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. Attempt to return function after an
- Worsening of vision caused by hot attack
temperature (increased temp: Prevent new attacks
slowed/blocked nerve TRANSMISSION Prevent disability
LHERMITTE’S SIGN – electric shock like Delay the progression of the disease
sensation radiating down the spine to the
Pharmacologic Therapy
legs and arms when neck is moved
Cognitive change Disease-Modifying therapies
Memory loss Immunosuppressants
Decreased concentration
Corticosteroids
Impaired cerebellar function (Charcot’s
- Prednisone (Deltasone, Liquid Pred,
Triad)
Deltasone, Orasone, Prednicen-M);
Scanning speech
methylprednisolone (Medrol, Depo-
Intention tremors
Medrol)
Nystagmus
Interferons: have the ability to regulate
Ataxia
the immune system & play an important
Dysarthria (poor speech articulation)\
role in protecting against intruders
Bladder, bowel & sexual dysfunctions including viruses
Diagnostic Findings - Beta interferons- found to be useful in
MRI- scattered patches of scar/plaque managing MS
(>5mm) in the CNS - Beta 1a: rebig; beta 1b: betasteron (SQ)
CSF Studies- protein electrophoresis., Igs Glatiramer acetate (Copaxone) – increase
are separated from csf, results (+) suppressor T cells, Admin sq daily (P3000/shot)
oligoclonal bonds
Symptoms Management
CT Scan
EEG Baclofen (Lioresal); (GABA agonist)- for
spasticity
Medical Management
Benzodiazepines (Valium), Tizanidine
No known cure for MS (Zanaflex) & dantrolene (Dantrium)
Goal of the treatments 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 Dysphonia- impaired ability to produce
voice Strabismus
muscles
Mask-like facial expression
BULBAR – affects muscles for breathing,
swallowing and speaking 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
