Med surg

According to Braddom, Guillain-Barre syndrome or GBS was first described almost a

century by French neurologists Guillain, Barre, and Strohl. It is the most common
cause of acute neuromuscular paralysis after polio has been eradicated. Guillain-
Barre Syndrome is a progressive, symmetrical weakness of the limbs. It also
includes hyporeflexia or areflexia, with or without sensory abnormalities. The
maxmimal weakness happens within 4 weeks. However, it reaches its peak at 2
weeks. GBS is currently recognized to be a group of conditions with varying
subtypes. Acute demyelinating polyradiculopathy or AIDP is the most common form.
There are also axonal forms such as the acute motor axonal neuropathy (AMAN) or
acute motor and sensory axonal neuropathy (AMSAN). Another variant is the Miller-
Fisher which is a triad of ataxia, areflexia, and ophthalmoplegia. Bulbar
abnormalities, pt0sis, facial weakness and papillary dysfunction are also present.

GBS appears with the progressive onset of limb weakness both proximally and
distally. It presents symmetrically and reaches peak in two-four weeks. Reflexes are
usually gone in the early phase of the disease. However, it can be stay or even brisk
in the axonal variants. Sensory loss is varying in individuals. The cranial nerves can
also be involved along with facial palsy and bulbar weakness. The muscles for
respiration are often affected with the decrease in vital capacity. The autonomic
system can be involved which can cause achycardia, hypertension, arrhythmias. A
significant complaint may be pain and can even be present prior to the onset of
weakness. During the acute stage, pain is usually described as deep and aching in
the following areas: the back, buttocks, and posterior thighs. The reason for this
might be because of the nociceptive pain from inflammation. Neuropathic pain can
be present later which is described with degeneration and regeneration of sensory
nerves. Aside from pain, fatigue is another common complaint. Some medications
have not been proven to help but bicycle exercise training has been shown to
decrease fatigue and improve functional outcome and quality of life.
Pathophysiology
Individuals wit GBS have an antecedent infection three weeks before the onset of
weakness. Campylobacter jejuni is the most commonly identified infectious agent.
Other agents are cytomegalovirus (CMV), Epstein-Barr virus, Mycoplasma
pneumoniae and Haemophilus influenzae. The strong association with antecedent
infection points out that in some cases there is an immune response to the
infectious agents that causes damage to peripheral nerves. The causative agent is
also connected with the subtype of GBS that develops.

Infectious agent GBS type

Campylobacter jejuni Axonal forms
Cytomegalovirus Cranial nerve respiratory and seve
sensory involvement
Esptein-Barr Milder disease

Diagnosis
The required clinical features for the diagnosis of GBS according to Braddom are
progressive weakness in both arms and legs, and areflexia. Other features include
progression of weakness over days to 4 weeks, symmetry of symptoms, mild
sensory symptoms, cranial nerve involvement, autonomic involvement, pain, high
protein concentration in the CSF, and typical electrodiagnostic findings.
Lumbar puncture is perfomed in individuals with a rapidly progressive weakness. In
GBS, there is an elevated CSF protein with normal white blood cell count. This is
usually referred to as albuminocytologic dissociation. The CSF protein may be noral
during the first week of the disease. Elevated WBC count should be suspected of
infection.