Introduction. Migraine is an important cause of disability that affects the quality of life producing a substantial social impairment. Objectives. The aim of this study was to evaluate the correlation between migraine severity and comorbidities in patients with episodic migraine. Methods. 2 groups of patients were included in the study: group 1 – control group (healthy subjects, n = 50), and group 2 – study group (patients with episodic migraine attacks, n = 65). Both groups were assessed for nonmodifiable risk factors (age), and modifiable risk factors: BMI (body mass index), lipids profiles (LDL-cholesterol, HDL-cholesterol, triglycerides), inflammatory parameters (C reactive protein and fibrinogen), and endothelial dysfunction (nitric oxide synthesis expressed as NOx). The migraine was diagnosed according to ICHD-2 (International Classification of Headache Disorders) and the severity was evaluated by MIDAS (Migraine Disability Assessment Scale). The study group was compared with control group. The parameters that showed statistic significance were correlated with MIDAS scale. Results. There was a significant correlation between the severity and frequency of migraine attacks (evaluated by MIDAS scale) and BMI. The subgroup with higher inflammatory parameters and decreased NOx had an increased MIDAS score. Conclusions. The connection between obesity, inflammatory parameters and migraine may be useful for new prophylaxis potent therapies. The individual personalized therapies according with particular risk factors of each patient may be a chance for better results. Identification and control of risk factors in migraine patients may be particularly important.

Multiple sclerosis (MS) is a demyelinating disease associated with a myriad of visual pathways pathology. These pathologies need to be assessed, even when asymptomatic, because they may represent an important index of disease course, severity and treatment response. This is a review of the importance of different visual pathways assessment methods such as classic ophthalmologic examination, cerebrospinal fluid analysis, Doppler ultrasonography of the orbital vessels, magnetic resonance imaging, optical coherence tomography, visual evoked potential, evaluating which may contribute to elucidate the pathophysiological process, structural and functional damage. The modern medical technology developed multiple methods which are trying to link their results to the overall brain damage in MS. A global analysis of these methods is needed, in order to a better evaluation of visual pathways damage associated with multiple sclerosis.

Group I had higher uDPD/uCr values (p < 0.05) compared to group II and group III (40.49 ± 11.1 vs 30.7 ± 16.3 and 24.78 ± 10.54). No differences were observed in other bone markers among all groups. The dietary calcium intake was adequate (> of EAR, Estimated Average Requirement) in only 19% of children, but no differences in both LS and TB BMD were revealed. Nevertheless, children with inadequate calcium intake had significant increased (p < 0.05) ALP/ bALP, compared to the rest of patients. Summary/Conclusion: In our study, 10% of children with Haemophilia A had low for chronological age LS BMD. Severe disease and history of FVIII inhibitor seem to burden bone health, as measured with DXA. Resorption markers were found to be impaired. Homeostasis of calcium seem to overweigh low dietary intake. Severe cases, especially those with history of inhibitor, are in higher risk to develop bone metabolic disturbances; thus, close monitoring of bone status seems to be necessitated.

Introduction. Hemodynamic changes of the cerebral arteries in ophthalmic migraine may be an important pathophysiological mechanism of the disease. The nitric oxide (NO) synthesis plays a significant role in hemodynamic changes due to vasodilatation effect. The purpose of this study is to evaluate the possible hemodynamic changes by Doppler measurements and their correlation with NO synthesis in ophthalmic migraine. Method. 37 ophthalmic migraine patients were compared with 35 healthy volunteers. Other cerebral and ophthalmic diseases were excluded by ophthalmological, neurological, and cranial MRI examinations. The migraine assessment scale (MIDAS) was used for clinical evaluation. Transcranial Doppler ultrasonography (TCD) was performed using 2 and 4 MHz frequencies transducers. The flow velocities of the internal carotid artery, middle cerebral artery, posterior cerebral artery, and NO plasma concentration were assessed 2 hours after migraine attacks. Results. The NO synthesis was significantly increased compared to the control group. The flow velocities decreased in internal carotid artery, middle cerebral artery, and posterior cerebral artery. The correlation between decreased flow velocities and NO plasma concentration was significant. Conclusions. Autonomic nervous system dysfunction in ophthalmic migraine is an important pathophysiological mechanism. The flow velocity status may reflect the vasomotor response and endothelial reactivity induced by NO synthesis. Further studies on the vasomotor response are necessary for the evaluation of this pathophysiological mechanism implication in ophthalmic migraine.

Traumatic vertebral artery (VA) dissection is a severe consequence of a cervical injury, which usually involves the vertebrae and spinal cord. Traumatic VA dissection has been frequently underdiagnosed or misdiagnosed, mainly because many patients remain asymptomatic. The consequence of VA dissection is ischemia in the territory supplied by the affected artery. The VA dissection presents most often as a vertebrobasilary transient ischemic attack or ischemic stroke, usually preceded by local symptoms such as neck pain or headache. Headache is a common symptom in patients with cervical artery dissection, but its characters are not specific. Diagnosis of VA dissection usually requires a CT-angiography. Delayed onset of symptoms with a variable asymptomatic interval, ranging from several days to 3 months, has been reported. The risk of stroke remains high, especially in the first weeks after the confirmation of VA dissection. Treatment of traumatic VA dissections include anticoagulation or antiplatelet therapy and revascularization techniques. We present the case of a patient with spinal cord injury and operated C5 fracture, who was diagnosed with unilateral VA dissection 6 months after the traumatic event, during the rehabilitation program.