Patients 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

Kernigs sign

Attempt to flex the head is

difficult because of spasm in
the ms
Thigh flexed on abdomen, leg
cannot be completely extended

Brudzinskis 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

Sensitized T cells
Pathophysiology
Enters and remains in CNS
Promotes
infiltration of
other agents
Damage to
immune system

Inflammation

Destroys myelin and oligodendroglial cells

Plaques of sclerotic tissue

s/s depending on
nerve affected

Interruption of impulse
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 nonexistent. 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

Evoked potential studies

Sclerotic plaques throughout white matter

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
mitoxantrone

Chemotherapeutic
agent
Iv infusion q3m
Reduces frequency of
clinical relapse in px
w/ secondary
progressive %
relapsing remitting
MS

spasticity

Ataxia

Anticholinergics, alpha
adrenergic blockers,
antispasmodics,

Fatigue

Beta adrenergic
blockers, anti-siezure
medication, BZD

Baclofen, BZD,
Dantrolene (centrally
acting ms relaxant)

amantadine
Symmetrel,
fluoexetine Prozac

Bladder & bowel

problems

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
Inhibits

T lymphocytes & Ach

receptor Ab levels Azathioprine
(Imuran)

Plasmapheresis

Plasma exchange
Patients plasma and
plasma components
are removed through a
centrally placed largebore 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
Cause

S/S

Myasthenic

Cholinergic

Disease
exarcerbation
Precipitating events
Generalized muscle
weakness
Sudden inability to
swallow, speak or
maintain a patent
airway( needs
artificial ventilation)

Anticholinergic
overmedication
Generalized
muscle weakness

Myasthenic
Response Improvement
to
Tensilon
Test
Treatment Neostigmine
methylsulfate
IV, IM

Cholinergic
Deterioration
No improvement
D/C all
anticholinergic
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

Demyelinationdegeneration of myelin

Insulation
Axons conduct impulses
rapidly

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
Axon unable to support nerve
conduction

Causes inflammation &

Degenerative changes in
post. & ant. nerve roots,
MOTOR and SENSORY
Losses occur
SIMULTANEOUSLY!

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

Reduction of circulating Ab

ECG

Ig

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

BELLS 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
Bells 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