In patients with SVD, independent predictors of VCI were baseline severity of WMH and total number of lacunar infarcts.

Baseline functional status and severity of WMH and development of cognitive decline predict the occurence of late-onset depression in patients with SVD.

Cluster headache (CH) is characterized by attacks of severe, strictly unilateral pain that is orbital, supraorbital, temporal, or any combination of these, lasts 15-180 min, and occurs from once every other day to eight times a day. The pain is associated with ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, miosis, ptosis and/or eyelid edema, and/or with restlessness or agitation. The understanding of the pathophysiological mechanisms behind CH is far from complete, but CH is considered to be a neurovascular and chronobiologic headache disorder, with a pivotal role played by the central brain mechanisms. The diagnosis of CH is based on a careful history that elicits the clinical features of attacks, ipsilateral autonomic phenomena, and the cyclical nature of the bouts in which the attacks occur. Additional diagnostic interventions are needed to rule out secondary causes of CH. The main focus of therapy is to abort attacks once they have begun and to prevent future attacks. Alternative interventions in patients with CH who have not experienced any meaningful benefit from preventive drugs are well defined. Although there have been advances in the diagnosis and therapy of CH, a significant number of CH patients experience misdiagnoses and diagnostic delay, which stalls the possibility of the timely application of adequate abortive and preventive therapy.

Although cerebral small vessel disease (SVD) is traditionally associated with aging and hypertension (HT), there are patients exhibiting sporadic SVD, free of HT. We aimed to investigate the differences in clinical and neuroradiological presentation in SVD patients in reference to the presence of HT as a risk factor (RF). Vascular RF, cognitive and functional status were evaluated in a cohort of 424 patients. Patients were classified in two groups based on the presence of HT. Severity of vascular lesions was assessed using 1.5 T magnetic resonance imaging with Age-Related White Matter Changes scale total score (tARWMC) and Fazekas scale periventricular (PV) and deep subcortical (DS) scores. No difference between groups in age and sex distribution was noted. In univariate analysis, HT was associated with vascular cognitive impairment (vCI) (OR 2.30, 1.53-3.45, P < 0.0001), functional status (OR 1.47, 1.11-1.95, P = 0.007), depression (OR 2.13, 1.23-3.70, P = 0.007), tARWMC (OR 1.10, 1.05-1.16 95% CI, P < 0.0001), Fazekas PV score (OR 1.34, 1.08-1.67 95% CI, P = 0.008), Fazekas DS score (OR 1.95, 1.44-2.63 95% CI, P < 0.0001) and total number of lacunes (OR 1.10, 1.02-1.18 95% CI, P = 0.009). Multivariate logistic regression analysis indicated that HT was an independent RF for vCI (OR 1.74, 1.09-2.76 95% CI, P = 0.020) and higher Fazekas DS score (OR 1.57, 1.11-2.22 95% CI, P = 0.011). The Kaplan-Meier curve of estimates of survival of SVD patients without vCI revealed a higher proportion of patients with HT progressing to vCI over time when compared to HT-free cases. In patients with sporadic SVD, HT is a contributing factor to worse clinical outcomes and neuroradiological presentation.