Javier Andrés Galnares-Olalde

BackgroundTrigeminal autonomic cephalalgias (TAC) are primary headache disorders characterized by unilateral craniofacial pain, usually periorbital or temporal, accompanied by ipsilateral autonomic symptoms such as tearing, nasal congestion, conjunctival injection, miosis, and ptosis. They include cluster headache, paroxysmal hemicrania, hemicrania continua, and short-lasting unilateral neuralgiform headache attacks (SUNCT and SUNA). Diagnosis depends on attack duration, frequency, and intensity, though clinical overlap may occur. Accurate identification is crucial, as treatment differs among subtypes. Understanding TAC pathophysiology, particularly trigeminal autonomic activation, is essential for improving diagnosis, distinguishing them from similar disorders like migraine, and optimizing therapeutic management.ResultsTrigeminal autonomic cephalalgias represent a group of rare but disabling primary headache disorders characterized by overlapping pathophysiological pathways involving the hypothalamus and trigemino-autonomic reflex. Advances in neuroimaging and neuromodulation have refined understanding of their mechanisms and expanded therapeutic options beyond traditional pharmacotherapy. Early recognition and tailored, mechanism-based interventions remain essential to improving outcomes.ConclusionsWe believe it is very important and necessary to offer a comprehensive and up-to-date review of trigeminal autonomic headaches, emphasizing their common and distinctive clinical features, the underlying neurobiological mechanisms, and current evidence-based approaches for timely diagnosis and treatment.

BackgroundMigraine is the most prevalent primary headache disorder in pregnancy, with unique clinical implications requiring specialized management approaches.ObjectiveTo provide a comprehensive review of migraine pathophysiology, clinical course, diagnosis, and management during pregnancy, postpartum, and lactation.MethodsSelective literature search of PubMed, Scopus, and Web of Science databases, complemented by AI-assisted tools (Elicit and Consensus) to ensure comprehensive coverage of emerging evidence, from 2003 to 2025.Key FindingsHormonal fluctuations drive migraine pathophysiology, with pregnancy's hormonal stability typically improving symptoms in 60-70% of women with migraine without aura during the second and third trimesters. However, migraine with aura shows less predictable improvement, and de novo attacks may occur. Maternal migraine, particularly with aura, is associated with hypertensive disorders, preterm birth, cesarean delivery, fetal growth restriction, and increased ischemic stroke risk. Psychiatric comorbidities, including depression and anxiety, are frequent and linked to poorer outcomes. Management Non-pharmacological interventions form the foundation of treatment. When pharmacological therapy is required, acetaminophen is first-line, NSAIDs may be used only in the second trimester, and sumatriptan is the safest triptan option. Preventive treatment should be reserved for severe, refractory cases, with magnesium, propranolol, and amitriptyline as evidence-based options.ConclusionMigraine during pregnancy and postpartum requires a multidisciplinary approach prioritizing safe pharmacological strategies, individualized monitoring, and lifestyle optimization to ensure optimal maternal and fetal outcomes.

Secondary headaches presenting similar clinical findings to migraine are known as migraine-like headaches. Currently, there is no broad consensus regarding their prevalence, characteristics, or underlying causes. Existing evidence is based primarily on descriptive studies and a single systematic review, with vascular, traumatic, and epileptic seizures as the most frequent causes. The aim of this systematic review was to describe and analyze secondary etiologies behind migraine-like headaches, including their epidemiological, clinical, and therapeutic characteristics. A database search of studies between 1977 and 2024 was conducted in February 2025 on EBSCO, SCOPUS, PubMed, and Web of Science using the terms “migraine-like” or “migraine mimic”. Included articles were human observational studies and case reports that documented a migraine-like headache with a diagnosed underlying cause. Articles lacking explicit causality, as well as review and experimental studies were excluded. Data on demographics, clinical features, etiology, imaging, and treatment were extracted and analyzed. Etiologies were categorized into vascular, neoplastic, traumatic, epileptic, autoimmune, infectious and others. Sensitivity analysis (SA) was performed using low-bias concern studies. Of 745 studies retrieved, 220 met inclusion criteria, totaling 4,422 patients (mean age 33.7 years, 63.4% female). Most presented severe (68.8%), unilateral (66.9%), gradual onset (56.6%) headaches with aura (52.5% and 47.8% in SA), primarily localized to frontal (29.3%) and temporal (22.8%) regions. Stroke (6.4% and 7.8% in SA), epilepsy (7.3%), and traumatic brain injury (5%) were the most frequent causes, while NSAIDs and triptans were the most common treatments (30.5 and 18.2%). After SA the associations between younger age and parietal pain (p = 0.023) and between imaging modality and etiology (p < 0.001) remained significant, where magnetic resonance imaging was predominantly used for autoimmune diseases and post-traumatic headaches frequently lacked imaging. Sudden onset and post-traumatic headaches were identified as frequent red flags. The present study findings underscore the importance of recognizing red flags in migraine-like headaches and early identification of underlying causes. Severe, sudden onset headaches alongside systemic symptoms or trauma history should prompt thorough evaluation. Future research should aim to refine the definition of migraine-like headache and to improve diagnostic precision and treatment timing in these patients.

Introduction: Low levels of Vitamin D are associated with severe manifestations of autoimmune or inflammatory diseases; there is limited information regarding Guillain-Barré Syndrome (GBS). Objective: To determine the serum levels of vitamin D in patients with GBS compared with healthy controls. Materials and Methods: A prospective observational study of consecutive patients with GBS based on EAN/PNS criteria over a year, from a single center was conducted. Clinical and paraclinical characteristics were obtained from the included patients upon admission; we determined the serum levels of Vitamin D (ng/ml) at admission and categorized them according to Vitamin D levels: sufficient >30 ng/mL, insufficient 20-30 ng/mL, and deficient P < 0.001]. Only 9% (95% CI 1-19%) of the GBS patients had sufficient levels of vitamin D. In correlation analysis, significant differences were found between Vitamin D levels and glucose levels (r2 = −.36, P = 0.007) and the glucose-leukocyte index (GLI) (r2 = −.42, P =<0.001). In comparative analysis (Vitamin D levels ≤15 ngs/ml/ vs ≥ 16 ng/mL), the presence of dysautonomias, facial diparesis, leukocytes, glucose-leukocyte index (GLI), and glucose levels were significant; in the Kaplan-Meier survival analysis, patients with Vitamin D levels ≤15 ngs/ml showed lesser recovery in independent walking at 3 months (log-rank = 0.047). Conclusion: Patients with GBS and low levels of Vitamin D exhibit a higher frequency of dysautonomias, higher GLI, and lesser recovery of independent walking.

Background: Up to 30% of patients with Guillain–Barré syndrome require mechanical ventilation and 5% die due to acute complications of mechanical ventilation. There is a considerable group of patients that will need prolonged mechanical ventilation (considered as >14 days) and should be considered for early tracheostomy. The objective of this study is to identify risk factors for prolonged mechanical ventilation.Methods: We prospectively analyzed patients with Guillain–Barré diagnosis with versus without prolonged mechanical ventilation. We considered clinical and electrophysiological characteristics and analyzed factors associated with prolonged mechanical ventilation.Results: Three hundred and three patients were included; 29% required mechanical ventilation. When comparing the groups, patients with prolonged invasive mechanical ventilation (IMV) have a lower score on the Medical Research Council score (19.5 ± 16.2 vs 27.4 ± 17.5, p = 0.03) and a higher frequency of dysautonomia (42.3% vs 19.4%, p = 0.037), as well as lower amplitudes of the distal compound muscle action potential (CMAP) of the median nerve [0.37 (RIQ 0.07–2.25) vs. 3.9 (RIQ1.2–6.4), p = p = p = 0.03, AUC of 0.774, (95%CI 0.66–0.88), p = < 0.001.Conclusions: Severe median nerve damage is an independent risk factor for prolonged mechanical ventilation.

Background:  Guillain-Barré syndrome (GBS) is the most common cause of acute flaccid paralysis worldwide. Lymphocytes and neutrophils are associated with systemic inflammation and production of proinflammatory mediators. GBS, as an autoimmune disease, elicits an upregulation in inflammatory and metabolic pathways, with increased production of lymphocytes and neutrophils. Serum markers such as the neutrophil-lymphocyte (NLR) and leuko-glycemic (LGR) ratios have been studied for the severity and prognosis of non-neurological disorders. Methods: A cross-sectional study from a prospective cohort of patients with GBS was conducted, from January 2018 to February 2021. Comparison between patients with or without ventilatory support was performed with student´s t test or Mann-Whitney U test based on distribution. Chi-square for was used for categorical variables, Fisher´s exact test was applied when necessary. A logistic regression analysis was performed. Results:  One hundred and twenty-three patients were included. Logistic regression analysis demonstrated NLI to be an independent factor for mechanical ventilation in GBS, but not for LGI and OR 2.0, respectively. Both LGI and NLI demonstrated a high performance for ventilatory support prediction, with 0.70 and 0.81, respectively. Best cut-off values, according to Youden index, are for LGI 1.12 (sensitivity 0.70, specificity 0.40) and for NLI 3.59 (sensitivity 0.78, specificity 0.33). Conclusions:  Despite the wide use of the EGRIS scale in estimating respiratory insufficiency in patients with GBS, we portray a new and easy to obtain laboratory tool that can further help non-neurologists and other clinicians to predict the risk for ventilatory support.

Background: Brain 18 FDG PET is very useful in the diagnosis of autoimmune encephalitides against post-synaptic receptors. However, little is known about the metabolic changes in other autoimmune encephalitides, such as Bickerstaff stem encephalitis (BBE). Objective: to report the case of a patient with BBE with an 18 FDG PET study and to review the literature. Results: A 20-year-old man with no relevant history presented to the emergency department due to a clinical picture of 7 days of evolution, characterized by non-painful distal paresthesias in the 4 extremities, diplopia, instability on gait and dysphagia. On the day of his hospital stay, he presented alterations in his awake state. The clinical diagnosis of Bikerstaff's stem encephalitis was made. In his paraclinical tests, the cerebrospinal fluid was normal. He received treatment with human immunoglobulin (2 grams/kg) for 5 days. An 18 FDG PET study reported hypermetabolism in the putamen and bilateral caudate nucleus and bilateral occipital hypometabolism. Conclusion: brain 18-FDG PET may be a subrogate marker for understanding CNS compromise in BBE.