Median and Ulnar Neuropathy Assessment in Parkinson's Disease regarding Symptom Severity and Asymmetry.

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.

The effects and interactions of APOE and APH-1A polymorphisms in Alzheimer disease.

BACKGROUND/AIM: Alzheimer disease (AD) is characterized by the accumulation of senile plaques composed of amyloid ß-peptide, which is derived from ß-amyloid precursor protein through degradation by ß-secretase and y-secretase complexes. One of the major components of y-secretase complex, anterior pharynx-defective-1 (APH-1), is responsible for the activity of the γ-secretase complex. In this study, we searched for not only the most known common genetic risk factor, APOE, but also the APH-1a gene polymorphism in AD patients in a Turkish population. MATERIALS AND METHODS: In this study, 49 AD patients and 45 healthy controls were included. The genetic polymorphisms and allele frequencies of APOE and APH-1a were investigated. Patients were evaluated for behavioral, cognitive, and functional domains by detailed neurocognitive tests, and comparison between the above-mentioned polymorphisms and disease severity was made. RESULTS: Although there was an increased tendency of the APO ε4 allele in the AD group, no statistically significant difference was detected either in APOE or APH-1a polymorphisms, not suggesting a strong susceptibility to the development of AD. CONCLUSION: While searching for the pathogenesis of AD in order to develop novel diagnostic as well as therapeutic approaches, analysis of other genes with a possible role in AD is warranted.

Bilateral facial nerve enhancement demonstrated by magnetic resonance imaging in Guillain-Barré syndrome.

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.

Can subdural hematoma be a trigger for Guillain-Barré syndrome?

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.

Neurologic complications after renal transplant.

OBJECTIVES: Neurologic complications are a significant cause of morbidity and mortality in patients who undergo transplants. We sought to evaluate the nature and incidence of neurologic complications in patients undergoing a renal transplant. PATIENTS AND METHODS: Between January 2005 and December 2007, 132 adults (35 women, 97 men; mean age, 34.32 -/+ 0.90 years) underwent a renal transplant at our institution. Associated comorbid medical conditions, presenting neurologic symptoms, and type of immunosuppression were obtained from patients' medical records. RESULTS: Major indications for renal transplant were hypertensive nephropathy (14.4%), vesicoureteral reflux (11.4%), and idiopathic causes (21.2%). Mean follow-up was 17.26 -/+ 0.89 months (range, 2 weeks to 40 months). Twenty neurologic complications were found in 18 patients (6 women, 12 men; mean age, 33.83 -/+ 2.37 years). Presenting symptoms included posterior leukoencephalopathy syndrome, 1 (5.6%); cephalgia, 10 (55.6%); cerebral infarcts, 2 (11.1%); seizure, 3 (16.7%); tremor, 2 (11.1%); encephalopathy, 1 (5.6%); and sinus thrombosis, 1 (5.6%). Immunosuppressive agents were the primary cause of 16 of the 20 neurologic complications. Effectiveness and complications of cyclosporinewere screened for a total of 1858.50 months, tacrolimus for 853.50 months, and sirolimus for 620 months; 50.2% of the neurologic complications appeared during the first 3 months after transplant; the blood level of immunosuppressive medications did not need to be higher than normal in every case. DISCUSSION: In addition to cyclosporine and tacrolimus, we suggest (for the first time) sirolimus as a cause of neurocomplications after renal transplant.

A diagnostic challenge of Parkinson's disease: intractable hiccups.

Parkinson's disease is a common neurodegenerative disorder and the diagnosis depends mostly on clinical assessment so it is important to be aware of less common symptoms of the disease for correct diagnosis and therapy. We describe a patient with intractable hiccups as a very unusual presentation of Parkinson's disease.