INFECTIOUS NEUROLOGIC

DISORDERS
MENINGITIS

Kenneth M. Sabido, RN, MN

 MENINGITIS
➢ inflammation of the meninges, which cover and
protect the brain and spinal cord.
MAJOR CAUSES:
1. Baterial ( Streptococcus pneumonia & Neisseria
meningitidis)
1. Viral (Enteroviruses)
2. Fungal Infections
N. meningitidis bacteria exists in the
throats and nasal passages PATHOPHYSIOLOGY
bacteremia

crosses blood brain barrier

proliferates in the CSF

inflammation of the
subarachnoid and pia mater

increased ICP
 CLINICAL MANIFESTATIONS
﴿ Fever & Headache
(steady/throbbing)
﴿ Neck immobility - stiff and painful
neck (nuchal rigidity)
﴿ Photophobia (extreme sensitivity
to light)
﴿ rash can be a striking feature of N.
meningitidis infection
 CLINICAL MANIFESTATIONS
﴿ Positive Kernig
sign
﴿ Positive
Brudzinski sign
﴿ Seizure
 DIAGNOSTICS
➢ CT SCAN
➢ Bacterial culture and Gram staining of CSF and blood
 PREVENTION

➢ Meningococcal conjugated vaccine - given at 11 to 12

years of age and booster dose at 16 years of age
➢ Chemoprophylaxis using rifampin (Rifadin),
ciprofloxacin hydrochloride (Cipro), or ceftriaxone
sodium (Rocephin) – start w/n 24hrs after exposure
➢ Vaccination against Haemophilus influenzae and S.
pneumonia – for children and adults who are at-risk
(CDC, 2016).
 MEDICAL MANAGEMENT
PHARMACOLOGIC:
1. Penicillin G + cephalosporins IV (e.g., ceftriaxone
sodium, cefotaxime sodium)
2. Dexamethasone
3. Fluid volume expanders - Dehydration
4. Anticonvulsant meds - seizure
 NURSING MANAGEMENT
1. Infection control precautions until 24 hours after
initiation of antibiotic therapy (oral and nasal
discharge is considered infectious)
2. Pain management due to overall body aches and
neck pain
3. Provide rest in a quiet, darkened room
4. Antipyretic agents and cooling blankets
5. Stay hydrated either orally or peripherally
 NURSING MANAGEMENT
6. Close neurologic monitoring
➢ O2 sat & ABG- identify need for respiratory support
➢ ET tube insertion- adequate tissue oxygenation
➢ BP monitoring- shock
➢ IV fluid replacement
➢ Temperature monitoring- Fever also increases the
workload of the heart and cerebral metabolism
BRAIN ABSCESS
 BRAIN ABSCESS
BRAIN ABSCESS
➢ Collection of infectious material
within the tissue of the brain
➢ Otogenic in origin
➢ Result from intracranial surgery,
penetrating head injury, or tongue
piercing
 CLINICAL MANIFESTATION
1. Headache
2. Fever
3. Vomiting
4. Focal neurologic deficits - weakness and
decreasing vision
5. Increase ICP – decreasing LOC & seizure
 NURSING ASSESSMENT
Be alert to the following signs and symptoms:
Frontal Lobe
➢ Expressive aphasia (inability to express oneself)
➢ Frontal headache
➢ Hemiparesis (weakness on one side of the body)
➢ Seizures
 NURSING ASSESSMENT
Temporal Lobe Cerebellar Abscess
➢ Changes in vision ➢ Ataxia (inability to
➢ Facial weakness coordinate movements)
➢ Localized headache ➢ Nystagmus (rhythmic,
Receptive aphasia involuntary movements
(inability to understand of the eye)
language) ➢ Occipital headache
 DIAGNOSTIC FINDINGS
➢ CT scan with contrast –Size and location
➢ Aspiration of the abscess- guided by CT or MRI
➢ MRI
➢ Blood cultures
➢ Chest X-ray
➢ EEG
 MEDICAL MANAGEMENT
PHARMACOLOGIC SURGICAL MANAGEMENT
1. Antibiotic – 1. Stereotactic CT-guided
Ceftriaxone aspiration - to drain the
2. Corticosteroids reduce abscess and identify the
cerebral edema causative organism
3. Anticonvulsant- treat
seizure
 NURSING MANAGEMENT

1. Neurologic assessment – be alert to changes in

ICP
2. Administer medications
3. Assess response to treatment – monitor blood
glucose and serum potassium levels
4. Provide safety and supportive care
Herpes Simplex
Encephalitis
Herpes Simplex Encephalitis
➢ acute inflammatory
process of the brain
tissue.
➢ Herpes simplex virus
(HSV) – causative
agent
 PATHOPHYSIOLOGY
Herpes simplex virus gains access through
mucous membranes and damaged skin

Causes local necrotizing hemorrhage in

the brain tissue that becomes more
generalized followed by edema

Progressive deterioration of nerve cell

bodies
CLINICAL MANIFESTATIONS
1. Fever
2. headache
3. confusion
4. hallucinations
 DIAGNOSTIC FINDINGS
1. Polymerase chain reaction (PCR) test –
standard test that identifies the
deoxyribonucleic acid (DNA) bands of HSV-
1 in the CSF
2. EEG -shows focal changes in the temporal
lobe
3. MRI -detect early changes caused by
herpes simplex
4. LUMBAR PUNCTURE- CSF examination for
causative agent
MEDICAL MANAGEMENT
Drug of choice:
Acyclovir (Zovirax)

Ganciclover (Cytovene)
 NURSING MANAGEMENT

1. Assessment of neurologic function is key to monitoring

the progression of disease.
2. Comfort measures to reduce headache:
✓ dimming the lights and limiting noise and visitors,
✓ grouping nursing interventions
✓ administering analgesic agents
3. Provide safety
4. Monitor blood chemistry test result and urinary output
 Arthropod-Borne
Virus Encephalitis
 Arthropod-Borne Virus Encephalitis

Inflammation of the brain

caused by Arthropod-
borne viruses, or
arboviruses by blood
feeding arthropods
(mosquitoes, psychodids,
ceratopogonids, and ticks).
5 main arboviral encephalitides:
1. eastern equine encephalitis,
2. western equine encephalitis,
3. St. Louis encephalitis,
4. La Crosse encephalitis,
5. West Nile virus encephalitis
 PATHOPHYSIOLOGY

Viral replication occurs at

Verimia
the site of the mosquito bite

virus gains access to the CNS via

Encephalitis
the olfactory tract
CLINICAL MANIFESTATION
1. Flulike symptoms (i.e.,
headache and fever)
2. SIADH with hyponatremia
3. CNS symptoms include stiff
neck, confusion, dizziness, and
tremors.
4. Coma can occur in severe cases
Assessment and Diagnostic Findings
MRI:
> Inflammation of the basal ganglia (SLE)
>Inflammation in the periventricular area (WNE)

EEG:
Identify abnormal brain waves to identify some viral infections

CSF EXAMINATION:
Presence of Immunoglobulin M antibodies for West Nile virus
MEDICAL MANAGEMENT
➢No specific
medication for
arboviral
encephalitis exists;
therefore, symptom
management is key
 NURSING MANAGEMENT
1. Monitor neurologic status
2. Injury prevention is key in light of the potential for falls or
seizures
3. Family support and education to cope with these outcomes.
4. Public education addressing the prevention of arboviral
encephalitis is a key nursing role
5. Wear clothing that provides coverage and insect repellents
containing 20% to 35% diethyltoluamide (DEET)
 NURSING MANAGEMENT
6. Remain indoors at dawn and dusk when mosquito
activity is highest.
7. Screens should be in good repair in the home
8. Standing water should be removed.
9. All cases of arboviral encephalitis must be reported
to the local health department.
Fungal Encephalitis
 Fungal Encephalitis
➢ Fungal infections of the CNS caused by Cryptococcus
neoformans, Blastomyces dermatitidis, Histoplasma
capsulatum, Aspergillus fumigatus, Candida, and
Coccidioides immitis
➢ People at risk are coal miners, construction workers,
and farmers.
➢ C. neoformans is associated with exposure to bird
droppings and may be seen in bird handlers.
 PATHOPHYSIOLOGY
fungal spores enter the body via inhalation

initially infect the lungs (Pneumonitis)

Fungemia
fungus may spread to the CNS
(Meningitis, Encephalitis, brain bscess, granuloma, arterial thrombus)
CLINICAL MANIFESTATIONS
1. Fever
2. Malaise
3. headache,
4. Meningeal signs
5. Change in LOC or cranial nerve
dysfunction.
6. Symptoms of increased ICP
related to hydrocephalus often
occur
Assessment and Diagnostic Findings
1. Fungal antibodies found in serologic tests
2. Elevated white cell and protein levels and
glucose levels are decreased in the CSF
examination
3. Blood or CSF culture to determine causative
agent
4. MRI shows area of hemorrhage, abscess, or
enhanced meninges indicating inflammation
MEDICAL MANAGEMENT
PHARMACOLOGIC SURGICAL
1. Anticonvulsant medication – MANAGEMENT
control seizure 1. Repeated Lumbar
2. Antifungal agents – puncture or shunting
Amphotericin B, of CSF –to control
Fluconazole, Flucytosine ICP
 NURSING MANAGEMENT
1. Administer non-opioid analgesic agents
2. Limit environmental stimuli
3. Positioning may optimize patient comfort.
4. Administer diphenhydramine (Benadryl) and acetaminophen
(Tylenol) approximately 30 minutes before giving amphotericin B
may prevent flulike side effects.
5. Providing support assists the patient and family to cope with the
illness because the recovery may be long
Creutzfeldt–Jakob and Variant
Creutzfeldt–Jakob Diseases
Creutzfeldt–Jakob(CJD) and Variant
Creutzfeldt–Jakob Diseases (vCJD)
➢ Belong to a group of
degenerative, infectious
neurologic disorders called
transmissible spongiform
encephalopathies (TSE).
➢ CJD is very rare and has no
identifiable cause
 Creutzfeldt–Jakob(CJD) and Variant
Creutzfeldt–Jakob Diseases (vCJD)
➢ human variation of
bovine spongiform
encephalopathy (BSE)
(commonly known as
mad cow disease) –
ingestion of prions in
infected meat
 PATHOPHYSIOLOGY

Ingestion
prion depo
by
crosses sited degener
humans ation of
the Cell
of prions
blood- in brain death
in
infected
brain brain tissue
barrier
meat. tissue
 CLINICAL MANIFESTATION
1. Affective symptoms (i.e., behavioral changes)
2. sensory disturbance, and limb pain
3. Muscle spasms and rigidity, dysarthria, incoordination,
cognitive impairment, and sleep disturbances
4. Patients with sporadic CJD present with mental
deterioration, ataxia, and visual disturbance.
5. Memory loss, involuntary movement, paralysis, and
mutism
 Assessment and Diagnostic Findings
1. Immunologic assessment of CSF - detects a protein
kinase inhibitor referred to as 14–3–3
2. EEG - reveals a characteristic pattern over the
duration of the disease
3. MRI scanning - demonstrates symmetric or
unilateral hyperintense signals arising from the
basal ganglia
MEDICAL MANAGEMENT
> Supportive and Palliative care
➢ Prevention of injury related to immobility and
dementia,
➢ Promotion of patient comfort
➢ Provision of support and education for the family.
NURSING MANAGEMENT
➢ Supportive and palliative
➢ Psychological and emotional support of the patient and
family
➢ Care extends to providing for a dignified death and
supporting the family through the processes of grief and
loss.
➢ Prevention of disease transmission- Standard Precautions
 NURSING MANAGEMENT
➢ Institutional protocols are followed for handling of brain,
spinal cord, pituitary gland, and eye tissue; and for exposure
and decontamination of equipment
➢ It is recommended that disposable instruments be used and
then incinerated, because conventional methods of
sterilization do not destroy the prion.
➢ If disposable instruments cannot be used, stringent
sterilization methods such as the use of bleach for cleaning
and extended sterilization time for instruments should be
used.
AUTOIMMUNE PROCESSES

MULTIPLE SCLEROSIS
 MULTIPLE SCLEROSIS
➢ Immune-mediated, progressive demyelinating
disease of the CNS.
➢ Demyelination- destruction of myelin—the fatty and
protein material that surrounds certain nerve fibers
in the brain and spinal cord; it results in impaired
transmission of nerve impulses
 PATHOPHYSIOLOGY
Sensitized T- and B Sensitized T cells remain in immune system attack
lymphocytes cross the blood– CNS and promote the leads to inflammation that
brain barrier; their function is infiltration of other agents destroy myelin and
to check the CNS for antigens that damage the immune oligodendroglial cells that
then leave system produce myelin in the CNS

Plaques appear on Axons begin to

Demyelinated axons
Demyelination demyelinated axons, degenerate,
are scattered
interrupts the flow further interrupting resulting in
irregularly in the
of nerve impulses the transmission of permanent and
CNS
impulses irreversible damage
 CLINICAL MANIFESTATION

➢ fatigue, depression, weakness, numbness, difficulty

in coordination, loss of balance, spasticity, and pain
➢ blurring of vision, diplopia (double vision), scotoma
(patchy blindness), and total blindness.
➢ Spasticity (muscle hypertonicity)
➢ Ataxia (impaired coordination of movement)
 CLINICAL MANIFESTATION
TYPES AND COURSES OF MULTIPLE SCLEROSIS
1. RELAPSING REMITTING
> characterized by clearly acute
attacks with full recovery or with
sequelae and residual deficit upon
recovery
 CLINICAL MANIFESTATION
2. Primary progressive MS
> characterized by disease
showing progression of
disability from onset, without
plateaus and temporary
minor improvements
CLINICAL MANIFESTATION
3. Secondary progressive MS
> begins with an initial RR
course, followed by
progression of variable rate,
which may also include
occasional relapses and minor
remissions.
 CLINICAL MANIFESTATION
4. Progressive relapsing MS
> shows progression from
onset but with clear acute
relapses with or without
recovery.
 Assessment and Diagnostic Findings
➢ MRI – presence of multiple plaques in the CNS
➢ Electrophoresis of CSF - presence of oligoclonal banding
(several bands of immunoglobulin G bonded together)
➢ Urodynamic studies - Underlying bladder dysfunction
➢ Neuropsychological testing - to assess cognitive
impairment.
➢ Sexual history - identify changes in sexual function.
 MEDICAL MANAGEMENT
➢ NO cure exists
➢ Symptomatic treatment and provide continuing
support
➢ Goals of treatment are to delay the progression of
the disease, manage chronic symptoms, and treat
acute exacerbations
 MEDICAL MANAGEMENT
PHARMACOLOGIC THERAPY
DISEASE-MODIFYING THERAPIES
❑ Reduce the frequency of relapse
➢ Interferon beta-1a (Rebif) and interferon beta-1b (Betaseron) SC – S/E:
flu-like symptoms
➢ Glatiramer acetate (Copaxone) SC – drug of choice for RR course
➢ Oral meds -Teriflunomide (Aubagio), fingolimod (Gilenya), and dimethyl
fumarate (Tecfidera) – to reduce disease activity and progression
➢ Methylprednisolone IV – acute relapse in RR course
➢ Mitoxantrone (Novantrone) IV q 3 months - reduce the frequency of
clinical relapses for secondary progressive or worsening RR MS.
 SYMPTOM MANAGEMENT:
1. Baclofen (Lioresal) – drug of choice for treating
spasticity
2. Benzodiazepines (e.g., diazepam [Valium]),
tizanidine (Zanaflex), and dantrolene (Dantrium) - to
treat spasticity
3. Amantadine (Symmetrel), pemoline (Cylert), or
dalfampridine (Ampyra) – treatment for fatigue that
interferes with ADL’s
 SYMPTOM MANAGEMENT:
4. Beta-adrenergic blockers (e.g., propranolol [Inderal])
– to treat Ataxia
5. Gabapentin (Neurontin), and benzodiazepines (e.g.,
clonazepam [Klonopin]) – anti-convulsant agent
6. Anticholinergic agents, alpha-adrenergic blockers,
antispasmodic agents – to treat bowel and bladder
problems
7. Ascorbic acid (vitamin C) – to acidify the urine,
making bacterial growth less likely to prevent UTI
 NURSING DIAGNOSIS AND INTERVENTIONS
Impaired bed and physical mobility related to weakness, muscle
paresis, spasticity, increased weight
1. EXERCISE - Walking improves the gait
2. Minimizing Spasticity and Contractures:
✓ Warm packs
✓ Muscle stretching in areas like hamstrings, gastrocnemius
muscles, hip adductors, biceps, and wrist and finger flexors
✓ stretch–hold–relax routine
✓ Swimming and stationary bicycling
✓ Progressive weight bearing
 NURSING DIAGNOSIS AND INTERVENTIONS

Impaired bed and physical mobility related to weakness, muscle

paresis, spasticity, increased weight
3. Activity and rest – take frequent short rest periods, preferably lying
down
4. Nutrition
✓ promote healthy eating and weight reduction
✓ include family members in interventions and nutrition education
5. Minimizing Effects of Immobility
✓ Perform coughing and deep-breathing exercises
✓ Turn to sides q 2 hrs
 NURSING DIAGNOSIS AND INTERVENTIONS

Risk for injury related to sensory and visual impairment

1. Walk with feet apart to widen the base of support and
to increase walking stability
2. Use of assistive devices (walker, cane, braces, crutches,
parallel bars)
3. Watch the feet while walking.
4. Use of weighted bracelets or wrist cuffs – help control
tremors
 NURSING DIAGNOSIS AND INTERVENTIONS
Impaired urinary elimination (urgency, frequency, incontinence),
constipation, and bowel incontinence related to nervous system
dysfunction
1. Bedpan or urinal should be readily available – need to void must be
heeded immediately
2. Voiding time schedule is set up (every 1.5 to 2 hours initially, with
gradual lengthening of the interval)
3. Patient is instructed to drink a measured amount of fluid every 2 hours
and then attempt to void 30 minutes after drinking.
4. Use of a timer or wristwatch with an alarm to signal the need to empty
the bladder
5. Adequate fluids, dietary fiber, and a bowel training program- for bowel
problem
 NURSING DIAGNOSIS AND INTERVENTIONS
Chronic confusion related to cerebral dysfunction
1. Use of eye patch or a covered eyeglass lens - to block
the visual impulses of one eye if the patient has
diplopia
2. Use of Prism glasses to patient’s with difficulty reading
in the supine position
3. Provide emotional support to patient and their families
to adapt to the changes and uncertainties
4. Set meaningful and realistic goals, to remain as active
as possible, and to maintain interests and activities.
 NURSING DIAGNOSIS AND INTERVENTIONS

Ineffective coping related to uncertainty of course of MS

1. Assist patients and families to manage or reduce stress
and making appropriate referrals for counseling and
support to minimize the adverse effects of dealing with
chronic illness
2. Initiates home care and coordinates a network of
services, including social services, speech therapy,
physical therapy, and homemaker services.
 NURSING DIAGNOSIS AND INTERVENTIONS

Impaired home maintenance management related to

physical, psychological, and social limits imposed by MS
➢ Promote independence in home management like
assistive eating devices, raised toilet seat, bathing aids,
telephone modifications, long-handled comb, tongs,
modified clothing
➢ Recommend air conditioning of at least one room -
Exposure to heat increases fatigue and muscle weakness
MYASTHENIA GRAVIS
 MYASTHENIA GRAVIS
➢ an autoimmune disorder
affecting the myoneural
junction, is characterized by
varying degrees of weakness
of the voluntary muscles
 antibodies directed at the PATHOPHYSIOLOGY
acetylcholine receptor sites

impair transmission of impulses

across the myoneural junction.

fewer receptors are

available for stimulation

Resulting in voluntary muscle

weakness that escalates with
continued activity
 CLINICAL MANIFESTATION

1. Diplopia and ptosis (drooping of the eyelids)

2. Weakness of the muscles of the face and throat
(bulbar symptoms)
3. Generalized weakness
4. Dysphonia (voice impairment)
5. Dysphagia
 Assessment and Diagnostic Findings

1. Acetylcholinesterase inhibitor test - administering

edrophonium chloride (Tensilon) IV; 30 seconds after
injection, facial muscle weakness and ptosis should
resolve for about 5 minutes
2. Ice Test - ice pack is held over the patient’s eyes for 1
minute; the ptosis should temporarily resolve in a patient
with MG
 Assessment and Diagnostic Findings

3. Acetylcholine antibodies test- used to confirm the

diagnosis
4. Repetitive nerve stimulation (RNS) demonstrates a
decrease in successive action potentials
5. Single-fiber electromyography (EMG) detects a delay
or failure of neuromuscular transmission
6. MRI scan – enlarged thymus gland is observed
MEDICAL MANAGEMENT
PHARMACOLOGIC:
1. Anticholinesterase medications (i.e Pyridostigmine bromide
(Mestinon) - inhibits the breakdown of acetylcholine and
increasing the relative concentration of available acetylcholine at
the neuromuscular junction.
2. Immunosuppressive therapy -to reduce production of the
antibody
3. Intravenous immune globulin (IVIG) - to treat exacerbations
4. Therapeutic plasma exchange (TPE) - to treat exacerbations
5. Prednisone - suppress the patient’s immune response, decreasing
the amount of antibody production
 MEDICAL MANAGEMENT
SURGICAL:
1. Thymectomy
➢ removal of thymus gland
➢ can produce antigen-
specific
immunosuppression and
result in clinical
improvement
 NURSING MANAGEMENT

1. Medication management
➢ Understanding the actions of the medications and taking
them on schedule is emphasized
➢ Determine the best times for daily dosing by keeping a
diary to determine fluctuation of symptoms and to learn
when the medication is wearing off.
➢ Regular administration of IVIG or subcutaneous
immunoglobulin (SCIG) as prescribed
2. Energy conservation
➢ schedule activities to coincide with peak energy and
strength levels
➢ scheduling periods of rest, monitoring for depression,
maintaining good sleep patterns, and incorporating
interventions to conserve energy are all strategies to
reduce fatigue
➢ mealtimes should coincide with the peak effects of
anticholinesterase medication to prevent aspiration
➢ sit upright during meals, with the neck slightly flexed to
facilitate swallowing
3. Strategies to help with ocular manifestations
➢ Tape the eyes closed for short intervals and to regularly
instill artificial tears to prevent corneal damage
➢ Patching of one eye can help with double vision
4. prevention and management of complications
➢ emotional stress, infections (particularly respiratory
infections), vigorous physical activity, some medications,
and high environmental temperature should be avoided
to prevent exacerbation of symptoms
 Myasthenic Crisis
➢ a life-threatening complication of myasthenia gravis
characterized by worsening of muscle weakness,
resulting in respiratory failure
➢ Symptoms include respiratory distress and varying
degrees of dysphagia, dysarthria (difficulty speaking),
eyelid ptosis, diplopia, and prominent muscle weakness
➢ Monitor signs of Respiratory failure. Endotracheal
intubation and mechanical ventilation may be needed
➢ Chest physiotherapy, including postural drainage to
mobilize secretions and suctioning to remove secretions
 SUPPORTIVE MEASURES:

1. Monitor Arterial blood gases, serum electrolytes,

input and output, and daily weight
2. If the patient cannot swallow, enteral tube feedings
may be prescribed
3. Sedative and tranquilizing agents are avoided,
because they aggravate hypoxia and hypercapnia
and can cause respiratory and cardiac depression.
Guillain–Barré Syndrome (GBS)
 Guillain–Barré Syndrome (GBS)
➢ also known as acute idiopathic polyneuritis, is an
autoimmune attack on the peripheral nerve
➢ acute, rapid segmental demyelination of peripheral
nerves and some cranial nerves, producing ascending
weakness with dyskinesia (inability to execute
voluntary movements), hyporeflexia, and paresthesias
(a sensation of numbness, tingling, or a “pins and
needles” sensation)
 Causative agent:
1. Campylobacter jejuni,
2. cytomegalovirus,
3. Epstein–Barr virus,
4. Mycoplasma pneumoniae,
5. H. influenzae,
6. HIV
 TYPES OF GBS
1. Weakness in the lower extremities, which progresses
upward and has the potential for respiratory failure.
2. Purely motor with no altered sensation
3. Descending GBS - more difficult to diagnose; it mostly
affects the head and neck muscles.
4. Miller–Fisher variant, presents with ataxia, areflexia,
and opthalmoplegia; Rarest type
 PATHOPHYSIOLOGY

Attack on peripheral
Viral infection nerve myelin proteins
(ganglioside GM1b)

Causes Inflammation and

Influx of macrophages and
destruction, interruption of
other immune-mediated
nerve conduction and
agents that attack myelin
axonal loss
 CLINICAL MANIFESTATION

➢ Muscle weakness and diminished reflexes of the lower

extremities
➢ Hyporeflexia and weakness may progress to tetraplegia.
➢ neuromuscular respiratory failure.
➢ Sensory symptoms: paresthesias of the hands and feet
➢ Optic nerve demyelination may result in blindness.
Bulbar muscle weakness
 Assessment and Diagnostic Findings

➢ Presents with symmetric weakness, diminished reflexes,

and upward progression of motor weakness.
➢ History of a viral illness in the previous few weeks.
➢ Assess Changes in vital capacity and negative inspiratory
force to identify impending neuromuscular respiratory
failure
➢ Elevated protein levels are detected in CSF evaluation,
without an increase in other cells
 MEDICAL MANAGEMENT

➢ mechanical ventilation may be necessary to support

pulmonary function and adequate oxygenation
➢ anticoagulant agents and sequential compression boots
to prevent venous thromboembolism (VTE), including
deep vein thrombosis (DVT) and PE.
➢ TPE and IVIG are used to directly affect the peripheral
nerve myelin antibody level
➢ Continuous ECG monitoring
Ineffective breathing pattern and impaired gas exchange related
to rapidly progressive weakness and impending respiratory
failure
1. Assess carefully for difficulty in coughing and swallowing,
which may cause aspiration of saliva and precipitate acute
respiratory failure
2. Encourage use of incentive spirometry, provide chest
physiotherapy and elevate head of bed to facilitate
respirations and promote coughing.
3. Suction to maintain a clear airway
4. Prepare patient for intubation and ventilator support when
signs of deteriorating respiratory function are noted
Impaired bed and physical mobility related to paralysis 1.
Perform passive range-of-motion exercises at least twice
daily.
2. Position the patient correctly to avoid further damage to
susceptible peripheral nerves, prevent contractures and
pressure sores.
3. Apply antiembolic stockings, and sequential compression
boots, and adequate hydration decrease the risk of VTE.
4. Padding may be placed over bony prominences, such as
the elbows and heels, to reduce the risk of pressure ulcers.
Imbalanced nutrition: less than body requirements
related to inability to swallow
1. If with paralytic ileus, provide intravenous fluids and
parenteral nutrition as prescribed, and monitor for
return of bowel sounds
2. Provide gastrostomy tube to administer nutrients if
patient cannot swallow
3. Collaborate with physician and dietician to meet
patient’s nutritional and hydration needs; Provide
adequate nutrition to prevent muscle wasting.
Impaired verbal communication related to cranial nerve
dysfunction
1. Establishing some form of communication with
picture cards or an eye blink system provides a
means of communication.
2. Collaboration with the speech therapist may be
helpful in developing a communication mechanism
that is most effective for a specific patient.
Fear and anxiety related to loss of control and
paralysis
1. Create a positive attitude and atmosphere.
2. Provide patient with information about the
condition
3. Provide instruction about relaxation exercises and
distraction techniques
4. Diversional activities are encouraged to decrease
loneliness and isolation
CRANIAL NERVE
DISORDERS
 TRIGEMINAL NEURALGIA
• Tic Douloureux (painful twitch) of the facial
muscles
• Condition of the 5th cranial nerve characterized
by paroxysms of pain in the area innervated by
any of the CN VII
• Pain ends as abruptly as it starts and is described
as a unilateral shooting and stabbing sensation
• Usually occur in the 5th-6th decade of life &
common among women and in people with MS
 TRIGEMINAL NEURALGIA
Paroxysms can occur with any stimulation of the terminals of the
affected nerve branches
a. Washing the face
b. Shaving
c. Brushing the teeth
d. Eating and Drinking & Talking
e. Draft of cold air or direct pressure
f. Combing hair
g. Hot or too cold
h. Light Touch
• Patients try not to do this activities that might cause the attack
• In between the attacks of pain, the patient will be pain free for
weeks to months.
 3 Branches of the
TRIGEMINAL nerve
Upper or 1st Branch (OPTHALMIC)
eye, eyebrow, forehead, & frontal portion of the
scalp

Middle or 2nd Branch (MAXILLARY)

Upper lip, upper teeth, upper gum, upper
cheek, lower eyelid & side of the nose
Lower or 3rd Branch (MANDIBULAR)
Lower lip, lower teeth, lower gum, & side of
the tongue, front of the ear & side of the
head
 MEDICAL MANAGEMENT
A.PHARMACOLOGIC
a.Carbamazepine (Tegretol) relieve pain by reducing
transmission of impulses at certain nerve terminals
–Taken with meals
–S/E: nauseas, dizziness, drowsiness & aplastic anemia
–CBC (blood dyscrasias) bone marrow depression-long term use
b.Gabapentin (Neurontin)and Baclofen (Lioresal)
c.Phenytoin (Dilantin) adjunct therapy if pain is not achieved
 MEDICAL MANAGEMENT
B. SURGICAL MANAGEMENT
a. Microvascular Decompression of the
Trigeminal Nerve
▪ Intracranial approach used to relieve the contact
between the cerebral vessels and trigeminal
nerve root
▪ Operating microscope-the artery loop is lifted
from the nerve to relieve the pressure and a
small prosthetic device is inserted to prevent
recurrence of impingement on the nerve.
 MEDICAL MANAGEMENT
B. SURGICAL MANAGEMENT
b. Radiofrequency Thermal Coagulation
• Percutaneous radiofrequency produces thermal lesion on
the
trigeminal nerve.
• Use of stereotactic MRI for identification of the trigeminal
nerve
followed by gamma knife radiosurgery
• Immediate pain relief but may experience dysesthesia of
the face
and loss of corneal reflex
• Pain recurrence rate is 25%-37% within 5years
 MEDICAL MANAGEMENT
B. SURGICAL MANAGEMENT
c. Percutaneous Balloon Microcompression
• Disrupts large myelinated fibers in all 3 branches of the
Trigeminal nerve
• After its placement the balloon is filled with a contrast
material fluoroscopic identification.
• The balloon compresses the nerve root for 1 minute and
provides Microvascular decompression.
• Provides immediate relief with recurrence of 25% within 3
years
 NURSING MANAGEMENT
PREVENTING PAIN
a. Provide cotton pads and room temperature water for
washing face, or tepid tub baths
b.Rinse with mouthwash after eating if tooth brushing causes
pain
c. Perform personal hygiene during pain-free intervals
d.Take foods and fluids at room temp.
e.Chew on unaffected side and ingest soft foods
 NURSING MANAGEMENT
POST OPERATIVE CARE
1. Neurologic assessments to evaluate for facial motor and sensory
deficits in each of the three branches of the trigeminal nerve.
2. Instructed not to rub the eye because the pain of a resulting injury
will not be detected.
3. Eye is assessed for irritation or redness.
4. Artificial tears may be prescribed to prevent dryness in the affected
eye.
5. Patient is cautioned not to chew on the affected side until
numbness has diminished.
6. Observed carefully for any difficulty in eating or swallowing foods
of different consistencies.
BELL’s PALSY
 BELL’s PALSY
FACIAL PARALYSIS
> due to unilateral inflammation
of the 7th cranial nerve resulting
into weakness & paralysis of the
facial muscle of the affected side
 PATHOPHYSIOLOGY
Inflammation within a
small bony tube

Increase pressure in the

FACIAL NERVE
▪Vascular ischemia
▪Viral disease Facial nerve gets
herpes simplex inflamed & edematous
herpes zoster
Epstein-Barr decrease blood supply
▪Autoimmune
disease ISCHEMIA
 CLINICAL MANIFESTATIONS
A. facial paralysis (masklike then sags) face
may appear asymmetric
B. Unable to close the eyelid
C. decreased lacrimation
D. painful sensations in the face, behind the
ear, and in the eye
E. Speech difficulties
F. unable to eat on the affected side
because of weakness or paralysis of the
facial muscles
 MEDICAL MANAGEMENT
*Objective of treatment are to maintain the muscle tone of the face
& to prevent or minimize denervation & prevent complications

A. PHARMACOLOGIC
a. Corticosteroid(Prednisone)-reduce inflammation & edema
i. Reduce vascular compression and permits restoration of blood circulation
to the nerve
ii. Early administration diminishes the severity relieve pain & prevent
minimize denervation
b. Analgesics for pain
c. Electrical stimulation to prevent muscle atrophy
 NURSING MANAGEMENT
PROTECTING THE EYE
does not close completely, blink reflex is diminished,
vulnerable to injury to dust & foreign particles

a. eye should be covered with a protective shield at night

b. Moisturizing eye drops during the day and eye ointment at
bedtime may help prevent injury
c. close the paralyzed eyelid manually before going to sleep.
 NURSING MANAGEMENT
d. Wraparound sunglasses or goggles may be worn during the
day to decrease evaporation from the eye
e. massaging the face several times daily, using a gentle
upward motion, to maintain muscle tone
f. Facial exercises, such as wrinkling the forehead,
blowing out the cheeks, and whistling, may be
performed with the aid of a mirror to prevent muscle
atrophy.
g. Exposure of the face to cold and drafts is avoided.
NOTABLE SUFFERER
 DISORDERS OF THE
PERIPHERAL NERVOUS
SYSTEM
 Peripheral Neuropathies
➢ Peripheral neuropathy (disorder of the nervous
system)- is a disorder affecting the peripheral motor
and sensory nerves
➢ Peripheral nerves connect the spinal cord and brain
to all other organs and transmit motor impulses
from the brain and relay sensory impulses to the
brain
 Peripheral Neuropathies
➢ characterized by bilateral and symmetric
disturbance of function, usually beginning in the
feet and hands.
➢ common cause of peripheral neuropathy is
diabetes with poor glycemic control.
CLINICAL MANIFESTATIONS

➢ loss of sensation
➢ muscle atrophy
➢ Weakness
➢ diminished reflexes
➢ pain, and paresthesia of the extremities.
 DIAGNOSTICS
1.History Taking
2. Physical examination
3. Electrodiagnostic studies such
as EEG

***No specific treatment exists

 NURSING MANAGEMENT

1. Inspection of the lower extremities for skin

breakdown.
2. Assistive devices such as a walker or cane may
decrease the risk of falls.
3. Bathwater temperature is checked to avoid thermal
injury.
4. Footwear should be accurately sized.
5. Driving may be limited or eliminated, thereby
disrupting the patient’s sense of independence.
 Mononeuropathy
➢ Mononeuropathy is limited to a single peripheral nerve
and its branches.
CAUSES:
➢ Trunk of the nerve is compressed or entrapped (as in
carpal tunnel syndrome)
➢ traumatized (as when bruised by a blow)
➢ overstretched (as in joint dislocation),
➢ punctured by a needle used to inject a drug or damaged
by the drugs thus injected, or inflamed because an
adjacent infectious process extends to the nerve trunk
 CLINICAL MANIFESATION
➢ Pain is increased with all body movements that tend to
stretch, strain, or cause pressure on the injured nerve
and sudden jarring of the body (e.g., from coughing or
sneezing).
➢ Skin in the areas supplied by nerves that are injured or
diseased may become reddened and glossy
➢ Subcutaneous tissue may become edematous, and the
nails and hair in this area are altered.
 MEDICAL MANAGEMENT

PHARMACOLOGIC:
1. Corticosteroid injections to reduce
inflammation and the pressure on the nerve.
2. Aspirin or codeine to relieve pain
3. Gabapentin – treat chronic pain
 NURSING MANAGEMENT
➢ Protection of the affected limb or area from injury,
➢ appropriate patient education about
mononeuropathy and its treatment.