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We report a patient with acute oropharyngeal palsy following enteritis. A 19-year-old woman developed increasing nasal voice over a few days. Neurological examination on day 7 of her course showed paretic dysarthria and mild weakness of neck flexion and quadriceps femoris muscle (Medical Research Council grade, 4+). Her palatal movement was diminished, whereas both palatal and pharyngeal reflex was normal. She could swallow water, although she had a slight amount of liquid reflux to her nose on swallowing. High titers of serum anti-Campylobacter jejuni, anti-GQ1b and anti-GT1a IgG antibodies were detected. Her symptoms improved gradually without any treatment, and disappeared by 40 days from neurological onset. Nasal voice with slight swallowing impairment as initial symptom has been rarely reported, but can occur in acute oropharyngeal palsy. Therefore, neurologists should take into account the possibility of Guillain-Barré syndrome and the regional variants in patients who show nasal voice during the initial stage.

A patient with Facial diplegia and paresthesias, a rare regional variant of Guillain-Barré syndrome (GBS), is described. A 37-year-old woman developed paresthesias in the distal limbs and subsequently bifacial weakness. She had had a preceding episode of laryngitis. Neurological examination showed severe facial diplegia with loss of taste sensation on the tip of the tongue. Limb muscle power was preserved. Deep tendon reflexes were generally absent. She complained of paresthesias in the distal limbs, but sensory examination was normal. Cerebrospinal fluid showed albuminocytological dissociation. Electrophysiological studies revealed severe facial nerve involvements and demyelinative findings in her limbs. Intravenous immunoglobulin rapidly improved the abnormal sensation in her limbs. Although facial diplegia gradually lessened after the therapy, mild residual weakness was noted 6 months after the neurological onset. To diagnose facial diplegia and paresthesias, it is important to clarify the findings common to typical GBS such as the antecedent illness, acute and monophasic course, distal paresthesias, areflexia, cerebrospinal fluid albuminocytological dissociation, and demyelinative conduction abnormalities in the limbs.

We described a patient with ataxic Guillain-Barré syndrome who subsequently developed facial diplegia. A 38-year-old man developed ataxia, distal limb paresthesias, mild dysphagia, urinary retention and orthostatic hypotension a week after an episode of laryngitis. He had high titers of serum anti-GQ1b, anti-GD1b, anti-GM1b, anti-GT1a, and anti-GD1a IgG antibodies during the acute phase. Although the initial symptoms markedly improved by intravenous immunoglobulin therapy, asymmetric facial diplegia subsequently occurred and remained longer than ataxia. Similar course of facial nerve palsy has been reported in patients with Fisher syndrome. Common pathophysiological mechanism may function in the development of delayed facial diplegia in Fisher syndrome and ataxic Guillain-Barre syndrome.

A 28-year-old man was admitted after developing acute onset unstable gait following acute enteritis. Neurological examination revealed mild weakness in four limbs, areflexia and ataxia. Serum obtained from the patient during the acute stage contained a high titer of anti-GD1b IgG antibody. Because the patient showed obvious cerebellar ataxia unrelated to muscle weakness, without ophthalmoplegia or proprioceptive sensory disturbance, we concluded that he had ataxic form of Guillain-Barré syndrome (GBS) (Richter, 1962). Although ataxic GBS is not an established conception, one should pay attention to the possible existence of such a rare GBS variant. It is necessary to accumulate additional case reports to clarify the association between ataxic GBS and anti-ganglioside antibodies.

We reported a 24-year-old man with right radial nerve palsy. He had suffered from a right humeral shaft fracture approximately three years before. The fracture was treated with intramedullary nailing. Our radiograph of the right upper limb showed callus around the fracture site. A nerve conduction study revealed conduction block of the radial nerve at the lateral side of the callus. Tinel's sign was present in the median nerve at the medial side of the callus. Surgical exploration revealed that the radial nerve trunk was compressed at the callus site. The median nerve trunk was close to the callus. We decompressed radial nerve trunk, and the patient's neurological symptoms improved gradually after the operation. Delayed radial nerve palsy has been reported only rarely, whereas acute compression of the nerve sometimes occurs after humeral shaft fractures. Morever, the median nerve also was vulnerable to compression at the site of callus. These findings underscore the importance of taking into account the possibility of delayed compression neuropathy after humeral shaft fracture.

We described a 62-year-old man with a 10 years history of chronic sensory ataxic neuropathy. His laboratory investigations revealed elevated serum IgM with IgM kappa paraproteinemia, IgM antibody against b-series gangliosides including GD3, GD2, GD1b, GT1b, GQ1b, GQ1b alpha, and high titer of cold agglutinin. The clinical and serological features in our patient were compatible with the diagnosis of CANOMAD (chronic ataxic neuropathy with ophthalmoplegia, M-protein, agglutination, and disialosyl antibodies), proposed by Willison et al. IgM antibody against b-series gangliosides including GD1b appeared to play an essential role in developing autoimmune sensory ataxic neuropathy.

Nerve conduction blocks (NCBs) in Guillain-Barré syndrome (GBS) are frequently found at the distal terminals, proximal segments, and common entrapment sites of peripheral nerves. NCBs at distal terminals and proximal segments are considered to be due to vulnerability of the sites to the humoral factors of GBS because of relative blood-nerve barrier deficiencies. In contrast, it is not clear whether NCBs at common entrapment sites in GBS are due to a vulnerability to humoral influences or to direct mechanical compression injuries. We report a case of a 22-year-old man with GBS. His electrophysiologic examination revealed NCBs at multiple common entrapment sites. All conduction blocks rapidly disappeared after plasmapheresis, in parallel with clinical improvement. The patient was ambulatory throughout the clinical course, suggesting that his common entrapment sites remained free from compression injuries. Rapid improvement by plasmapheresis suggested that there were no demyelinative histologic changes in the NCB sites. Such NCBs may be caused by some humoral factor that is removed by plasmapheresis. Therefore, the common entrapment sites in our patient may have been especially vulnerable to the humoral factor of GBS.