(1) Background: Increased attention has lately been given to polyneuropathy in Parkinson’s Disease (PD). Several papers postulated that large-fiber neuropathy (PNP) in PD is related to vitamin B12 deficiency and L-Dopa exposure. (2) Methods: Using a cross-sectional, observational study, we evaluated 73 PD patients without a previously known cause of PNP using clinical scores (UPDRS II and III and Toronto Clinical Scoring System), biological evaluation of vitamin B12 and folic acid, and nerve conduction studies to assess the prevalence and features of PNP. (3) Results: The prevalence of PNP was 49.3% in the study group. In the L-Dopa group, the frequency of PNP was 67.3% as compared to PNP in the non-L-Dopa group, where one subject had PNP (χ2 = 23.41, p < 0.01). PNP was predominantly sensory with mild to moderate axonal loss. Cyanocobalamin correlated with L-Dopa daily dose (r = −0.287, p < 0.05) and L-Dopa duration of administration (r = −0.316, p < 0.05). L-Dopa daily dose correlated with the amplitudes of sensory nerve action potentials of the superficial peroneal and radial nerves (r = −0.312, p < 0.05) (r = −0.336, p < 0.05), respectively. (4) Conclusions: PNP is more frequent in L-Dopa-treated patients than in L-Dopa-naïve patients. The results imply that longer exposure to high doses of L-Dopa may cause vitamin B12 and folate imbalance and PNP, secondarily.

background. Recent studies described a higher prevalence of peripheral neuropathy (PN) in Parkinson's disease that was linked to L-Dopa exposure. Peripheral neuropathies are known causes of a decreased health-related quality of life (HrQoL). Until now, no studies addressed the issue of how or if associated PN in PD affects HrQoL. Methods. In a cross-sectional, observational study, 73 non-demented PD patients, from which 36 with confirmed PN based on clinical (using the Toronto Clinical Neuropathy Scale-TCSS) and nerve conduction studies completed the Romanian version of PDQ-39. results. Significant differences between mean scores in Motor (49.86 (27.61) vs. 31.50 (26.24), p = 0.005), Activities of daily living (49.86 (27.61) vs. 31.75 (30.10), p = 0.003) and body discomfort (52.54 (29.54) vs. 23.64 (18.48), p = 0.002) domains of PDQ-39 in the PN-PD group versus non-PN group were observed. TCSS significantly correlated to motor, emotional well-being and body discomfort domains (r = 0.406 p< 0.001; r = 0.316 p = 0.007; r = 0.356 p = 0.002, respectively). The multivariate linear regression model showed that motor impairment and PN correlated to motor domain (beta = 0.601, p = 0.000; beta = 0.211 p = 0.041, respectively) and PN significantly correlated to body discomfort domain (beta = 0.314, p = 0.020) of PDQ-39. conclusions. The presence of associated PN in PD determines a further deterioration of HrQol in subjects with already a poorer HrQol.

Gayet-Wernicke encephalopathy is an acute neuropsychiatric condition caused by thiamine deficiency. Only a small percentage of patients experience all three symptoms, with ophtalmoplegia, ataxia and confusion, and the full triad occurs more frequently among those who have overused alcohol. The evolution is toward full recovery, Korsakoff syndrome, dementia or death. We present the case of a 56-year-old patient, known with a diagnostic of alcoholism, who was admitted for a complicated withdrawal syndrome with delirium and who developed encephalopathy and dementia syndrome.

Rasmunssen encephalitis is a rare disease characterized by focal cortical inflammation with progressive extension and diffusion. Clinical features are continuous partial epilepsy non responsive to usual anti-epileptic therapy and unilateral motor deficit, corresponding with the IRM imaging to cerebral hemiatrophy. The disease mainly affects children but there are some acknowledged cases described in adolescent and adult life. This report aims to present a clinical case of a young female with seven years personal history of generalized epilepsy. Having a clinical and paraclinical evolution a suspicion of chronic focal Rasmunssen encephalitis took shape. During admission she suffered of weakness and involuntary movements in her left side, which gradually worsened in the last month and memory impairment also. Routine laboratory blood evaluation, inflammatory and infectious tests were within the normal range. Magnetic resonance imaging of the brain reveals T2 atrophy of the right cerebral hemisphere with a low displacement of median structures to the left and an abnormal hyper intensity signal on T2-weighted, along with FLAIR images. Electroencephalography showed a profoundly altered, slowed, asymmetrically with paroxysmal unilateral right slow activity record with high amplitude. Based on clinical criteria, MRI imaging and EEG we supported the diagnosis of Rassmunsen encephalitis.