GUILLAIN BARRE SYNDROME  lower extremities) - Ascending paralysis

 Muscle weakness of the legs

Definition: An autoimmune condition where the
(Dyskinesia)
immune system attacks nerves in PNS and CNS.
 Persistent pain in the back, calves of the
Also called Landry’s Paralysis. The immune
legs and may progress to upper
system attacks the myelin sheath.
extremities, trunk
Cause: Unknown Diagnostics:

Predisposing Factors: • CSF studies- elevated CHON levels

• EMG- diminish electrical activity of
- Antecedent viral infection
skeletal muscles
- Immunization- flu vaccine
• Nerve conduction studies progressive
- Autoimmune Disorders
deterioration of nerve
Types of GBS: conduction velocity
 Acute inflammatory demyelinating
Complications
Polyradiculoneuropathy
 Miller Fisher syndrome ❖ ARF
 Acute motor axonal neuropathy
❖ Cardiac dysrhythmia
 Acute Motor-Sensory Axonal
Neuropathy ❖ DVT and pulmonary embolism

Pathophysiology ❖ Paralysis

- Segmental demyelination of peripheral ❖ Pressure ulcers

nerves cause inflammation and
❖ Contractures
degeneration in sensory and motor
nerve roots ❖ Muscle wasting
- Most clients experience spontaneous
❖ Aspiration
and complete recovery although mild
deficits may persist. Medical Management
Manifestations: • Mechanical ventilation if respiratory
 Paresthesia problems are present
 Generalized muscle weakness (starts • Plasmapheresis- decrease circulating
from antibody
• Continuous ECG monitoring

Drugs:
• Propranolol for HPN
• Atropine – for bradycardia
• Corticosteroids- depress immune
response
• Antiarrhythmic agents

Nursing Interventions
 Maintain adequate ventilation
 Check individual muscle groups every 2
hours
 Assess cranial nerve function
 Monitor vital signs and observe for
signs of autonomic dysfunction
 Prevent complications of immobility
ROMs, anticoagulants, antiembolism
stockings
 Promote comfort
 Promote optimum nutrition
(TPN/Gastrostomy)
 Provide psychological support and
encouragement to client/significant
MULTIPLE SCLEROSIS ↓

Permanent & irreversible damage

Definition: An autoimmune disease that affects
Clinical Manifestation
the myelin sheath of neurons in the CNS.
 During EXACERBATIONS, new symptoms
Inflammation and scarring of neuron. There will
appear & existing ones worsen
be a decrease in nerve transmission.
 During REMISSIONS, symptoms decrease
Cause: Unknown
or disappear
Predisposing Factors:
 Signs & symptoms are varied & multiple,
 Genetics: indicates the presence of a
reflecting the location of lesion or
specific cluster (haplotype- DNA
combination of lesions
variation)
 Primary symptoms
 Infections
 Fatigue, weakness
 Environmental factors - geographic
 Depression
 Severe stress
 Numbness
 Smoking
 difficulty in coordination, loss of balance
 Intake of aspartame
& Pain
Pathophysiology  Visual disturbances (demyelination of CN

Sensitized T&B lymphocytes cross the BBB 2)

↓  Blurring of vision
 Diplopia
In MS, sensitized T cells remain in the CNS
 Patchy blindness- scotoma
↓
 Total blindness
T cells recognize myelin as foreign
 Heat, Depression
↓  Anemia, Deconditioning (weakness)
Inflammatory processes is triggered  Sensory manifestations

Attacks the myelin as if it were an invading virus  Pain

 Paresthesias
↓
 Dysesthesias
Plaques & demyelinated axons occur
 Spasticity of the extremities
↓
 Behavioral- emotional lability, euphoria,
Axons begin to degenerate depression
 Uhthoff – often the first sign of M.S.
- Worsening of vision caused by hot
temperature (increased temp:
slowed/blocked nerve TRANSMISSION
 LHERMITTE’S SIGN – electric shock like
sensation radiating down the spine to the
legs and arms when neck is moved
 Cognitive change
 Memory loss
 Decreased concentration
 Impaired cerebellar function (Charcot’s
Triad)
 Scanning speech
 Intention tremors
 Nystagmus
 Ataxia
 Dysarthria (poor speech articulation)\
Bladder, bowel & sexual dysfunctions
Diagnostic Findings
 MRI- scattered patches of scar/plaque
(>5mm) in the CNS
 CSF Studies- protein electrophoresis., Igs
are separated from csf, results (+)
oligoclonal bonds
 CT Scan
 EEG
Medical Management
 No known cure for MS
 Goal of the treatments
 Attempt to return function after an
attack
 Prevent new attacks
 Prevent disability
 Delay the progression of the disease
Pharmacologic Therapy
Disease-Modifying therapies
Immunosuppressants
 Corticosteroids
- Prednisone (Deltasone, Liquid Pred,
Deltasone, Orasone, Prednicen-M);
methylprednisolone (Medrol, Depo-
Medrol)
 Interferons: have the ability to regulate
the immune system & play an important
role in protecting against intruders
including viruses
- Beta interferons- found to be useful in
managing MS
- Beta 1a: rebig; beta 1b: betasteron (SQ)
Glatiramer acetate (Copaxone) – increase
suppressor T cells, Admin sq daily (P3000/shot)
Symptoms Management
 Baclofen (Lioresal); (GABA agonist)- for
spasticity
 Benzodiazepines (Valium), Tizanidine
(Zanaflex) & dantrolene (Dantrium)
 Fatigue: amantadine (symmetrel),
pemoline (Cylert), fluoxetine (prozac)
  Ataxia: beta adrenergic blockers (Inderal);
antiseizure agents (Neurontin) &
benzodiazepines (Klonopin)
 BOWEL AND BLADDER PROB:
 Anticholinergic (incontinence/frequency) –
probanthine; oxybutynin
 Cholinergic (retention)– Bethanecol;
Neostigmine
 PAIN – gabapentin; carbamazepine;
amitriptyline

Nursing Interventions
 Promoting physical mobility Exercises:
 Minimizing Spasticity and Contractures
 Activity and Rest
 Preventing Injury
 Enhancing Bladder and Bowel Control
 Enhancing Communication and Managing
Swallowing Difficulties
 Improving Sensory and Cognitive Function
 Promoting Sexual Functioning

Complications

 Complications of Immobility
 Blindness
MYASTHENIA GRAVIS  Dysphagia
 Diplopia- caused by weakening of
Definition: An autoimmune condition where the
extraocular muscles
body attacks muscle receptors that control
 Dysarthria
voluntary muscles that will lead to muscle
 Dyspnea
weakness. Literally means grave muscle
weakness. Objective

3 Types of Muscles affected in MG  Ptosis

 OCULAR – affects only eye and lid
muscles
 BULBAR – affects muscles for breathing,
swallowing and speaking
 Dysphonia- impaired ability to produce
voice 􀂇 Strabismus
 Mask-like facial expression
 Myasthenic smile- SNARLING SMILE

 GENERALIZED – OCULAR, BULBAR +  Drooling

NECK and LIMB MUSCLES (most  Decreasing vital capacity and

common) respiratory failure

Causes: Unknown Diagnostic Test

1. Tensilon test
Pathophysiology
- Edrophonium chloride- a fast acting
Antibodies block, alter or destroy the receptors AChE inhibitor, is administered IV to
for acetylcholine at the neuromuscular junction
diagnose MG.
↓
- (+) test: immediate improvement in
Communication between the nerve & muscle is
muscle strength after administration of
interrupted
this agent.
↓
2. Ice pack Test
Muscle contraction is prevented
ice is applied to the eyes for 1-2
↓ minutes; (+) if there’s improvement in
Skeletal muscle weakness & fatigability lid strength

Clinical Manifestations 3. MRI – CHECK THYMUS GLAND

4. EMG – delayed/ failed nerve -
Subjective
transmission
 Extreme muscle weakness
 Fatigue
Medical Management cells and a plasma substitute are
reinfused
 Directed at improving function and
reducing and removing circulating Surgical Management
antibodies
 THYMECTOMY: surgical removal of the
 NO CURE: treatment does not stop
thymus gland; after thymus gland is
production of Ach receptor antibodies
removed, it may take up to 3 years for
Pharmacological Management the patient to benefit from the
procedure, because of the long life of
 Pyridostigmine Bromide (Mestinon):
circulating T cells
anticholinesterase medication; provides
symptomatic relief Nursing Management
 Adverse effects: fasciculations,
 Medication management- 30 mins.
abdominal pain, diarrhea,
before meals
increased oropharyngeal
secretions MEDICATIONS TO AVOID:

 Immunosuppressive drugs: to reduce  Barbiturates

the production of the antibody  Muscle relaxants
 Corticosteroid, Monitor CBC  Morphine Sulfate
 Azathioprine (Imuran)  Neomycin
 Intravenous immune globulin: used to  Tranquilizers
treat exacerbations and long- term
adjunctive basis  Energy conservation - Identify the

Plasmapheresis optimal time for rest throughout the day

 Minimize the risk of aspiration
 a technique used to treat
 Mealtimes should coincide with the
exacerbations.
peak effects of anti-cholinesterase
 patient’s plasma and plasma
medications
components are removed through a
 Rest before meals
centrally placed large-bore double-
 Sit upright during meals
lumen catheter
 oft foods- encourage gravy and sauce
 the blood cells & antibody containing
 Suction should be available at home
plasma are separated, after which the
  Supplemental feedings
 Strategies to help with ocular
manifestations - Tape the eyes closed for
short intervals - Regularly instill artificial
tears

Management

 Patient is placed in ICU

 ET intubation and mechanical
ventilation
 Provide ventilator assistance
 Ongoing assessment of respiratory
failure
 Chest physical therapy
 Monitor ABG, serum electrolytes, input
and output
 NGT feeding
 Avoid sedative and tranquilizers

Clinical Manifestations

 Nausea and vomiting, diarrhea and

abdominal cramps
 Pallor
 Facial muscle twitching
 Hypotension
PARKINSON’S DISEASE Imbalance of acetylcholine & dopamine
neurotransmitters in the corpus striatum
Definition: A neuro disease that affects
movement. Dopaminergic neurons die in ↓

substantia nigra. Impairment of extrapyramidal tracts controlling

complex body movements
CAUSE ↓

• Unknown for most cases (idiopathic) Tremors, Rigidity, Bradykinesia, Postural

changes
• Dopamine - acetylcholine disequilibrium CLINICAL MANIFESTATIONS

RISK FACTORS Early onset- the most obvious symptoms are

• Age is the largest risk factor (Older than 50-60 movement-related include:
years of age)
• Shaking
• Men are affected about 1.5 to 2 times more
• Rigidity
often than women.
• slowness of movement
• Genetics; A small number of individuals are at
• difficulty with walking & gait.
increased risk because of a family history of the
disorder Later

• Head trauma & illness • Cognitive & behavioral problems

• Exposure to environmental toxins (pesticides • Dementia; occurring in the advanced stages

& herbicides)
of the disease
PATHOPHYSIOLOGY
• Sensory, sleep & emotional problem
Dopaminergic neuronal cells are destroyed.
4 CARDINAL SIGNS OF PD
↓
 Tremor
Depletion of dopamine stores
 Rigidity
↓
 Bradykinesia
Degeneration of the dopaminergic nigrostriatal
pathway  Postural Instability

↓
Other Manifestations admitted to the hospital only for complications
or to initiate new treatments
• Psychiatric changes- depression, dementia
(progressive PHARMACOLOGIC THERAPY

mental deterioration), delirium, hallucinations - Antiparkinsonian medications act by:

• Mental changes- cognitive, perceptual & ▪ Increasing striatal dopaminergic activity

memory deficits; intellect is not usually
▪ Restoring a balance between dopaminergic &
affected.
cholinergic activities
• Dysphonia (soft, slurred, low-pitched, less
▪ Acting on neurotransmitter pathways other
audible speech)
than the dopaminergic pathway
• Dysphagia, begins to drool, & at risk for
- Levodopa (Larodopa)/ Carbidopa with
choking & aspiration
levodopa
DIAGNOSTIC TESTS
(Sinemet)- the most effective agent & the
• PET & Single Photon Emission Computed mainstay treatment
Tomography (SPECT)- FINDINGS: nigrostriatal
- Converted to dopamine in the basal ganglia,
dysfunction
producing symptom relief
• EEG
- Avoid the following when on Levodopa ▪
• No tests are diagnostic of PD Tyramine rich foods (prevent hypertensive
crisis) ▪ B6 (pyridoxine)
MEDICAL MANAGEMENT
SURGICAL MANAGEMENT
• Treatment are directed at controlling
symptoms & maintaining functional • Surgery provides symptom relief in selected
independence patients

• Care in individualized for each patient based 1. Stereotactic procedures: To interrupt the
on presenting symptoms & social, occupational, nerve
& emotional needs

• Patient are usually cared for at home & are

NURSING DIAGNOSES

• Impaired physical mobility related to muscle

rigidity & motor weakness

• Self-care deficits related to tremor & motor

disturbance

• Constipation related to medication & reduced

activity

• Imbalanced nutrition

• Impaired verbal communication

• Ineffective coping

NURSING INTERVENTIONS

✔ Improving mobility (progressive program of

daily exercise)

✔ Enhancing self-care activities (independence)

✔ Improving bowel elimination

✔ Improving nutrition (high residue, high

caloric, soft diet)

✔ Encouraging the use of assistive devices

✔ Improving communication (refer to speech

therapy)

✔ Supporting coping abilities

✔ Promoting Home & community based care

TRIGEMINAL NEURALGIA or applying makeup, brushing teeth,
eating, drinking, talking, or being
Definition: A.K.A. Tic douloureux. Is a neurologic
exposed to the wind
condition involving recurrent episodes of facial
 cheek twitch
pain.
 a tearing eye or salivation on the same
Causes: side of the face

•vascular compression and pressure Diagnostics:

-as the brain changes with age, a loop of a  X-rays of the skull, teeth and sinuses
cerebral artery or vein may compress the nerve
 MRI
root entry point
Medical Management:
Occurrence:
 Pharmacologic Therapy
 occurs most often before 35 years of
 Antiseizure agents i.e.
age
Carbamazepine (Tegretol)
 more common in women
 relieve pain by reducing the
 common in people with MS compared
transmission of impulses at certain
with the general population
nerve terminals
Patho:  Should be taken with meals
 Serum levels should be monitored
Vascular compression and pressure in
trigeminal nerve which would cause heightened  Monitor for bone marrow depression
sensation in innervated areas that will trigger during long-term therapy
spot that leads to pain.  Muscle relaxants i.e. Gabapentin
(Neurontin),Baclofen (Lioresal)-used for
Clinical Manifestations:
pain control
 episodes of sudden, intense, "stabbing"  Sedatives
or "shocklike" facial pain  Antidepressants
 pain typically felt on one side of the jaw
Surgical Management
or cheek
 intense flashes of pain can be triggered If pharmacologic management fails to relieve

by vibration or contact with the cheek pain.

such as when shaving, washing the face

•Microvascular decompression of the trigeminal
nerve-artery loop is lifted from the nerve using
silicon foam

•Radiofrequency thermal coagulation

-Produces thermal lesion on the trigeminal

nerve

•Percutaneous balloon microcompression

-Disrupts large myelinatedfibers in all three

branches ofthe trigeminal nerve

•Retrogasserian Rhizotomy-Sensory root of CNV

is surgical severed

•Radiosurgery with stereotatictechnique

•-uses GAMMA KNIFE to severe CNV 5

•Alcohol or phenol block-injection of alcohol

into a CN5 branch for pain relief (transient: 1 yr)

Nursing Management

 Preventing Pain
 Providing postoperative care
MENINGITIS