
1, Coup injury: impact against object;
-a, site of impact and direct trauma to brain;
-b, shearing of subdural veins;
-c, trauma to base of brain.
2, Contrecoup injury: impact within skull;
-a, site of impact from brain hitting opposite side of skull;
-b, shearing forces through brain. These injuries occur in one continuous motion—the head strikes the wall (coup) and then rebounds (contrecoup).

Diffuse axonal injury (DAI)
-Widespread axonal damage occurring after a mild, moderate, or severe TBI
-Process takes approximately 12 to 24 hours

Damage occurs around
-Axons in subcortical white matter of the cerebral hemispheres
-Basal ganglia

Clinical signs
-Decreased LOC
-Increased ICP
-Decerebration or decortication
-Global cerebral edema

Warning signs after a head injury: (the first 24 hours):
-changes in LOC (increased drowsiness, confusion, difficult to arouse)
-bleeding or water drainage from nose or ears
-pupils slow to react or unequal
-visual problems
-loss of sensation to any extremity
-slurred speech
-projectile vomiting

Epidural hematoma
-Results from bleeding between the dura and the inner surface of the skull
-Neurologic emergency
-Venous or arterial origin

Classic signs include
-Initial period of unconsciousness
-Brief lucid interval followed by decrease in LOC
-Nausea, vomiting
-Focal findings

Subdural hematoma
-Occurs from bleeding between the dura mater and arachnoid layer of the meningeal covering of the brain
-Most common source is the veins that drain the brain surface into the sagittal sinus
-Usually venous in origin
--Much slower to develop into a mass large enough to produce symptoms
-May be caused by an arterial hemorrhage

Acute subdural hematoma
-Signs within 48 hours of the injury
-Similar signs and symptoms to brain tissue compression in increased ICP
-Patient appears drowsy and confused
-Ipsilateral pupil dilates and becomes fixed

Subacute subdural hematoma
-Occurs within 2 to 14 days of the injury
-After initial bleeding, subdural hematoma may appear to enlarge over time

Chronic subdural hematoma
-Develops over weeks or months after a seemingly minor head injury
-Peak incidence in sixth and seventh decades of life
-Presenting complaint often focal symptoms, not signs of increased ICP
-Delay in diagnosis in older adults because symptoms mimic those of vascular disease and dementia

Intracerebral Hematoma
-Occurs from bleeding within the parenchyma
-Usually occurs within the frontal and temporal lobes
-Size and location of hematoma determine patient outcome

Diagnostic Studies and Collaborative Care
-CT scan
--Best diagnostic test to determine craniocerebral trauma
-Transcranial Doppler studies
-Cervical spine x-ray
-Glasgow Coma Scale (GCS)

Treatment principles
-Prevent secondary injury
-Timely diagnosis
-Surgery if necessary

Nursing management:
-Glasgow Coma Scale score
-Neurologic status
-Presence of CSF leak

Nursing Diagnosis:
-Ineffective tissue perfusion
-Acute pain
-Impaired physical mobility
-Collaborative problem: Increased ICP

-Maintain adequate cerebral perfusion
-Remain normothermic
-Be free from pain, discomfort, and infection
-Attain maximal cognitive, motor, and sensory function

Nursing Implementation:
Health Promotion
-Prevent car and motorcycle accidents
-Wear safety helmets and seat belts

Acute Intervention
-Maintain cerebral perfusion
-Prevent secondary cerebral ischemia
-Monitor for changes in neurologic status
-Treatment of life-threatening conditions will initially take priority in nursing care
-Major focus of nursing care relates to increased ICP
-Eye problems
-Raise the head of patients leaking CSF

Ambulatory and Home Care
-Bowel and bladder management
-Seizure disorders
-Personality changes
-Family participation and education

-Expected Outcomes
-Maintain normal cerebral perfusion pressure
-Achieve maximal cognitive, motor, and sensory function
-Experience no infection or hyperthermia
-Achieve pain control
Acute inflammation of meningeal tissue
-Always arachnoid mater and cerebrospinal infection

Bacterial meningitis is a medical emergency
-Untreated, mortality rate near 100%

Organisms enter CNS from respiratory tract or bloodstream
-May enter through wounds of skull or fractured sinuses
-Often secondary to viral respiratory disease

Streptococcus pneumoniae and Neisseria meningitidis

Haemophilus influenzae no longer large contributor because of vaccine

Inflammatory response increases CSF production, with moderate increase in ICP

Purulent secretions spread to other areas of brain through CSF

If process extends into parenchyma or if concurrent encephalitis is present, edema and increased ICP become problematic

Clinical Manifestations:
-Severe headache
-Nausea, vomiting
-Nuchal rigidity
-Positive Kernig's sign
-Positive Brudzinski's sign
-↓ LOC
-Signs of ↑ ICP
-Coma has poor prognosis
--Occurs in 5% to 10% of bacterial cases
-Seizures occur in one third of cases
-Headache becomes progressively worse
--Vomiting and irritability may accompany

Acute complication is ↑ ICP
-Major cause of unconsciousness

Residual neurologic dysfunction
-Cranial nerves III, IV, VI, VII, or VIII can become dysfunctional
-Hearing loss may be permanent

Optic nerve is compressed by increased ICP

Ocular movements affected with irritation to nerves III, IV, and VI

CN V irritation includes sensory loss and loss of corneal reflex

Irritation of CN VII results in facial paresis

Irritation of CN VIII causes tinnitus, vertigo, and deafness

Hemiparesis, dysphagia, and hemianopsia may occur and resolve over time

Acute cerebral edema causes
-CN III palsy
-Hypertensive coma

Noncommunicating hydrocephalus if CSF flow obstructed

Waterhouse-Friderichsen syndrome

Diagnostic studies:
-Blood culture
-Lumbar puncture and analysis of CSF
-Gram-stained smear to detect bacteria
-X-rays of skull
-CT scan

Don't do lumbar puncture if any chance of ICP

Collaborative Care:
-Rapid diagnosis based on history and PE
-Antibiotic therapy instituted after collection of specimens
--Able to cross blood-brain barrier
-Examine fundus of eyes before lumbar puncture to identify increased ICP

Nursing Assessment:
-Vital signs
-Oxygenation status
-Motor responses
-Elimination patterns
-F and E balance

Nursing Diagnosis:
-Disturbed sensory pattern
-Acute pain
-Ineffective therapeutic regimen management

Nursing Implementation:
-Vaccination against respiratory infections
-Early treatment of respiratory infections
-Prophylactic antibiotics for those exposed to meningitis
-Careful recording of assessment
-Assist patient to comfortable position
-Administer pain medication
-Darkened room
-Cool cover for eyes
-Low lightning to decrease hallucinations
-Observe and record seizures
-Administer anti-seizure medications
-Manage fever
-Frequent assessments for dehydration
-Initial respiratory isolation
-Aseptic technique
-Small, frequent feedings
-Progressive ROM exercises
-Increase activity as tolerated

Patient will
-Have minimal disorientation
-Lack evidence of agitation
-Have satisfactory pain relief
-Participate in treatment
-Have normal body temperature
Although 30,000 to 70,000 people die each year from rabies worldwide, only 1 to 3 people die annually in the United States. The threat is much greater for developing countries, and the rabies vaccine is encouraged for individuals who will travel globally, as it remains a serious public health concern, and ultimately will result in death if contracted.

The etiology of rabies is an RNA virus that causes an acute, progressive viral encephalitis.

Transmitted via saliva from the bite of an infected animal.

Also spread by scratches, mucous membrane contact with infected secretions, and inhalation of aerosolized virus into the respiratory tract.

Any warm-blooded mammal can carry rabies, including livestock. Throughout the world, rabid dogs are the most common disease vector. However, in developed countries, raccoons, skunks, bats, and foxes are the primary animal carriers.

Clinical Manifestations:
Spreads from the contact site through the CNS via peripheral nerve and possibly muscle fibers.

2 to 14 days after exposure, experience flu-like symptoms, pain, paresthesias, or numbness.

An acute neurologic syndrome occurs 2 to 7 days later and is manifested by agitation, hypersalivation, hydrophobia, dysarthria, vertigo, diplopia, hallucinations, and other neurologic sequelae (e.g., hyperactive reflexes, nuchal rigidity, and a positive Babinski's sign).

Coma develops within 7 to 10 days of the neurologic syndrome. Experience flaccid paralysis, apnea, hydrophobia, and seizures. Death ensues as a result of respiratory and cardiovascular collapse within a few days after the onset of coma.

Because rabies is nearly always fatal, management efforts are directed at preventing the transmission and onset of the disease. Rabies postexposure prophylaxis is discussed in Chapter 69.
Probably the most common type of pain experienced by humans

Majority of people have functional headaches
-Migraine or tension-type headaches

Not all cranium tissues are sensitive to pain

Pain-sensitive structures include venous sinuses, dura, cranial blood vessels, divisions of the trigeminal nerve, facial nerve, glossopharyngeal nerve, vagus nerve, and the first 3 cervical nerves

Classification from the International Headache Society diagnostic criteria

Primary classifications

Can be first symptom of a more serious illness

Can accompany subarachnoid hemorrhage; brain tumors; other intracranial masses; arteritis; vascular abnormalities; trigeminal neuralgia; diseases of the eyes, nose, and teeth; and systemic illness

Symptoms may vary greatly

Clinical evaluation must be thorough
-Life adjustment
-Family situation

Collaborative Care:
If no systemic underlying disease is found, therapy is directed toward functional type of headache

Symptomatic and prophylactic therapies are used
-Including drugs, medications, yoga, biofeedback, cognitive-behavioral therapy, and relaxation training

Nursing Management:
Nursing Assessment
Health history
-Seizures, cancer, stroke, trauma, asthma or allergies, mental illness, stress, menstruation, exercise, food, bright lights, noxious stimuli
-Surgery and other treatments

Specific details about the headache
-Type of pain
-Duration, time of day
-Relation to outside events

Objective Data
-Anxiety or apprehension
-Diaphoresis, pallor, unilateral flushing with cheek edema, conjunctivitis

Nursing Diagnosis:
-Acute pain

-Have decreased or no pain
-Experience increased comfort and reduced anxiety
-Demonstrate understanding of triggering events and treatment strategies
-Use positive coping strategies to deal with chronic pain
-Experience increased quality of life

Nursing Implementation
-Daily exercise, relaxation periods, and socializing help reduce recurrence and should be encouraged
-Suggest alternative pain management such as relaxation, meditation, yoga, and self-hypnosis
-Help patient examine lifestyle, recognize stressful situations, and learn to cope with them more appropriately
-Massage and heat packs can help with tension-type
-Patient should make a written note of medications to prevent accidental overdose
-Teach patient about prophylactic treatment
-Dietary counseling for food triggers
-Avoid smoking and smoke exposure and other environmental triggers

Characterized by unilateral or bilateral throbbing pain

Triggering event or factor

Strong family history

Manifestations associated with neurologic and autoimmune nervous system function

More common in females than males

In United States, prevalence highest in those of lower socioeconomic status

Evidence suggests that vascular, muscular, and biochemical factors are involved

Exact cause is unknown

Can be preceded by an aura and prodrome
-May precede by days or hours
-Aura associated with wave of oligemia beginning at occipital lobe and spreading forward

May be precipitated or triggered by
-Hormonal fluctuations
-Head trauma
-Physical exertion
-Pharmacologic agents

Clinical Manifestations:
Subdivided into five categories

Two most important are
-Migraine with aura
-Migraine without aura

Migraine without aura is the most common

-May start 10 to 30 minutes before the start of headache
-May include sensory dysfunction, motor dysfunction, dizziness, confusion, and even loss of consciousness

Clinical manifestations with migraines
-Generalized edema
-Nausea, vomiting

During headache, some patients "hibernate"
-Seek shelter from noise, light, odors, people, and problems

Headache is described as steady, throbbing pain that matches with the pulse

Pain is usually unilateral but may switch to other side in another episode

Symptoms may worsen over time

Severity is varied
-Not all migraines are disabling

Diagnostic Studies:
-No specific laboratory or radiologic tests
-Diagnosis is usually made from history
-Neurologic and diagnostic examinations are normal
-IHS criteria used as clinical basis
-Neuroimaging techniques are not recommended unless abnormal findings are found on examination

Drug therapy:
-Goal is to terminate or reduce symptoms
-Mild to moderate headache can obtain relief with aspirin or acetaminophen

For moderate to severe, triptans have become first line of therapy
-Affect selected serotonin receptors
-Reduce neurogenic inflammation of cerebral blood vessels
-Produce vasoconstriction

Preventive treatment
-Topiramate (Topamax)
-β-Adrenergic blockers
-Selective serotonin reuptake inhibitors
-Calcium channel blockers
-Divalproex, clonidine, and thiazides
Rare form of headache

Characterized by repeated headaches that occur for weeks or months at a time, followed by periods of remission

One of the most severe forms of head pain

Neither cause nor pathophysiologic mechanism is known

Extracranial vasodilation occurs in affected part of face

Trigeminal nerve is implicated

Involve dysfunction of intracranial blood vessels, sympathetic nervous system, and pain modulation systems

Genetic component has been noted in some families

Smoking and alcohol may be associated with headaches

Clinical Manifestations
Sharp stabbing

Intense pain typically lasting about 1 hour

Pain is usually located around the eye, radiating to the temple, forehead, cheek, nose, or gums

Other manifestations include
-Swelling around the eye
-Facial flushing or pallor
-Constriction of the pupil

During the headache, patient is often agitated and restless

Headaches occur with regularity
-Usually occur at same time of day

Typically last daily for 4 to 8 weeks then into remission for months or years

Diagnostic Studies:
-Diagnosis may be based primarily on history
-Headache diaries are helpful
-CT scan, MRI, or MRA may be performed to rule out aneurysm, tumor, or infection

Drug Therapy:
Drug therapy not as useful as for other headaches

Prophylactic drugs may include verapamil, lithium, ergotamine, divalproex, or NSAIDs

Acute treatment is inhalation of 100% oxygen delivered at a rate of 7 to 9 L per minute for 15 to 20 minutes

Sumatriptan also effective for acute cluster headache

Overuse of analgesics can lead to chronic daily headache or drug-induced headache
Condition in which a person has spontaneously recurring seizures caused by underlying chronic condition

5 to 10 per 1000 persons

Higher incidence in first year of life and in elderly

Common causes during first 6 months of life
-Severe birth injury
-Congenital birth defects involving CNS
-Inborn errors of metabolism

Common causes between 2 and 20 years of age
-Birth injury
-Genetic factors

Common causes between 20 and 30 years of age
Structural lesions
-Brain tumors
-Vascular disease

Common causes after 50 years of age
-Cerebrovascular lesions
-Metastatic brain tumors

75% of seizure disorders are considered idiopathic

Role of heredity in seizure disorders is difficult to determine

Some families carry predisposition in the form of low threshold to seizure-producing stimuli
-High fever

In epilepsy, abnormal neurons undergo spontaneous firing

Cause of abnormal firing is unclear

Firing spreads to adjacent or distant areas of the brain
-If activity involves whole brain, generalized seizure occurs

Often area of brain from which epileptic activity arises is found to have gliosis
-Thought to interfere with normal chemical and structural environment of neurons
-Therefore making them more likely to fire abnormally
-Astrocytes are now believed to play a key role in recurring seizures

Clinical Manifestations
-Determined by site of electrical disturbance
-Divided into two major classes: Generalized and partial

May progress through several phases
-Prodromal phase
-Aural phase
-Ictal phase
-Postictal phase

Prodromal phase precedes seizure with signs or activity

Aural phase with sensory warning

Ictal phase with full seizure

Postictal phase with rest and recovery

Collaborative Care:
Drug therapy aimed at prevention
-Stabilize nerve cell membranes and prevent spread of epileptic discharge
-70% of patients controlled with medication
-Monitor drug serum levels
-Serum levels of medication should be monitored

Primary drugs for treatment of generalized tonic-clonic and partial seizures

-Phenytoin (Dilantin)
-Carbamazepine (Tegretol)
-Divalproex (Depakote)

-Gabapentin (Neurontin)
-Lamotrigine (Lamictal)
-Topiramate (Topamax)
-Tiagabine (Gabitril)
-Levetiracetam (Keppra)
-Zonisamide (Zonegran)

For absence, akinetic, and myoclonic
-Ethosuximide (Zarontin), Depakote, and clonazepam (Klonopin)

Status epilepticus treated with IV lorazepam (Ativan) and diazepam (Valium)
-Must be followed with long-acting drugs

Antiseizure drugs should not be discontinued abruptly because it can precipitate seizures

Side effects include diplopia, drowsiness, ataxia, and mental slowing

Neurologic assessment involves testing for
-Hand and gait coordination
-Cognitive functioning
-General alertness

Side effects outside of CNS include
-Hyperplasia of gingiva
-Blood dyscrasias
-Effects on liver and kidneys

Gerontologic Considerations
-Phenytoin may be problematic for older adults with compromised liver function

Newer antiseizure medications offer better treatment for older adults

Surgical removal of epileptic focus or to prevent spread of epileptic activity in brain
-Removal of one lobe (usually temporal), cortex, or separation of two hemispheres (corpus callosotomy)

Benefits of surgery are reduction or cessation in frequency of seizures

Not all types benefit from surgery

Requirements for surgery
-Diagnosis of epilepsy confirmed
-Adequate trial with drug therapy without satisfactory results
-Electroclinical syndrome defined

Vagal nerve stimulation gives intermittent stimulation to brain to reduce frequency and intensity of seizures

Biofeedback to control seizures teaches patient to maintain a certain brainwave frequency that is refractory to seizure activity

Nursing Assessment:
-Birth defects or injuries at birth
-Anoxic episodes
-CNS trauma
-Metabolic disorders
-Exposure to metals or carbon monoxide
-Hepatic or renal failure
-Compliance with antiseizure medications, barbiturate or alcohol withdrawal, cocaine/amphetamines
-Family history
-Headaches, aura, mood or behavioral changes before seizure
-Anxiety, depression, loss of self-esteem, social isolation
-Decreased sexual drive, ED
-Metabolic acidosis or alkalosis
-Water intoxication
-Bitten tongue, soft-tissue damage, cyanosis
-Abnormal respiratory rate
-Apnea (ictal)
-Absent or abnormal breath sounds
-Airway occlusion
-Hypertension, tachy/bradycardia
-Bowel/urinary incontinence, excessive salivation
-Weakness, paralysis, ataxia (postictal)
-Abnormal CT, MRI, EEG

Tonic-clonic: Loss of consciousness, muscle tightening then jerking, dilated pupils, hyperventilation then apnea, postictal somnolence

Absence: Altered consciousness, minor facial motor activity

Simple: Aura; focal sensory, motor, cognitive, or emotional phenomena; unilateral "marching"; motor seizure

Complex: Altered consciousness with inappropriate behaviors, amnesia of event

Nursing Diagnosis:
-Ineffective breathing pattern
-Risk for injury
-Ineffective coping
-Ineffective therapeutic regimen management

Overall goals are that patient will
-Be free from injury during seizure
-Have optimal mental and physical functioning while taking antiseizure medications
-Have satisfactory psychosocial functioning

Nursing Implementation
-Wearing helmet if risk for head injury
-General health habits (diet, exercise)
-Assist to identify events or situations precipitating seizures and avoidance if possible
-Instruct to avoid excessive alcohol, fatigue, and loss of sleep

Acute Intervention
Observation and treatment of seizure
-Maintain patent airway, support head, turn to side, loosen constrictive clothing, ease to floor
-May require suctioning or oxygen after seizure
Assess level of understanding

Ambulatory and Home Care:
-Instruct on importance of adherence to medication, not to adjust dose without physician
-Keep regular appointments
-Teach family members emergency management
-Emotional support and identification of coping mechanisms
-Medical alert bracelets
-Referrals to agencies and organizations

Dilantin: when given in the hospital is incompatible with everything
When given PO can cause hyperplasia
Has to be on a pump, can push it
Need to be on cardiac monitoring

-Appropriate HR/rhythm, depth of respirations
-No injury
-Verbalization of knowledge of potential injury
-Arrangement of environment to minimize injury
-Acceptance of disorder
-Acknowledgment that a seizure has occurred
-Therapeutic drug levels
-Compliance with therapeutic regimen
Characterized by bilateral, synchronous, epileptic discharges in brain from seizure onset

No warning or aura because entire brain is affected

Loss of consciousness from seconds to minutes

Tonic-clonic seizures (grand mal)
-Characterized by loss of consciousness and falling
-Body stiffens (tonic) with subsequent jerking of extremities (clonic)
-Cyanosis, excessive salivation, tongue or cheek biting may occur
-Postictal phase for tonic-clonic characterized by muscle soreness, fatigue; patient may sleep for hours
-May not feel normal for days
-No memory of seizure

Typical absence seizures (petit mal)
-Occurs only in children and rarely into adolescence
-May cease or develop into another type
-Typical symptom is staring spell for only a few seconds and usually goes unnoticed
-Brief loss of consciousness
-May occur up to 100 times/day if untreated
-EEG demonstrates pattern unique to this type of seizure
-Often precipitated by hyperventilation and flashing lights

Atypical absence seizures characterized by staring spell with other signs and symptoms
-Brief warnings
-Peculiar behavior during seizure
-Confusion after

Myoclonic seizure
-Characterized by sudden, excessive jerk of body and extremities
-Can be forceful enough to cause fall
-Brief and may occur in clusters

Atonic seizure involves tonic episode or paroxysmal loss of muscle tone and person falls

Consciousness usually returns by time person hits ground and can resume normal activity

Great risk for head injury

Tonic seizures involve sudden onset of decreased exterior muscle tone
-Patients often fall

Clonic seizures begin with loss of consciousness and sudden loss of muscle tone
-Followed by limb jerking
Disease of basal ganglia characterized by
-Slowing down in the initiation and execution of movement
-↑ Muscle tone
-Tremor at rest
-Impaired postural reflexes

Diagnosis increases with age, with peak onset being in the sixth decade

More common in men, ratio of 3:2

Other causes of parkinsonism
-Encephalitis lethargica (type A encephalitis) has been associated with onset
--Incidence has dwindled since 1920s
-Symptoms have occurred after intoxication with a variety of chemicals
-Can also been seen after use of illicit drugs, including amphetamines and methamphetamines
-Hydroencephalus, hypoxia, infections, stroke, tumor, and trauma

Pathologic process of PD involves degeneration of dopamine-producing neurons in substantia nigra of the midbrain

Disrupts dopamine-acetylcholine balance in basal ganglia

Symptoms of the disease
-Do not occur until 80% of neurons in the substantia nigra are lost

Clinical Manifestations:
-Onset is gradual and insidious
-Classic triad of PD
--Tremor; Rigidity; Bradykinesia
-Progression may involve only one side of the body initially
-Beginning stages may involve only mild tremor, slight limp, or ↓ arm swing
-Later stages may have shuffling, propulsive gait with arms flexed, and loss of postural reflexes

-So minimal initially that only the patient may notice it
-More prominent at rest and is aggravated by emotional stress or ↑ 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 (PD)

-Increased resistance to passive motion when limbs are moved through ROM
-Rigidity is typified by a jerky quality when the joint is moved
-Rigidity is similar to intermittent catches in the movement of a cogwheel

Caused by sustained muscle contraction and consequently elicits the following
-Complaint of soreness
-Feeling tired and achy
-Pain in the head, upper body, spine, or legs

Inhibits the alternating contraction and relaxation in opposite muscle groups, thus slowing movement

-Slowing down in initiation and execution of movement

Evident in loss of autonomic movements
-Swinging of arms while walking
-Swallowing of saliva
-Self-expression with facial movements

Nonmotor symptoms
-Short-term memory impairment

As disease progresses, complications increase
-Motor symptoms
-Neurologic problems
-Neuropsychiatric problems

Dementia occurs in 40% of patients

Dysphagia may result in malnutrition and aspiration

General debilitation may lead to pneumonia, UTIs, and skin breakdown

Orthostatic hypotension may occur
-Could result in falls and injuries

Sleep disorders are common and potentially severe
-Effective management of sleep disturbances can greatly improve quality of life

Diagnostic Tests
No specific tests

Diagnosis based solely on history and clinical features
-Firm diagnosis can be made when at least 2 of 3 characteristics of the classic triad (tremor, rigidity, and bradykinesia) are present
-Ultimate confirmation of the disease is a positive response to antiparkinsonian drugs

Drug Therapy:
Aimed at correcting imbalances of neurotransmitters within the CNS

Antiparkinsonian drugs either
-Enhance or release supply of DA
-Antagonize or block the effects of overactive cholinergic neurons in the striatum

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

Carbidopa/levodopa is also available as Paracopa
-Rapidly dissolves in the mouth without water

Effectiveness of Sinemet could wear off after a few years of therapy
-Therefore initiation of therapy is with a DA receptor agonist instead
-Sinemet is added when moderate to severe symptoms develop

DA receptor agonists
-Bromocriptine (Parlodel)
-Pergolide (Permax)
-Ropinirole (Requip)
-Pramipexole (Mirapex)

Anticholinergics are also used in management
-↓ Activity of acetylcholine

Antihistamines with anticholinergic or β-adrenergic blockers are used to manage tremors

Antiviral agent amantadine is effective, although exact mechanism is unknown

MAO inhibitor selegiline may be combined with Sinemet

Entacapone and tolcapone block the enzyme that breaks down levodopa in the peripheral circulation
-Prolongs the effects of Sinemet

Initially, only one drug is typically used

As disease progresses, combination therapy is often required

Excessive dopaminergic drugs can lead to paradoxic intoxication

Within 3 to 5 years of treatment, patients experience episodes of hypomobility
-Treated with apomorphine (Apokyn)
--Needs to be taken with an antiemetic drug

Collaborative Care
Surgical therapy
-Procedures aimed at relieving symptoms
-Used in patients who are usually unresponsive to drug therapy or have developed severe motor complications

Ablation surgery
-Has been used to treat PD for over 50 years
-However, has been recently replaced by deep brain stimulation (DBS)

Deep brain stimulation
-Involves placing an electrode in the thalamus, globus pallidus, or subthalamic nucleus
-Connected to a generator placed in the upper chest
-Device is programmed to deliver specific current to targeted brain location

Transplantation of fetal neural tissue into the basal ganglia provides DA-producing cells in the brains of patients
-Still in experimental stages

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

Nursing Management :
Nursing Assessment
Health history
-CNS trauma
-Cerebrovascular disorders
-Exposure to metals and CO2


-Excessive salivation
-Weight loss
-Difficulty initiating movements, falls, loss of dexterity
-Diffuse pain in head, shoulders, neck, back, legs, and hips
-Mood swings

Objective Data
-Blank faces, infrequent blinking
-Ankle edema
-Postural hypotension
-Tremor at rest
-"Pill rolling"
-Poor coordination
-Subtle dementia
-Cogwheel rigidity

Nursing Diagnoses
-Impaired physical mobility
-Imbalanced nutrition: Less than body requirements
-Impaired verbal communication
-Deficient diversional activity

-Maximize neurologic function
-Maintain independence in activities of daily living (ADLs) for as long as possible
-Optimize psychosocial well-being

Nursing Implementation:
Promotion of physical exercise and well-balanced diet
-Limits the consequences from decreased mobility
-Specific exercises to strengthen muscles involved with speaking and swallowing

Teach maintenance of good health, independence, and avoidance of complications

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

Get out of a 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 seats

Assist patients as they make adjustments to their lifestyle to accommodate symptoms

Caregivers may also experience stress associated with the disease progression (i.e., dementia)
Chronic, progressive, degenerative disorder of the central nervous system (CNS)

Characterized by disseminated demyelination of nerve fibers of the brain and spinal cord

Disease usually affects young to middle-aged adults

Onset between 15 and 50 years of age

Women are affected more than men

Cause is unknown

Related to infectious, immunologic, and genetic factors

Multiple genes confer susceptibility to multiple sclerosis (MS)

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

Possible precipitating factors
-Infection; Physical injury; Emotional stress; Excessive fatigue; Pregnancy; Poor state of health

Characterized by chronic inflammation, demyelination, and gliosis in the CNS

Primary neuropathologic condition is an autoimmune disease orchestrated by autoreactive T cells

Initially triggered by a virus in genetically susceptible individuals

Activated T cells migrate to CNS causing blood-brain disruption

Subsequent antigen-antibody reaction leads to demyelination of axons

Disease process consists of
-Loss of myelin
-Disappearance of oligodendrocytes
-Proliferation of astrocytes

Changes result in plaque formation
-Plaques scattered throughout the CNS

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

Myelin can be replaced by glial scar tissue

Nerve impulses slow down without myelin

With destruction of axons, impulses are totally blocked

Results in permanent loss of nerve function

Clinical Manifestations:
Vague symptoms occur intermittently over months and years

Disease may not be diagnosed until long after the onset of the first symptom

Characterized by
-Chronic, progressive deterioration in some
-Remissions and exacerbations in others





Common signs and symptoms
-Motor problems
-Sensory problems
-Cerebellar problems
-Emotional problems

Motor manifestations
-Weakness or paralysis of limbs, trunk, and head
-Scanning speech
-Spasticity of muscles

Sensory manifestations
-Numbness and tingling
-Blurred vision
-Vertigo and tinnitus
-↓ Hearing
-Chronic neuropathic pain

Cerebellar manifestations

Bowel and bladder functions may be impaired
-Spastic bladder
--Small capacity for urine results in incontinence

Flaccid bladder
-Large capacity for urine and no sensation to urinate

Sexual dysfunction can occur in MS
-Erectile dysfunction
-Decreased libido
-Difficulty with orgasmic response
-Painful intercourse
-Decreased lubrication

Emotional manifestations

Diagnostic Studies:
Based primarily on history, clinical manifestations, and presence of multiple lesions over time measured by MRI

Certain laboratory tests are used as adjuncts to clinical examination

Cerebral spinal fluid (CSF) analysis
-↑ In oligoclonal immunoglobulin G
-Contains a higher number of lymphocytes and monocytes

Evoked responses are often delayed because of ↓ nerve conduction from the eye and ear to the brain

Magnetic resonance spectroscopy may also be used to evaluate patients with MS

Drug Therapy:
-Treat acute exacerbations by reducing edema and inflammation at the site of demyelination
-Do not affect the ultimate outcome or degree of residual neurologic impairment from exacerbation

Immunosuppressive Therapy
-Beneficial effects in patients with progressive-relapsing, secondary-progressive, and primary-progressive MS
-Potential benefits counterbalanced against potentially serious side effects

-Interferon -1b (Betaseron)
-Interferon -1a (Avonex, Rebif)
-Glatiramer (Copaxone)
-Mitoxantrone (Novantrone)

Other Drug Therapy
-CNS stimulants
-Tricyclic antidepressants and antiseizure drugs
-Dorsal-column electrical stimulation
-Intrathecal baclofen pump

Physical therapy
-Relieve spasticity
-Improve coordination
-Train patient to substitute unaffected muscles for impaired muscles

Nutritional Therapy
-Include megavitamins and diets consisting of low-fat, gluten-free food and raw vegetables
-High-protein diet with supplementary vitamins is often prescribed

Subjective Data
Health history
-Viral infections or vaccinations
-Residence in cold or temperate climates
-Physical and emotional stress
-Elimination problems
-Weight loss, dysphagia
-Muscle weakness or fatigue, tingling or numbness, muscle spasms
-Blurred or lost vision, diplopia, vertigo, tinnitus
-Decreased libido, impotence
-Anger, depression, euphoria, isolation

Objective Data
-Apathy, inattentiveness
-Pressure ulcers
-Scanning speech
-↓ Hearing
-Muscular weakness
-Foot dragging

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

-Maximize neuromuscular function
-Maintain independence in activities of daily living for as long as possible
-Optimize psychosocial well-being
-Adjust to the illness
-Decrease factors that precipitate exacerbations

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

Focus teaching on building general resistance to illness
-Avoiding fatigue, extremes of hot and cold, exposure to infection

Teach patient
-Good balance of exercise and rest
-Avoiding the hazards of immobility

Teach self-catheterization if necessary

Teach adequate intake of fiber to aid in regular bowel habits
an autoimmune disease of the neuromuscular junction characterized by the fluctuating weakness of certain skeletal muscle groups.

In MG, antibodies attack acetylcholine receptors (AChRs), resulting in a decreased number of AChR sites at the neuromuscular junction.

Clinical Manifestations:
The muscles most often affected by the fluctuating weakness are those used for moving the eyes and eyelids, chewing, swallowing, speaking, and breathing.

The course of this disease is highly variable. Some patients may have short-term remissions, others may stabilize, and others may have severe, progressive involvement.

Myasthenic crisis is an acute exacerbation of muscle weakness triggered by infection, surgery, emotional distress, drug overdose, or inadequate drugs. The major complications of MG result from muscle weakness in areas that affect swallowing and breathing.

Collaborative Care:
Drug therapy includes anticholinesterase drugs, corticosteroids, and immunosuppressants.

Because the presence of the thymus gland in the patient with MG appears to enhance the production of AChR antibodies, removal of the thymus gland results in improvement in a majority of patients.

Plasmapheresis can yield a short-term improvement in symptoms and is indicated for patients in crisis or in preparation for surgery when corticosteroids must be avoided.

The patient with MG who is admitted to the hospital usually has a respiratory tract infection or is in an acute myasthenic crisis. Nursing care is aimed at maintaining adequate ventilation, continuing drug therapy, and watching for side effects of therapy.
Syndrome characterized by dysfunction or loss of

Other characteristics that can manifest
-Personality changes
-Behavioral problems such as

Problems disrupt individual's
-Social responsibilities
-Family responsibilities

Physicians usually diagnose when 2 or more brain functions are significantly impaired

Not a normal part of aging

Affects 15% of older Americans

Half of the patients in long-term care facilities have dementia

~100 causes of dementia

Due to treatable and nontreatable conditions

Two most common causes
-Neurodegenerative conditions
-Vascular disorders

Dementia Patients:
-Lewy Body Disease
-Vascular Dementia
-Alzheimer's Disease
-Other Types
• Pick's disease
• Normal pressure
• Creutzfeldt-Jakob

Important risk factors
-Advanced age
-Family history

Infectious diseases can result in vascular and neurodegenerative changes that can lead to dementia
-Bacterial meningitis
-Viral encephalitis

Dementia sometimes caused by treatable conditions can be reversed

But prolonged exposure may make dementia irreversible

Vascular dementia
-Loss of cognitive function due to brain lesions caused by cardiovascular disease
-Result of decreased blood supply from narrowing and blocking of arteries that supply brain

Predisposed risks of vascular dementia
-Cardiac dysrhythmias
-Diabetes mellitus
-Coronary artery disease

Clinical Manifestations:
Onset of dementia depends on cause
-Insidious and gradual
--Neurologic degeneration dementia is usually gradual and progressive over time
--Vascular dementia tends to be abrupt or progress in a stepwise pattern


Early Stage (Mild)
-Forgetfulness beyond what is seen in a normal person
-Short-term memory impairment
-Geographic disorientation

Clinical Manifestations:
Initial symptoms are related to changes in cognitive function

Family members often report to doctor
-Memory loss
-Mild disorientation
-Trouble with words and/or numbers

Middle Stage (Moderate)
-Impaired ability to recognize close friends and family
-Wandering, getting lost
-Forgets how to do simple tasks
-Delusions, hallucinations

Late Stage (Severe)
-Little memory, unable to process information
-Difficulty eating, swallowing
-Cannot understand words

Dementia vs. Depression
Depression often mistaken for dementia and vice versa

Manifestations of depression, especially in older adults
-Difficulty thinking and concentrating
-Feelings of despair

Dementia and depression occurring together can cause extreme intellectual deterioration

Depression alone or with dementia is treatable

Diagnostic Studies
First focused on determining cause
-Reversible or nonreversible

Thoroughly evaluate patient history

Physical examination to rule out other medical conditions

Screen for
-Cobalamin (vitamin B12) deficiencies
-Possibly neurosyphilis

Mental status testing is important
-Those with mild dementia may be able to compensate, making diagnosis difficult through just conversation

The Mini-Mental State Examination is most commonly used tool for assessing cognitive function

Computed tomography (CT)

Magnetic resonance imaging (MRI)

To monitor changes:
-Single-photon emission computed tomography (SPECT)
-Positron emission tomography (PET)
Chronic, progressive, degenerative disease of the brain

~5.3 million Americans suffer from AD

Most live 8-10 years after being diagnosed

Incidence slightly higher is African and Hispanic Americans
-May be related to socioeconomic status or access to health care, not ethnicity

Women more likely to develop AD
-Have longer life expectancy than men

Exact etiology is unknown

Age of onset determines type:
-Early onset
-Late onset

Familial Alzheimer's disease
-Earlier onset
-More rapid disease course

Changes in brain structure and function
-Amyloid plaques
-Neurofibrillary tangles
-Loss of connections between cells and cell death

Clinical Manifestations:
-Pathologic changes precede clinical manifestations by 5 to 20 years
-Alzheimer's Association has developed a list of 10 warning signs

Early Signs of Alzheimer's Disease:
1. Memory loss that affects job skills
-Frequent forgetfulness or confusion that goes beyond forgetting names or phone numbers
2. Difficulty performing familiar tasks
-Such as cooking a meal then forgetting that they made it
3. Problems with language
-Forget simple words or substitute inappropriate words, making speech hard to understand
4. Disorientation to time and place
-Become lost on their own street: not know where they are, how they got there, or how to get back home
5. Poor or decreased judgment
-May dress inappropriately in noticeable ways, such as wearing a bathrobe to the store or sweater on a hot day
6. Problems with abstract thinking
-Difficulty recognizing numbers or doing basic calculations
7. Misplacing things
-May put items in inappropriate place (such as eating utensils in a clothing drawer) and have no memory of how they got there
8. Changes in mood or behavior
-Exhibit rapid mood swings for no apparent reason
9. Changes in personality
-Such as an easygoing person becoming angry, suspicious, or fearful
-Can change dramatically, either suddenly or over time
10. Loss of initiative
-May become and remain uninterested in many of their usual pursuits

Clinical Manifestations
-Progression is variable from person to person and ranges from 3 to 20 years
-Initial sign is subtle deterioration in memory
-Inevitably progresses to more profound memory loss
-Recent events and new information cannot be recalled
-Behavioral manifestations are not intentional or controllable because of ongoing loss of neurons
-Some develop psychotic manifestations

In AD that has progressed
-Visual agnosia
-Some long-term memory loss

Late stages
-Unable to communicate
-Cannot perform activities of daily living
-Patient may be unresponsive and incontinent, requiring total care

Decreasing the Risk of AD
Early findings show people who engage in activities that involve information processing have a decreased risk of developing AD
-Crossword puzzles
-Learning a new language
Ischemia is inadequate blood flow

Stroke occurs when there is ischemia to a part of the brain that results in death of brain cells

Also known as brain attack

Functions are lost or impaired
-Such as movement, sensation, or emotions that were controlled by the affected area of the brain

Severity of the loss of function varies according to the location and extent of the brain involved

Third most common cause of death in the United States and Canada

Leading cause of serious, long-term disability

Approximately 35% of individuals who have an initial stroke die within 1 year

Blood is supplied to the brain by two major pairs of arteries
-Internal carotid arteries
-Vertebral arteries

Carotid arteries branch to supply most of the
-Frontal, parietal, and temporal lobes
-Basal ganglia
-Part of the diencephalon

Vertebral arteries join to form the basilar artery, which supplies
-Middle and lower temporal lobes
-Occipital lobes
-Part of the diencephalon

Brain requires a continuous supply of blood to provide the oxygen and glucose that neurons need to function

If blood flow to brain is totally interrupted
-Neurologic metabolism is altered in 30 seconds
-Metabolism stops in 2 minutes
-Cellular death occurs in 5 minutes

Brain is normally well protected from changes in mean systemic arterial blood pressure by a mechanism known as cerebral autoregulation

Cerebral autoregulation involves
-Changes in the diameter of cerebral blood vessels in response to changes in pressure so that the blood flow to the brain stays constant

Factors affecting blood flow to brain
-Systemic blood pressure
-Cardiac output
-Blood viscosity

Collateral circulation may develop to compensate for a decrease in cerebral blood flow

An area of the brain can potentially receive blood supply from another blood vessel if its original blood supply is cut off

Atherosclerosis is the hardening and thickening of arteries and is a major cause of stroke

Can lead to thrombus formation and contribute to emboli

In response to ischemia, a series of metabolic events (ischemic cascade) occur
-Inadequate adenosine triphosphate (ATP) production
-Loss of ion homeostasis
-Release of excitatory amino acids
-Free radical formation
-Cell death

Around the core area of ischemia is a border zone of decreased blood flow

Ischemia is potentially reversible

If adequate blood flow can be restored early (<3 hours) and the ischemic cascade can be interrupted
-Less brain damage and less neurologic function lost

Transient ischemic attack (TIA) is a temporary focal loss of neurologic function caused by ischemia

Most TIAs resolve within 3 hours

TIAs may be due to microemboli that temporarily block the blood flow

TIAs are a warning sign of progressive cerebrovascular disease

Computed tomography (CT) of the brain without contrast is the most important initial diagnostic study

Cardiac monitoring and tests may reveal an underlying cardiac condition that is responsible for clot formation

Risk Factors:
-Most effective way to decrease the burden of stroke is prevention
-Risk factors can be divided into nonmodifiable and modifiable

Nonmodifiable Risk Factors:
-Heredity/family history

Modifiable Risk Factors:
-Metabolic syndrome
-Heart disease
-Heavy alcohol consumption
-Poor diet
-Drug abuse
-Sleep apnea
-Physical inactivity

-stroke is more common in men than women
-in most age-groups, more men than women will have a stroke in a given year
-more likely to have a thrombotic stroke
-more likely to have an embolic stroke
-have better chance of surviving from a stroke

-at all ages, more women than men die from strokes
-more likely to have a hemorrhagic stroke
-oral contraceptive use and pregnancy contribute to stroke risk
-tPA used less frequently to treat women who have strokes

Cultural and Ethnic Health Disparities:
•African Americans have a higher incidence of strokes than whites.
•The rate of first strokes in African Americans is almost twice that of whites.
•African Americans are three times more likely than whites to have an ischemic stroke and four times as likely to have a hemorrhagic stroke.
•This high incidence may be related to increased rates of hypertension, diabetes mellitus, and sickle cell anemia in African Americans.
•African Americans also have a higher incidence of smoking and obesity than whites, which are two other risk factors for stroke.
•African Americans are twice as likely to die from a stroke as whites.
•Hispanics, Native Americans, and Asian Americans have a higher incidence of strokes than whites.

Strokes are classified based on the underlying pathophysiologic findings

Clinical Manifestations:
-Affects many body functions
-Motor activity
-Intellectual function
-Spatial-perceptual alterations

Motor Function:
Most obvious effect of stroke

Include impairment of
-Mobility; Respiratory function; Swallowing and speech; Gag reflex; Self-care abilities

Characteristic motor deficits
-Loss of skilled voluntary movement
-Impairment of integration of movements
-Alterations in muscle tone
-Alterations in reflexes

An initial period of flaccidity
-May last from days to several weeks
-Related to nerve damage

Spasticity of the muscles follows the flaccid stage
-Related to interruptions of upper motor neuron influence

Patient may experience aphasia when a stroke damages dominant hemisphere of the brain
-Aphasia is a total loss of comprehension and use of language

Results from damage to different language areas in brain.

Some people may have difficulty repeating words and sentences even though they can speak and they understand the meaning of the word or sentence.

Others may have difficulty naming objects even though they know what the object is and what its use is.

Dysphasia refers to difficulty related to the comprehension or use of language and is due to partial disruption or loss

Dysphasia can be classified as nonfluent or fluent

Many patients experience dysarthria
-Disturbance in the muscular control of speech

Impairments may involve

Dysarthria does not affect the meaning of communications or the comprehension of language

It does affect the mechanics of speech

-Patients who suffer a stroke may have difficulty controlling their emotions
-Emotional responses may be exaggerated or unpredictable
-Depression and feelings associated with changes in body image and loss of function can make this worse

Intellectual Function:
-Patients may also be frustrated by mobility and communication problems
-Both memory and judgment may be impaired as a result of stroke
-A left-brain stroke is more likely to result in memory problems related to language

Spatial-Perceptual Alterations:
-Stroke on the right side of the brain is more likely to cause problems in spatial-perceptual orientation
-However, this may occur with left-brain stroke

Four categories
-Incorrect perception of self and illness
-Erroneous perception of self in space
-Inability to recognize an object by sight, touch, or hearing
-Inability to carry out learned sequential movements on

Sensory-perceptual alterations
-Blindness in same half of each visual field is a common problem after stroke.
--Known as homonymous hemianopsia
-Other visual problems may include
--Diplopia (double vision)
--Loss of the corneal reflex
--Ptosis (drooping eyelid)c

Most problems with urinary and bowel elimination occur initially and are temporary

When a stroke affects one hemisphere of the brain, the prognosis for normal bladder function is excellent

Diagnostic Studies:
When symptoms of a stroke occur, diagnostic studies are done to
-Confirm that it is a stroke
-Identify the likely cause of the stroke

CT is the primary diagnostic test used after a stroke

CT should btained within 25 minutes and read within 45 minutes of arrival at ER

CT will
-Indicate size and location of lesion
-Differentiate between ischemic and hemorrhagic stroke

Other studies to diagnose a stroke, including extent of involvement
-Cerebral angiography
-Digital subtraction angiography
-Transcranial Doppler ultrasonography
-Lumbar puncture
-LICOX system

To measure cerebral blood flow
-Cerebral angiography
-Digital subtraction angiography
-Doppler ultrasonography
-Transcranial Doppler
-Carotid duplex
-Carotid angiography

For cardiac assessment
-Chest x-ray
-Cardiac enzymes
-Holter monitor

Additional studies:
-Complete blood count (CBC)
-Platelets, prothrombin time, activated partial thromboplastin time
-Electrolytes, blood glucose
-Renal and hepatic studies
-Lipid profile

•Reduce salt and sodium intake.
•Maintain a normal body weight.
•Maintain a normal blood pressure.
•Increase level of physical exercise.
•Avoid cigarette smoking or tobacco products.
•Limit consumption of alcohol to moderate levels.
•Use a diet that is low in saturated fat, total fat, and dietary cholesterol and high in fruits and vegetables

Priority for decreasing morbidity and mortality from stroke

Goals of stroke prevention include
-Health promotion for the well individual
-Education and management of modifiable risk factors to prevent a stroke

Patients with known risk factors require close management
-Diabetes mellitus
-High serum lipids
-Cardiac dysfunction

Smoking should be discontinued

Limited alcohol intake

Healthy diet , Weight control

Regular exercise

Routine health examinations

Antiplatelet drugs are usually the chosen treatment to prevent further stroke in patients who have had a TIA

Aspirin is the most frequently used anti platelet agent

Surgical interventions for the patient with TIAs from carotid disease include
-Carotid endarterectomy
-Transluminal angioplasty
-Extracranial-intracranial bypass

Endarterectomy for TIA's (those at risk for stroke - or after a stroke to prevent recurrence)
-Removal of atherosclerotic plaque occluding the central core of the artery

Extracranial/ Intracranial bypass (EC-IC bypass)
-Anastamosing (surgically reconnecting) a branch of an extracranial artery to an intracranial artery beyond the area of obstruction

Acute Care:
-Preserving life
-Preventing further brain damage
-Reducing disability

Treatment differs according to type of stroke and as patient changes:
Begins with managing the ABCs

-Sudden vascular compromise causing disruption of blood flow to the brain
-Arterial venous malformation

Assessment findings
-Altered level of consciousness
-Weakness, numbness, or paralysis
-Speech or visual disturbances
-Severe headache
-↑ or ↓ heart rate
-Respiratory distress
-Unequal pupils
-Facial drooping on affected side
-Difficulty swallowing
-Bladder or bowel incontinence
-Nausea and vomiting

Interventions: Initial
-Ensure patent airway.
-Call stroke code or stroke team.
-Remove dentures.
-Perform pulse oximetry; Maintain adequate oxygenation (SaO2 >95%) with supplemental O2, if necessary.
-Establish IV access with normal saline.
-Maintain BP according to guidelines (e.g., Cardiac Life Support).
-Remove clothing.
-Obtain CT scan immediately.
-Perform baseline laboratory tests (including blood glucose) immediately, and treat if hypoglycemic.
-Position head midline; Elevate head of bed 30 degrees if no symptoms of shock or injury.
-Institute seizure precautions.
-Anticipate thrombolytic therapy for ischemic stroke.
-Keep patient NPO until swallow reflex evaluated.
-Hypertension is common immediately after stroke
--Drugs to lower BP are used only if BP is markedly increased
-Fluid and electrolyte balance must be controlled carefully
--Adequate hydration promotes perfusion and decreases further brain injury

Interventions: Ongoing
Monitor vital signs and neurologic status
-Level of consciousness
-Motor and sensory function
-Pupil size and reactivity
-O2 saturation
-Cardiac rhythm
-NIH Stroke Scale
-Reassure patient and family

Recombinant tissue plasminogen activator (tPA)
-Used to reestablish blood flow through a blocked artery to prevent cell death in patients with acute onset of ischemic stroke symptoms
-Must be administered within 3 to 4.5 hours of onset of clinical signs of ischemic stroke

Aspirin is used within 24 to 48 hours of stroke

Platelet inhibitors and anticoagulants may be used in thrombus and embolus stroke patients after stabilization
-Contraindicated for patients with hemorrhagic stroke

Approximately 5% to 7% of patients who experience a stroke will have seizures, usually within 24 hours
-Phenytoin is given if seizures occur

After stroke has stabilized for 12 to 24 hours, collaborative care shifts from preserving life to lessening disability and attaining optimal functioning

Patient may be transferred to a rehabilitation unit, outpatient therapy, or home care-based rehabilitation

Rehabilitation Unit
-Goal: promote optimal function of the patient and family
-Fall and Injury Prevention
-Prevent Aspiration and Malnutrition
-Lifestyle Modification
-Bowel and Bladder Care
-Medication Management
-Communication and Coping Strategies

Lifestyle changes
-Increase activities
-Change diet
-Stop smoking
-Decrease weight
-Decrease alcohol intake
-Decrease B/P
-Decrease stress
result from:
-Inadequate blood flow to the brain from partial or complete occlusion of an artery

80% of all strokes are ischemic strokes

Ischemic strokes can be
-Transient Ischemic Attack
-Thrombotic Stroke
-Embolic Stroke

Transient ischemic attack
-Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction of the brain
-Symptoms last <1 hour

Thrombotic stroke
-Thrombosis occurs in relation to injury to a blood vessel wall and formation of a blood clot
-Result of thrombosis or narrowing of the blood vessel
-Most common cause of stroke
-Two-thirds are associated with hypertension and diabetes mellitus
-Often preceded by a TIA

Embolic stroke
-Occurs when an embolus lodges in and occludes a cerebral artery
-Results in infarction and edema of the area supplied by the involved vessel
-Second most common cause of stroke
-Majority of emboli originate in the inside layer of the heart, with plaque breaking off from the endocardium and entering the circulation
-Patient with an embolic stroke commonly has a rapid occurrence of severe clinical symptoms
-Onset of embolic stroke is usually sudden and may or may not be related to activity
-Patient usually remains conscious although may have a headache
-Often occurs rapidly
-Recurrence is common unless the underlying cause is aggressively treated

Surgical interventions for stroke
-Ischemic stroke
-Hemorrhagic stroke
--Immediate evacuation of aneurysm-induced hematomas
--Cerebellar hematomas >3 cm

Clipping or coiling of an aneurysm
-Administration of nimodipine (Nimotop) before or after clipping or coiling to decrease vasospasm and minimize cerebral damage
--Restricts the influx of calcium ions into the cells by reducing the number of open calcium channels
--Take BP and apical pulse before admin and hold if pulse < 60 or SBP < 90 and notify primary healthcare provider
Acetylsalicylic Acid

•Analgesic, antipyretic, antiplatelet; NSAID

Inhibits formation of prostaglandins involved in the production of inflammation, pain, and fever. Inhibits platelet aggregation.

•Relieves low-to-moderate pain.
•Decreases inflammation in conditions: systemic lupus erythematosus, rheumatoid arthritis, osteoarthritis, bursitis, and tendonitis.
•Prophylaxis against or reduction of the recurrence of transient ischemic attack and myocardial infarction.

•Hypersensitivity to salicylates
•Clients with diagnosed bleeding disorders
•Do not use during pregnancy
•History of gastrointestinal (GI) ulceration, bleeding problems
•Recent history of viral infection (influenza and chickenpox) in children has been associated with Reyes syndrome.

•Decreases platelet aggregation; **increases bleeding potential
•**Epigastric distress, heartburn, and nausea
•Aspirin overdose or toxicity—**tinnitus, generalized pruritus, headache that may progress to further deterioration with respiratory changes, hyperthermia, sweating, and dehydration with electrolyte imbalance

1. Give with milk or full glass of water to decrease gastric irritation.
2. Teach safety measures to parents regarding medications at home.
3. *The potential for toxicity is high in older adults and children.
4. Teach to avoid concurrent use of alcohol to decrease GI irritation.
5. Client should not take aspirin for at least 1 week before surgery.
6. Evaluate client to determine purpose of medication—pain, inflammation, or antiplatelet action.

Anti-platelet aggregation

Watch for:
-bleeding tendencies
-stomach pain
Candidate for:
-18 yrs or older
-Dx of ischemic stroke causing a measurable neuro defecit
-Time of symptom onset well established to be less than 180 minutes before treatment would begin

*tissue plasminogen activator

-Evidence of intracranial hemorrhage on pretreatment CT
-Only minor or rapidly improving stroke
-Clinical presentation suggestive of subarachnoid hemorrhage, even with normal CT
-Active Internal bleeding
-Known bleeding diathesis
-Surgery or serious trama excluding head trauma in previous 14 days
-Hx of GI or urinary tract hemorrhage within 21 days
-Recent arterial puncture at a noncompresible site
-Recent lumbar puncture
-Severe HTN requiring aggessive treatment
-HX intracranial hemorrhage
-Blood glucose <50 or >400
-Post MI pericarditis
-Seizure occurred with symptoms of stroke

Administration of tPA:
0.9 mg/kg (*maximum of 90mg*) IV infused over 60 minutes with 10% of the total dose administered as an IV bolus over 1 minute

Sequence of Events:
-Determine whether time is available to start treatment with rt-PA before 3 hrs.
-Draw blood for tests while preparations are made to perform non-contrast CT scan
-Start recording B/P
-Neuro exam
-CT scan without contrast
-Determine if CT has evidence of hemorrhage
-If pt has severe head or neck pain, or is somnolent or stuporous, be sure there is no eveidenc eof subarachnoid hemorrhage
-Review required test results (HCT,PLT,BG, PT, or aPTT

-Review patient selection criteria
-Infuse tPA
-Give 0.9 mg/kg, 10% as a bolus, IV
-Do not use the cardiac dose
-Do not exceed the 90 mg maximum dose
-Do not give aspirin, heparin or warfarin for 24 hours
-Monitor the pt carefully, especially b/p. Follow specific b/p treatment protocol
-Monitor neuro status
sudden, usually unilateral, severe, brief, stabbing, recurrent, episodes of pain in the distribution of the trigeminal nerve

relatively uncommon cranial nerve disorder

most commonly diagnosed neuralgic condition

seen twice as often in women as men

majority of cases in persons older than 40

Risk factors
-multiple sclerosis
-herpes virus infection
-infection of the teeth and jaw
-brainstem infarct.

Trigeminal nerve is the fifth cranial nerve (CN V)
-both motor and sensory branches
-sensory branches, primarily the maxillary and mandibular branches, are involved.

No specific cause has been identified
-one theory is that compression of blood vessels, especially the superior cerebellar artery, occurs and results in chronic irritation of the trigeminal nerve at the root entry zone.

Clinicial Manifestations:
Described as a burning or knifelike or a lightning-like shock in the lips, upper or lower gums, cheek, forehead, or side of the nose.

Classic feature
Abrupt onset of paroxysms of excruciating pain

Described as:
-Intense pain, twitching, grimacing, and frequent blinking and tearing of the eye occur during the acute attack (giving rise to the term tic).
-The brief attacks, lasting seconds to 2 or 3 minutes, generally unilateral.
-Attack ends as abruptly as it begins.
-Recurrences are unpredictable; they may occur several times each day or weeks or months apart.
-After the refractory (pain-free) period, a phenomenon known as clustering can occur; it is characterized by a cycle of pain and refractoriness that continues for hours.

The painful episodes are usually initiated by a triggering mechanism of light cutaneous stimulation at specific points (trigger zones) along the distribution of the nerve branches.
Precipitating stimuli include:
-teeth brushing
-a hot or cold blast of air on the face
-washing the face
-touch and tickle seem to predominate as causative triggers rather than pain or changes in temperature.

As a result, the patient may:
-not eat properly
-neglect hygienic practices
-wear a cloth over the face
-withdraw from interaction with other individuals
-may sleep excessively as a means of coping with the pain

Although this condition is considered benign, the severity of the pain and the disruption of lifestyle can result in almost total physical and psychologic dysfunction or even suicide.

Because of the severe pain caused by the condition, clients are susceptible to severe depression and suicide.

Diagnostic Studies:
-Computed tomography (CT) scan to rule out any lesions, tumors, or vascular abnormalities.
-Magnetic resonance imaging (MRI) to rule out multiple sclerosis
-Neurologic assessment including audiologic evaluation, although results are usually normal.

Drug Therapy:
Antiseizure drug therapy
-stabilize the neuronal membrane
-decrease paroxysmal afferent impulses of the nerve.

Usual first-line therapy for trigeminal neuralgia
-carbamazepine (Tegretol) or oxcarbazepine (Trileptal)
-act on sodium channels
-lengthen the time for neuron repolarization, resulting in decreased neuron firing
-may prevent an acute attack or promote remission of symptoms

Drug therapy may not provide permanent pain relief, some patients may seek help from otolaryngologists or acupuncture and megavitamins.

Conservative Therapy
Nerve blocking with local anesthetics is a treatment option. Local nerve blocking results in complete anesthesia of the area supplied by the injected branches. Relief of pain is temporary, lasting 6 to 18 months.

Biofeedback is another strategy for pain management. In addition to controlling the pain, the patient may experience a strong sense of personal control by mastering the technique and altering certain body functions.

Surgical Therapy:
If a conservative approach is not effective, surgical therapy is available.
-Glycerol rhizotomy is a percutaneous procedure that consists of an injection of glycerol through the foramen ovale into the trigeminal cistern.
-Percutaneous radiofrequency rhizotomy (electrocoagulation) consists of placing a needle into the trigeminal rootlets that are adjacent to the pons and destroying the area by means of a radiofrequency current. Can result in facial numbness (some degree of sensation may be retained) or trigeminal motor weakness. Destroys some of the nerve fibers, assists to manage the pain
-Microvascular decompression of the trigeminal nerve is performed by displacing and repositioning blood vessels that appear to be compressing the nerve at the root-entry zone where it exits the pons. Relieves pain without residual sensory---is potentially dangerous since near the brainstem.
-Other procedures include gamma knife radiosurgery, retrogasserian rhizotomy, and suboccipital craniotomy.
palsy (peripheral facial paralysis, acute benign cranial polyneuritis)
-characterized by a disruption of motor branches of the facial nerve (CN VII) on one side of the face in the absence of any other disease, such as a stroke
-can affect any age group, but it is more commonly seen in the 20- to 60-year-old age range
-Despite its good prognosis, Bell's palsy leaves more than 8000 people a year in the United States with permanent, potentially disfiguring facial weakness.
-Bell's palsy is considered benign, with full recovery after 6 months in most patients, especially if treatment is instituted immediately.

The exact etiology is not known
-activation of herpes simplex virus (HSV) may be involved with
inflammation --> edema --> ischemia --> eventual demyelination of the nerve --> creating pain and alterations in motor and sensory function

Clinical Manifestations:
Paralysis of the motor branches of the facial nerve
typically results in:
-flaccidity of the affected side of the face
--with drooping of the mouth accompanied by drooling
-inability to close the eyelid
--with an upward movement of the eyeball when closure is attempted
-widened palpebral fissure (opening between the eyelids)
-flattening of the nasolabial fold
-unilateral loss of taste; decreased muscle movement may alter chewing ability
-inability to smile, frown, or whistle
-some patients may experience a loss of tearing or excessive tearing.
-pain may be present behind the ear on the affected side, especially before the onset of paralysis.

Complications can include psychologic withdrawal because of changes in appearance, malnutrition and dehydration, mucous membrane trauma, corneal abrasions, and facial spasms and contractures.

Diagnosis of Bell's palsy is one of exclusion. Diagnosis and prognosis are indicated by observation of the typical pattern of onset and the testing of percutaneous nerve excitability by electromyogram (EMG).

Methods of treatment include:
-moist heat
-gentle massage
-electrical stimulation of the nerve
--stimulation may maintain muscle tone and prevent atrophy

Care is primarily focused on:
-relief of symptoms
-protection of the eye on the affected side
-prevention of complications

Drug therapy:
Corticosteroids, especially prednisone, are started immediately
-best results are obtained if corticosteroids are initiated before paralysis is complete
-decreases edema and pain, but mild analgesics can be used if necessary
-when the patient improves to the point that corticosteroids are no longer necessary, they should be tapered off over 2 weeks

HSV is implicated in many cases of Bell's palsy
-treatment with acyclovir (Zovirax) alone or in conjunction with prednisone
-valacyclovir (Valtrex)
-famciclovir (Famvir)

Eye care
-Instill methylcellulose drops frequently during the day
-Ophthalmic ointment and eye patches may be required at night
an acute, rapidly progressing, and potentially fatal form of polyneuritis

It is also called postinfectious polyneuropathy and ascending polyneuropathic paralysis.

It is characterized by ascending, symmetric paralysis that usually affects cranial nerves and the peripheral nervous system.

With adequate supportive care, 85% to 95% of these patients recover completely.

The etiology is unknown.

Both cellular and humoral immune mechanisms play a role in the immune reaction directed at the nerves.

The result is a loss of myelin (a segmental demyelination) and edema and inflammation of the affected nerves.

As demyelination occurs, the transmission of nerve impulses is stopped or slowed down.

The muscles innervated by the damaged peripheral nerves undergo denervation and atrophy.

In the recovery phase, remyelination occurs slowly, and neurologic function returns in a proximal-to-distal pattern.

The syndrome is often preceded by immune system stimulation from a viral infection, trauma, surgery, viral immunizations, or human immunodeficiency virus (HIV).

Campylobacter jejuni Is the most recognized organism associated with Guillain-Barré syndrome.

C. jejuni gastroenteritis is thought to precede Guillain-Barré syndrome in approximately 30% of cases.

Other potential pathogens include Mycoplasma pneumoniae, cytomegalovirus, Epstein-Barr virus, varicella-zoster virus, and vaccines (rabies, swine influenza).

a heterogeneous condition with symptoms ranging from mild to severe. Symptoms usually develop 1 to 3 weeks after an upper respiratory or gastrointestinal (GI) infection.
-Weakness of the lower extremities (evolving more or less symmetrically) occurs over hours to days to weeks, usually peaking about day 14. Distal muscles are more severely affected.
-Paresthesia (numbness and -tingling) is frequent, and paralysis usually follows in the extremities. Hypotonia and areflexia are common, persistent symptoms. Sensory loss is variable, with deep sensation more affected than superficial sensations.
-Autonomic nervous system dysfunction is usually seen in patients with severe muscle involvement and respiratory muscle paralysis. The most dangerous autonomic dysfunctions include orthostatic hypotension, hypertension, and abnormal vagal responses (bradycardia, heart block, and asystole).

Other autonomic dysfunctions include bowel and bladder dysfunction, facial flushing, and diaphoresis.

Patients may also have the syndrome of inappropriate antidiuretic hormone (SIADH) secretion

Progression of Guillain-Barré syndrome to include the lower brainstem involves the facial, abducens, oculomotor, hypoglossal, trigeminal, and vagus cranial nerves. This involvement manifests itself through facial weakness, extraocular eye movement difficulties, dysphagia, and facial paresthesia.

Pain is a common finding; the pain can be categorized as paresthesias, muscular aches and cramps, and hyperesthesias. Pain appears to be worse at night. Opioids may be indicated for those experiencing severe pain. Pain may lead to a decrease in appetite and interfere with sleep.

The most serious complication is respiratory failure, which occurs as paralysis progresses to the nerves that innervate the thoracic area.

Respiratory infections or urinary tract infections (UTIs) may occur.

Fever is generally the first sign of infection, and treatment is directed at the infecting organism.

Immobility from the paralysis can cause problems such as paralytic ileus, muscle atrophy, deep vein thrombosis, pulmonary emboli, skin breakdown, and orthostatic hypotension.

Diagnosis is based primarily on patient history and clinical signs.

Cerebrospinal fluid
-normal or has a low protein content initially, but after 7 to 10 days it shows a greatly elevated protein level (700 mg/dL [7 g/L]).

Electromyographic (EMG) and nerve conduction studies
-markedly abnormal (showing reduced nerve conduction velocity) in affected extremities.

Management is aimed at supportive care, particularly ventilatory support, during the acute phase.

Plasmapheresis is used in the first 2 weeks. In patients with severe disease treated within 2 weeks of onset, there is a distinct reduction in length of stay, length of time on ventilator, and time required to resume walking.

Intravenous (IV) administration of high-dose immunoglobulin (Sandoglobulin) has been as effective as plasmapheresis and has the advantage of immediate availability and increased safety. After 3 weeks past disease onset, plasmapheresis and immunoglobin therapies have little value

Corticosteroids appear to have little effect on the disease prognosis or duration.
(lockjaw) is an extremely severe polyradiculitis and polyneuritis affecting spinal and cranial nerves.

It results from the effects of a potent neurotoxin released by the anaerobic bacillus Clostridium tetani.

The toxin interferes with the function of the reflex arc by blocking inhibitory transmitters at the presynaptic sites in the spinal cord and brainstem.

The spores of the bacillus are present in soil, garden mold, and manure.

Worldwide, the number of cases per year is estimated to be 1 million.

In the United States the number of individuals under the age of 40 years with tetanus is increasing, most likely related to intravenous (IV) drug use.

C. tetani enters the body through a traumatic or suppurative wound
-which provides an appropriate low-oxygen environment for the organisms to mature and produce toxin

Other possible sources include dental infection, chronic otitis media, injections of heroin, human and animal bites, frostbite, open fractures, and gunshot wounds.

Incubation period is usually 7 days but can range from 3 to 21 days
-symptoms frequently appearing after the original wound is healed
-the longer the incubation period, the milder the illness and the better the prognosis.

Clinical Manifestations:
Initial manifestations of generalized tetanus include:
-a feeling of stiffness in the jaw (trismus) or neck
-a slight fever
-symptoms of general infection
-generalized tonic spasms occur because of the lack of reciprocal innervation

As the disease progresses, symptoms include:
-progressive ridgidity of the neck muscles, back, abdomen, and extremities

In severe forms, continuous tonic convulsions may occur with opisthotonos (extreme arching of the back and retraction of the head).

Laryngeal and respiratory spasms cause apnea and anoxia.

Additional effects are manifested by overstimulation of the sympathetic nervous system; these include:
-profuse diaphoresis
-labile hypertension
-episodic tachycardia

The slightest noise, jarring motion, or bright light can set off a seizure
-seizures are agonizingly painful
-mortality is almost 100% in the severe form.

Health teaching is aimed at ensuring tetanus prophylaxis, which is the most important factor influencing the incidence of this disease. Adults should receive a tetanus and diphtheria toxoid booster every 10 years.
-Teach the patient that immediate, thorough cleansing of all wounds with soap and water is important in prevention.
-If an open wound occurs and the patient has not been immunized within 5 years, the health care provider should be contacted so that a tetanus booster can be given.

Tetanus toxoid, adsorbed/tetanus toxoid

No trade name

Uses: Tetanus toxoid: Used for prophylactic treatment of wounds

Adult and child: IM 0.5 ml q4-6wk × 2 doses, then 0.5 ml 1 yr after dose 2 (adsorbed); SUBCUT/IM 0.5 ml q4-8wk × 3 doses, then 0.5 ml -1 yr after dose 3, booster dose 0.5 ml ½ q10yr

CONTRAINDICATIONS: Hypersensitivity, active infection, poliomyelitis outbreak, immuno-suppression

Management includes:
administration of tetanus and diphtheria toxoid booster (Td) and tetanus immune globulin (TIG) in different sites before the onset of symptoms to neutralize circulating toxins
a much larger dose of TIG is given to patients with manifestations of clinical tetanus

If equine tetanus antitoxin is to be used, the patient should be tested for sensitivity. Administration of equine antitoxin is not recommended if sensitivity occurs; anaphylactic shock is potentially life threatening, and desensitization is ineffective. The side effects of routine administration of the antitoxin are mild and include a sore arm, swelling at the site, and itching. Serious side effects rarely occur. Routine administration of a booster shot to an adequately immunized patient can cause arm swelling and lymphadenopathy

Equine tetanus antitoxin (horse derived) was the only product available for the prevention of tetanus prior to the development of tetanus toxoid in the 1940s. Equine antitoxin was also used for passive postexposure prophylaxis of tetanus (e.g., after a tetanus-prone wound) until the development of human tetanus immune globulin in the late 1950s. Equine tetanus antitoxin has not been available in the U.S. for at least 40 years

Management includes:
Control of spasms is essential and is managed by:
-deep sedation, usually with diazepam (Valium), barbiturates
-in severe cases, neuromuscular blocking agents such as vecuronium that act to paralyze skeletal muscles

A 10- to 14-day course of penicillin, tetracycline, or doxycycline is recommended to inhibit further growth of C. tetani.

Tracheostomy is usually performed early and the patient is maintained on mechanical ventilation because of laryngospasm and potential need for neuromuscular blocking drugs

Sedative agents and opioid analgesics are given concomitantly to all patients who are pharmacologically paralyzed

Any recognized wound should be debrided or an abscess drained.

Antibiotics may be given to prevent secondary infections.
Bactericidal disrupts and weakens the cell wall, leading to cell lysis and death.

Based on type of penicillin, treatment of infections caused by bacteria

•Narrow spectrum that are penicillinase sensitive—penicillin G (Bicillin), penicillin V (Veetids)
•Penicillinase-resistant (antistaphylococcal penicillins)—nafcillin, oxacillin, dicloxacillin
•Broad-spectrum (aminopenicillins)—ampicillin (Principen), amoxicillin (Amoxil)
•Extended spectrum penicillins (antipseudomonal penicillins)—ticarcillin (Ticar), carbenicillin (Geocillin), piperacillin (Zosyn)

•Hypersensitivity to penicillin, cephalosporins, or carbepenems

•Allergic response (all types)—**rash, itching, hives, anaphylaxis
•With ticarcillin and carbenicillin—sodium overload (heart failure), bleeding as a result of the interference with platelet function

1. Instruct client to check label with regard to administering with food.
2. Instruct client to wear medication-alert bracelet if allergic to penicillin.
3. Monitor renal function to avoid toxic levels.
4. *Monitor client for 30 minutes when given parenterally; administer epinephrine if anaphylaxis occurs.
5. *Collect any laboratory culture specimens before initiating penicillin therapy.
6. Do not mix aminoglycosides with penicillin in the same intravenous (IV) infusion—deactivates the aminoglycoside.
7. *Monitor for circulatory overload and bleeding tendencies when client receives ticarcillin and carbenicillin.
Even young patients with spinal cord injuries can anticipate a long life
-Prognosis for life ~5 years less than persons without spinal cord injuries
-Cause of premature death usually related to compromised respiratory function

Spinal cord injuries can cause major problems
-Potential disruption of individual growth and development
-Economic loss
-High cost of rehabilitation and long-term health care

Estimates from CDC
-12,000 Americans suffer spinal cord injuries each year
-259,000 Americans live with spinal cord injuries

Cost of spinal cord injury care is high

For patient with high cervical injury
-First year: $682,957
-Subsequent years: $122,334

Many spinal cord patients remain independent
-90% are discharged to their home or another noninstitutional residence
-10% are discharged to nursing homes, chronic care facilities, or group homes

Young adult men between ages 16 and 30 are at greatest risk

81% of spinal cord injury patients are 19-year-old males

-42% Motor vehicle crashes
-27% Falls
-15% Violence
--In large urban areas, gunshot wounds may surpass falls
-7% Sport injuries
-8% Other miscellaneous

Increase in number of injuries from 1970s (4.7%) to today (11%) in older adults

Older adults with traumatic spinal cord injuries experience
-More complications
-Longer hospitalizations

Initial Injury
Spinal cord is wrapped in tough layers of dura

Rarely torn or transected by direct trauma

Spinal cord injury due to cord compression by
-Bone displacement
-Interruption of blood supply to cord
-Traction resulting from pulling on cord

Penetrating trauma (gunshot wound or stab wounds)

Primary injury
-Initial mechanical disruption of axons as a result of stretch or laceration

Secondary injury
-Ongoing, progressive damage that occurs after initial injury

Several theories on what causes ongoing damage at molecular and cellular levels
-Free radical formation
-Uncontrolled calcium influx
-Lipid peroxidation

Apoptosis occurs and may continue for weeks or months after initial injury

Complete cord damage in severe trauma related to autodestruction of cord
-Petechial hemorrhages are in central gray matter of cord shortly after injury

Hemorrhagic areas in center of spinal cord
-Appear within 1 hour
-4 hours later may be infarction in gray matter

Ongoing destruction process makes initial care and management of spinal cord injuries critical

Resulting hypoxia, ↓ oxygen tension below level that meets metabolic needs of spinal cord

Lactate metabolites

↑ Vasoactive substances

At high levels, vasoactive substances cause

Leading to subsequent necrosis

Spinal cord has minimal ability to adapt to vasospasm

By ≤24 hours, permanent damage may occur because of edema

Edema secondary to inflammatory response is harmful because of lack of space for tissue expansion

Resultant compression of cord and extension of edema above and below injury increase ischemic damage

Extent of neurologic damage caused by spinal cord injury results from
Primary injury damage
-Actual physical disruption of axons

Secondary damage
-Ischemia, hypoxia, microhemorrhage, and edema

Extent of injury and prognosis for recovery most accurately determined at least 72 hours or more after injury

Classified by mechanism of
-Skeletal level of injury
-Neurologic level of injury
-Completeness or degree of injury

Clinical Manifestations:
Generally direct result of trauma that causes cord compression, ischemia, edema, and possible cord transection

Related to level and degree of injury

Patient with an incomplete lesion may demonstrate a mixture of symptoms

Higher the injury, the more serious the sequelae
-Proximity of cervical cord to medulla and brainstem

Immediate postinjury problems include
-Maintaining a patent airway
-Adequate ventilation
-Adequate circulating blood volume
-Preventing extension of cord damage (secondary damage)

Movement and rehabilitation potential related to specific locations of spinal cord injury

High cervical injury caused by flexion-rotation is the most complex SCI
-Halo fixation apparatus (most frequently used method of stabilization)
-Skeletal traction (Crutchfield, Vinke, or Gardner-Wells tongs)
-Kinetic therapy
-Cervical fusion (cervical collar, sternal-occipital-mandibular immobilizer)

Thoracic or lumbar spine injuries
-Thoracolumbar orthosis ("body jacket")

Return of reflexes may complicate rehabilitation.
-Exaggerated responses
-Penile erections

-Antispasmodic drugs most commonly prescribed are baclofen (Lioresal) and dantrolene (Dantrium) to relax external sphincter and decrease spasticity of pelvic floor muscles.
--Monitor for weakness due to muscle relaxantion effect.
--Avoid driving and similar activities because of sedative effects.
--Do not abruptly stop therapy because of potential CNS irritability.
--Avoid use with tranquilizers and alcohol.

Botulism toxin injections may also be given to treat severe spasticity.

Patient or family may see this as return of function.

Respiratory complications closely correspond to level of injury

During first 48 hours, spinal cord edema ↑ level of dysfunction and respiratory distress may occur.

Cervical injury
Above level of C4
-Presents special problems because of total loss of respiratory muscle function
-Patient is exhausted.
-Labored breathing/ABGs deteriorate.
-Endotracheal intubation/tracheostomy/ mechanical ventilation

Below level of C4
-Diaphragmatic breathing if phrenic nerve is functioning
-Spinal cord edema and hemorrhage can affect function of phrenic nerve and cause respiratory insufficiency
-Hypoventilation almost always occurs with diaphragmatic breathing

Cervical and thoracic injuries cause paralysis of
-Abdominal muscles
-Intercostal muscles

Patient cannot cough effectively
-Leads to atelectasis or pneumonia

Artificial airway provides direct access for pathogens
Important to decrease infections

Neurogenic pulmonary edema may occur

Pulmonary edema may occur in response to fluid overload

Collaborative Care:
-Aggressive chest physiotherapy, incentive spirometry
-Oxygen therapy
-Pain management

*Physical assessment should concentrate on respiratory status, especially in clients with injury at C-3 to C-5, because the cervical plexus innervates the diaphragm.

Any cord injury above level T6 greatly ↓ the influence of the sympathetic nervous system

Bradycardia occurs because of unopposed vagal response.
-Any ↑ in vagal stimulation can result in cardiac arrest
-Anticholinergic (atropine) for marked bradycardia (<40 beats/min)
-Temporary/permanent pacemaker

Peripheral vasodilation results in hypotension

Relative hypovolemia exists due to↑ in venous capacitance

Cardiac monitoring is necessary

Peripheral vasodilation
-↓ Venous return of blood to heart
-↓ Cardiac output

IV fluids or vasopressor drugs (dopamine or norepinephrine) may be required to support BP and manage hypotension

Pulmonary embolism a leading cause of death

Deep vein thrombosis (DVT) problem during first 3 months

Usual signs of pain and tenderness will not be present due to the SCI injury

DVT assessments
-Doppler examination
-Impedance plethysmograph
-Measurement of legs and thigh girth

DVT prophylactic measures
-Compression gradient stockings
-Remove every 8 hours for skin care.

Prophylactic heparin or low-molecular-weight heparin (enoxaparin [Lovenox})

Urinary retention common immediately after injury

Bladder is atonic and overdistended due to loss of autonomic and reflex control of bladder and sphinctermay (may even result in rupture of the bladder).

Bladder overdistention can result in reflux into kidney with eventual renal failure

Indwelling catheter inserted --- Increased risk of infection / UTIs

Bladder may become hyperirritable
-Loss of inhibition from brain
-Reflex emptying

**A common cause of death after spinal cord injury is urinary tract infection. Bacteria grow best in alkaline media, so keeping urine dilute and acidic is prophylactic against infection. Also, keeping the bladder emptied assists in avoiding bacterial growth in urine that has stagnated in the bladder.

If cord injury is above T5, primary GI problems related to hypomotility

Decreased GI motor activity contributes to development of
-Paralytic ileus
-Gastric distention
--Nasogastric tube may relieve gastric distention

Intraabdominal bleeding may occur
-Difficult to diagnose
-Indications of bleeding
--Continued hypotension despite treatment
--Decreased hemoglobin and hematocrit

Expanding girth may also be noted

Stress ulcers common
-Physiologic response to severe trauma or physiologic stress
-High-dose corticosteroids
-Peak incidence occurs 6 to 14 days after injury.
-Drug therapy
--Corticosteroids: should be given with antacids or food to decrease physiological response to high-dose corticosteroids.
Histamine (H2)-receptor blockers (e.g., ranitidine [Zantac], famotidine [Pepcid]) or proton pump inhibitors (e.g., pantoprazole [Protonix], omeprazole [Prilosec]) given prophylactically to decrease the secretion of hydrochloric acid.

Less voluntary neurogenic control over bowel results in neurogenic bowel

Injury level of T12 or below
-Bowel is areflexic; ↓ Sphincter tone

As reflexes return
-Bowel becomes reflexic; Sphincter tone is enhanced; Reflex emptying occurs

-Voluntary or involuntary (reflex) evacuation of bowel control may be lost.
-High-fiber diet and adequate fluid intake
-Stool evacuation measures
--Suppositories (bisacodyl [Dulcolax] or glycerin), small-volume enemas, or digital stimulation by patient or nurse
Stool softner (docusate sodium [Colace]) used to regulate stool consistency

Consequence of lack of movement is skin breakdown

Pressure ulcers can occur quickly
-Prevention of pressure ulcers and other types of injury to insensitive skin is essential.

Can lead to major infection or sepsis

Below level of injury there is no vasoconstriction, piloerection, or heat loss through perspiration;therefore, temperature control is largely external to the patient.

-Adjustment of body temperature to room temperature
-Occurs in spinal cord injuries because sympathetic nervous system interruption prevents peripheral temperature sensations from reaching hypothalamus

With spinal cord disruption, there is also
-Decreased ability to sweat
-Decreased ability to shiver

Degree of poikilothermism depends on level of injury

During first 48 to 72 hours, GI tract may stop functioning (paralytic ileus).

Nasogastric tube may be inserted.
-Nasogastric suctioning may lead to metabolic alkalosis
-Monitor electrolyte levels until suctioning is discontinued and normal diet is resumed
--Diet: (high-protein, high-calorie for energy and tissue repair)

Decreased Tissue perfusion may lead to acidosis

Nutritional needs much greater than expected for immobilized person
-Positive nitrogen and high-protein diet
--Prevents skin breakdown and infection
--Decreases rate of muscle atrophy

Loss of body weight is common

Fluid and electrolyte needs must be carefully monitored.

Oral foods and liquids can be given once bowel sounds are present or flatus has passed.

Female Reproductive Problems
-Effects of spinal cord injury on female sexual response are less clear.
-Woman of child-bearing age remains fertile and has the ability to become pregnant or to deliver normally through birth canal.

Male Reproductive Problems
-Injury level and completeness of injury are needed to understand the male patient's potential for orgasm, erection, and fertility, and the patient's capacity for sexual satisfaction.
-Treatments for erectile dysfunction include drugs, vacuum devices, and surgical procedures.

-Clinically depressed patients require drug treatment or psychotherapy.

-May feel an overwhelming sense of loss
-May believe they are useless and burdens to their families
-Response and recovery differ from those experiencing loss from amputation or terminal illness.

Diagnostic Studies:
-History and physical examination, including comprehensive neurologic examination
-Complete x-rays of spine are performed to assess for vertebral fracture
-Anteroposterior, lateral, and odontoid spinal x-ray studies
-CT scan may be used to assess stability of injury, location, and degree of bone injury
-MRI used where there is unexplained neurologic deficit
-Electrolytes, glucose level, coagulation profile, hemoglobin and hematocrit levels
-Serial bedside PFTs
-EMG to measure evoked potentials
-Venous duplex studies

-Immobilization of vertebral column by skeletal traction
-Maintenance of heart rate (e.g., atropine) and blood pressure (e.g., dopamine [Intropin])
-Methylprednisolone high-dose therapy
-Insertion of nasogastric tube and attachment to suction
-Intubation (if indicated by ABGs and PFTs)
-O2 by high-humidity mask
-Indwelling urinary catheter
-Administration of IV fluids
-Stress ulcer prophylaxis
-Deep vein thrombosis prophylaxis
-Bowel and bladder training

Physical therapy
-Range-of-motion exercises
-Mobility training
-Muscle strengthening

Occupational therapy (splints, activities of daily living training)

Bowel and bladder training

Autonomic dysreflexia prevention

Pressure ulcer prevention

Recreational therapy

Patient and caregiver teaching

Initial goals are to
Sustain life
-Patent airway
-Adequate ventilation
-Adequate circulating blood volume
Prevent further cord damage

Systemic and neurogenic shock must be treated to maintain BP

At cervical level, all body systems must be maintained until full extent of damage is known

Thoracic and lumbar vertebrae injuries
-Systemic support less intense
-Respiratory compromise not as severe
-Bradycardia is not a problem
-Specific problems treated symptomatically

After stabilization, history is obtained
-Emphasis on how injury occurred
-Extent of injury as perceived by patient immediately after event

-Test muscle groups with and against gravity
-Note spontaneous movement
-Sensory examination
-Position sense and vibration
-Brain injury may have occurred—assess history for
--Signs of concussion
--Increased intracranial pressure
-Musculoskeletal injuries
-Trauma to internal organs

Nonoperative Stabilization:
-Focused on stabilization of injured spinal segment and decompression
-Through traction or realignment
-Eliminate damaging motion at injury site
-Intended to prevent secondary damage

Surgical Therapy:
Criteria for early surgery
-Cord decompression may result in ↓ secondary injury
-Evidence of cord compression
-Progressive neurologic deficit
-Compound fracture
-Bony fragments
-Penetrating wounds of spinal cord or surrounding structures

Common surgical procedures
-Decompression laminectomy by anterior cervical and thoracic approaches with fusion
-Posterior laminectomy with use of acrylic wire mesh and fusion
-Insertion of stabilizing rods (Harrington rods for the correction and stabilization of thoracic deformities)

Drug Therapy:
Vasopressor agents
-Used in acute phase
-Maintain mean arterial pressure

When administering vasopressors or adrenergic stimulants, such as dopamine (Intropin):
-Administer through volume-controlled pump.
-Monitor BP every 5 to 15 minutes.
-Watch intravenous site carefully for extravasation and tissue damage.
-Ask health care provider for target mean systolic BP (> 90 mm Hg) so that perfusion to the spinal cord is improved

**All vasopressor drugs are potent and dangerous and require that the client be weaned onto and off them.

Methylprednisolone (MP)
-Administered early and in large doses there is greater recovery of neurologic function
-Commonly used treatment option
-No benefit 8 hours postinjury
-Blocker of lipid peroxidation by-products, is thought to improve blood flow and reduce edema in the spinal cord.
-Side effects include immunosuppression, increased frequency of upper GI bleeding, and increased risk of infection.

Drug interactions may occur

Pharmacologic agents
-Used to treat specific autonomic dysfunctions