Guillain-Barré syndrome (GBS) is an acute inflammatory demyelinating peripheral nerve disorder. It is known that gadolinium enhancement on magnetic resonance imaging (MRI) reflects alteration of the blood-nerve barrier secondary to inflammation. Enhancement of the cauda equina roots with gadolinium on lumbosacral magnetic resonance imaging have been demonstrated in several reports. Although about 50% of GBS patients clinically exhibit facial nerve involvement, it has never been demonstrated on MRI. We aimed to observe facial nerve involvement in a GBS patient who has prominent facial diplegia. With the guidance of the literature, we predict that MRI in selected GBS patients may be an adjunct tool for the clinician in both diagnosis and monitoring the treatment response.

Background. While increasing evidence suggests comorbidity of peripheral neuropathy (PNP) and Parkinson's disease (PD), the pathogenesis of PNP in PD is still a debate. The aim of this article is to search the core PD symptoms such as rigidity and tremor as contributing factors to mononeuropathy development while emphasizing each individual patient's asymmetric symptom severity. Methods. We studied 62 wrists and 62 elbows of 31 patients (mean age 66.48 ± 10.67) and 64 wrists and 64 elbows of 32 age-gender matched healthy controls (mean age 62.03 ± 10.40, p = 0.145). The Hoehn and Yahr disability scale and Unified Parkinson's Disease Rated Scale were used to determine the severity of the disease. Results. According to electrodiagnostic criteria, we confirmed median neuropathy in 16.12% (bilateral in two-thirds of the patients) and ulnar neuropathy in 3.22% of the PD group. While mean age (p = 0.003), age at PD onset (p = 0.019), and H&Y scores (p = 0.016) were significant, tremor and rigidity scores were not. The comparison of the mean indices of electrophysiologic parameters indicated subclinical median and ulnar nerve demyelination both at the wrist and at the elbow in the patient groups where a longer disease duration and mild tremor and rigidity scores are prominent, remarkably. Conclusion. A disease related peripheral neurodegeneration beyond symptom severity occurs in PD.

Guillain-Barré syndrome (GBS) is an acute inflammatory polyneuropathy which follows a precipitating event in approximately two thirds of cases. Although its pathogenesis is unclear, it is likely to be a consequence of an immune-mediated process. In the literature there are three case reports of GBS following subarachnoid hemorrhage, subdural hematoma, and facial bone fracture after head trauma.The unique feature of our case with GBS after subdural hematoma is the presence of cerebellar symptoms. We believe that GBS results from an aberrant immune response following trauma that somehow mistakenly attacks the nerve tissue of its host, and we discuss the effects of the trauma of head injury on cellular and humoral immunities and the absence of antiganglioside antibody (anti-GD1b IgG, which is accused of ataxia and cerebellar symptoms) in this case report.

The spontaneous occurrence of blepharospasm and dystonic movements in face muscles, particularly those of the perioral and mandibular regions, has been named as Meige's disease which was first described by Henry Meige in 1910. We report the case of a woman with Meige's syndrome whose symptoms improved with the use of levetiracetam.

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