Management of Patient’s

with Neurologic
Infections, Autoimmune
Disorders & Neuropathies
By Esperancita A. Ferrer RN MD
Infectious Neurologic
Disorders
Meningitis
 Is an inflammation of the pia
mater, the arachnoid & the
cerebrospinal fluid.
Classification:
 Septic – Bacteria (N.
meningitidis & S. pneumoniae)
 Aseptic – Virus MC or lymphoma

(nonpolio enterovirus)
Clinical Manifestations
 High grade fever
 Headache
 Nuchal rigidity – early sign
 Attempt to flex the head is
difficult because of spasm in
the ms
 Kernig’s sign –
 Thigh flexed on abdomen, leg
cannot be completely extended
 Brudzinski’s sign –
 When neck is flexed, flexion of
the knees & hips is produced
 Sensitive indicator of
meningeal irritation
 Petechial rash w/
purpuric lesions
 Photophobia
 Disorientation
 Lethargy
 Seizures
 ↑ ICP – sec.
accumulation of purulent
exudate
Diagnostic Evaluation
 Bacterial Culture & Gram Staining of CSF

Prevention
 Vaccination
 Antimicrobial Prophylaxis rifampin,
ciprofloxacin hcl, ceftriaxone Na (24h)
 For close contact
Medical Management
Antibiotics that cross the BBB
 Penicillin antibiotics (Ampicillin,
Piperacillin)
 Cephalosphorins (ceftriaxone Na,
cefotaxime Na)
 Vancomycin & Rifampin resistant cases
Nursing Management
 Assessment & management of meningitis
should be a collaborative effort
 Institute infection control precautions until
24h after initiation of antibiotic therapy
(oral & nasal discharge is considered
infectious)
 Cooling measures, antipyretics
 Rapid IV fluid tx prescribed caution fluid
overload
 Observe for ↑ ICP
 Quiet calm environment
 Darken room
 Assist on position of comfort
 Administer Antibiotics on time &
Analgesics as prescribed
Encephalitis
 Inflammation of Cerebral tissue, typically
accompanied by meningeal inflammation
 Heres Simplex Virus (HSV) MC
 HSV-1 children & adults
 HSV-2 neonates
Clinical Manifestations
 High grade fever
 Headache
 Disorientation
 Neurologic deficits
 Seizure
 Motor weakness hemiparesis
 ↑ DTR & extensor plantar response
 Visual field defects, aphasia, dysphagia,
ataxia & paresthesia
Diagnostic Evaluation
 EEG
 CSF Examination
 MRI

Medical Management
 Acyclovir (Zovirax) x 3 wks IV
Nursing Management
 Assessment & management of encephalitis
should be a collaborative effort
 Cooling measures, antipyretics
 Observe for ↑ ICP
 Quiet calm environment
 Darken room
 Assist on position of comfort
 Administer Antiviral agent on time &
Analgesics as prescribed
 Reorient
Autoimmune Nervous
System Disorders
Multiple Sclerosis
 An auto-immune
mediated progressive
demyelinating disease
of the CNS
 Causes impaired
transmission of nerve
impulses from the
brain to the peripheral
nervous system.
 Destruction of myelin
in optic nerve, brain &
SC
Cause:
 Unkown
 Possibly related to autoimmune
dysfunction, genetic susceptibility, or an
infectious process
 Multiple factors
 viral infection
 environmental factors
 geographic location and
 genetic predisposition

Common in WOMEN ages 20-40

Pathophysiology Sensitized T cells

Enters and remains in CNS

Promotes
infiltration of Inflammation
other agents

Damage to Destroys myelin and oligodendroglial cells

immune system

Plaques of sclerotic tissue

s/s depending on Interruption of impulse

nerve affected transmission
Relapsing Remitting MS
 Mild infrequent sensory exacerbations with full
recovery.
 Lack of disease progression
Primary Progressive MS
 Episodes of exacerbations and remissions during
which not all symptoms resolve completely. The
patient may be left with permanent disability
which may vary in severity. relapses are often
more severe than in the previous group. Relapses
also become more severe with time.
Secondary Chronic Progressive
 Condition of patients with relapsing/remitting
disease begins to gradually worsen over time with
resulting accumulation of neurologic signs and
symptoms. In this form of the disease, relapses
become more severe while remissions are less
complete, shorter in duration, and eventually
non-existent. The course of MS becomes steadily
progressive.
Progressive Relapsing
 Progression of neurologic deficits. But w/ clear
acute relapses w/ or w/o recovery. Problems
appear and gradually worsen over time. Common
problems include spastic paraparesis, cerebellar
ataxia, urinary incontinence.
Increasing Disability

Time
Clinical Manifestations
 Symptoms reflect area of demyelination
 Visual Disturbances- blurring of vision,
double vision (diplopia), patchy blindness
(scotoma), & total blindness; Retrobulbar
Optic Neuritis
Visual Disturbances
 Clinical Manifestations
FRONTAL LOBE MOTOR CORTEX
 Spasticity of extremities & loss of abdominal reflexes (motor
pathway, corticospinal tract)
 Bladder bowel & sexual dysfunction(corticospinal tract)
 Fatigue (most disabling)
 Weakness
FRONTAL LOBE
 Cognitive (memory) psychsocial problem, Depression
(frontal/parietal lobe)
PARIETAL LOBE
 Paresthesia, loss of proprioception (sensory pathway, posterior
column
 Pain (lesions on sensory pathways)
CEREBELLAR Signs
 Ataxia & tremor
 Difficulty in coordination
 Loss of balance
Diagnostic Evaluation
 MRI
 Sclerotic plaques throughout white matter
 Evoked potential studies
 Slowed conduction
 CSF electropheresis
 IgG Ab
 Pharmacologic Therapy
Interferon A- B –C
 AVonex (beta 1a Interferon)
 Decreases T-cell
proliferation
 IM, once a week
 Betaseron (Interferon beta
1b)
 Decreases frequency of
relapse
 Decreases appearance of
new lesions
 SQ, every other day
 Copaxone (Glatiramer Acetate)
 Decreases number of lesions
 Decreases relapse rate
 SQ, once a day
 Avonex & Betaseron – rapidly
progressive
 Copaxone –immunomodulator,
relapsing-remitting disease
Corticosteroids
 Methylprednisolone
 IV 1g x 3d tapered w/
prednisone po
 Shortens duration of relapse
 Tx acute relapse
 Relieves Sx acute attack
 Novantrone  amantadine
mitoxantrone Symmetrel,
 Chemotherapeutic fluoexetine Prozac
agent  Fatigue
 Iv infusion q3m  Beta adrenergic
 Reduces frequency of blockers, anti-siezure
clinical relapse in px
w/ secondary medication, BZD
progressive %  Ataxia
relapsing – remitting  Anticholinergics, alpha
MS
adrenergic blockers,
 Baclofen, BZD, antispasmodics,
Dantrolene (centrally  Bladder & bowel
acting ms relaxant) problems
 spasticity  Ascorbic acid
 UTI
Nursing Interventions
Promote Physical Mobility
 Exercise
 walking improves gait
 Stretching (stretch-hold-relax)
 Apply ice packs before stretching
 Progressive weight bearing
 Schedule activity and rest periods
 Warm packs over the spastic area
 Swimming and cycling are very
useful
Prevent injuries
 Wide stance walking
 Use of walking aids
 Wheelchair, motorizes scooters
 If with loss of position sense,
walk while watching feet
Enhance bladder and bowel control
 Set a voiding schedule
 q 1.5 – 2hr initially
 Intermittent bladder catheterization
 Use of condom catheter
 Adequate fluids, dietary fibers and
bowel training program
Manage speech and swallowing
difficulties
 Careful feeding,
 proper positioning,
 suction machine availability
 Speech therapist
 Improve Sensory and Cognitive
function
VISION
 use eye patch on one eye for diplopia
 Obtain large printed reading materials

COGNITION & EMOTIONAL RESPONSES

 Offer emotional support
 Involve the family in the care
Build general resistance to
infection
 Avoid
 Fatigue
 Extremes of temperature
 Exposure to infection
Myasthenia Gravis
A chronic autoimmune d/o effecting
the neuromuscular transmission of
impulses in the voluntary ms. of the
body
 It is due to an antibody mediated
attack against Ach receptors at the
NMJ
 Loss of Ach receptors leads to a defect
in neuromuscular transmission.
When the nerve impulse reaches the presynaptic terminal at
the NMJ, Synaptic vesicles discharge Ach into the synaptic
cleft
Release of Ach from
vesicles(Myoneural junction)
↓
Ach attaches to receptor
sites(Motor end plate)
↓
Muscle contraction

Continuous binding of Ach

to receptor site necessary
for ms contraction to be
sustained
Pathophysiology
Antibodies attack
receptor sites
↓
Ach attaches to receptor
sites (Motor end plate)
↓
Transmission of nerve
impulse impaired
↓
Poor Muscle contraction
↓
Voluntary ms weakness
Pathophysiology

 Follows an unpredictable course of periodic

exacerbations and remissions

 Purely motor, no effect on sensation and

coordination
Etiology
Autoimmune
Thymoma

Women suffer at an earlier

age and are more affected
MYASTHENIA GRAVIS
 Clinical Manisfestations:
 Gradually progressive skeletal muscle
weakness and fatigue; partially reversed by
rest
 Weakness that worsens during the day;
muscles are stronger in the morning
 Ptosis (CN III), diplopia and weak eye closure
 Blank, mask-like facies
 Difficulty chewing, swallowing, talking
 Respiratory difficulty
 Dysphonia(nasal voice)
Diagnostic Tests
 EMG
 decremental response to repetetive
nerve stimulation
 Serum anti- Ach Receptor antibodies
 CT scan/MRI
 enlarged thymus gland
 Acetylcholinesterase
Inhibitor Test:
TENSILON TEST (Edrophonium)
TENSILON TEST (Edrophonium)
 Tensilon IV (2mg at a time, total of 10
mg)
 30 sec after injection, facial weakness
and ptosis should resolve for 5 min
 Atropine sulfate should be available to
counteract side effects
 Bradycardia
 Sweating
 cramping
Medical Management
 BASIS OF DRUG TREATMENT IS TO
INACTIVATE ACETYLCHOLINESTERASE
ANTICHOLINESTERASE
 DOC: Pyridostigmine bromide (Mestinon)
 Neostigmine bromide (Prostigmin)
 Inhibit breakdown of Ach
 ↑ conc. of available acetylcholine at NMJ
 Dose is gradually increased
 Should be administered on time
 AE:
 Abdominal pain
 Diarrhea
 Fasciculations
 Increase oropharyngeal secretions
Immunomodulating Drugs
 Corticosteriods
 Suppress immune response thus
decreasing the amount of Ab
production
 Eg. Prednisone
 Immunosuppresant
 InhibitsT lymphocytes & ↓ Ach
receptor Ab levels Azathioprine
(Imuran)
Plasmapheresis
 Plasma exchange
 Patient’s plasma and
plasma components
are removed through
a centrally placed
large-bore double
lumen
 Blood cells and
antibody-containing
plasma are separated
 Cells and plasma
substitute are
reinfused
 Effects is temporary
Surgical Management
 Thymectomy
Myasthenic Vs Cholinergic Crisis
Myasthenic Cholinergic
Cause Disease Anticholinergic
exarcerbation overmedication
Precipitating events
S/S Generalized muscle Generalized
weakness muscle weakness
Sudden inability to
swallow, speak or
maintain a patent
airway( needs
artificial ventilation)
 Myasthenic Cholinergic
Response Improvement Deterioration
to No improvement
Tensilon
Test
Treatment Neostigmine D/C all
methylsulfate anticholinergic
IV, IM Atropine sulfate

DANGER:
•Respiratory muscle weakness
•Bulbar muscle weakness
•Inadequate cough and gag
Bulbar muscle weakness
 Weakness of palatal muscles can result in a nasal
twang to the voice and nasal regurgitation of food
and especially liquids.
 Chewing may become difficult.
 Severe jaw weakness may cause the jaw to hang
open (the patient may sit with a hand on the chin
for support).
 Swallowing may become difficult and aspiration
may occur with fluids, giving rise to coughing or
choking while drinking.
 Weakness of neck muscles is common and neck
flexors usually are affected more severely than
neck extensors.
 Respiratory muscle weakness
 May produce acute respiratory failure. True
neuromuscular emergency, immediate intubation
may be necessary. Weakness of the intercostal
muscles and the diaphragm may result in carbon
dioxide retention due to hypoventilation.
 Weak pharyngeal muscles may collapse the upper
airway. Careful monitoring of respiratory status is
necessary in the acute phase of MG.
 Negative inspiratory force (NIF), vital capacity (VC), and
tidal volume must be monitored carefully.
 Relying on pulse oximetry to monitor respiratory status can
be dangerous.
 During the initial phase of neuromuscular hypoventilation,
carbon dioxide is retained but arterial blood oxygenation is
maintained.
Nursing Interventions
 Administer prescribed medication as
scheduled
 Prevent problems with chewing and
swallowing
 Administer Medications 30-45 ac; sit up right
w/ neck slightly flexed
 Soft food; pureed food
 Suction standby
 Rest before mealtimes
 Prevention of aspiration
 Mealtimes should coincide with peak effects of
anticholinesterase
 Prepare for complications like myasthenic crisis
and cholinergic crisis
 Prevent problems associated with impaired
vision resulting from ptosis of eyelids
 Tape eyes
 Artificial tears
 Eye patching
 Promote respiratory function
 Encourage adjustments in lifestyle to prevent
fatigue
 Maximize functional abilities
Guillain – Barre
Syndrome
Polyradiculoneuritis
Definition
 An auto-immune attack of the peripheral
nerve myelin

 Acute, rapid segmental demyelination of

peripheral nerves and some cranial nerves

 Rapidly progressive ascending inflammatory

demyelinating polyneuropathy of the
peripheral sensory & motor nerves & nerve
roots
Antecedent Events:
 Viral Infection (C. pneumoniae, CMV, EBV,
H. Influenzae)
 Influenza Vaccination
 Infectious Diarrheal Illness
(Campylobacter)
 Schwann cells-produce
myelin
 Myelin- fatlike subs, that
sheaths around certain
nerve fibers
 Insulation
 Axons conduct impulses
rapidly
 Demyelination-
degeneration of myelin
 Dysfunction in conduction of
impulses
 Axons- impulses away
from the cell
 Dendrites- impulses
toward the cell body
 The dorsal root are
sensory and transmit
sensory impulses from
specific areas of the
body known as
dermatomes
 Sensory fibers may
be:
 Somatic – carrying
information about pain,
temperature, touch,
position sense
(proprioception) from
tendons, joints, and
body surfaces
 Visceral – carrying
information from the
internal organs
 The ventral roots are
motor and transmit
impulses from the
spinal cord to the
body.
 Either:
 Somatic
 Visceral – includes
autonomic fibers that
control the cardiac
muscles and glandular
secretions
Pathophysiology
Infectious organism contains amino acid that
mimics the peripheral nerve

Antibody cannot distinguish

between the 2 proteins
Antibody attacks peripheral nerve
myelin
Inflammation and destruction of
peripheral nerve myelin
Causes inflammation &
Degenerative changes in
post. & ant. nerve roots,
MOTOR and SENSORY
Losses occur
SIMULTANEOUSLY!

Axon unable to support nerve

conduction
Clinical Manifestations:
 Symmetric ms weakness beginning in the
LE ascending to involve the trunk, UE &
facial ms. Paralysis may develop
 Hyporeflexia → Areflexia
 Paresthesia
 Dyskinesia
 Pain
 Blindness
 Difficulty w/ swallowing, speech, chewing
 Autonomic Dysfunction (↓or↑ BP, HR)
 Decreased Vital Capacity, depth of respirations
& breath sounds
Diagnostic Tests:
 Lumbar Puncture - CSF protein level
is INCREASED but the WBC remains
normal in the CSF

 Electrophysiologic
Studies - nerve
conduction velocity ↓ conduction
Medical Management:
 Plasmapharesis
 Intravenous Ig
 Reduction of circulating Ab
 ECG monitoring
 Short acting alpha adrenergic blocking
agents
 Intubation & Mechanical ventilation
 Analgesics & muscle relaxants
 Anticoagulant
 Thigh-high elastic compression stockings
Sequential Compression Boots
Mechanical Ventilator
Nursing Interventions
Maintain respiratory function
 Chest physiotherapy
 Incentive spirometry
 Elevate HOB
 Monitor for signs of respiratory
failure: Tachycardia, Tachypnea
 Monitor for Respiratory Fatigue:
Breathlessness when talking, ↓ VC,
PaO2 <70 mmHg, Bulbar weakness
 Mechanical ventilator
 Suction
Enhance physical mobility
 Paralyzed extremities functional
positions
 PROM 2x/d
 Prevent DVT & PE
 ROM, position changes,
anticoagulation, thigh high elastic
compression stockings, adequate
hydration
 Prevent Pressure Ulcers
 Padding over bony prominences,
turning q2h
Provide adequate nutrition
Problem: Paralytic Ileus
 insufficient parasympathetic activity
 Auscultate BS- hold feeding if absent
to prevent gastric distention
 Assess CN V & IX
 IVF & Parenteral nutrition
 Gastrostomy Tube
Improve communication
 Use other means of communication,
picture cards, eye blink system
 Px call system. Standard call lights
cannot be activated by the severely
weak GBS px. Constant monitoring &
surveillance.
Patient Education & Health
Maintenance
 Acute phase 1-4wks, afterwards pax
stabilizes, rehabilitation can begin
 Instruct: Breathing exercises, incentive
spirometer
 Wear good supportive & protective shoes
while out of bed
 Check feet routinely
 Scheduled rest periods
Monitor and manage complications
Respiratory Failure- major cause of
Mortality

 DVT
 Urinary retention
 Pulmonary embolism
 Respiratory failure
Cranial Nerve Disorders:
Trigeminal Neuralgia
 A.k.a Tic
Douloureux
 Condition of the
fifth cranial nerve
 Characterized by
paroxysms of pain
in the area
innervated by any
of the three
branches of
trigeminal nerve
Cause:
 Not certain
 May be due to
chronic
compression or
irritation of the
trigeminal nerve
Clinical Manifestations:
 Unilateral, shooting/stabbing pain
 Starts and end abruptly
 May last for 1 – 15 minutes
 Associated symptom:
 Involuntary contraction of the facial
muscle
Stimuli that can trigger pain:

 Washing of face
 Shaving
 Brushing of the teeth
 Eating
 Drinking
 Draft of cold air
 Direct pressure on the nerve
Medical Management
 Antiseizure agents
 CARBAMAZEPINE (Tegretol)
 Relieves pain by decreasing the transmission
of impulses at certain nerve terminals
 Should be taken with meals
 Side effects:
 Nausea
 Dizziness
 Drowsiness
 Aplastic anemia
 Mgt Pain
 Gabapentin (Neurontin), Baclofen,
phenytoin (Dilantin)
Surgical Management
 Microvascular Decompression of the
Trigeminal Nerve
 Intracranial approach
 Relieve contact between cerebral
vessel & trigeminal nerve root
 Relieves pain while preserving normal
sensation
 Radio frequency thermal
coagulation
 Thermal lesion on trigeminal nerve
 Dysesthesia of the face & loss of
corneal reflex occurs
 Percutaneous Balloon
Microcompression
 Balloon compresses the nerve root for
1 minute
 Microvascular compression
 Masseter ms weakness & facial
dysesthesia results
Nursing Interventions:
 Prevent pain
 Help recognize precipitating/aggravating
factors
 Chew on the unaffected side
 Ingest soft foods
 Provide emotional support
 Encourage to express feelings
 Provide adequate nutrition in small frequent
meals at room temperature
 Post-op
 Assess for motor and sensory deficit in the
trigeminal nerve
 BELL’S PALSY
 Dysfunction of the facial
nerve
 Due to unilateral
inflammation of the 7th
cranial nerve
 Cause: unknown
 May be related to
 Vascular ischemia
 Viral disease
 Autoimmune disease
 Combination of the
these factors
Pathophysiology
Inflammation

Compression of the nerve

Damage
“Bell’s smile”
 Clinical Manifestations:
 Unilateral facial weakness
 Mouth drooping
 Distorted taste perception
 Smooth forehead
 Inability to close eyelid on the affected side
 Incomplete eye closure
 Excessive tearing when attempting to close the
eyes
 Inability to raise eyebrows, puff out the cheek
 Painful sensation in the face, behind the ear and
in the eye
Medical Management
Recovery 3-5 wks
 Prednisone
 To decrease inflammation and edema
 To decrease vascular compression
 To permit restoration of blood
circulation
 Artificial Tears
 Analgesics
 TENS
Nursing Intervention
 Apply moist heat to reduce pain
 Massage the face to maintain muscle
tone
 Give frequent mouth care
 Protect the eye with an eye patch. Eyelid
can be taped at night
 Instruct to chew on unaffected side