`MULTIPLE SCLEROSIS  Age 10-11: 698-1560 mg/dl

MEDICAL MANAGEMENT
Diplopia

CLINICAL MANIFESTATIONS GOAL: delay progression, manage chronic symptoms, treat acute
exacerbations
 Relapsing-Remitting Course
Disease Modifying agents
 S/sx depends on the location of lesion (plaque)
 Interferon 1a and Interferon 1b
 PRIMARY symptoms:
 Side effect: FLu-like symptoms
 Fatigue Desce
 Aceteaminophen/ibuprofen
 Depression Paraly
 Glatiramer Acetate (Copaxone)- subcutaneous
 Weakness
 Reduces rate of relapse
 Numbness difficulty in coordination
 Reduces plaques noted in MRI
 Ataxia (cerebellar and basal ganglia involvement)
MEDICAL MANAGEMENT
 Pain (lesion on sensory pathways)
IV methylpredinisolone

 Key agent for acute relapse

Optic never lesion or their connection:
 Anti-inflammatory effect
 Blurring of vision
Mitoxantrone (Novantrone)/anti neoplastic
 Diplopia (double vision)
 Check for cardiac toxicity (ecg before administration)
 Scotoma (patchy blindness)
Symptom Mng:
 Total blindness
 Baclofen (Lioseral) - muscle relaxant
Spaticity (muscle hypertonicity)
 Medication of choice SPASTICITY
 Involvement of motor pathways
MEDICAL MANAGEMENT
Frontal and Parietal lobe involvement
 Amantadine (symmetrel)
 Cognitive and psychosocial involvement
 Treatment of fatigue
CHARCOT’S TRIAD
 Beta-blockers, antiseizures agents, benzodiazepines
 Scanning of speech
 Ataxia
 INTENTION tremors
 UTI
 Nystagmus
 Vitamin C (increases the acidity of urine)
DIAGNOSTICS FINDINGS

MRI

 Multiple plaque in CNS

NURSING MANAGMENT
CSF eletrophoresis
Promote physical mobility
 Presence of oligocional bonding (bands of IgG)
 Walking (improves gait and loss of position sense)
 Ref.ranfe of immunoglobulin-
 Daily exercise
 Age 0-1: 231-1411 mg/dl
Minimize spasticity
 Age 1-3: 453-916 mg/dl
 Warm packs
 Age 4-6: 504-1464 mg/dl
OCULAR MUSCLES
Hot baths (avoided:risk of burn injury secondary to sensory loss)
 Age 7-9: 572-1474 mg/dl
Minimize effects of immobility
 Coughing and deep breathing exercises

Prevent injury

 Walking with feet apart (widens the base) DIAGNOSTICS FINDING

Enhance bowel and bladder function Acetycholinesterase inhibitor test

 Encouraged schedule toileting rounds a.k.a TENSILON TEST

Respiratory
Enhance communication and manage swallowing difficulties  Stops acetylcholine breakdown making it available for binding in
myoneural junction Failure
 Suctioning
Endrophonium Chloride (Tensilon)
 Careful feeding
 Fast acting anticholinesterase is administered IV
 Proper position for eating
 30 secs after injection:
Vision problem (Diplopia)
 Resolution of symptoms (facial muscle weakness and ptosis)
 Patch one eye after 5 mins CONFIRMS the diagnosis.

 ATROPINE (anticholinergic) antidote for side effects

MYESTHENIA GRAVIS

Autoimmune disease affecting the MYONEURAL junction that cause

weakness of voluntary muscles

 Women are more affected than men

 Purely motor disorder (no effect on sensation and coordination)

PATHOPHYSIOLOGY

Antibodies attacks acetlycholine receptors

MEDICAL MANAGEMENT

Fewer available receptors for
Stimulation
IMMUNOSUPPRESIVE THERAPY
Impaired transmission of
Corticosteroid
impulses on myoneural junction
 Supresses immune response

 Decreasing amount of antibodies

Voluntary muscle weakness
IV immunoglobulin (IVIG)

Azathioprine-immunosupressant
Throat and facial Generalized  Inhibits T lymphocytes and reduce antibody level
muscles muscles weakness
 Procaine is avoided

 Dentist is informed diagnosis

Ptosis

(drooping Bland Dysphonia Weakness on GUILLAIN-BARRE SYNDROME

of eyelid) facial
(voice extremities Autoimmune demyelinating disease of the PNS
Expression impairment)
 Resulting to acute, rapid segmental demyelination of peripheral
nerves and some cranial nerves producing ASCENDING
WEAKNESS

 Viral infection: common antecedent effect

 Major caused if the patient is infected before

  Prevent immobility complications:

PATHOPHISIOLOGY  Anticoagulants

Cell mediated and humoral immune  Anti embolic stockings

Attack on PNS sheath  Plasmapheresis Therapeutic Plasma Exchange

 IVIG (therapy of choice: fewer side effects)

Inflammatory demyelination

Segmental demyelination

Delayed impulse transmission

hypereflexia dyskinesia ASCENDI parasthesias Respiratory

NURSING MANAGEMENT
NG
Failure
PARALYS Enhancing physical mobility
IS
 AROMEs in paralyzed extremities twice a day

 Position changes

 Anticoagulation administration

 Anti-embolic stockings

\  Padding bony prominences

ASCENDING
Nutrition
PARALYSIS*
Improve communication

 Picture cards/eye-blink system

CLINICAL MANIFESTATIONS Decrease fear and anxiety

 Dyskinesia (inability to execute voluntary movements) Diversional activity

 Hyporeflexia

 Paresthesia (numbness) DEGENERATIVE NEUROLOGIC DISORDER: PARKINSON’S DISEASE

 Weakness beginning from LEGS and progresses UPWARD  Slowly progressing neurologic MOVEMENT DISORDER

 Does not affect cognitive function  Affects MEN more than WOMEN

DIAGNOSTICS FINDINGS

 History of viral illness in the previous week suggest the diagnosis PATHOPHYSIOLOGY

 Elevated protein in CSF

Destruction of pigmented neuronal cells in basal ganglia (SUBSTANTIA

NIGRA)
 Other serum labs are not useful

MEDICAL MANAGEMENT

 Considered a MEDICAL EMERGENCY!

DECREASED DOPAMINE RELEASE
 Mechanical ventilation:respiratory failure
 Impaired control of refine motor movements

CLINICAL MANIFESTATIONS

CARDINAL SIGNS
Tremors Rigidity bradykkinesia Postural
 RESTING tremors instability
 Rigidity

 Bradykinesia- (muscle weakness)

 Postural instability (shuffling gait*)

 Mask-like facies (expressionless)

 Dysphonia (soft,slured,low-pitched,and less audible speech)

 Dysphagia and drooling

SURGICAL MANAGEMENT

THALAMOTOMY AND PALLIDOTOMY

 Inadequate response to medical therapy

 Interrupts application of stereotactic electrical stimulator that

destroys the ventrolateral portion of hypothalamus and medical
globus pallidus

Neural transplantation

Deep Brain stimulation

Pacemaker-like implants

MEDICAL MANAGEMENT

Antiparkinsonian medications

LEVADOPA (most effective and mainstay treatment)

>Converted in dopamine in the basal ganglia

Combined with CARBIDOPA (prevents conversion of levadopa to

dopamine in the PNS)