Background: The impact of Levodopa on the gut microbiota of Parkinson's disease (PD) patients has not been sufficiently addressed.Methods: We conducted a longitudinal study to examine the impact of Levodopa initiation on the gut microbiota composition of 19 PD patients who had not previously been exposed to Levodopa. Patients provided two stool samples prior to and two samples 90 days after starting Levodopa. Motor impairment (MDS-UPDRS Part III), diet, and other patient characteristics were assessed. 16S rRNA gene amplicon sequencing was used to characterize the microbiota. We examined, cross-sectionally and longitudinally, the associations between Levodopa use and alpha and beta diversity and performed feature-wise, multivariate modeling to identify taxa associated longitudinally with Levodopa use and with improvement in motor function after Levodopa administration.Results: We did not observe significant differences in alpha or beta diversity before vs. after initiation of Levodopa. In longitudinal feature-wise analyses, at the genus level, no taxa were significantly associated with Levodopa use after false discovery rate (FDR) correction (q < 0.05). We observed a marginally lower relative abundance of bacteria belonging to Clostridium group IV in PD patients who experienced a medium or large improvement in motor impairment in response to Levodopa compared to those with a small response [β = −0.64 (SE: 0.18), p-trend: 0.00015 p-FDR: 0.019].Conclusions: In this study, Levodopa was not associated with changes in microbiota composition in this longitudinal analysis. The association between abundance of Clostridium group IV and short-term motor symptom response to Levodopa is preliminary and should be investigated in larger, longer-term studies, that include a control group.
There are only six cases in literature that describe development of dystonia with Sjogren's syndrome (SS). We describe a case of a 43-year-old woman who presented with symptoms including movement disorder, sensory neurogenic bladder, sensory loss and neuropathic pain, migraine like headaches, musculoskeletal pain, Raynaud's phenomenon and dysautonomia. Symptoms started in 2000, with weakness that progressed to dystonia in 2003. Diagnostic work-up was inconclusive with negative inflammatory serologies, cerebrospinal fluid and MRI for many years. After patient developed sicca syndrome with dry eyes and mouth in 2009, her rheumatoid factor titre was elevated (550 IU/mL), erythrocyte sedimentation rate, anti-Sjogrens syndrome-related antigen A (anti-Ro/SSA) and anti-SSB/La: anti-Sjogrens syndrome-related antigen B (anti-La/SSB) became positive. Lip biopsy confirmed diagnosis of SS. She was diagnosed with primary SS with neurological involvement. Her symptoms responded well to intravenous methylprednisolone. Symptoms stabilised with trials of immune-suppressive therapy. This is a case that demonstrates the delay of diagnosing SS with preceding unique neurological association.
Background: Hydrocephalus is a common complication in patients with aneurysmal subarachnoid hemorrhage (aSAH) and is one of the predictors of poor outcome. Currently the only treatment modality for hydrocephalus is shunting; there is no known prophylactic therapy. Limited pre-clinical data suggest that anti-inflammatory effect of steroids could be used to prevent arachnoiditis and subarachnoid fibrosis after aSAH, which in turn may reduce the rate of hydrocephalus that requires shunting. Methods: A retrospective study of patients with aSAH admitted to two tertiary care centers from 2009 to 2017 was performed. Age, sex, hypertension, Glasgow coma scale [GCS], Hunt Hess [HH] grade, administration of steroids (dexamethasone [DXM], methylprednisolone [MTP] or none), presence of hydrocephalus and ventriculoperitoneal shunt (VPS) as well as occurrence of adverse events such as hyperglycemia, delirium and infection were recorded for each patient. Results: A total number of 288 patients were included. Mean age was 56.9±13.9 years, 186 (64.6%) patients were female and 145 (50.5%) patients had hypertension. Median GCS score was 14 (IQR 7-15) and median HH grade was 3 (IQR 2-4). 204 (71%) patients received DXM, 23 (8%) patients received MTP and 61 (21%) patients were not administered any steroids during hospital stay. Hydrocephalus was present in 114 (56.4%) patients who received DXM, 13 (56.5%) who received MTP and 37 (61.6%) who did not receive steroids (p>0.05; χ 2 -test). The incidence of VPS placement did not differ between the groups (p>0.05; χ 2 -test). Patients who received steroids were more likely to develop pneumonia (63 [31%] vs. 7 [31.8%] vs. 5 [8.2%] in DMX, MTP and no steroids group, respectively; p=0.008; χ 2 -test). Patients who received DXM (but not MTP) more frequently were treated for a urinary tract infection (48 [23.5%] vs. 6 [9.8%]; p=0.019; χ 2 -test). There was no difference in the ratio of hyperglycemia or delirium between the groups. Conclusion: Our results support the evidence that, although commonly used in clinical practice, steroids administered in patients with aSAH do not decrease the risk of developing hydrocephalus and subsequent VPS. In addition, steroids may increase the risk of infections such as pneumonia and urinary tract infection.
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