Neuropathy in Parkinson's disease patients with intestinal levodopa infusion versus oral drugs.

BACKGROUND: Severe polyneuropathy has been observed in a number of patients treated for Parkinson's disease with Levodopa/Carbidopa intestinal gel infusion. This may reflect a rare individual complication or a systematic side effect. OBJECTIVE: To investigate whether peripheral nerve function differed between patients with oral treatment versus Levodopa/Carbidopa intestinal gel infusion. METHODS: In an observational design, data from median, tibial, and peroneal neurography were prospectively assessed and compared between patients with conventional drug treatment (n = 15) and with Levodopa/Carbidopa intestinal gel infusion (n = 15). The groups were matched for age and disease duration. In view of the medical risk profile for polyneuropathy, comorbidity and basic serological parameters were assessed. RESULTS: Axonal neuropathy was common in both patient groups. However, although group differences in risk factors for polyneuropathy were not evident, neurographic abnormalities were more severe in the patients treated with Levodopa/Carbidopa intestinal gel infusion than in the orally treated patients. In the group with Levodopa/Carbidopa intestinal gel infusion, the degree of neuropathic change correlated with weight lost since therapy initiation and with the drug dose. In contrast to the axonal abnormalities, conduction velocity was found normal in both groups. CONCLUSION: The results are compatible with the promotion of axonal neuropathy by Levodopa/Carbidopa intestinal gel infusion. This could be due to the intrinsically high levodopa doses associated with the therapy and/or malnutritional effects from intestinal drug application. The results should be corroborated by a larger longitudinal and controlled trial

Preserved Responsiveness of Secondary Somatosensory Cortex in Patients with Thalamic Stroke

Cortical representations may change when somatosensory input is altered. Here, we investigated the functional consequences of partial ‘‘central’ ’ deafferentation of the somatosensory cortex due to a lesion of the ventroposterior lateral nucleus (VPL) in patients at a chronic stage after solitary infarction of the thalamus. Event-related functional magnetic resonance imaging during electrical index finger stimulation of the affected and nonaffected side was performed in 6 patients exhibiting contralesional sensory deficits (mainly hypesthesia). Involvement of the VPL and additional nuclei was determined by high-resolution magnetic resonance imaging (MRI) and subsequent MRI-to-atlas coregistration. For the group, statistical parametric maps showed a reduced activation of contralateral primary somatosensory cortex (SI) in response to stimulation of the affected side. However, no significant difference in the activation of contralateral secondary somatosensory cortex (SII) compared with stimulation of the nonaffected side was detected. Correspondingly, the ratio of SII-to-SI activation for the ipsilesional hemisphere was markedly elevated as compared with the contralesional hemisphere. For preserved responsiveness of SII in thalamic stroke comparable with that of the contralesional hemisphere, possible explanations are a direct thalamocortical input to SII mediating parallel information processing, nonlinear response behavior of SII in serial processing, or reorganizational processes that evolved over time

Effects of Laparoscopic Gastric Band Applications on Plasma and Fundic Acylated Ghrelin Levels in Morbidly Obese Patients

It has been proposed that laparoscopic adjustable gastric banding (LAGB) procedure might play a role in modulation of fundic ghrelin production. To test this hypothesis, we examined plasma and tissue concentrations of acylated ghrelin in morbidly obese patients before and 6 months after LAGB. Baseline levels of acylated ghrelin in morbidly obese patients were also compared with those in age-matched, healthy, non-obese controls

Correlation of daily levodopa dose and the number of neurographically impaired nerves.

<p>The daily levodopa dose is indicated on the abscissa, the number of neurographically impaired nerves on the ordinate. Triangles and dots reflect the values of the orally treated and LCIG patients respectively. The regression line is provided for the data from the LCIG group for which the correlation coefficient (r) was significantly higher than in the orally treated group.</p

Correlations between the number of impaired nerves and patient parameters.

<p>The first two data columns provide the correlation values per parameter in each group. The last column indicates the p-values for the comparisons of the correlation coefficients between the groups (reflecting the probability of erroneously assuming distinct correlations in LCIG versus orally treated patients).</p><p>LD: levodopa dose.</p><p>LED: levodopa equivalence dose.</p><p>numbers: Spearman rank correlation (with asterisk: p<0.05).</p><p>Δ (p-value): probability of erroneously assuming different correlations between the groups.</p

Laboratory results in LCIG and orally treated patients.

<p>ESR: erythrocyte sedimentation rate; HbA₁c: glycated haemoglobin, TSH: thyroid-stimulating hormone; ALT: alanine transaminase, AST: aspartate transaminase; GGT: gamma-glutamyltransferase; ANA: anti-nuclear antibodies last column: p-values for group comparisons per parameter Data provided as mean values ± standard deviation.</p