Guillain-Barré syndrome other diagnostic studies: Difference between revisions
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'''Guillain-Barré syndrome''' ('''GBS''') is an acute, autoimmune, [[neuropathy|polyradiculoneuropathy]] affecting the [[peripheral nervous system]], usually triggered by an acute infectious process. It is included in the wider group of [[peripheral neuropathy|peripheral neuropathies]]. There are several types of GBS, but unless otherwise stated, GBS refers to the most common form, acute inflammatory demyelinating polyneuropathy (AIDP). It is frequently severe and usually exhibits as an ascending paralysis noted by weakness in the legs that spreads to the upper limbs and the face along with complete loss of deep tendon reflexes. With prompt treatment of [[plasmapheresis]] followed by [[immunoglobulins]] and supportive care, the majority of patients will regain full functional capacity. However, death may occur if severe pulmonary complications and [[dysautonomia]] are present. | '''Guillain-Barré syndrome''' ('''GBS''') is an acute, autoimmune, [[neuropathy|polyradiculoneuropathy]] affecting the [[peripheral nervous system]], usually triggered by an acute infectious process. It is included in the wider group of [[peripheral neuropathy|peripheral neuropathies]]. There are several types of GBS, but unless otherwise stated, GBS refers to the most common form, acute inflammatory demyelinating polyneuropathy (AIDP). It is frequently severe and usually exhibits as an ascending paralysis noted by weakness in the legs that spreads to the upper limbs and the face along with complete loss of deep tendon reflexes. With prompt treatment of [[plasmapheresis]] followed by [[immunoglobulins]] and supportive care, the majority of patients will regain full functional capacity. However, death may occur if severe pulmonary complications and [[dysautonomia]] are present. | ||
==Other diagnostic studies== | ==Other diagnostic studies== | ||
CSF and ECD is used almost every time to verify symptoms, but because of the acute nature of the disease, they may not become abnormal until after the first week of onset of signs and symptoms. | |||
* '''[[cerebrospinal fluid|CSF]]''' - typical CSF findings include an elevated protein level (100 - 1000 mg/dL) without an accompanying pleocytosis (increased cell count). A sustained pleocytosis may indicate an alternative diagnosis such as infection. | * '''[[cerebrospinal fluid|CSF]]''' - typical CSF findings include an elevated protein level (100 - 1000 mg/dL) without an accompanying pleocytosis (increased cell count). A sustained pleocytosis may indicate an alternative diagnosis such as infection. | ||
The diagnosis is confirmed by the presence of Albuminocytological dissociation in the CSF | The diagnosis is confirmed by the presence of Albuminocytological dissociation in the CSF | ||
* '''Electrodiagnostics''' - [[electromyography]] (EMG) and [[nerve conduction study]] (NCS) may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound action potential in demyelinating cases. In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing. | * '''Electrodiagnostics''' - [[electromyography]] (EMG) and [[nerve conduction study]] (NCS) may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound action potential in demyelinating cases. In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing. | ||
The following tests may be ordered: | The following tests may be ordered: | ||
Revision as of 20:46, 24 February 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Priyamvada Singh, MBBS [2]
Overview
Guillain-Barré syndrome (GBS) is an acute, autoimmune, polyradiculoneuropathy affecting the peripheral nervous system, usually triggered by an acute infectious process. It is included in the wider group of peripheral neuropathies. There are several types of GBS, but unless otherwise stated, GBS refers to the most common form, acute inflammatory demyelinating polyneuropathy (AIDP). It is frequently severe and usually exhibits as an ascending paralysis noted by weakness in the legs that spreads to the upper limbs and the face along with complete loss of deep tendon reflexes. With prompt treatment of plasmapheresis followed by immunoglobulins and supportive care, the majority of patients will regain full functional capacity. However, death may occur if severe pulmonary complications and dysautonomia are present.
Other diagnostic studies
CSF and ECD is used almost every time to verify symptoms, but because of the acute nature of the disease, they may not become abnormal until after the first week of onset of signs and symptoms.
- CSF - typical CSF findings include an elevated protein level (100 - 1000 mg/dL) without an accompanying pleocytosis (increased cell count). A sustained pleocytosis may indicate an alternative diagnosis such as infection.
The diagnosis is confirmed by the presence of Albuminocytological dissociation in the CSF
- Electrodiagnostics - electromyography (EMG) and nerve conduction study (NCS) may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound action potential in demyelinating cases. In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing.
The following tests may be ordered:
- Cerebrospinal fluid sample ("spinal tap") may have increased levels of protein without an increase in white blood cells.
- ECG may show heart problems in some cases.
- EMG tests the electrical activity in muscles. It may show that nerves do not react properly to stimulation.
- Nerve conduction velocity test shows that electrical activity along the nerves is slowed or blocked.