Retinal and peripapillary vascular density in episodic and chronic migraine cases without aura.

BACKGROUND: Migraine is a neurovascular disease that can cause ocular and systemic ischemic damage. Despite from aura, a limited number of studies have considered the effect of the chronic migraine in cases without aura. Our aim was to evaluate the differences in the retinal and optic disk microvasculature among episodic and chronic migraine cases without aura using optical coherence tomography angiography (OCTA) imaging. METHODS: 45 cases with migraine, and 25 control subjects were included in this prospective, cross-sectional study. OCTA was performed at 3 × 3 mm and 6 × 6 mm of the macula and at 4.5 × 4.5 mm of the optic disk. Retinal nerve fiber layer (RNFL) thickness, ganglion cell complex thickness, and vessel densities of the optic nerve and macula were compared among the three groups: a control group, an episodic migraine without aura (EMWOA) group, and a chronic migraine without aura (CMWOA) group. RESULTS: In EMWOA group, circumpapillary vascular density (cpVD) was not decreased significantly in any quadrants (all, p>0.05). Compared to the control group, CMWOA group had significantly lower RNFL thickness in superior-temporal quadrants (p = 0.002 and 0.006, respectively), while cpVD differed only in the temporal quadrant and temporal inferior sector (p = 0.002 and p = 0.009, respectively). CONCLUSIONS: Temporal peripapillary perfusion is valuable in the follow-up of chronic migraine cases. Longitudinal studies are needed to determine the place of OCTA in the follow-up of migraine.

Analysis of determinants of treatment change in adult paediatric-onset MS patients.

BACKGROUND: Paediatric-onset multiple sclerosis (POMS) is increasing worldwide and represents approximately 5% of all MS cases. Although this patient group has similar characteristics to the adult group, it is important for this patient group to receive effective treatment due to the early onset of cognitive involvement, higher lesion burden, and secondary progression at an earlier age than adults. In this study, we aimed to evaluate the factors that cause treatment change in POMS patients. MATERIAL AND METHOD: Adult patients with a first MS attack at age 18 years or younger who were followed up with the diagnosis of MS at the Clinical Neuroimmunology and Demyelinating Diseases outpatient clinic of Cerrahpasa Medical School between 1987 and 2020 were included in our study. Patient files were reviewed retrospectively, and demographic and clinical characteristics, imaging, first attack characteristics, and treatment change were noted. We included 269 patients with a definite diagnosis of MS in the study, and these patients were evaluated in two groups: negative for treatment change and positive for treatment change. RESULTS: Multifocal involvement was detected more frequently in the group with treatment change (p = 0,049). Cerebellar involvement as a first attack symptom was more common in male patients (p = 0,023) The age at first MS attack was found to be younger (p = 0,006), and the disease duration was longer in the positive for treatment change group (p = 0,003). Spinal cord involvement was more common in the positive for treatment change group (p = 0,016). Abnormal VEP findings were observed more frequently in the group without treatment change (p = 0.018). In multivariant analysis, spinal cord involvement, younger age at first attack, and abnormal VEP findings in the group without treatment change were found to be significant. Among the reasons for treatment change, the most common reason was radiological and clinical progression. CONCLUSION: The higher inflammatory load in POMS patients compared with adults necessitates early initiation of treatment in this group and timely treatment change to prevent disability. Furthermore, this patient group should be followed closely and receive effective treatment.

Analysis of neurology consultations in hospitalized patients with COVID-19.

OBJECTIVE: The aim of this study was to evaluate patients who were hospitalized with a diagnosis of COVID-19 and were consulted by neurology during their hospital stay. METHODS: All files of patients with COVID-19 who were admitted to Cerrahpasa Medical Faculty Hospital between March 11th and December 31st, 2020 were retrospectively reviewed, and files of patients who consulted by neurology during their stay were included. Demographic and clinical characteristics, neurologic diagnosis, outcome and related laboratory data were extracted from electronic medical records and analyzed. Patients were categorized into the first wave and second wave according to the date of hospitalization. RESULTS: A total of 2257 patients were hospitalized for COVID-19; among them, 127 were consulted by a neurologist during their hospital stay. Fifteen patients received a consultation for possible drug interactions. Among the remaining 112 patients, the reason for neurology consultation was i. exacerbation of a neurological comorbidity vs ii. new-onset neurological manifestations. The median age was 68.5 ± 14.2 years, and 60.7% were men. Dementia and stroke were the leading neurological comorbidities. COVID-19 disease was more severe in the patients with the new-onset neurological comorbidity than in patients with exacerbation of a neurological comorbidity (p = 0.07). Serum creatinine kinase levels were higher in the new-onset patient group (p < 0.05). Exacerbation of previous neurological disease or new neurological impairment were jointly and severely related to high mortality (overall 35/112 vs 275/2145, p < 0.001; exacerbation 12/45 vs 275/2145 p < 0.01; new-onset 23/67 vs 275/2145, p < 0.001). CONCLUSION: Serious neurological involvement is relatively uncommon in hospitalized patients with COVID-19 and is associated with increased mortality.

Altered Transcriptional Profile of Mitochondrial DNA-Encoded OXPHOS Subunits, Mitochondria Quality Control Genes, and Intracellular ATP Levels in Blood Samples of Patients with Parkinson's Disease.

Mitochondrial dysfunctions are significant contributors to neurodegeneration. One result or a cause of mitochondrial dysfunction might be the disruption of mtDNA transcription. Limited data indicated an altered expression of mtDNA encoded transcripts in Alzheimer's disease (AD) or Parkinson's disease (PD). The number of mitochondria is high in cells with a high energy demand, such as muscle or nerve cells. AD or PD involves increased risk of cardiomyopathy, suggesting that mitochondrial dysfunction might be systemic. If it is systemic, we should observe it in different cell types. Given that, we wanted to investigate any disruption in the regulation of mtDNA encoded gene expression in addition to PINK1, PARKIN, and ATP levels in peripheral blood samples of PD cases who are affected by a neurodegenerative disorder that is very well known by its mitochondrial aspects. Our results showed for the first time that: 1) age of onset > 50 PD sporadic (PDS) cases: mtDNA transcription and quality control genes were affected; 2) age of onset <50 PDS cases: only mtDNA transcription was affected; and 3) PD cases with familial background: only quality control genes were affected. mtDNA copy number was not a confounder. Intracellular ATP levels of PD case subgroups were significantly higher than those of healthy subjects. We suggest that a systemic dysregulation of transcription of mtDNA or mitochondrial quality control genes might result in the development of a sporadic form of the disease. Additionally, ATP elevation might be an independent compensatory and response mechanism. Hyperactive cells in AD and PD require further investigation.