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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)

Meningitis  Is an inflammation of the pia mater, the arachnoid & the cerebrospinal fluid. Classification:

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

Clinical Manifestations  High grade fever  Headache  Nuchal rigidity – early sign  Attempt
Clinical Manifestations  High grade fever  Headache  Nuchal rigidity – early sign  Attempt

Petechial rash w/ purpuric lesions

Photophobia Disorientation Lethargy Seizures

↑ ICP – sec. accumulation of purulent exudate

 Petechial rash w/ purpuric lesions  Photophobia  Disorientation  Lethargy  Seizures  ↑

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
Multiple Sclerosis  An auto-immune mediated progressive demyelinating disease of the CNS  Causes impaired transmission

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

Pathophysiology

Sensitized T cells
Sensitized T cells
Enters and remains in CNS Inflammation Destroys myelin and oligodendroglial cells Plaques of sclerotic tissue
Enters and remains in CNS
Inflammation
Destroys myelin and oligodendroglial cells
Plaques of sclerotic tissue
Sensitized T cells Enters and remains in CNS Inflammation Destroys myelin and oligodendroglial cells Plaques of

Promotes infiltration of other agents

   
Sensitized T cells Enters and remains in CNS Inflammation Destroys myelin and oligodendroglial cells Plaques of

Damage to immune system

 

Interruption of impulse

 

transmission

Sensitized T cells Enters and remains in CNS Inflammation Destroys myelin and oligodendroglial cells Plaques of

s/s depending on nerve affected

Relapsing Remitting MS

Mild infrequent sensory exacerbations with full recovery.

Lack of disease progression

Relapsing Remitting MS  Mild infrequent sensory exacerbations with full recovery.  Lack of disease progression
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.

Primary Progressive MS  Episodes of exacerbations and remissions during which not all symptoms resolve completely.
Primary Progressive MS  Episodes of exacerbations and remissions during which not all symptoms resolve completely.

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.

Secondary Chronic Progressive  Condition of patients with relapsing/remitting disease begins to gradually worsen over time
Secondary Chronic Progressive  Condition of patients with relapsing/remitting disease begins to gradually worsen over time

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
Increasing Disability
Progressive Relapsing  Progression of neurologic deficits. But w/ clear acute relapses w/ or w/o recovery.

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

Visual Disturbances
Visual Disturbances
Visual Disturbances
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 mitoxantrone

amantadine Symmetrel, fluoexetine Prozac

Chemotherapeutic agent Iv infusion q3m

Fatigue

Beta adrenergic blockers, anti-siezure medication, BZD

Ataxia

Anticholinergics, alpha adrenergic blockers, antispasmodics,

Bladder & bowel

 Novantrone mitoxantrone   amantadine Symmetrel, fluoexetine Prozac Chemotherapeutic agent Iv infusion q3m  

problems

Reduces frequency of clinical relapse in px w/ secondary progressive % relapsing – remitting MS

Baclofen, BZD, Dantrolene (centrally acting ms relaxant)

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

Prevent injuries  Wide stance walking  Use of walking aids  Wheelchair, motorizes scooters 

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

Enhance bladder and bowel control  Set a voiding schedule  q 1.5 – 2hr initially

Manage speech and swallowing difficulties

Careful feeding, proper positioning, suction machine availability Speech therapist

Manage speech and swallowing difficulties  Careful feeding,  proper positioning,  suction machine availability 

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

Improve Sensory and Cognitive function VISION  use eye patch on one eye for diplopia 

Build general resistance

to infection

Avoid

Fatigue Extremes of temperature Exposure to infection

Build general resistance to infection  Avoid  Fatigue  Extremes of temperature  Exposure to

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
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
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

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

Plasmapheresis  Plasma exchange  Patient’s plasma and plasma components are removed through a centrally placed

Surgical Management

Thymectomy

Surgical Management  Thymectomy

Myasthenic Vs Cholinergic Crisis

 

Myasthenic

Cholinergic

Cause

Disease

Anticholinergic

exarcerbation

overmedication

Precipitating events

S/S

Generalized muscle weakness

Sudden inability to swallow, speak or maintain a patent airway( needs

artificial ventilation)

Generalized muscle weakness

 

Myasthenic

Cholinergic

Response

Improvement

Deterioration

to

 

No improvement

Tensilon

Test

 

Treatment

Neostigmine methylsulfate

D/C all 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

 Schwann cells-produce myelin  Myelin- fatlike subs, that sheaths around certain nerve fibers  Insulation

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

The ventral roots are motor and transmit impulses from the spinal cord to the body.

Either:

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

Somatic

Visceral – includes autonomic fibers that control the cardiac muscles and glandular secretions

 The dorsal root are sensory and transmit sensory impulses from specific areas of the body

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

Antibody cannot distinguish between the 2 proteins

Antibody attacks peripheral nerve myelin

Inflammation and destruction of peripheral nerve myelin

   
Antibody cannot distinguish between the 2 proteins Antibody attacks peripheral nerve myelin Inflammation and destruction of
 

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 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

Sequential Compression Boots
Sequential Compression Boots
Sequential Compression Boots

Mechanical Ventilator

Mechanical Ventilator
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

Trigeminal Neuralgia  A.k.a Tic Douloureux  Condition of the fifth cranial nerve  Characterized by

Cause:

Not certain

May be due to chronic compression or irritation of the trigeminal nerve

Cause:  Not certain  May be due to chronic compression or irritation of the trigeminal

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 7 th cranial nerve

Cause: unknown

May be related to

Vascular ischemia Viral disease Autoimmune disease

Combination of the these factors

BELL’S PALSY  Dysfunction of the facial nerve  Due to unilateral inflammation of the 7

Pathophysiology

Inflammation

Compression of the nerve

Damage

Pathophysiology Inflammation Compression of the nerve Damage “Bell’s smile”

“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