The Relationship between Polyneuropathy and Cognitive Functions in Type 2 Diabetes Mellitus Patients.

OBJECTIVES: Type 2 Diabetes Mellitus (DM) is a risk factor for mild cognitive impairment (MCI), Alzheimer's disease and vascular dementia. However, it is not known which pathophysiological mechanisms lead to impairment in cognitive functions in Type 2 DM. This study aims to compare the cognitive functions of diabetic patients with and without polyneuropathy using standardized Mini-Mental Test (MMSE) and the Montreal Cognitive Assessment Scale (MoCA) and to assess whether the presence of polyneuropathy is a predictive factor for the development of cognitive impairment. METHODS: Patients with DM who underwent our EMG laboratory for polyneuropathy between January 2014 and January 2015 were included in this study. Patients who underwent electrophysiological examinations were evaluated for polyneuropathy. Patients with polyneuropathy were classified as a patient group and other patients as a control group. In all cases, MMSE and MoCA were administered. The demographic data and educational status of the patients were recorded. Hypertension, coronary artery disease, smoking and alcohol use were questioned. Their complaints, duration of illness and the treatment they were receiving were questioned. Glycosylated hemoglobin (HBA1C) values in the last three months and physical examination findings of patients were recorded. Patients with and without polyneuropathy were compared with statistical methods. RESULTS: Polyneuropathy was detected in 34 (42%) of the 81 patients who participated in our study. The age, disease duration and HBA1C levels were statistically higher in the polyneuropathy group than in the control group (p=0.024, p=0.000, p=0.016). However, there was no statistically significant difference between MMSE and MoCA scores of these groups. In both groups, there were no patients scoring below the MMSE cut-off value of 24. Seventeen of the 34 patients (50%) in the polyneuropathic group and 19 (40,4%) of the 47 patients in the control group had scores below the MoCA cut-off value 21. However, there was no statistically significant difference between the two groups. We also found that the mean MoCA value of all DM patients was 21, which was the MoCA cut-off value. Also, factors affecting cognitive functions in all Type 2 DM patients were evaluated by logistic regression analysis, and it was found that duration of education was an independent factor affecting cognitive impairment (OR=8.167; p=0.001). CONCLUSION: In our study, we did not observe significant differences between MMSE and MoCA scores of Type 2 DM patients with and without polyneuropathy. However, the cross-sectional nature of our study makes it impossible to comment on this issue. To clarify whether the presence of polyneuropathy is a predictive factor in the development of cognitive impairment in Type 2 DM, there is a need for a larger sample group and long-term follow-up studies. It has also been shown that patients with Type 2 DM may have low scores according to the MOBID cut-off value even though peripheral neurologic involvement findings are not observed. In the Type 2 DM population, it has also been shown that MoCA may be affected by education level.

A database for screening and registering late onset Pompe disease in Turkey.

The aim of this study was to search for the frequency of late onset Pompe disease (LOPD) among patients who had a myopathy with unknown diagnosis registered in the pre-diagnostic part of a novel registry for LOPD within a collaborative study of neurologists working throughout Turkey. Included in the study were 350 patients older than 18 years who have a myopathic syndrome without a proven diagnosis by serum creatine kinase (CK) levels, electrodiagnostic studies, and/or muscle pathology, and/or genetic tests for myopathies other than LOPD. Acid alpha glucosidase (GAA) in dried blood spot was measured in each patient at two different university laboratories. LOPD was confirmed by mutation analysis in patients with decreased GAA levels from either both or one of the laboratories. Pre-diagnostic data, recorded by 45 investigators from 32 centers on 350 patients revealed low GAA levels in a total of 21 patients; from both laboratories in 6 and from either one of the laboratories in 15. Among them, genetic testing proved LOPD in 3 of 6 patients and 1 of 15 patients with decreased GAA levels from both or one of the laboratories respectively. Registry was transferred to Turkish Neurological Association after completion of the study for possible future use and development. Our collaborative study enabled collection of a considerable amount of data on the registry in a short time. GAA levels by dried blood spot even from two different laboratories in the same patient may not prove LOPD. LOPD seemed to be rarer in Turkey than in Europe.

Peripheral component of laryngeal and pharyngeal motor evoked potentials.

In this study, the responses of thyroarytenoid (TA) and cricopharyngeus (CP) muscles were simultaneously recorded to peripheral magnetic stimulation of the vagus nerve. Recordings were performed in 13 subjects by means of concentric needle EMG electrodes inserted in the TA and CP. Magnetic shocks were delivered to the vagus nerve with a round coil placed occipitally, while EMG was silent in the TA. In all subjects, clear-cut responses were obtained simultaneously in both muscles. In TA compared to CP, the maximum amplitude of the responses were higher, whereas the onset latency was shorter. Our results revealed that simultaneous recordings of TA and CP motor responses to occipital magnetic stimulation enabled a reliable evaluation of their peripheral innervation by the vagus nerve.

The presentation of a transient hyperintense lesion with Legionnaires disease in a patient--is it a coincidence or an incidental finding?

Up to date the presentation of transient splenial lesions in corpus callosum were reported in diffusion weighted magnetic resonance imaging (MRI) only in epileptic patients and patients under antiepileptic therapy. A 41 year old male with no previous medical history was admitted to our clinic with symptoms of pneumonia. The neurological exam revealed stupor, but when awake his speech and orientation were normal. There were no meningeal irritation signs, cranial nerves, piramidal and cerebellar functions were normal. He had moderate respiratory distress and had bilateral rales in lower lobes while on auscultation. Laboratory tests revealed high liver function levels and high acute phase reactants. Arterial blood levels showed hypoxemia. A brain MRI showed a hypointensity in the splenium of corpus callosum on T1 weighted images. There was markedly increased signal in this region on diffusion weighted imaging and hypointense on ADC. The lesion was slightly hyperintense on T2 and FLAIR weighted images. A repeat brain MRI was done 30 days after the initial study and showed a complete resolution of the splenial lesion. Transient splenial lesions can be seen due to different mechanisms in different clinical settings. It should be noted that these lesions are mostly reversible. Unnecessary therapies and procedures should be avoided in these lesions.