The diagnosis of<unk>  depends on findings such as rapid development of muscle paralysis, absent reflexes, absence of fever, and absence of a likely cause. Cerebrospinal fluid analysis (through a lumbar spinal puncture) and nerve conduction studies are supportive investigations commonly performed in the diagnosis of<unk> . Testing for antiganglioside antibodies is often performed, but their contribution to diagnosis is usually limited. Blood tests are generally performed to exclude the possibility of another cause for weakness, such as a low level of potassium in the blood. An abnormally low level of sodium in the blood is often encountered in<unk> . This has been attributed to the inappropriate secretion of antidiuretic hormone, leading to relative retention of water. In many cases, magnetic resonance imaging of the spinal cord is performed to distinguish between<unk>  and other conditions causing limb weakness, such as spinal cord compression. If an MRI scan shows enhancement of the nerve roots, this may be indicative of<unk> . In children, this feature is present in 95% of scans, but it is not specific to<unk> , so other confirmation is also needed. Spinal fluid Cerebrospinal fluid envelops the brain and the spine, and lumbar puncture or spinal tap is the removal of a small amount of fluid using a needle inserted between the lumbar vertebrae. Characteristic findings in<unk>  are an elevated protein level, usually greater than 0.55 g/L, and fewer than 10 white blood cells per cubic millimeter of fluid ("albuminocytological dissociation"). This pattern distinguishes<unk>  from other conditions (such as lymphoma and poliomyelitis) in which both the protein and the cell count are elevated. Elevated CSF protein levels are found in approximately 50% of patients in the first 3 days after onset of weakness, which increases to 80% after the first week. Repeating the lumbar puncture during the disease course is not recommended. The protein levels may rise after treatment has been administered. Neurophysiology Directly assessing nerve conduction of electrical impulses can exclude other causes of acute muscle weakness, as well as distinguish the different types of<unk> . Needle electromyography (EMG) and nerve conduction studies may be performed. In the first two weeks, these investigations may not show any abnormality. Neurophysiology studies are not required for the diagnosis. Formal criteria exist for each of the main subtypes of<unk>  (AIDP and AMAN/AMSAN, see below), but these may misclassify some cases (particularly where there is reversible conduction failure) and therefore changes to these criteria have been proposed. Sometimes, repeated testing may be helpful. Clinical subtypes A number of subtypes of<unk>  are recognized. Despite this, many people have overlapping symptoms that can make the classification difficult in individual cases. All types have partial forms. For instance, some people experience only isolated eye-movement or coordination problems; these are thought to be a subtype of Miller Fisher syndrome and have similar antiganglioside antibody patterns. Type Symptoms Population affected Nerve conduction studies Antiganglioside antibodies Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) Sensory symptoms and muscle weakness, often with cranial nerve weakness and autonomic involvement Most common in Europe and North America Demyelinating polyneuropathy No clear association Acute motor axonal neuropathy (AMAN) Isolated muscle weakness without sensory symptoms in less than 10%; cranial nerve involvement uncommon Rare in Europe and North America, a substantial proportion (30–65%) in Asia and Central and South America; sometimes called "Chinese paralytic syndrome" Axonal polyneuropathy, normal sensory action potential GM1a/b, GD1a & GalNac-GD1a Acute motor and sensory axonal neuropathy (AMSAN) Severe muscle weakness similar to AMAN but with sensory loss - Axonal polyneuropathy, reduced or absent sensory action potential GM1, GD1a Pharyngeal-cervical-brachial variant Weakness particularly of the throat muscles, and face, neck, and shoulder muscles - Generally normal, sometimes axonal neuropathy in arms Mostly GT1a, occasionally GQ1b, rarely GD1a Miller Fisher syndrome Ataxia, eye muscle weakness, areflexia but usually no limb weakness This variant occurs more commonly in men than in women (2:1 ratio). Cases typically occur in the spring and the average age of occurrence is 43 years old. Generally normal, sometimes discrete changes in sensory conduction or H-reflex detected GQ1b, GT1a Other diagnostic entities are often included in the spectrum of<unk> . Bickerstaff's brainstem encephalitis (BBE), for instance, is part of the group of conditions now regarded as forms of Miller Fisher syndrome (anti-GQ1b antibody syndrome), as well as a related condition labelled "acute ataxic hypersomnolence"where coordination problems and drowsiness are present but no muscle weakness can be detected. BBE is characterized by the rapid onset of ophthalmoplegia, ataxia, and disturbance of consciousness, and may be associated with absent or decreased tendon reflexes and as well as Babinski's sign. The course of the disease is usually monophasic, but recurrent episodes have been reported. MRI abnormalities in the brainstem have been reported in 11%. Whether isolated acute sensory loss can be regarded as a form of<unk>  is a matter of dispute; this is a rare occurrence compared to<unk>  with muscle weakness but no sensory symptoms.
Guillain–Barré syndrome
Myasthenia gravis
Tension myositis syndrome
Botulism
Lambert–Eaton myasthenic syndrome
Acute flaccid myelitis
FACES syndrome
CMV polyradiculomyelopathy