GUILLAIN-BARRÉ

SYNDROME
by
SAIDA SADIQ
 GUILLAIN-BARRÉ SYNDROME

• Guillain-Barré syndrome is an autoimmune attack of the

peripheral nerve myelin. The result is acute, rapid
segmental demyelination of peripheral nerves and some
cranial nerves, producing ascending weakness with
dyskinesia (inability to execute voluntary movements),
hyporeflexia, and paresthesias (numbness).
• There is a predisposing event, most often a respiratory or
gastrointestinal infection, although vaccination, pregnancy,
and surgery have also been identified as antecedent
events
• The antecedent event usually occurs 2 weeks before
symptoms begin. Weakness usually begins in the legs and
progresses upward for about 1 month. Maximum weakness
varies but usually includes neuromuscular respiratory failure
and bulbar weakness. The duration of the symptoms is
variable: complete functional recovery may take up to 2
years . Any residual symptoms are permanent and reflect
axonal damage from demyelination.
 Pathophysiology
• Myelin is a complex substance that covers nerves, providing insulation and
speeding the conduction of impulses from the cell body to the dendrites.
The cell that produces myelin in the peripheral nervous system is the
Schwann cell. In Guillain-Barré the Schwann cell is spared, allowing for
remyelination in the recovery phase of the disease.
• Guillain-Barré is the result of a cell-mediated immune attack on peripheral
nerve myelin proteins. The best-accepted theory is that an infectious
organism contains an amino acid that mimics the peripheral nerve myelin
protein. The immune system cannot distinguish between the two proteins
and attacks and destroys peripheral nerve myelin. With the autoimmune
attack there is an influx of macrophages and other immune-mediated
agents that attack myelin, cause inflammation and destruction, and leave
the axon unable to support nerve conduction.
Clinical Manifestations
• Classic Guillain-Barré begins with muscle weakness and diminished
reflexes of the lower extremities. Hyporeflexia and weakness
progress and may result in quadriplegia
• Demyelination of the nerves that innervate the diaphragm and
intercostal muscles results in neuromuscular respiratory failure.
• Sensory symptoms include paresthesias of the hands and feet and
pain related to the demyelination of sensory fibers.
• Cranial nerve demyelination can result in a variety of clinical
manifestations. Optic nerve demyelination may result in blindness.
• Bulbar muscle weakness related to demyelination of the
glossopharyngeal and vagus nerves results in an inability to
swallow or clear secretions.
• Vagus nerve demyelination results in autonomic dysfunction,
manifested by instability of the cardiovascular system. The
presentation is variable and may include tachycardia, bradycardia,
hypertension, or orthostatic hypotension.
• Guillain-Barré does not affect cognitive function or level of
consciousness.
• While the classic clinical features include areflexia and ascending
weakness, variation in presentation occurs. There may be a
sensory presentation, with progressive sensory symptoms, an
atypical axonal destruction, and the Miller-Fisher variant, which
includes paralysis of the ocular muscles, ataxia, and areflexia
• Miller Fisher syndrome (MFS) is a rare variant of Guillain-Barré
syndrome (GBS), characterized by a triad of ophthalmoplegia (eye
muscle paralysis), ataxia (loss of coordination), and areflexia
(absent reflexes)
Assessment and Diagnostic
Findings
• The patient presents with symmetric weakness, diminished
reflexes, and upward progression of motor weakness. A
history of a viral illness in the previous few weeks suggests
the diagnosis.
• Changes in vital capacity and negative inspiratory force are
assessed to identify impending neuromuscular respiratory
failure.
• Serum laboratory tests are not useful in the diagnosis.
However, elevated protein levels are detected in CSF
evaluation, without an increase in other cells.
Medical Management
• Because of the possibility of rapid progression and
neuromuscular respiratory failure, Guillain-Barré is a medical
emergency, requiring intensive care unit management. Careful
assessment of changes in motor weakness and respiratory
function alert the clinician to the physical and respiratory needs
of the patient.
• Respiratory therapy or mechanical ventilation may be necessary
to support pulmonary function and adequate oxygenation.
Mechanical ventilation may be required for an extended period.
The patient is weaned from mechanical ventilation when the
respiratory muscles can again support spontaneous respiration
and maintain adequate tissue oxygenation
• Other interventions are aimed at preventing the complications of
immobility. These may include the use of anticoagulant agents and thigh-
high elastic compression stockings or sequential compression boots to
prevent thrombosis and pulmonary emboli.
• Plasmapheresis and IVIG are used to directly affect the peripheral nerve
myelin antibody level. Both therapies decrease circulating antibody levels
and reduce the amount of time the patient is immobilized and dependent
on mechanical ventilation. Studies indicate that IVIG and plasmapheresis
are equally effective in treating Guillain-Barré
• The cardiovascular risks posed by autonomic dysfunction require
continuous ECG monitoring. Tachycardia and hypertension are treated with
short-acting medications such as alpha-adrenergic blocking agents.
Hypotension is managed by increasing the amount of IV fluid administered.
The use of short-acting agents is important because autonomic dysfunction
is very labile
Nursing Interventions
• MAINTAINING RESPIRATORY FUNCTION
• IMPROVING COMMUNICATION
• PROVIDING ADEQUATE NUTRITION
• DECREASING FEAR AND ANXIETY
• MONITORING AND MANAGING POTENTIAL COMPLICATIONS
• TEACHING PATIENTS SELF-CARE
 TRIGEMINAL NEURALGIA
• Trigeminal neuralgia is a condition of the fifth cranial nerve characterized by
paroxysms of pain in the area innervated by any of the three branches, but it
most commonly occurs in the second and third branches of the trigeminal
nerve
• The pain ends as abruptly as it starts and is described as a unilateral shooting
and stabbing sensation. The unilateral nature of the pain is an important
diagnostic characteristic
• Associated involuntary contraction of the facial muscles can cause sudden
closing of the eye or a twitch of the mouth, hence the name tic douloureux
(painful twitch)
• The cause is not certain, but chronic compression or irritation of the
trigeminal nerve or degenerative changes in the ganglion are suggested
causes. Vascular pressure from structural abnormalities (loop of an artery)
encroaching on the trigeminal nerve has also been suggested as a cause.
Medical Management
• PHARMACOLOGIC THERAPY
1. Antiseizure agents
2. Gabapentin (Neurontin) and baclofen (Lioresal)
3. If pain control is still not achieved, phenytoin (Dilantin) may
be used
• SURGICAL MANAGEMENT
• When these methods fail to relieve pain, a number of
surgical options are available. The choice of procedure
depends on the patient’s preference and health status
• Microvascular Decompression of the Trigeminal Nerve.
An intracranial approach can be used to decompress the
trigeminal nerve. The pain may be caused by vascular
compression of the entry zone of the trigeminal root by
an arterial loop and occasionally by a vein .
• With the aid of an operating microscope, the artery loop
is lifted from the nerve to relieve the pressure, and a
small prosthetic device is inserted to prevent recurrence
of impingement on the nerve. This procedure relieves
facial pain while preserving normal sensation, but it is a
major procedure, involving a craniotomy.
• Percutaneous Radiofrequency Trigeminal Gangliolysis.
Percutaneous radiofrequency interruption of the gasserian
ganglion, in which the small unmyelinated and thinly myelinated
fibers that conduct pain are thermally destroyed, is the surgical
procedure of choice for trigeminal neuralgia
Use of stereotactic MRI for identification of the trigeminal nerve
followed by gamma knife radiosurgery is being used at some
centers with good results
 Nursing Management
• PREVENTING PAIN
• Preoperative management of a patient with trigeminal neuralgia occurs mostly on
an outpatient basis and includes recognizing factors that may aggravate
excruciating facial pain, such as food that is too hot or too cold or jarring the
patient’s bed or chair. Even washing the face, combing the hair, or brushing the
teeth may produce acute pain.
• The nurse can assist the patient in preventing or reducing this pain by providing
instructions about preventive strategies. Providing cotton pads and room-
temperature water for washing the face, instructing the patient to rinse with
mouthwash after eating when tooth-brushing causes pain, and performing
personal hygiene during pain-free intervals are all effective strategies. The patient
is instructed to take food and fluids at room temperature, to chew on the
unaffected side, and to ingest soft foods. The nurse recognizes that anxiety,
depression, and insomnia often accompany chronic painful conditions and uses
appropriate interventions and referrals.
• PROVIDING POSTOPERATIVE CARE
• Postoperative neurologic assessments are conducted to evaluate
the patient for facial motor and sensory deficits in each of the
three branches of the trigeminal nerve.
• If the surgery results in sensory deficits to the affected side of the
face, the patient is instructed not to rub the eye, because pain will
not be felt if there is injury. The eye is assessed for irritation or
redness. Artificial tears may be prescribed to prevent dryness in the
affected eye.
• The patient is cautioned not to chew on the affected side until
numbness has diminished. The patient is observed carefully for any
difficulty in eating and swallowing foods of different consistency