NEUROLOGICAL SYSTEM DISORDERS

NERVOUS SYSTEM
Cells of the Nervous System
● Neuron
○ Transmits and receives electrical and chemical impulses
■ Insulates and allows quick impulses

Synaptic Transmission

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NEUROTRANSMITTER FUNCTIONS

Adrenaline Fight or Flight

Noradrenaline Concentration

Dopamine Pleasure

GABA Calming

Acetylcholine Learning

Serotonin Calming and Sleep

Histamine Immunity

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Lobes of the brain

• Occipital: Vision
• Temporal: Memory, understanding language
• Parietal: Perception, math, spelling, logic
• Frontal: Thinking, planning, organizing, problem solving, emotions, behavioral control,
personality
• Cerebellum: Balance
• Medulla: HR, BP, reflexes (swallowing, vomiting)
*Language centers:
• Broca’s area: expressive language
• Wernicke’s area: receptive language

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Meninges
• Connective tissue covering the CNS

Cerebrospinal fluid
• A clear, odorless liquid found in your brain and spinal cord.
• CSF is produced mainly by the choroid plexus epithelium and ependymal cells of the ventricles
and flows into interconnecting chambers; namely, the cisterns and the subarachnoid spaces.

STROKE
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What is a stroke?
• “A disease that affects the arteries leading to and within the brain. It is the No. 5 cause of death
and a leading cause of disability in the United States. A stroke occurs when a blood vessel that
carries oxygen and nutrients to the brain is either blocked by a clot or bursts”.

• There is a lack of oxygen to the brain, and that causes damage!

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• This lack of oxygen can be:

● Hemorrhagic
● Ischemic
○ Embolic
○ Thrombotic

Pathophysiology - Hemorrhagic stroke

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● A vessel ruptures and bleeds into the brain.

● As the blood accumulates, there is increased pressure on the brain
● The rupture can be caused by a weakened vessel, such as in an aneurysm.
“Worst headache of my life”

Pathophysiology - Ischemic stroke

● Blood flow to the brain is blocked by a blood clot.
○ Thrombotic - a blood clot (thrombus) in an artery going to the brain. Onset in a stepwise
fashion.
○ Embolic - a clot that’s formed elsewhere (usually in the heart or neck arteries) travels in the
bloodstream and clogs a blood vessel in or leading to the brain. Sudden onset!
● There is a loss of blood circulating to this area of the brain.
● The lack of blood leads to a lack of oxygen, causing ischemia and damage.

Assessment
● Warning signs:
○ Balance
■ Dizzy → loss of balance
○ Eyes
■ Blurry vision
■ Abnormal pupil response
■ Hemianopia-loss of half of a visual field
● Facial droop
■ Unilateral
● Arms
■Arm drift or weakness
● Speech
■ Aphasia
■ Dysphagia

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■ Altered LOC/Confusion

DIAGNOSTIC PROCEDURES

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• A non-contrast computed tomography (CT) scan is the initial diagnostic test and should be
performed within 25 min from the time of client arrival to the emergency department. This will
assist with the determination of type of stroke (ischemic versus hemorrhagic) and whether the
client is a candidate for thrombolytic therapy.

• A magnetic resonance imaging (MRI) can be used to identify edema, ischemia, and necrosis. A
magnetic resonance angiography or a cerebral angiography are used to identify the presence of a
cerebral hemorrhage, abnormal vessel structures (AV malformation, aneurysms), vessel ruptures,
and regional perfusion of blood flow in the carotid arteries and brain.

• A lumbar puncture is used to assess for the presence of blood in the cerebrospinal fluid. A
positive finding is consistent with a cerebral hemorrhage or ruptured aneurysm.

• The Glasgow Coma Scale is used when the client has a decreased level of consciousness or
orientation. The risk for increased intracranial pressure (ICP) exists related to the swelling of the
brain that can occur secondary to ischemic insul

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DOOR TO NEEDLE TIME

• This time is commonly referred to as the 'door to needle' (DTN)
time. Our standard, set by the Clinical Commissioning Group (CCG) is to achieve a median time
of scanning and thrombolysis within 60 minutes from the time that the patient enters the hospital.

To receive tPA the patient should have a:

• CT of head that is NEGATIVE for hemorrhage
• labs within normal limits (glucose, INR, platelets)
• BP needs to be controlled SBP <185 and DBP <110
• glucose controlled (increases rise of hemorrhage)
• not receiving heparin or other types of anticoagulants
• It must be given within 3 hours from the onset of stroke symptoms.

• Nurse’s Role: monitor for BLEEDING, neuro checks around the clock, blood pressure
medication if needed for hypertension, vital signs, labs, glucose, preventing injury (bedrest), avoid
unnecessary venipunctures, avoid IM injections, will go to ICU to be monitored

Nursing Interventions for Stroke

• Monitor vital signs and neuro status:
• especially blood pressure (notify MD is hypertensive)
• airway (difficulty swallowing….at risk for aspiration HOB 30’ with suction at bedside)
• turn every 2 hours with proper alignment and watch for increased ICP (intracranial pressure)
during acute stage
- headache, nausea and vomiting, increased blood pressure and decreased HR
and decreased RR, decrease in mental status from baseline, pupils don’t respond.

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Assess with NIH Stroke Scale

• Score ranges from 0 to 42
• 0: no stroke symptoms
• 21-42: severe symptoms
• 11 assessments area are scored

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• Assesses:
- Level of consciousness, gaze, visual, facial palsy, motor function of extremities, sensory,
best language, dysarthria, extinction/inattention
- Check cranial nerves: pupil responses, motor function, gag reflex
- Monitor bowel and bladder function (may be incontinent or retaining)
- Passive ROM with extremities and preventing contractions

Interventions for aphasia

• Communication is key (just because the patient can’t communicate doesn’t mean they have a
mental deficit). They just can’t get it out and it takes them time. The nurse’s role is to help bridge
the gap and make it less frustrating for the patient.

Receptive Aphasia: unable to comprehend speech (Wernicke’s area)

-use short phrases
-use gestures or point while giving a command
-be patient and not expect a fast response
-remove distractions

Expressive Aphasia: comprehends speech but can’t respond back with speech (Broca’s area)
-be patient and let them speak
-be direct and simple when asking questions…..give options
-communication via a dry erase board

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Stroke care is a multidisciplinary approach: need to involve family as much as possible because
they will be providing care when patient is discharged. In addition, it is important to be always be
communicating with the speech language pathologist, physical therapy, occupational therapy etc.

Diet: evaluated by speech language pathologist

• may need thicken liquids and mechanical soft foods
• assist with eating and monitor for pouching of food in cheek (on the affected side). This
increases risk of aspiration.
• Have patient tuck in chin to their chest while swallowing.

Watch for neglect syndrome: (tends to happen in right side brain damage). The patient is at
risk for injury because patient ignores the affected side.
• Remind patient to use and touch both sides of body daily (must make a conscious effort to do
so).
• Educate the patient about the importance of turning head side-to-side to prevent injuring the
affected side.

Hemianopsia interventions: turning head side-to-side to see all visual fields to prevent injury

CLIENT EDUCATION
● Use the unaffected side to exercise the affected side of the body.
● For edema of the extremities, massage by stroking from the fingertips or toes back toward the
body to encourage fluid movement.
● Support the arm while in bed, the wheelchair, or during ambulation with an arm sling or
strategically placed pillows

HEALTH PROMOTION AND DISEASE PREVENTION

● Hypertension, diabetes mellitus, smoking, and other related disorders can increase a client’s risk
for a stroke.
● Early treatment of hypertension, maintenance of blood glucose within expected range, and
refraining from smoking will decrease
these risk factors.

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● Maintaining a healthy weight and getting regular exercise can also decrease the risk of a stroke.

SEIZURES AND EPILEPSY

• Seizures are an abrupt, abnormal, excessive, and uncontrolled electrical discharge of neurons
within the brain that can cause alterations in the level of consciousness and/or changes in
motor and sensory ability and/or behavior.
• Epilepsy is the term used to define chronic recurring abnormal brain electrical activity resulting
in two or more seizures. Seizures resulting from identifiable causes, such as substance withdrawal
or fever, are not considered epilepsy.
• The International Classification of Epileptic Seizures uses three broad categories to describe
seizures: generalized, partial, and unclassified.

Risk factors
● Genetic predisposition: Absence seizures are more common in children and tend to occur in
families.
● Acute febrile state: Particularly among infants and children younger than 2 years old.

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● Head trauma: Can be early or late onset (up to 9 months), and incidence is increased when the
head trauma includes a skull fracture.
● Cerebral edema: Especially when it occurs acutely and seizure activity tends to disappear when
the edema is successfully treated.
● Abrupt cessation of antiepileptic drugs (AEDs): As a rebound activity.
● Infection: If intracranial, a result of increased intracranial pressure; if systemic, a result of the
persistent febrile state.
● Metabolic disorder: A result of insufficient or excessive chemicals within the brain, such as
occurring with hypoglycemia or hyponatremia.
● Exposure to toxins: Especially those associated with pesticides, carbon monoxide, and lead
poisoning.
● Stroke: Most likely to occur within the first 24 hr following a stroke as a result of increased
intracranial pressure.
● Heart disease: Common cause of new-onset seizures in older adults.
● Brain tumor: If benign, seizures caused by the increased bulk associated with the tumor; if
malignant, associated with the ability of the brain tissue to function.
● Hypoxia: Results in a decreased oxygen level of the brain; necessary for neuronal activity.
● Acute substance withdrawal: Dehydration accompanies withdrawal, creating a toxic level of the
substance in the body.
● Fluid and electrolyte imbalances: Results in abnormal levels of nutrients required for neuronal
function.
● With older adult clients, increased seizure incidence is associated with cerebrovascular diseases

Nursing Management
During a seizure
● Protect the client’s privacy and the client from injury (move furniture away, hold head in lap if
on the floor).
● Position the client to provide a patent airway.
● Be prepared to suction oral secretions.
● Turn the client to the side to decrease the risk of aspiration.
● Loosen restrictive clothing.
● Do not attempt to restrain the client.

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● Do not attempt to open the jaw or insert airway during seizure activity (can damage teeth, lips,
and tongue).
● Do not use padded tongue blades.
● Document onset and duration of seizure and findings (level of consciousness, apnea, cyanosis,
motor activity, incontinence) prior to, during, and following the seizure.

After a seizure
● This is the postictal phase of the seizure episode.
● Maintain the client in a side-lying position to prevent aspiration and to facilitate drainage of oral
secretions.
● Check vital signs.
● Assess for injuries.
● Perform neurological checks.
● Allow the client to rest if necessary.
● Reorient and calm the client, who might be agitated or confused.
● Determine if client experienced an aura, which can indicate the origin of seizure in the brain.
● Try to determine possible trigger (such as fatigue)

• Seizure precautions may include:

- at bedside have suction and oxygen ready
- IV access (to given anti-seizure medication, if needed)
- padded side rails
- pillow under head (to protect head)
- bed in the lowest position
- remove objects that can cause injury (remove any restrictive clothing or items
- the patient may be wearing….eye glasses etc. )

EEG may be ordered:

• What’s an EEG?: assesses brain activity
• Painless
• Hold seizure medications or medications that are stimulants or depressants prior to EEG (these
medications can prevent the proper assessment of abnormal brain waves associated with a seizure)

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• No caffeine products (a stimulant) 8 hours before

• Can eat before
• Make sure patient’s hair is clean (needs good attachment to scalp)
• Different types of EEGs: some patients will need to experience sleep deprivation before the test
by not sleeping the night before the test or only part of the night….always ask about this.

Education to patient about factors that can trigger a seizure:

Treatment
● Anticonvulsants
○ Rapid acting - lorazepam
○ Long acting - phenytoin
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● Very important to monitor for therapeutic levels

● Never stop taking suddenly - can cause a seizure

• Barbiturates: Phenobarbital (used tonic-clonic or focal seizures & status epilepticus)

•Side effects: drowsiness, uncoordinated movements (ataxia) etc.
• watch for: respiratory depression and hypotension
• drug level 15 to 40 mcg/mL

• Hydantoins: Phenytoin (used in tonic-clonic or focal seizures)

• watch the gums: will enlarge and easily bleed (called gingival hyperplasia….teach about good
mouth care, gum gingival hyperplasiamay cause bone marrow suppression (watch platelets and
WBCs)
• tell patient to watch for rash or Steven-Johnson’s Syndrome and to REPORT it to their doctor
immediately
• don’t give with milk or antacids (interferes with absorption)
• 10 to 20 mcg/mL

Benzodiazepines: absence seizures, tonic clonic, focal

• Diazepam or Lorazepam: status epilepticus (fast acting)
• Very drowsy, tolerance can develop where it isn’t as effective, impair liver (monitor liver
studies)
• Reversal agent: Flumazenil (*used with extreme caution due to its risks)

Valproates: Valproic Acid

• all types….monitor liver, WBC and platelets, GI issues

Other treatments:

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• surgery: to remove an area of the brain that is causing the seizure….example: focal seizures that
arise from temporal lobe (temporal lobectomy)
• Meds not working: placement of a vagus nerve stimulator: an electrical device that sends
electrical signals to the vagus nerve
• Ketogenic diet (used in pediatric patient who have epilepsy): high fat, low carb, diet….used
when seizures not controlled by medication.

CLIENT EDUCATION
● Take medications at the same time every day to enhance effectiveness.
● The potential to develop tolerance to anti seizure medications over time is called drug decline.
This can lead to an increase in seizures. Some clients develop sensitivity with age. If drug decline
or sensitivity occurs, clients will need blood levels drawn frequently and medication dosages
adjusted

Complications
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Status epilepticus
• This is repeated seizure activity within a 30-min time frame or a single prolonged seizure lasting
more than 5 min.
• The complications associated with this condition are related to decreased oxygen levels, inability
of the brain to return to normal functioning, and continued assault on neuronal tissue.
• This acute condition requires immediate treatment to prevent permanent loss of brain function
and death.
• The usual causes are substance withdrawal, sudden withdrawal from AEDs(automated external
defibrillator), head injury, cerebral edema, infection, and metabolic disturbances

NURSING ACTIONS
● Maintain an airway, provide oxygen, establish IV access, perform ECG monitoring, and monitor
pulse oximetry and ABG results.
● Administer diazepam or lorazepam IV push followed by IV phenytoin or fosphenytoin.

MENINGITIS
1. An inflammation of the arachnoid and pia mater of the brain and spinal cord
2. It is caused by bacterial and viral organisms, although fungal and protozoan meningitis also
occur.
3. Predisposing factors include skull fractures, brain or spinal surgery, sinus or upper respiratory
infections, the use of nasal sprays, and a compromised immune system.
4. CSF is analyzed to determine the diagnosis and type of meningitis. In meningitis, CSF is cloudy,
with increased protein, increased white blood cells, and decreased glucose counts.

Transmission
• Transmission occurs in areas of high population density and in crowded living areas such as
college dormitories and prisons.
• Transmission of meningitis is by direct contact, including droplet spread.
Assessment
1. Sudden onset of fever, nuchal rigidity, and mild lethargy are the most common signs.
2. Deterioration in the level of consciousness
3. Photophobia
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4. Signs of meningeal irritation, such as nuchal rigidity and a positive Kernig’s sign and
Brudzinski’s sign
5. Red, macular rash with meningococcal meningitis
6. Abdominal and chest pain with viral meningitis

Treatment
● Steroids
● Analgesics
● Antibiotics - only if bacterial!!
● Isolation precautions
○ Viral - standard
○ Bacterial - standard
○ Hib or meningococcal - Droplet
● Prevention
○ Hib vaccine
○ Recommended for college students due to living in close quarters in dorms

Interventions
1. Monitor vital signs and neurological signs.
2. Assess for signs of increased ICP.
3. Initiate seizure precautions.

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4. Monitor for seizure activity.

5. Monitor for signs of meningeal irritation.
6. Perform cranial nerve assessment.
7. Assess peripheral vascular status (septic emboli may block circulation).
8. Maintain isolation precautions as necessary with bacterial meningitis.
9. Maintain urine and stool precautions with viral meningitis.
10. Maintain respiratory isolation for the client with pneumococcal meningitis.
11. Elevate the head of the bed 30 degrees, and avoid neck flexion and extreme hip flexion.
12. Prevent stimulation and restrict visitors.
13. Administer analgesics and/or antibiotics as prescribed.

COMPLICATIONS
Increased ICP
• Increased ICP Meningitis can cause ICP to increase, possibly to the point of brain herniation.

NURSING ACTIONS
● Monitor for indications of increasing ICP (decreased level of consciousness, pupillary changes,
impaired extraocular movements).
● Provide interventions to reduce ICP (positioning with head of the bed elevation at 30° and
avoidance of coughing and straining).
● Mannitol can be administered via IV

SIADH
• SIADH can be a complication of meningitis due to abnormal stimulation to the hypothalamic
area of the brain, causing excess secretion of antidiuretic hormone (vasopressin).
NURSING ACTIONS
● Monitor for manifestations (dilute blood, concentrated urine).
● Provide interventions, such as the administration of demeclocycline and restriction of fluid.
● Monitor the client’s weight daily.
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SEPTIC EMBOLI
● Septic emboli can form during meningitis and travel to other parts of the body, particularly the
hands, but can occur in the feet as well.
● Development of gangrene can necessitate an amputation.
● Septic emboli can lead to disseminated intravascular coagulation or stroke.

NURSING ACTIONS
● Monitor circulatory status of extremities and coagulation studies.
● Report any alterations immediately to the provider

ENCEPHALITIS
1. An inflammation of the brain parenchyma and often of the meninges.
2. It affects the cerebrum, brainstem, and cerebellum.
3. It most often is caused by a viral agent, although bacteria, fungi, or parasites also may be
involved.
4. Viral encephalitis is almost always preceded by a viral infection.

Transmission
1. Arboviruses can be transmitted to human beings through the bite of an infected mosquito or
tick.
2. Echovirus, coxsackievirus, poliovirus, herpes zoster virus, and viruses that cause mumps and
chicken pox are common enteroviruses associated with encephalitis.
3. Herpes simplex type 1 virus can cause viral encephalitis.
4. The organism that causes amebic meningoencephalitis can enter the nasal mucosa of persons
swimming in warm fresh water, such as a pond or lake.
Assessment
1. Changes in level of consciousness and mental status
2. Presence of cold sores, lesions, or ulcerations of the oral cavity
3. History of insect bites and swimming in fresh water

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4. Exposure to infectious diseases

5. Travel to areas where the disease is prevalent
6. Fever
7. Nausea and vomiting
8. Nuchal rigidity
9. Signs of increased ICP
10. Motor dysfunction and focal neurological deficits

Interventions
1. Monitor vital and neurological signs.
2. Assess level of consciousness using the Glasgow Coma Scale.
3. Assess for mental status changes and personality and behavioral changes.
4. Assess for signs of increased ICP.
5. Assess for the presence of nuchal rigidity and a positive Kernig’s sign or Brudzinski’s sign,
indicating meningeal irritation.
6. Assist the client to turn, cough, and deep breathe frequently.
7. Elevate the head of the bed 30 to 45 degrees.
8. Assess for muscle and neurological deficits.
9. Administer acyclovir as prescribed (usually the medication of choice for herpes encephalitis).
10. Initiate rehabilitation as needed for motor dysfunction or neurological deficits.

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MULTIPLE SCLEROSIS
1. A degenerative disorder of the CNS that is characterized by demyelinization of the neurons. It is
a chronic, progressive, and noncontagious disorder.
2. It usually occurs between the ages of 20 and 50 years and consists of periods of remissions and
exacerbations.
3. The causes are unknown, but the disease is thought to be the result of an autoimmune response
or viral infection.
4. Precipitating factors include pregnancy, fatigue, stress, infection, and trauma.
5. Electroencephalographic findings are abnormal.
6. Assessment of a lumbar puncture indicates an increased gammaglobulin level, but the serum
globulin level is normal.

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Assessment

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Treatment
● No cure
● Corticosteroids
○ Decrease inflammation
● Plasmapheresis

Interventions
1. The client with multiple sclerosis should be aware of triggers that cause worsening of the
disease and avoid them where possible.
2. Provide energy conservation measures during exacerbation.
3. Protect the client from injury by providing safety measures.
4. Place an eye patch on the eye for diplopia.
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5. Monitor for potential complications such as urinary tract infections, calculi, pressure ulcers,
respiratory tract infections, and contractures.
6. Promote regular elimination by bladder and bowel training.
7. Encourage independence.
8. Assist the client to establish a regular exercise and rest program and to balance moderate
activity with rest periods.
9. Assess the need for assistive devices, and provide as needed.
10. Initiate physical and speech therapy.
11. Instruct the client to avoid fatigue, stress, infection, overheating, and chilling.
12. Instruct the client to increase fluid intake and eat a balanced diet, including low-fat, high-fiber
foods and foods high in potassium.
13. Instruct the client in safety measures related to sensory loss, such as regulating the temperature
of bath water and avoiding heating pads.
14. Instruct the client in safety measures related to motor loss, such as avoiding the use of scatter
rugs and using assistive devices.
15. Instruct the client in the self-administration of prescribed medications.
16. Anticholinergic agents are used for bladder spasticity and intravenous glucocorticoids for
acute flare-ups.
17. Provide information about the National Multiple Sclerosis Society.

MYASTHENIA GRAVIS
1. A neuromuscular autoimmune disorder of the neuromuscular junction characterized by
considerable weakness and abnormal fatigue of the voluntary muscles
2. A defect in the transmission of nerve impulses at the myoneural junction occurs.
3. Causes include insufficient secretion of acetylcholine, excessive secretion of cholinesterase, and
unresponsiveness of the muscle fibers to acetylcholine.

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Assessment
1. Weakness and fatigue
2. Difficulty chewing and swallowing
3. Dysphagia
4. Ptosis

5. Diplopia
6. Weak, hoarse voice
7. Difficulty breathing
8. Diminished breath sounds
9. Respiratory paralysis and failure

**HALLMARK: muscle weakness becomes worse with activity (especially repetitive

activity) but will improve after resting the muscle.

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Diagnosis
• Tensilon Test

Treatment
● Cholinesterase inhibitors
● Corticosteroids
● Immunosuppressants (Prednisone, Azathioprine, and Mycophenolate Mofetil)

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Interventions
1. Monitor respiratory status and ability to cough and deep-breathe adequately.
2. Monitor for respiratory failure.
3. Maintain suctioning and emergency equipment at the bedside.
4. Monitor vital signs.
5. Monitor speech and swallowing abilities to prevent aspiration.
6. Encourage the client to sit up when eating.
7. Assess muscle status.
8. Instruct the client to conserve strength.
9. Plan short activities that coincide with times of maximal muscle strength.
10. Monitor for myasthenic and cholinergic crises.
11. Administer anticholinesterase medications as prescribed.
12. Instruct the client to avoid stress, infection, fatigue, and over-the-counter medications.
13. Many medications are known to exacerbate MS, such as fluoroquinolones, beta blockers, and
magnesium; the nurse needs to conduct a careful medication reconciliation.
14. Instruct the client to wear a MedicAlert bracelet.
15. Inform the client about services from the Myasthenia Gravis Foundation

MYASTHENIC CRISIS
a. An acute exacerbation of the disease
b. The crisis is caused by a rapid, unrecognized progression of the disease, inadequate amount of
medication, infection, fatigue, or stress.

Assessment
a. Increased pulse, respirations, and blood pressure
b. Dyspnea, anoxia, and cyanosis
c. Bowel and bladder incontinence
d. Decreased urine output
e. Absent cough and swallow reflex

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Interventions
a. Assess for signs of myasthenic crisis.
b. Increase anticholinesterase medication, as prescribed.

Cholinergic crisis
a. The crisis is caused by overmedication with anticholinesterase.
Assessment
a. Abdominal cramps
b. Nausea, vomiting, and diarrhea
c. Blurred vision
d. Pallor
e. Pupillary miosis
f. Facial muscle twitching
g. Hypotension
h. Increased bronchial secretions, tearing, perspiration
i. Bronchospasm, wheezing, and bradycardia

Interventions
a. Withhold anticholinesterase medication.
b. Prepare to administer the antidote, atropine sulfate, if prescribed.
c. Monitor vital signs and respiratory status closely; intubation may be necessary.
d. Frequent monitoring of respiratory status is needed, and elective intubation may be initiated.

GUILLAIN-BARRÉ SYNDROME
1. An acute infectious autoimmune neuronitis of the cranial and peripheral nerves. Generally
occurs a few days to weeks after viral or bacterial infection.
2. The immune system overreacts to the infection and destroys the myelin sheath.
3. The syndrome usually is preceded by a mild upper respiratory infection or gastroenteritis.
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4. The recovery is a slow process and can take years.

• The major concern in Guillain-Barré syndrome is difficulty breathing; monitor respiratory status
closely.
Mnemonic for Guillain-Barré syndrome: “GBS”
∙ Gradual
∙ Blocking of
∙ Sensation

Assessment
1. Paresthesias
2. Pain and/or hypersensitivity such as with the weight of bedsheets or other items touching the
body
3. Weakness of lower extremities
4. Gradual progressive weakness of the upper extremities and facial muscles
5. Possible progression to respiratory failure
6. Cardiac dysrhythmias
7. CSF that reveals an elevated protein level
8. Abnormal electroencephalogram

Treatment
● Client will gradually recover as antibodies clear
● Plasmapheresis
○ Filter blood and remove antibodies attacking the nerves
○ Helps symptoms
● Immunoglobulin therapy
○ Stops the antibodies that are attacking the myelin sheath

Interventions

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1. Care is directed toward the treatment of symptoms, including pain management.

2. Monitor respiratory status closely.
3. Provide respiratory treatments.
4. Prepare to initiate respiratory support. During the acute phase of illness, ventilatory support is
often a critical component of treatment.
5. Monitor cardiac status.
6. Assess for complications of immobility.
7. Provide the client and family with support.

WEST NILE VIRUS INFECTION

1. A potentially serious illness that affects the CNS.
2. The virus is contracted primarily by the bite of an infected mosquito ,culex (mosquitoes become
carriers when they feed on infected birds).
3. Symptoms typically develop between 3 and 14 days after being bitten by the infected mosquito.
4. Neurological effects can be permanent.

Assessment
1. Many individuals will experience no symptoms.
2. Mild symptoms include fever; headache and body aches; nausea; vomiting; swollen glands; or a
rash on the chest, stomach, or back.
3. Severe symptoms include a high fever, headache, neck stiffness, stupor, disorientation, tremors,
muscle weakness, vision loss, numbness, paralysis, seizures, or coma.
• Interventions are supportive; there is no specific treatment for the virus.

Prevention
1. Use insect repellents containing DEET (diethyltoluamide) when outdoors, and wear long
sleeves and pants and light-colored clothing.
2. Stay indoors at dusk and dawn, when mosquitoes are most active.
3. Ensure that breeding sites for mosquitoes, such as standing water and water in bird baths, are
eliminated. Keep wading pools empty and on their sides when not in use.

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PARKINSON DISEASE
Parkinson’s disease is a progressive neurological disorder affecting movement and balance. It’s
caused by a loss of nerve cells in specific areas of the brain. The dopaminergic neurons in the part
of the brain called substantia nigra have started to die.

• Significance of this area? This area is part of the basal ganglia which is part of the midbrain
that controls movements.

• What is the role of these dopaminergic neurons? They release the neurotransmitter
dopamine, which allows us to have accuracy with movement. Therefore, if they are dying this
will lower the amounts of dopamine available to our body for normal movement.

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• Why is there the signs and symptoms of tremors, rigidity etc.? Normally in the nervous system
there is a balance between acetylcholine (an excitatory neurotransmitter) and dopamine (an
inhibitory neurotransmitter).
• Therefore, the loss of dopamine leads to more acetylcholine being able to produce more
excitatory affects to the neurons in the basal ganglia and this leads to overstimulation…..tremors,
rigidity (increased cholinergic activity) etc.

Key Points about Parkinson’s Disease

• The disease tends to occur in older age 60+ (however it can affect younger people.There is
currently no cure (there are medications to relieve signs and symptoms).
• Signs and symptoms are subtle (some patients don’t notice them at first) and they will become
worse overtime.
• Signs and symptoms may present on one side or one extremity and progress to the others
overtime.

Signs and Symptoms of Parkinson’s Disease

• Mainly motor symptoms: affects how the patient is able to move
• Tremors at rest (most common): hands, arms, legs (even lips and tongue)… improves with
movement
• Pill-rolling: tremors of the hands and fingers….looks like the patient is rolling a pill between
fingers and hands.

• Stiffness of extremities (arms DON’T swing with gait)…. akinesia: inability to move the
muscles voluntarily….”freeze up”
• Shuffling of gait (extremities can freeze while walking)
• Cogwheel rigidity: when moving the patient’s arms passively toward the body they jerk or
push back slightly
• Bradykinesia: movements are slow, difficulty swallowing (drooling), Face mask-like:
expressionless
• Coordination issues…..so the patient will stoop to compensate.
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• Issues with the muscles used for chewing food, swallowing, and speaking: soft or slurred speech,
problems swallowing (aspiration)
• Other signs and symptoms that are non-motor:
• Depression
• Constipation: digestion slows down
• Loss of smell

Medications for Parkinson’s Disease (side effects and teaching)

• NO cure but medications can help make signs and symptoms more manageable
• Carbidopa/Levodopa (combination)….most common “Sinemet”: adds more dopamine to the
brain
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• Carbidopa helps to prevent levodopa from being broken down in the blood before it enters the
brain (hence more enters the brain) and lessens the side effect of nausea and when levodopa enters
the brain it turns into dopamine
Education:
• takes up to 3 weeks to notice a decrease in symptoms when beginning treatment
• don’t be alarm if body fluids turn a dark color
• Don’t take with MAO inhibitors….hypertensive crisis!!
• Don’t take with high amounts of food or supplements with Vitamin B6: decreases
effectiveness
• Avoid taking with high protein foods like cheese, milk, meat etc…decreases the amount
of drug absorbed (competes with protein in the small intestines)
Side effects: nausea, involuntary movements

• Ropinirole “Requip”: stimulates dopamine receptors ….dopamine agonists: helps with

improving movement
Side effects: drowsiness major side effect (educate NOT to take when about to drive, cook, or
operative machinery etc.)

• Amantadine (antiviral: prevents influenza A…antiparkison as well): helps with symptoms by

stimulating dopaminergic activity in the CNS

Anticholinergic:
• Remember acetylcholine (causes cholinergic activity) is exceeding dopamine, which is
producing an excitatory affect on the neurons. Therefore, ANTI cholinergics can be prescribed to
decrease these effects. These medications are usually for younger adults who have extreme
tremors and avoided in older adults because for the side effects.

Benztropine “Cogentin”: blocks acetylcholine by decreasing rigidity, saliva (drooling), improved

movements
• NOT for people with GLAUCOMA!!
• Education: never abruptly stop taking (increases signs and symptoms seen in Parkinson
disease), dry mouth (sugar less candy or gum), NO alcohol.

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MAO Inhibitor Type B (Monoamine Oxidase Inhibitor Type B):

• Rasagiline “Azilect”: increases dopamine by stopping the activity of MOA…improvement of
symptoms
• Educate about limiting foods with tyramine: hypertensive crisis
- aged cheese
- smoked or cured meats (pepperoni, bacon, hot dogs)
- fermented food
- beer

Nursing Interventions for Parkinson’s Disease

• Safety issues (balance coordination, swallowing, freezing episodes can lead to falls)
• Psychosocial issues (low self-esteem, loses ability to care for self, depression, isolation)
• Digestion issues/nutrition issues
• Side effects and teaching with medications

Safety Issues:
• Patient needs to wear low heel shoes and avoid rubber soles (they tend to stick to the floor
and can cause tripping). The soles should be smooth (not slick).
• For balance: move slowly when changing positions…rubber tip cane that is single point can
help.
• Education on how to deal with freezing episodes (some patients have them and they can occur
randomly). For example, it can occur in the legs, and it feels like the shoes suddenly become stuck
to the ground and they can’t move.
• Try to change direction of movement….rather then continue going to the side go forward.
• Use cane or walker with a laser…it provides a laser line on the floor that will help the patient
find a landmark for when freezing episode happens and helps the patient coordinate their next
step.

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• Consciously lift the legs (as in marching) with each step or pretend they are walking over an
object.
• DON’T push through the freeze up.
• Use handrails in bathroom and shower, elevated toilet seat, non-slip shoes and socks, removes
rugs and make sure pets are away from feet etc.
Psychosocial Issues: autonomy very important!
• Help them with locating utensils for eating, cooking etc….. there are special types of cookware
for PD like spoons, forks, bowls, knives to maintain autonomy
isolation:
• local support groups with other people who have PD
• exercise
• Don’t stress patient about activities or hurry them…stress increases symptoms….wait for
medication to peak so the most dopamine will be the most available.
• Dress patient in shirts without buttons or zippers…easy to put on…replace articles of clothing
with Velcro and shoes that don’t have to be tied.

Digestion/Nutrition:
• Avoid taking antiparkinson’s medication (Carbidopa/Levodopa) with a high protein meal
(meats, eggs, dairy, beans) because they interfere with how the body can absorb the medication
(makes medication less effective).
• At risk for weight loss because of the struggle with swallowing, chewing, depression, and hard
to feed self due to rigidity
• Needs foods that are soft, easy to swallow, and chew…speech therapy to evaluate…recommend
consistency of fluids

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• Prevent constipation: drink plenty of fluids 2 L per day (unless contraindicated) with high fiber
foods….example fresh fruits and vegetable and stool softner per order
• Assess last bowel movement and bowel sounds along with palpation of abdomen.
.

ALZHEIMER’S DISEASE

• It’s a chronic brain disease that is a type of dementia. It occurs because neurons in the brain lose
the ability to communicate and eventually die. This is mainly due to the development of plaques
and tangles.
• These plaques and tangles lead to a progressive loss of the ability to:
• problem solve, communicate, recall memories, perform everyday tasks, and care for one self.

• It’s thought to be caused by an abnormal buildup of proteins. This buildup of naturally occurring
proteins clump together to form plaques that collect between neurons and disrupt cell function.
Another protein forms tangles within the cells, which disrupts connections.
• Alzheimer’s disease is the most common cause of dementia which causes a persistent decline in
thinking, behavioral and social skills that affects a person’s ability to carry out activities of daily
living consistently.

Risk Factors & Causes

• Family history
Stages
• Stage 1 – No impairment

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• Stage 2 – Forgetfulness and short-term memory loss

• Stage 3 – Long-term memory loss
• Stage 4 – Bedridden

4 A’s For Alzheimer’s Disease

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Nursing Interventions for Alzheimer’s Disease

Fall Safety
• Remove throw rugs and clutter from the floor
• Assist in showers & tubs
• Utilize night lights

Location & Locked Down

• Provide safe return bracelet on wrist
• Lock doors
• Including hazards: toxic chemicals, gas, sharp objects, medications

Living Areas
• Allow for free movement
• Place frequently used items within easy reach
• Install pictures or symbols:
• Bathrooms
• Hot vs. cold water
Simple Communication
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• Avoid open-ended questions, yes or no questions instead

• Limit choices, not too many options
• Do not rush the client
• Allow plenty of time for ADLs and tasks

Wandering
a. Provide the client with a safe environment free of clutter and hazardous items.
b. Provide safe ambulation, including mobility aids and comfortable and well-fitting shoes.
c. Provide close and frequent supervision.
d. Close and secure doors.
e. Use identification bracelets and electronic surveillance.
f. Encourage rest periods in the afternoon, because wandering worsens at night.
g. Provide regular supervised exercise or walking programs.
h. Sundown syndrome (sundowning) is characterized by a pronounced increase in symptoms and
problem behaviors in the evening. Providing a safe environment is a priority in the care of a client
with Alzheimer’s disease.
• Providing a safe environment is a priority in the care of a client with Alzheimer’s disease.

Communication disorders
a. Disorders include language disorder (expressive–receptive disorder), speech sound disorder
(phonological disorder), childhood onset fluency disorder (stuttering disorder), and social
communication disorder (impaired social communication).
b. Adapt to the communication level of the client.
c. Pay attention to nonverbal cues.
d. Use a firm volume and a low-pitched voice to communicate.
e. Stand directly in front of the client and maintain eye contact.
f. Give ample time for the client to respond.
g. Use a calm and reassuring voice. Do not speak loudly unless the client is hearing impaired.
h. Use pantomime gestures if the client is unable to understand spoken words.
i. Speak slowly and clearly, using short words and simple sentences.

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j. Ask only one question at a time and give one direction at a time.
k. Repeat questions if necessary, but do not rephrase.
l. Provide alternative means of communication.
m. Minimize external noise or distractions when communicating.

Impaired judgment
a. Remove throw rugs, toxic substances, and dangerous electrical appliances from the
environment.
b. Reduce hot water heater temperature.

Altered thought processes

a. Call the client by name.
b. Orient the client frequently.
c. Use familiar objects in the room.
d. Place a calendar and clock in a visible place.
e. Maintain familiar routines.
f. Allow the client to reminisce.recall.
g. Make tasks simple.
h. Allow time for the client to complete a task.
i. Provide positive reinforcement for positive behaviors.

Altered sleep patterns

a. Allow the client to wander in a safe place until the client becomes tired.
b. Prevent shadows in the room by using indirect light.
c. Avoid the use of hypnotics because they cause confusion and aggravate the sundown effect.
confusion, anxiety, aggression or ignoring directions occurring in the late afternoon and lasting
into the night- SUNDOWN EFFECT

Agitation

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a. Assess the precipitant of the agitation.

b. Reassure the client.
c. Remove items that can be hazardous when the client is agitated.
d. Approach the client slowly and calmly from the front, and speak, gesture, and move slowly.
e. Remove the client to a less stressful environment; decrease excess stimuli.
f. Use touch gently.
g. Do not argue with or force the client to do something.

HUNGTINGTON DISEASE
• Huntington’s disease is an inherited genetic disorder affecting muscles and coordination. It’s
caused by a breakdown (degeneration) of the nerve cells of the brain.
• Huntington’s disease is a genetic disorder in which the brain degenerates over time. It’s
characterized by uncontrolled movements and loss of intellectual abilities, which are often
accompanied by behavioral changes.
• Huntington’s affects each individual differently. Symptoms can begin as early as thirty years old
or as late as the eighth decade. The disease typically progresses in stages and eventually leads to
death within fifteen to twenty years after symptoms appear (if left untreated).

Medications used to treat Huntington’s Disease

• There are currently no cures for Huntington’s disease, but some medications can help manage
symptoms:
• Antipsychotics (typical or atypical) to control agitation, anxiety, and psychosis.
• Antidepressants for depression and anxiety disorders.

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• Anti-anxiety medications such as benzodiazepines (e.g., Valium) to treat severe anxiety

episodes.
• Anticonvulsants to prevent seizures.

Huntington’s Disease Nursing Interventions

Assess
• Client’s physical status (including weight loss, muscle wasting, and tremors)
Encourage
• Client to engage in social interactions with family and friends.
Assist
• In meal preparation, housekeeping, transportation, and other activities of daily living.

AMYOTROPHIC LATERAL SCLEROSIS

• Amyotrophic lateral sclerosis (ALS) is a disease of unknown cause in which there is a loss of
motor neurons (nerve cells controlling muscles) in the anterior horns of the spinal cord and
the motor nuclei of the lower brain stem.
• It is often referred to as Lou Gehrig’s disease.

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Risk Factors
• Autoimmune
• Free radical damage
• Oxidative stress
• Cigarette smoking

Pathophysiology
• As motor neuron cells die, the muscle fibers that they supply undergo atrophic changes.
Neuronal degeneration may occur in both the upper and lower motor neuron systems.
• The leading theory held by researchers is that over excitation of nerve cells by the
neurotransmitter glutamate leads to cell injury and neuronal degeneration.

Signs & Symptoms

• Difficulty breathing (Dyspnea)
• Progressive muscle weakness
• Difficulty swallowing (Dysphagia)
• Constipation
• Difficulty speaking (Dysphasia)
• Respiratory failure
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ALS Nursing Interventions

• Monitor for pneumonia, infection, fever, and lung sounds (Rhonchi).
• Provide comfort and emotional support.
• Encourage independence, communication, and self-expression.

ALS Medications
• The main types of ALS medications include: anticholinesterases and riluzole.
• Anticholinesterases work by slowing the breakdown of acetylcholine in the body, which
prevents its effects from being too strong.
• Riluzole works by inhibiting glutamate receptors in the brain that cause neuronal death. It can
cause side effects such as dizziness, gastrointestinal conditions and liver function changes. It is
important to monitor blood counts and liver functions while on the drug.
∙ Edaravone (Radicava). This drug, given by intravenous infusion, has been shown to reduce the
decline in daily functioning. Its effect on life span isn't yet known. Side effects can include
bruising, headache and shortness of breath. This medication is given daily for two weeks a month

CEREBRAL ANEURYSM
• Dilation of the walls of a weakened cerebral artery; can lead to rupture.

Assessment
1. Headache and pain
2. Irritability

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3. Visual changes
4. Tinnitus
5. Hemiparesis
6. Nuchal rigidity
7. Seizures

Surgical Management
• The goal of surgery is to prevent bleeding in an unruptured aneurysm or further bleeding in an
already ruptured aneurysm.
• Craniotomy. Surgical evacuation is most frequently accomplished via a craniotomy.
• Aneurysm coiling. This is the obstruction of the aneurysm site with a coil.

Interventions
1. Maintain a patent airway (suction only with a PHCP’s prescription).
2. Administer oxygen as prescribed.
3. Monitor vital signs and for hypertension or dysrhythmias.
4. Avoid taking temperatures via the rectum.
5. Initiate aneurysm precautions

Precautions
■ Maintain the client on bed rest in a semi-Fowler’s or a side-lying position.
■ Maintain a darkened room (subdued lighting and avoid direct, bright, artificial lights) without
stimulation (a private room is optimal).
■ Provide a quiet environment (avoid activities or startling noises); a telephone in the room is not
usually allowed.
■ Reading, watching television, and listening to music are permitted, provided that they do not
overstimulate the client.
■ Limit visitors.
■ Maintain fluid restrictions.
■ Provide diet as prescribed; avoid stimulants in the diet.

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■ Prevent any activities that initiate the Valsalva maneuver (straining at stool, coughing); provide
stool softeners to prevent straining.
■ Administer care gently (such as the bath, back rub, range of motion).
■ Limit invasive procedures.
■ Maintain normothermia.
■ Prevent hypertension.
■ Provide sedation.
■ Provide pain control.
■ Administer prophylactic antiseizure medications.
■ Provide deep vein thrombosis (DVT) prophylaxis as prescribed.

TRIGEMINAL NEURALGIA
• A sensory disorder of the trigeminal (fifth cranial) nerve.
• It results in severe, recurrent, sharp facial pain along the trigeminal nerve.

Assessment
1. The client has severe pain on the lips, gums, or nose, or across the cheeks.
2. Situations that stimulate symptoms include cold, washing the face, chewing, or food or fluids of
extreme temperatures.

Interventions
1. Instruct the client to avoid hot or cold foods and fluids.
2. Provide small feedings of liquid and soft foods.
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3. Instruct the client to chew food on the unaffected side.

4. Administer medications as prescribed.

Surgical interventions
1. Microvascular decompression: Surgical relocation of the artery that compresses the trigeminal
nerve as it enters the pons, which may relieve pain without compromising facial sensation.

2. Radiofrequency waveforms: Create lesions that provide relief of pain without compromising
touch or motor function.

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3. Rhizotomy: Resection of the root of the nerve to relieve pain.

4. Glycerol injection: Destroys the myelinated fibers of the trigeminal nerve (may take up to 3
weeks for pain relief to occur)

BELL’S PALSY (FACIAL PARALYSIS)

1. Caused by a lower motor neuron lesion of cranial nerve VII that may result from infection,
trauma, hemorrhage, meningitis, or tumor.
2. It results in paralysis of one side of the face.
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3. Recovery usually occurs in a few weeks, without residual effects.

Assessment
1. Flaccid facial muscles
2. Frequently results in inability to raise the eyebrows, frown, smile, close the eyelids, or puff out
the cheeks
3. Upward movement of the eye when attempting to close the eyelid
4. Loss of taste

Management
• The objectives of management are to maintain facial muscle tone and to prevent or minimize
denervation (loss of nerve supply).
• Corticosteroid therapy (prednisone) may be initiated to reduce inflammation and edema, which
reduces vascular compression and permits restoration of blood circulation to the nerve.
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• Early administration of corticosteroids appears to diminish severity, relieve pain, and minimize
denervation.
• Facial pain is controlled with analgesic agents or heat applied to the involved side of the face.
• Additional modalities may include electrical stimulation applied to the face to prevent muscle
atrophy, or surgical exploration of the facial nerve.
• Surgery may be performed if a tumor is suspected, for surgical decompression of the facial
nerve, and for surgical rehabilitation of a paralyzed face.

Nursing Management
• Patients need reassurance that a stroke has not occurred and that spontaneous recovery occurs
within 3 to 5 weeks in most patients. Teaching patients with Bell’s palsy to care for themselves at
home is an important nursing priority.

Teaching Eye Care

• Because the eye usually does not close completely, the blink reflex is diminished, so the eye is
vulnerable to injury from dust and foreign particles. Corneal irritation and ulceration may occur.
Distortion of the lower lid alters the proper drainage of tears. Key teaching points include the
following:
• Cover the eye with a protective shield at night.
• Apply eye ointment to keep eyelids closed during sleep.
• Close the paralyzed eyelid manually before going to sleep.
• Wear wrap around sunglasses or goggles to decrease normal evaporation from the eye.

Teaching About Maintaining Muscle Tone

• Show patient how to perform facial massage with gentle
• upward motion several times daily when the patient can tolerate the massage.
• Demonstrate facial exercises, such as wrinkling the forehead, blowing out the cheeks, and
whistling, in an effort to prevent muscle atrophy.
• Instruct patient to avoid exposing the face to cold and drafts (warm air)

Neuropathy
“Weakness, numbness, and pain from nerve damage”
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● There has been injury to the peripheral nerve

○ Injuries
○ Infections
○ Toxin exposure
○ Diabetes
Pain is often described as “pins and needles”, numbness, or weakness.

Pain
• An unpleasant sensory and emotional experience associated with actual or potential tissue
damage, or described in terms of such damage.
• Pain occurs when something hurts. It can be severe or mild, and is often an indicator that
something is wrong.

• Most types of pain are caused by damage to the tissue or damage to the nerves. Some pain is
idiopathic, which means it has an unknown cause.
• Pain is most often grouped into one of four distinct types, based on the damage that causes it.
The four types of pain are acute pain, chronic pain, breakthrough pain, and pain related to cancer.

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Acute pain
• Acute pain is pain that is new or comes on suddenly, often caused by something specific. It alters
the vital signs, for instance, raising the patient's heart rate and/or blood pressure.
• Acute pain is not long-lasting and resolves when the cause of pain is addressed. Consider a
patient with appendicitis. They will be in great pain, often guarding or holding their abdomen,
possibly sweating. They will appear tense and their vital signs will be affected. Surgery
would alleviate the pain in the case of appendicitis.

Chronic pain
• Chronic pain is pain that persists for a long time, longer than three months. Chronic pain can
affect a patient's psychological status and quality of life — it can affect how they sleep, their
appetite, or their ability to work.
• The vital signs of a patient dealing with chronic pain are often not affected. That is because the
body learns to adapt to deal with that pain — the patient has become used to the constant
discomfort. However, just because a patient has normal vital signs, that doesn't mean they aren't in
pain.
• For example, a patient with scoliosis might report their back hurting every day, at a constant
level of severity of 3 (out of 10), but they carry on with their life regardless of their discomfort
because they have learned to live with their pain.

Breakthrough pain
• Just like it sounds, breakthrough pain is pain that breaks through. It is intense, transient pain that
occurs despite taking pain medication. For instance, a patient who has had surgery might feel well
until they get up and walk around, at which point they may feel intense pain.

Cancer pain
• Cancer pain can be related to both the cancer and the cancer treatment. It may be acute and/or
chronic and is often a very intense kind of pain.

Etiology Of Pain
• Etiology means cause or set of causes. Etiology of pain refers to the cause or origin of the pain,
which can be classified as one of three distinct categories: nociceptive, neuropathic, and
idiopathic.

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Nociceptive pain
• Nociceptive pain is caused by injury or damage to body tissue. It is often described as aching or
throbbing. Most pain is nociceptive and results when pain receptors (nociceptors) discern painful
or noxious stimuli. A sports injury or broken tooth are examples of nociceptive pain.

Neuropathic pain
• Neuropathic pain is caused by damage to the nerves ("neuro-" meaning nerves and "-pathic"
meaning disorder). It is often chronic. Patients might describe their pain as burning or shooting, or
they might report “being on pins and needles.” Phantom limb syndrome (pain that is felt in the
area where an arm or leg has been amputated) is an extreme example of neuropathic pain.

Idiopathic pain
• Idiopathic pain is pain that comes from an unknown cause that defies explanation, even after
examination. Idiopathic pain may be psychological or physiological in origin.
• A migraine may be considered an idiopathic pain

PAIN LOCATIONS
• Another way that pain is classified is by location. Different locations of pain indicate different
problems from which a patient may be suffering.
• Location of pain is broken into four possible areas: cutaneous, somatic, visceral, and referred.

Cutaneous pain
• Cutaneous pain involves the skin (the Latin word “cutis” means skin). Cutaneous pain is caused
by stimulation of structures in the skin that sense pain (nociceptors). A paper cut is an example of
something that causes cutaneous pain.

Somatic pain
• Somatic pain is pain that involves deeper tissues, like joints, tendons, or bones. It is localized, it
may be either intermittent or constant, and patients will often describe this sort of pain as aching,
gnawing, throbbing, or cramping. Spraining an ankle is an example of something that causes
somatic pain.

Visceral pain
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• Visceral pain refers to organ-related pain, when pain receptors in the pelvis, abdomen, chest, or
intestines are activated. A patient may experience this type of pain if their internal organs and
tissues are damaged or injured. Visceral pain is vague and not localized. Someone suffering
visceral pain might not be able to clearly define it, and instead report feeling a deep squeeze,
pressure, or aching.

Referred pain
• Referred pain is pain that is perceived at a location other than the site of the painful stimulus or
origin of the pain. The body has networks of interconnected sensory nerves, which supply many
different tissues. An injury to one site in the network might send a signal to the brain, which then
interprets the pain as occurring elsewhere in the body. An example of referred pain is shoulder
pain following a heart attack.

Nonpharmacological therapies
• Nonpharmacological therapies are therapies that do not involve medications and may be
categorized as complementary and alternative medicine (CAM). These include:
• Physical therapy: the treatment of disease, injury, or deformity by physical methods such as
massage, heat treatment, and exercise rather than by drugs or surgery.
• Massage: the manipulation of the body's soft tissues
• Guided imagery: a type of focused relaxation or meditation, often led by a trained practitioner or
teacher.
• Distraction: shifting or moving one's attention away; in distraction therapy, one trains the brain
to focus its attention onto something other than the pain (even though the pain is still there).
• Biofeedback: a mind-body therapy that can improve physical and mental health; during a
biofeedback session, a practitioner will use painless sensors to measure certain bodily functions.
• Acupuncture: A therapy that involves the insertion of very thin needles through the skin at
strategic points on the body; deriving from Chinese medicine, acupuncture can be used to alleviate
stress a well as pain.

PATIENT-CONTROLLED ANALGESIA
• Patient-controlled analgesia (PCA) is a means of delivering individualized analgesia, prescribed
by a provider for pain control, where it is the patient who controls the amount of medication they
are receiving.
• Medication is administered via a pump, intravenously. It is administered in small doses, which
the patient receives at certain intervals.
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• The most common medications administered via PCA are opioid analgesics.
• Note that only the patient should press the button that administers a dosage. Neither nurses nor
visitors should do this.

Lockout interval
• The interval for doses is called the lockout interval. If, for example, a dose is 0.2 mg of
hydromorphone every 10 minutes, that is the most frequently the patient can self-administer. It is
not automatic — the patient has to push the button on the pump to deliver the medication.
Bolus vs. basal doses
• A bolus dose is what we call the administration of the single dose of medication via the PCA,
also called the demand dose. It gets administered when the patient pushes the button on the pump.
• Basal doses are administered continuously, in small amounts. The PCA pump can be
programmed to deliver pain medication continuously, if needed.

Nursing care best practices for PCA

Engage another nurse to verify PCA settings
• When a patient is set up with a PCA pump, it is important to engage another RN to verify the
pump settings. It is vital to make sure that the medication the provider ordered is indeed what is in
the pump.

Only the patient administers medication via the PCA

• As mentioned above, only the patient operates the PCA. Educate patients and their family
members so they know that only the patient touches the delivery button and nobody else
(including nurses!)

Monitor your patient for signs of toxic effects

• Finally, it is equally important to understand that the patient can suffer toxic effects of
medication, even when following provider's orders.
• For example, if the patient is pushing the button every 10 minutes, it is possible that they are
receiving too much medication, that is, more than their body can tolerate. Assess the patient
frequently, checking that their vital signs are as expected, depending on their condition.
• And always check on the status of the patient's pain level.

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Pharmacological therapies
• Pharmacological therapies make use of medication to treat the patient’s pain. These include
nonopioid analgesics, opioid analgesics, and adjuvant analgesics.
Nonopioid analgesics
• Nonopioid analgesics are used to treat mild to moderate pain and include acetaminophen,
NSAIDs (nonsteroidal anti-inflammatory drugs, such as ibuprofen or naproxen), and aspirin.

Opioid analgesics
• Opioid analgesics are used to treat moderate to severe pain and can include fentanyl, morphine,
dilaudid, and oxycodone.

Adjuvant analgesics
• Adjuvant analgesics are drugs with a primary indication other than pain but have analgesic
properties and can alleviate pain in some conditions. Adjuvant analgesics include antidepressants
(e.g., amitriptyline), anticonvulsants (e.g., carbamazepine or pregabalin, known commercially as
Lyrica), and topical analgesics (e.g., lidocaine).

BOTULISM

● Botulinum toxin released by Clostridium botulinum

○ Found in soil and dust
○ Can contaminate honey
Children under 1 year old should never have honey

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● Inhibits acetylcholine release at the junction between peripheral nerves and muscles
● This causes life-threatening flaccid paralysis.

The most common forms of botulism include:

• Infant botulism
• Foodborne botulism
• Wound botulism

• Infant botulism, the most common form, occurs after a baby consumes the bacterial spores,
typically by eating contaminated honey. It’s most often diagnosed in babies age 1 year and
younger (infants’ digestive systems aren’t mature enough to move the botulism-containing honey
out of their body quickly).

• Foodborne botulism is caused by consuming foods contaminated with the botulinum toxin —
most commonly home-canned vegetables, cured pork, smoked or raw fish, honey, and corn syrup.

• Wound botulism develops if Clostridium botulinum enters an open wound and releases its toxins.

• There are other, even more rare forms of botulism, including iatrogenic botulism. This occurs
following an accidental overdose of botulinum toxin during Botox injections, which are used
during cosmetic procedures as well as to treat certain neuromuscular disorders. Fortunately, this is
a rare occurrence, according to research.
• All types of botulism can be fatal and are considered medical emergencies.

Assessment Findings
● Blurry vision
● Difficulty breathing
● Respiratory failure
● Symmetric, descending flaccid paralysis

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Signs of botulism in infants include:

• Poor feeding
• Lethargy and weakness

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• Constipation
• Weak cry
• Poor muscle tone and head control
• Poor gag and sucking reflexes
• The signs and symptoms of foodborne botulism typically appear 12 to 36 hours after consuming
contaminated food, but can begin anytime between a few hours after ingestion to a few days,
according to the Mayo Clinic. You may test toxin-positive as late as 12 days after ingestion.

Medication Options for Botulism

• Botulinus antitoxin, which is administered by injection, is the only effective drug treatment for
foodborne and wound botulism. The antitoxin works by attaching itself to the Clostridium
botulinum toxin that’s still circulating in your bloodstream, preventing it from damaging your
nerves.
• Treatment with the antitoxin won’t resolve any nerve damage that’s already been caused by the
toxin, but your nerves may eventually regenerate on their own during and after treatment.
• For wound botulism, your doctor may also recommend additional antibiotics to help the wound
heal and clear up any infection
• For infant botulism, doctors use a different type of antitoxin called botulism immune globulin.

Prevention of Botulism
There are steps you can take to help prevent most types of botulism.
• To prevent foodborne botulism, be sure to:
• Keep foods refrigerated even after cooking.
• Check to see that you’ve cooked food thoroughly prior to eating with use of proper cooking
techniques and prompt refrigeration.
• Avoid prepackaged foods in containers — cans, cartons, or boxes — that are damaged or
bulging.
• Properly storing and refrigerating foods, ideally within two hours after cooking, prevents the
Clostridium botulinum bacteria from producing spores. In addition, cooking food thoroughly can
help kill any Clostridium botulinum bacteria.

• To prevent wound botulism:

o Don’t abuse injectable drugs.
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o Seek medical treatment for a wound with signs of infection.

o Clean and bandage any open wounds.
o Using injectable drugs can expose you to Clostridium botulinum bacteria through
contaminated needles.
• Wound botulism can also occur after traumatic injuries and surgeries. To prevent wound
botulism:
o Don’t use illicit injectable drugs. Seek drug and mental health treatment
centers for help.
o Seek medical treatment for a wound with signs of infection.
o Clean and bandage any open wounds.
• The only known way to prevent infant botulism is to avoid feeding babies honey. However, in
general, it’s best to take the same precautions designed to prevent foodborne botulism with any
meals you prepare for your child.

Complications of Botulism
Botulism can lead to several health complications, mostly related to the muscle paralysis and
weakness it causes. These include:
• Difficulty breathing (the most common cause of death in botulism)
• Problems speaking and/or swallowing
• Long-lasting muscle weakness
• If left untreated, botulism can lead to death due to respiratory failure

TRAUMATIC HEAD INJURIES

Head injury is the pathological result of any mechanical force to the skull, scalp, meninges, or
brain.

Risk Factors
● Motor vehicle or motorcycle crashes
● Illicit drug and alcohol use
● Sports injuries
● Assault
● Gunshot wounds
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● Falls

Expected Findings
● Amnesia (loss of memory) before or after the injury.
● Loss of consciousness: Length of time the client is unconscious is significant.
● CSF leakage from the nose and ears can indicate a basilar skull fracture. Test for the “halo
sign,” clear or yellow-tinted ring surrounding a drop of blood when bloody drainage is placed on
a piece of gauze

Manifestations of increased intracranial pressure

✓ Severe headache, nausea, vomiting

✓ Deteriorating level of consciousness, restlessness, irritability
✓ Dilated or pinpoint nonreactive pupils
✓ Cranial nerve dysfunction
✓ Alteration in breathing pattern (Cheyne-Stokes respirations, central neurogenic
hyperventilation, apnea)
✓ Deterioration in motor function, abnormal posturing (decerebrate, decorticate, flaccidity)
✓ Cushing’s triad: a late finding characterized by severe hypertension with a widening pulse
pressure (systolic – diastolic) and bradycardia
✓ Seizure

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Types
Head injuries are classified as open or closed.

 Open Head Injury - When a patient has an open head injury, they are at high risk for
infection because trauma has caused the skull to open up, allowing different types of
harmful elements like bacteria to enter the site and cause infection. On the other hand,
people who have open head injuries are less likely to develop severe complications
because the pressure from the swelling can easily be drained from the brain.

 Closed Head Injury- Traumatic closed head injuries, compared to open head injuries,
are more serious and damaging. Getting a brain swelling is similar to getting a bruise on
any part of your body. If there’s a bruise in your brain, it will immediately swell up and
result in numerous adverse consequences, mainly:
- Increased risk for intracranial pressure
- Increased risk for spinal cord pressure

Types of brain injury include concussion, contusion, diffuse axonal injury, and
intracranial hemorrhage.
A concussion, or mild traumatic brain injury , occurs after head trauma that results in a
change in the client’s neurologic function but no identified brain damage and usually
resolves within 72 hr. Post-concussion syndrome includes persistence of cognitive and
physical manifestations for an unknown period of time.

✓ A contusion occurs when the brain is bruised and the client has a period of
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unconsciousness associated with stupor and or confusion.

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✓ Diffuse axonal injury is a widespread injury to the brain that results in coma and
is seen in severe head trauma.
✓ Intracranial hemorrhage can occur in the epidural, subdural, or intracerebral
space. It is a collection of blood following head trauma. There can be a delay of
weeks to months in presenting manifestations for a subacute or chronic subdural
hematoma.

The danger of closed head injuries is that there isn’t enough room to
accommodate the swelling and the fluid has to be drained. Otherwise, it will lead
to increased intracranial pressure. Increased intracranial pressure will cause a
series of complications and can eventually lead to death.

Cerebrospinal Fluid Leak

One of the major complications of traumatic head injuries is cerebrospinal fluid
(CSF) leaking from the brain. Cerebrospinal fluid, in copious amounts, can leak
from the ears and even around the neck.

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Basilar Skull Fracture

A basilar fracture is a trauma aimed at the base of the cranium that causes nose or

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ear CSF leak.

Battle’s sign → Bruising over the mastoid process
Raccoon eyes → Periorbital bruising

Cerebrospinal rhinorrhea

■ Test drainage for CSF

● Halo test
● Glucose (Glucose oxidized test)

NEVER INSERT AN NG TUBE IN A CLIENT WITH A BASILAR SKULL

FRACTURE

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Management Planning Technique

When making a care plan for a patient with traumatic head injury, always consider
the state that can be detrimental to the patient. What is the first situation that can
kill the patient the fastest? Whatever the answer is, it should be the top priority.
And usually, in answering major exam questions, it’s always the ABC (airway,
breathing, and circulation).

Nursing Interventions
✓ Monitor airway and respiratory status.
✓ Swelling in the face or brain can cause compromised airway or breathing.
✓ Cranial nerve damage may also impair swallowing.
✓ Assess drainage for CSF, avoid nose blowing.
✓ Halo’s sign (yellow ring around blood spot on gauze) indicates a CSF leak from
nose/ears or through a fracture. Nose blowing can cause a CSF leak or bleed.
✓ Assess cranial nerve function : Facial fractures and basilar skull fractures carry a
high risk of cranial nerve damage, including sensation to the face and ability to
swallow.
✓ Assess LOC and ICP/CPP with frequent neuro checks.
✓ CPP = MAP – ICP (monitor hemodynamics)
✓ What is a normal Cerebral perfusion pressue (CPP)? 60-100 mmHg NOTE: When
CPP falls too low the brain is not perfused and brain tissue dies. If the patient’s
mean arterial pressure (MAP) starts to fall to the patient’s ICP, then the cerebral
perfusion pressure will drop. Therefore, maintaining a sufficient MAP is essential.

✓ Neurological changes related to increasing ICP may be subtle or may occur

rapidly. Frequent detailed neuro checks allow changes to be recognized quickly so
that interventions can be initiated.

✓ Perform interventions to minimize ICP:

o Maintain HOB 30-45°
o Decrease stimuli

✓ Maintain HOB 30-45°

o HOB < 30 = increased blood flow to brain → Increased ICP
o HOB > 45 = increased intrathoracic pressure → decreased venous outflow from
brain → increased ICP

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✓ Decrease stimuli
o Agitation or stress can cause increased ICP

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✓ Avoid Valsalva maneuvers

o Coughing or bearing down can cause increased ICP

✓ Assess swallow before giving anything by mouth – involve Speech Therapy as

appropriate.

- Due to muscle weakness, patients may experience difficulty swallowing. It

may be appropriate to have ST assess for appropriate interventions to prevent
aspiration.

✓ Administer analgesics as ordered

Severe pain can cause increased ICP, among other complications. Give pain
medications as ordered and as needed.

INCREASED INTRACRANIAL PRESSURE (ICP)

1. Increased ICP may be caused by trauma, hemorrhage, growths or tumors,

hydrocephalus, edema, or inflammation.
2. Increased ICP can impede circulation to the brain, impede the absorption of
CSF, affect the functioning of nerve cells, and lead to brainstem compression and
death

Assessment
1. Altered level of consciousness, which is the most sensitive and earliest
indication of increasing ICP
2. Headache
3. Abnormal respirations
4. Rise in blood pressure with widening pulse pressure
5. Slowing of pulse
6. Elevated temperature
7. Vomiting
8. Pupil changes
9. Late signs of increased ICP include increased systolic blood pressure, widened
pulse pressure, and slowed heart rate.
10. Other late signs include changes in motor function from weakness to
hemiplegia, a positive Babinski’s reflex, decorticate or decerebrate posturing, and
seizure.

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Interventions
1. Monitor respiratory status and prevent hypoxia.
2. Monitor ICP if a pressure device is in place.
3. Avoid the administration of morphine sulfate to prevent the occurrence of
hypoxia.
4. Maintain mechanical ventilation as prescribed; maintaining the PaCO2 at 30 to
35 mm Hg will result in vasoconstriction of the cerebral blood vessels, decreased
blood flow, and therefore decreased ICP.
5. Maintain body temperature.
6. Prevent shivering, which can increase ICP.
7. Decrease environmental stimuli.
8. Monitor electrolyte levels and acid–base balance.
9. Monitor intake and output.
10. Limit fluid intake to 1200 mL/day.
11. Instruct the client to avoid straining activities, such as coughing and sneezing.
12. Instruct the client to avoid Valsalva’s maneuver.

For the client with increased ICP, elevate the head of the bed 30 to 40
degrees, avoid the Trendelenburg’s position, and prevent flexion of the neck
and hips.

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Medications:
Antiseizure
■ Seizures increase metabolic requirements and cerebral blood flow and volume,
thus increasing intracranial pressure (ICP).

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■ Medications may be given prophylactically to prevent seizures.

Antipyretics and Muscle Relaxants

■ Temperature reduction decreases metabolism, cerebral blood flow, and thus
ICP.
■ Antipyretics prevent temperature elevations.
■ Muscle relaxants prevent shivering.

Blood Pressure Medication

■ Blood pressure medication may be required to maintain cerebral perfusion at a
normal level.
■ Notify the primary health care provider if the blood pressure range is lower than
100 or higher than 150 mm Hg systolic.

Corticosteroids
■ Corticosteroids stabilize the cell membrane and reduce leakiness of the blood-
brain barrier.
■ Corticosteroids decrease cerebral edema.
■ A histamine blocker may be administered to counteract the excess gastric
secretion that occurs with the corticosteroid.
■ Clients must be withdrawn slowly from corticosteroid therapy to reduce the risk
of adrenal crisis.

Intravenous Fluids
■ Fluids are administered intravenously via an infusion pump to control the
amount administered.
■ Infusions are monitored closely because of the risk of promoting additional
cerebral edema and fluid overload.

Hyperosmotic Agent (Osmotic Diuretic)

■ A hyperosmotic agent increases intravascular pressure by drawing fluid from
the interstitial spaces and from the brain cells.
■ Monitor renal function.
■ Diuresis is expected.

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PHENYLKETONURIA
Phenylketonuria is a genetic disorder (autosomal recessive disorder) that results in
central nervous system damage . The child lacks in enzyme (phenylalanine
hydroxylase ) that converts amino acid phenylalanine into amino acid tyrosine . lack
of enzyme prevents the conversion causing accumulation of phenylalanine in the
blood leading to irreversible neurological damage .

It is characterized by blood phenylalanine levels greater than 20 mg/dL ; normal

level is 0 to 2 mg/dL
All 50 states require routine screening of all newborns for phenylketonuria.

Signs and symptoms

1. In all children
a. Digestive problems and vomiting
b. Seizures
c. Musty odor of the urine , breath and skin
d. Mental retardation
e. irritability of failure to thrive

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2. In older children
a. Eczema
b. Hypertonia
c. Hypopigmentation of the hair, skin, and irises
d. Hyperactive behavior

Management :
Screening of newborn infants for phenylketonuria:.

✓ The infant should have begun formula or breast milk feeding before specimen
collection.
✓ The serum level of phenylalanine is monitored.If initial screening is positive, a repeat
test is performed, and further diagnostic
evaluation is required to verify the diagnosis.
✓ Rescreen newborns by 14 days of age if the initial screening was done before 48
hours of age.

If phenylketonuria is diagnosed, prepare to implement the following:

✓ Restrict phenylalanine intake; high protein foods (meats, eggs and dairy products)
and aspartame as in artificial sweeteners are avoided because they contain large
amounts of phenylalanine.
✓ Monitor physical, neurological, and intellectual development.
✓ Stress the importance of follow-up treatment.
✓ Encourage the parents to express their feelings about the diagnosis and discuss the
risk of phenylketonuria in future children.
✓ Educate the parents about the use of special preparation formulas and about the
foods that contain phenylalanine. Include synthetic proteins and special formula eg
Lofenalac , phenyl-free
✓ Encourage consumption of natural food low in phenylalanine (most fruit and
veggie )
✓ Consult with social care services to assist the parents with the financial burdens of
purchasing special prepared formulas
✓ Genetic counseling before pregnancy to determine the risk
✓ Tyrosine is low or normal and is not usually restricted .

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CRANIAL NERVE EXAMINATION

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Cranial Nerve I
To test cranial nerve I..….olfactory nerve: Have the patient close their eyes and place
something with a pleasant smell under the nose and have them identify it.

Cranial Nerve II

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To test cranial nerve II….optic nerve: Perform the confrontation visual field test and visual
acuity test with a Snellen chart.

Confrontation Visual Field Test

Assesses peripheral vision:

 Stand arm’s length from the patient.

 Cover your left eye, while the patient covers their right eye.
 Have the patient look at your nose (tell the patient NOT to look at your fingers)
 In the top and bottom of the visual field (test it with yours) hold up random numbers
with your fingers and have the patient recite them back to you.
 Repeat again with the other eye (cover your right eye while the patient covers their left
eye).

Visual Acuity: use a Snellen chart and have patient wear glasses or contact lenses if they
normally wear them

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 Have patient stand 20 feet from chart

 First the patient will cover the right eye, then left eye, and lastly read the chart with both
eyes.
 Covering the right eye first, have the patient recite the lowest line they can read with
ease.
 Repeat this with the left eye and then both eyes.
Results: If the patient can read line 8, their vision is 20/20, which means that the patient can
see the same line of letters at 20 feet that a person with normal vision can see at 20 feet.

However, let’s say the patient can only read line 6 with the left eye, which means the
patient has 20/30 in this eye. This means the patient can see at 20 feet what a person with
normal vision can see at 30 feet.

Cranial Nerve III, IV, VI

To test cranial nerve III (oculomotor nerve), IV (trochlear), VI (abducens):

 Have the patient follow your pen light by moving it 12-14 inches from the patient’s
face in the six cardinal fields of gaze (start in the midline)
 Watch for any nystagmus (involuntary movements of the eye)

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 Reactive to light?
 Dim the lights and have the patient look at a distant object (this dilates the
pupils)
 Shine the light in from the side in each eye.
 Note the pupil response: The eye with the light shining in it should
constrict (note the dilatation size and response size (ex: pupil size goes
from 3 to 1 mm) and the other side should constrict as well.

 Accommodation?
 Make the lights normal and have patient look at a distant object to dilate pupils,
and then have patient stare at pen light and slowly move it closer to the patient’s
nose.
 Watch the pupil response: The pupils should constrict and equally move
to cross.

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If all these findings are normal you can document PERRLA.(pupil equally round and
reactive to light and accomodation )

Cranial Nerve V

To test Cranial Nerve V…..trigeminal nerve: This nerve is responsible for many functions
and mastication is one of them.

 Have the patient bite down and feel the masseter muscle and temporal muscle
 Then have the patient try to open the mouth against resistance

Cranial Nerve VII

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 To test cranial nerve VII…facial nerve: have the patient close their eyes tightly,
smile, frown, puff out cheek. Can they do this will ease?

Cranial Nerve VIII

To test cranial nerve VIII…vestibulocochlear nerve:

 Test the hearing by occluding one ear and whispering two words and have the
patient repeat them back. Repeat this for the other ear.

Cranial Nerve IX and X

To test cranial nerve IX (glossopharyngeal) and X (vagus) have patient say “ah”…the uvula
will move up (cranial nerve IX intact) and if the patient can swallow with ease and has no
hoarseness when talking, cranial nerve X is intact.

Cranial Nerve XI

Test cranial nerve XI….accessory nerve: Have the patient move head from side to side
and up and down and shrug shoulders against resistance.

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Cranial Nerve XII

Test cranial nerve XII….hypoglossal: have patient stick tongue out and move it side to side

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SPINAL CORD INJURY (SCI)

• Spinal cord injury (SCI) is damage to any part of the spinal cord or nerves at the end of the
spinal canal. The condition often causes permanent changes in strength, sensation, and other
body functions below the site of the injury.

Sign and symptoms

• Physical findings vary, depending on the level of injury, degree of spinal shock, and phase and
degree of recovery, but in general, are classified as follows:
� C-1 to C-3: Tetraplegia with total loss of muscular/respiratory function.
� C-4 to C-5: Tetraplegia with impairment, reduced pulmonary capacity, complete dependency
for ADLs.
� C-6 to C-7: Tetraplegia with some arm/hand movement allowing some independence in
ADLs.
� C-7 to T-1: Tetraplegia with limited use of thumb/fingers, increasing independence.
� T-2 to L-1: Paraplegia with intact arm function and varying function of intercostal and
abdominal muscles.
� L-1 to L-2 or below: Mixed motor-sensory loss; bowel and bladder dysfunction

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1. Central cord syndrome

 Occurs from a lesion in the central portion of the spinal cord
 Loss of motor function is more pronounced in the upper extremities, and varying degrees
and patterns of sensation remain intact.

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2. Anterior cord syndrome

a. Caused by damage to the anterior portion of the gray and white matter of the spinal cord
b. Motor function, pain, and temperature sensation are lost below the level of injury;
however, the sensations of position, vibration, and touch remain intact.

3. Posterior cord syndrome

a. Caused by damage to the posterior portion of the gray and white matter of the spinal cord
b. Motor function remains intact, but the client experiences a loss of vibratory sense, crude
touch, and position sensation.

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4.Brown-Sequard syndrome
a. Results from penetrating injuries that cause hemisection of the spinal cord or injuries that
affect half of the cord
b. Motor function, vibration, proprioception (sense of position), and deep touch sensations are
lost on the same side of the body as the lesion or cord damage.
c. On the opposite side of the body (contralateral) from the lesion or cord damage, the sensations
of pain, temperature, and light touch are affected.

Assessment of spinal cord injuries

1. Dependent on the level of the cord injury

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2. Level of spinal cord injury: Lowest spinal cord segment with intact motor and sensory
function
3. Respiratory status changes
4. Motor and sensory changes below the level of injury
5. Total sensory loss and motor paralysis below the level of injury
6. Loss of reflexes below the level of injury
7. Loss of bladder and bowel control
8. Urinary retention and bladder distention
9. Presence of sweat, which does not occur on paralyzed areas
Manifestations of Neurogenic Shock , Spinal Shock and Autonomic Dysreflexia

Always suspect spinal cord injury when trauma occurs until this injury is ruled out.
Immobilize the client on the spinal backboard with the head in a neutral position to prevent an
incomplete injury from becoming complete.

Nursing Management:

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Spinal immobilization
Initial assessment
• Be aware the loss of thoracic sympathetic innervation (T1-T5) may inhibit tachycardia and
vasoconstriction as signs of hypovolaemia. Thus haemorraghic injuries may not be indicated by
the usual signs.

Initial care - Immobilisation:

o Immobilize the entire spine of any patient with known or potential SCI
o Immobilize neck with a hard collar.
o Use log roll with adequate personnel to turn patient while maintaining spine alignment.
Maintain neck in neutral position by use of a foam collar, but change to two-piece semi-rigid
collar for comfort and avoidance of complications (e.g. pressure area, venous obstruction,
aspiration) following assessment or early surgery.
• Surgery may be required in the situation of a reversible compression injury or
deteriorating neurology with a spinal injury amenable to some form of reduction and or
fixation.

Halo & Orthotic devices:

o Some patients may have Halo devices applied by surgeons, or a brace made by orthotics to
maintain correct alignment of the spine. These devices are fixed to the chest.
o Ensure you know how to open devices to perform chest compressions in the event of a cardiac
arrest, and that spinal immobilisation is maintained manually throughout any resuscitation.
• Move patient using slide sheets or pat slide with adequate number of personnel to maintain
spinal alignment.

Neurological assessment
� Neurological assessment and documentation
o Sensory level
o Motor function

� Glasgow coma score

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� Pupil response
Perform hourly for 1st 24 hours then decrease to 4 hourly if condition stabilized.
Note evidence of brain injury as well as spinal cord injury

Vital signs (and autonomic control)

• Vital signs can be quite abnormal following SCI. In addition to the usual causes in trauma such
as pain, bleeding and distress, this can be due to loss of autonomic control, which occurs
particularly in cervical or high thoracic injuries. The autonomic nervous system controls our HR,
BP temperature etc. Autonomic instability is most acute in the first few days to weeks of the
injury
AUTONOMIC DYSREFLEXIA
• Autonomic dysreflexia is a condition that emerges after a spinal cord injury, usually when the
damage has occurred above the T6 level.
• The higher the level of the spinal cord injury, the greater the risk, with up to 90% of patients
with cervical spinal or high-thoracic spinal cord injury being susceptible.
• Autonomic hyperreflexia (dysreflexia) is an exaggerated (excessive) reflex response by the
autonomic system (specifically the sympathetic nervous system).
• This reflex response by the sympathetic nervous system will be unopposed by the
parasympathetic nervous system, which makes it dangerous.

What causes this exaggerated reflex response?

• It occurs due to an irritating (potentially harmful) stimulus below the site of injury in patients
who have a spinal cord injury, and it results in severe hypertension.
• It’s a medical emergency that must be PREVENTED and quickly DETECTED. It can lead to
a stroke or seizure and be fatal.

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Main BIG causes of Autonomic Dysreflexia

• Anything that is an irritating stimulus that occurs BELOW the site of the spinal cord injury can
lead to it, BUT there are 3 big causes you need to remember.

Remember the 3 Big B’s….

• Bladder issue: example would be a distended or urinary tract infection
• Bowel issue: like hard stool that collects in the rectum leading to impaction
• Break down of skin: due to any type of binding devices or clothing, pressure injury, burns,
infection, cuts etc.
• Miscellaneous causes: birthing process, sexual intercourse, menstruation, or anything procedure
that causes stimulation below the site of injury.

Signs and Symptoms of Autonomic Dysreflexia

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• Throbbing Headache
• Hypertension: normal blood pressure for a patient with a T6 or higher spinal cord injury is
usually a systolic 90-110 mmHg….watch for systolic 20-40 mmHg higher than their baseline
because this is worrisome
• Flushing of skin ABOVE the spinal injury site (vasodilation)
• Bradycardia (heart rate less than 60 bpm)
• Pale, cool, clammy BELOW the spinal injury site (vasoconstriction)
• Goosebumps on the skin
• Sweating
• Dilated pupils/blurred vision
• Nasal stuffiness
• Anxiety

Nursing Interventions for Autonomic Dysreflexia

• Think PDA (Prevention, Detection and action)

PREVENTION:
• Think of the 3 BIG B’s (Bladder, Bowel, Break down of Skin)
• Bladder: prevent distention by making sure the bladder stays emptied, assess urinary output,
perform a bladder scans to make sure the bladder is not retaining urine (this is non-invasive),
take steps to prevent urinary tract infections, if patient has a Foley catheter make sure it is
draining properly (not kinked or blocked)
• Bowel: assess last bowel movement, bowel sounds, and palpate abdomen for distention. If
impacted, use an anesthetic jelly prior to manually removing the stool.

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• Break down of skin: remove any binding clothing or devices, turns every 2 hours, assess skin
regularly, keep skin protected from injury etc.

DETECTION and ACTION:

• Remember patients who’ve experience at T6 or higher spinal cord injury are at HIGHEST risk.
Always assess blood pressure and monitor for any elevation (remember 20-40 mmHg higher
from baseline could indicate AD).
• If patient reports a headache, INVESTIGATE it by checking blood pressure immediately.
• Monitor for the signs and symptoms.

What to do if this develops: It’s a medical emergency!

• Get help (call rapid response), get help, and stay with the patient.
• Position the patient in High Fowler’s….90 degree angle with legs lowered….this will cause
blood to pool in the lower extremities and help decrease blood pressure.
• Check blood pressure every 2-5 minutes.
• Remove any binding clothing or devices.
• Investigate and correct the problem….it could be any of the three Big B’s.
• Start with bladder (most common cause): assess that catheter is draining properly or if
patient doesn’t have a Foley may need to be catheterize to drain urine (use anesthetic jelly
to prevent more stimulation).
• Check for bowel impaction: need to use anesthetic jelly prior to prevent causing
stimulation to the rectum and increase AD symptoms…remove stool if present.
• Check skin for injury or break down.
• If blood pressure still high may need medications:
• Nitropaste (topical application)….do NOT give Nitropaste if patient has taken a
phosphodiesterase inhibitor within the past 24 hours (Sildenafil or Tadalafil) because this
could lead to life-threatening hypotension.
• Nifedipine (sublingual for immediate release)…calcium channel blocker

NEUROGENIC BLADDER

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• Neurogenic Bladder, also known as Neurogenic Lower Urinary Tract Dysfunction, is when a
person lacks bladder control due to brain, spinal cord or nerve problems.
• Bladder relies on muscles to contract and release when you’re ready to urinate. Brain typically
regulates this process, but sometimes the message that you need to urinate isn’t sent from your
brain to your bladder. This is a condition known as neurogenic bladder. Treatment for this
condition can help you regain control.

Causes
• Neurogenic bladder is a condition caused by the nerves along the pathway between the bladder
and the brain not working properly. This can be due to a brain disorder or bladder nerve damage.

Examples of brain disorders that can cause neurogenic bladder include:

� Alzheimer’s disease
� tumors of the brain or spinal cord
� multiple sclerosis
� Parkinson’s disease
� injury to the spinal cord
� spinal cord birth defects, such as spina bifida
� stroke

Conditions that affect the bladder muscles include:

� diabetes, which can cause nerve damage
� long-term alcohol abuse
� pelvic surgery, which can cause nerve damage
� spinal nerve damage

Neurogenic bladder symptoms include:

� a dribbling stream when urinating
� an inability to fully empty your bladder
� straining during urination

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� a loss of bladder control

� increased urinary tract infections (UTIs)
� leaking urine
� difficulty determining when your bladder is full

Effects of Neurogenic Bladder

• Incontinence and urinary retention can both cause a variety of problems, with often unpleasant
consequences.

Effects of incontinence (urinary leaking):

� Wetting clothes
� Unpleasant odor from urine leaks
� Skin irritation from urine leaks
� Sores on the skin that may be painful and can become infected
� Unpredictability of urinary urges
� Embarrassment due to leaking small or large amounts of urine when around other people
Effects of urinary retention (bladder retention):
� Physical discomfort
� Abdominal pain or pressure
� Urinary tract infection resulting from urine remaining in the bladder for too long, which can
allow infectious bacteria to thrive. A urinary tract infection often requires treatment with
prescription-strength medications.
� Kidney damage due to pressure from the bladder, which may lead to kidney dilation
(hydronephrosis), increased creatinine, or other issues as a result of incomplete emptying of the
bladder.

Complication
• Because this condition causes you to lose the sensation to urinate, your bladder can fill beyond
typical capacity and leak.

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• But your bladder may not empty fully. This is called urinary retention. Urinary retention
increases your risk of a UTI.
• Infection can result when urine remains in your bladder or kidneys for too long. Frequent
urinary tract and kidney infections can lead to damage over time.
• This can ultimately lead to kidney failure, which can be fatal.

Treatment
• Suggest to urinate at regular intervals, which will prevent bladder from becoming too full. Ask
to keep a journal to record any leakage incidents. This can help determine the best intervals for
urinating. Suggest therapies such as Kegel exercises and pelvic floor muscle strengthening

Electrical stimulation therapy

• Another treatment option is electrical stimulation therapy. This therapy involves placing small
electrodes on the bladder. When stimulated, the electrodes can send impulses to the brain, telling
the need to urinate.

Medications
• There are no medications to treat or control neurogenic bladder specifically. However, some
medications can reduce or enhance muscle contractions. These help to ensure proper
emptying of the urinary tract
• A number of medications are available to help control the bladder muscles. They include the
following.

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� Anticholinergics: oxybutynin, tolterodine, fesoterodine, darifenacin, trospium, and solifenacin.

Trospium does not cross the blood-brain barrier and may be best suited for older patients or those
with confusion.
� Beta-3 adrenergic receptor agonist: mirabegron, the only drug currently available of this type,
relaxes the bladder muscle and increases bladder capacity.
� Other medications: estrogen therapy, imipramine, and amitriptyline. These medications act on
the nerves or muscles to help regain some control of the urination process.

Catheterization
In some instances, doctor may recommend catheterization to ensure complete bladder emptying.
This painless process involves inserting a thin plastic tube into the bladder to release urine.
However, this procedure carries the risk for increased UTIs. doctor may prescribe antibiotics at
low doses to minimize the risk for UTIs

Surgery
Your doctor can insert an artificial sphincter into body that compresses the urethra to prevent
urinary leakage which can then be manually released to allow emptying of the bladder. Other
surgical options include bladder reconstruction surgery which may help with bladder control.

CEREBRAL PALSY

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1. Disorder characterized by impaired movement, posture, and/or muscle tone, resulting from an
abnormality in the extrapyramidal or pyramidal motor system
2. The most common clinical type is spastic cerebral palsy, which represents an upper motor
neuron type of muscle weakness.

Assessment
1. Extreme irritability and crying
2. Feeding difficulties
3. Abnormal motor performance
4. Alterations of muscle tone; stiff and rigid arms or legs
5. Delayed developmental milestones
6. Persistence of primitive infantile reflexes (Moro, tonic neck) after 6 months (most primitive
re- flexes disappear by 3 to 4 months of age)
7. Abnormal posturing, such as opisthotonos (exaggerated arching of the back)
8. Seizures may occur.

Figure: Abnormal posturing : opisthotonos

Interventions
1. The goal of management is to recognize the disorder early and implement interventions to
maximize the child’s abilities.
2. An interprofessional team approach is implemented to meet the many needs of the child.

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3. Therapeutic management includes physical therapy, occupational therapy, speech therapy,

education, and recreation.
4. Assess the child’s developmental level and intelligence.
5. Encourage early intervention and participation in school programs.
6. Prepare for using mobilizing devices to help prevent or reduce deformities.
7. Encourage communication and interaction that correspond with the child’s developmental age
level, rather than chronological age level.
8. Provide a safe environment by removing sharp objects, using a protective helmet if the child
falls frequently, and implementing seizure precautions if necessary.
9. Provide safe, appropriate toys for the child’s age and developmental level.
10. Position the child upright after meals.
11. Medications may be prescribed to relieve muscle spasms, which cause intense pain;
antiseizure medications may also be prescribed.
12. Provide the parents with information about the disorder and the treatment plan; encourage
support groups for parents.

NEURAL TUBE DEFECTS

1. This central nervous system defect results from failure of the neural tube to close during
embryonic development.
2. Folic acid is recommended during childbearing years and pregnancy to reduce the occurrence
of these conditions.
3. Associated deficits include sensorimotor disturbance, dislocated hips, talipes equinovarus
(clubfoot), and hydrocephalus.
4. Defect closure is performed soon after birth.

Spina Bifida
• Spina bifida is part of a group of birth defects called neural tube defects.
• Caused by a defect in the neural arch generally in the lumbosacral region, spina bifida is a
failure of the posterior laminae of the vertebrae to close; this leaves an opening through which
the spinal meninges and spinal cord may protrude.

Types

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• Spina bifida occulta. A bony defect that occurs without soft tissue involvement is called spina
bifida occulta.

• Spina bifida with meningocele. When part of the spinal meninges protrudes through the bony
defect and forms a cystic sac, the condition is termed spina bifida with meningocele.

• Spina bifida with myelomeningocele. In spina bifida with myelomeningocele, there is a

protrusion of the spinal cord and the meninges, with nerve roots embedded in the wall of the
cyst.

Causes
• The etiology in most cases of spina bifida is multifactorial, involving genetic, racial, and
environmental factors, in which nutrition, particularly folic acid intake, is key.
• Low folic acid intake. Research indicates folate can reduce the incidence of neural tube
defects by about 70% and can also decrease the severity of these defects when they occur.
• Genetics. If a woman gives birth to a baby with spina bifida, she has a higher-than-normal risk
of having another baby with spina bifida too (about 5% risk).
• Certain medications. Some medications (Valproate and carbamazepine) , such as some for
treating epilepsy or bipolar disorder have been associated with a higher risk of giving birth
to babies with congenital defects, such as spina bifida.
• Diabetes. Women with diabetes are more likely to have a baby with spina bifida, compared to
other females.

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• Obesity. Obese women, those whose BMI (body mass index) is 30 or more have a higher risk
of having a baby with spina bifida. The higher the woman’s BMI is over 30, the higher the risk.

Clinical Manifestations

1. Depends on the spinal cord involvement

2. Visible spinal defect
3. Flaccid paralysis of the legs
4. Altered bladder and bowel function
5. Hip and joint deformities
6. Hydrocephalus

Interventions:
1. Evaluate the sac and measure the lesion.
2. Perform neurological assessment.
3. Monitor for increased ICP, which might indicate developing hydrocephalus.
4. Measure head circumference; assess anterior fontanel for bulging.
5. Protect the sac; as prescribed, cover with a sterile, moist (normal saline), nonadherent dressing
to maintain the moisture of the sac and contents.

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6. Change the dressing covering the sac on a regular schedule or whenever it becomes soiled
because of the risk of infection; diapering may be contraindicated until the defect has been
repaired.
7. Use aseptic technique to prevent infection.
8. Assess the sac for redness, clear or purulent drainage, abrasions, irritation, and signs of
infection.
9. Early signs of infection include elevated temperature (axillary), irritability, lethargy, and
nuchal rigidity.
10. Place in a prone position to minimize tension on the sac and the risk of trauma; the head is
turned to one side for feeding.
11. Assess for physical impairments such as hip and joint deformities.
12. Prepare the child and family for surgery.
13. Administer antibiotics preoperatively and postoperatively, as prescribed, to prevent infection.
14. Teach the parents and eventually the child about long-term home care.
a. Positioning, feeding, skin care, and range-of motion exercises
b. Instituting a bladder elimination program and performing clean intermittent
catheterization technique if necessary
c. Administering antispasmodics (that act on the smooth muscle of the bladder) as
prescribed to increase bladder capacity and improve continence
d. Implementing a bowel program, including a high-fiber diet, increased fluids, and
suppositories as needed.
e. The child is at high risk for allergy to latex and rubber products because of the frequent
exposure to latex during implementation of care measures.

Surgical Management
• Many specialists are involved in the treatment of these newborns, especially in the case of
myelomeningocele.
• Surgery. Surgery is required to close the open defect but may not be performed immediately,
depending on the surgeon’s decision.
• Prenatal surgery. In this procedure — which takes place before the 26th week of pregnancy
— surgeons expose a pregnant mother’s uterus surgically, open the uterus and repair the baby’s
spinal cord.

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• Ongoing care. Babies with myelomeningocele may also start exercises that will prepare their
legs for walking with braces or crutches when they’re older.
• Cesarean birth. Cesarean birth may be part of the treatment for spina bifida; many babies with
myelomeningocele tend to be in a feet-first (breech) position.

Nursing Interventions
• Prevent infection. Monitor the newborn’s vital signs, neurologic signs, and behavior
frequently; administer prophylactic antibiotic as ordered; carry out routine aseptic technique;
cover the sac with a sterile dressing moistened in a warm sterile solution and change it every 2
hours; the dressings may be covered with a plastic protective covering.

• Promote skin integrity. Placing a protective barrier between the anus and the sac may prevent
contamination with fecal material, and diapering is not advisable with a low defect.

• Prevent contractures of lower extremities. Newborns with spina bifida often have talipes
equinovarus (clubfoot) and congenital hip dysplasia (dislocation of the hips); if there is loss of
motion in the lower limbs because of the defect conduct range-of-motion exercises to prevent
contractures; position the newborn so that the hips are abducted and the feet are in a neutral
position; massage the knees and other bony prominences with lotion regularly, then pad them,
and protect them from irritation.

• Proper positioning of the newborn. Maintain the newborn in a prone position so that no
pressure is placed on the sac; after surgery, continue this positioning until the surgical site is well
healed.

• Promote family coping. Be especially sensitive to their needs and emotions; encourage family
members to express their feelings and emotions as openly as possible; provide privacy as needed
for the family to mourn together over their loss; encourage the family members to cuddle and
touch the newborn using proper precautions for the safety of the defect.

• Provide family teaching. Give family members information about the defect and encourage
them to discuss their concerns and ask questions; provide information about the newborn’s
present state, the proposed surgery, and follow-up care; information shall be provided in small
segments to facilitate comprehension; after the surgery, teach the family to hold the newborn’s
head, neck, and chest slightly raised in one hand during feeding; also teach them that stroking the
newborn’s cheeks helps stimulate sucking.

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HYDROCEPHALUS
1. An imbalance of CSF absorption or production that is either the result of congenital
complication or an acquired condition such as tumors, hemorrhage, infections, or trauma
2. Results in head enlargement and increased ICP

Types
1. Communicating: Hydrocephalus occurs as a result of impaired absorption within the
subarachnoid space, obliteration of the subarachnoid cisterns, or malfunction of the arachnoid
villi.
2. Noncommunicating (obstructive): Hydrocephalus occurs as a result of excess cerebrospinal
fluid (CSF) due to structural blockage within the ventricular system.

Assessment
1. Infant
a. Increased head circumference
b. Thin, widely separated bones of the head that produce a cracked-pot sound (Macewen’s sign)
on percussion
c. Anterior fontanel tense, bulging, and nonpulsating; sutures will separate prior to fontanel
bulging.
d. Pupils become sluggish and have an unequal response to light
e. Increased irritability

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f. Changes in LOC
g. Lower extremity spasticity
h. Poor feeding
i. Dilated scalp veins
j. Frontal bossing
k. “Setting sun” eyes

2. Child
a. Signs and symptoms seen in early to late childhood are caused by the increase in intracranial
pressure and are dependent upon the location of the focal lesion.
b. Behavioral changes, such as irritability and lethargy
c. Headache on awakening
d. Nausea and vomiting
e. Ataxia
f. Strabismus
g. Papilledema

3. Late signs: High, shrill cry and seizure

Surgical interventions
1. The goal of surgical treatment is to prevent further CSF accumulation by bypassing the
blockage and draining the fluid from the ventricles to a location where it may be reabsorbed.
2. In a ventriculoperitoneal shunt, the CSF drains into the peritoneal cavity from the lateral
ventricle.

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Figure: Ventriculo-peritoneal shunt

3. In a ventriculoatrial shunt, CSF drains into the right atrium of the heart from the lateral
ventricle, bypassing the obstruction (used in older children and in children with pathological
conditions of the abdomen).
4. Shunt revision may be necessary as the child grows.

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5. An alternative to shunt placement is endoscopic third ventriculostomy, in which a small

opening in the floor of the third ventricle is made that allows CSF to bypass the fourth ventricle
and return to the circulation to be absorbed; this treatment may not be appropriate for some types
of hydrocephalus.

Preoperative interventions
1. Monitor intake and output; give small, frequent feedings as tolerated until preoperative NPO
status is prescribed.
2. Reposition the head frequently and use special devices such as an egg crate mattress under the
head to prevent pressure sores.

Figure: Egg Crate Mattress

3. Prepare the child and family for diagnostic procedures and surgery.

Postoperative interventions
1. Monitor vital signs and neurological signs.

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2. Position the child on the unoperated side to prevent pressure on the shunt valve.
3. Keep the child flat if prescribed to avoid rapid reduction of intracranial fluid.
4. Observe for increased ICP; if increased ICP occurs, elevate the head of the bed to 15 to 30
degrees to enhance gravity flow through the shunt.
5. Measure head circumference.
6. Monitor for signs of infection, and assess dressings for drainage.
7. Monitor intake and output.
8. Provide comfort measures and administer medications as prescribed.
9. Instruct parents on how to recognize shunt infection or malfunction.
10. In an infant, irritability, lethargy, feeding poorly, and a high, shrill cry may indicate shunt
malfunction or infection.
11. In a toddler, headache and a lack of appetite are the earliest common signs of shunt
malfunction.
12. In older children, an indicator of shunt malfunction is an alteration in the child’s level of
consciousness.
13. Monitor for shunt presence behind the ear.

A high, shrill cry in an infant can be a sign of increased ICP.

REYE’S SYNDROME
1. Reye’s syndrome is an acute encephalopathy that follows a viral illness and is characterized
pathologically by cerebral edema and fatty changes in the liver, fluid and electrolyte imbalance,
acidbase imbalance, and coagulopathies; diagnosis is made by laboratory studies and liver
biopsy.
2. The exact cause is unclear; it most commonly follows a viral illness such as influenza or
varicella
3. Administration of aspirin or aspirin-containing products is not recommended for children with
a febrile illness or children with varicella or influenza or other viral illnesses because of its
association with Reye’s syndrome.
4. Acetaminophen and ibuprofen are considered the medications of choice.
5. Early diagnosis and aggressive treatment are important; the goal of treatment is to maintain
effective cerebral perfusion and to control increasing ICP.

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Assessment
1. History of systemic viral illness 4 to 7 days before the onset of symptoms
2. Fever
3. Nausea and vomiting
4. Signs of altered hepatic function such as lethargy
5. Progressive neurological deterioration
6. Increased blood ammonia levels

Interventions
1. Provide rest and decrease stimulation in the environment.
2. Assess neurological status.
3. Monitor for altered level of consciousness and signs of increased ICP.
4. Monitor for signs of altered hepatic function and results of liver function studies.
5. Monitor intake and output.
6. Monitor for signs of bleeding and signs of impaired coagulation, such as a prolonged bleeding
time.

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