Binge eating disorder (BED) is characterized by recurrent episodes of excessive intake within a limited time period, accompanied by loss of control and distress. These behaviors may overstimulate and desensitize the dopaminergic system, leading to the search for palatable foods to reactivate a hypofunctional reward circuit. Dopamine release activates GABAergic pathways, which exert inhibitory control by reducing dopamine release, suggesting that this system may be altered in the context of BED. The objective of this systematic review was to gather research conducted between 2013 and 2023 on GABAergic functioning in eating behavior and binge episodes, focusing exclusively on rodent models (rats and mice). The review followed PRISMA 2020 guidelines, using ScienceDirect and PubMed as data sources. The initial search yielded 488 results. After screening, 23 articles were selected, and five met the inclusion criteria. Of these, 60% (n = 3) were conducted in mice and 40% (n = 2) in rats. In 80% of cases (n = 4), only male animals were used, while 20% (n = 1) included both sexes. Likewise, 80% (n = 4) used adult animals, and 20% (n = 1) did not report age. Contradictory results emerged regarding GABA involvement in feeding behavior: some studies showed increased intake associated with both lower and higher GABAergic activation, while others reported the opposite pattern. These inconsistencies may reflect interactions between distinct neuroanatomical regions and procedural differences. Most studies focused on general food intake modulation rather than binge-specific behaviors, limiting the direct applicability of findings to BED.
Guillain-Barr & eacute; syndrome (GBS) is the leading cause of flaccid paralysis and significantly affects functionality and health-related quality of life (HRQoL). While disability and muscle strength scales remain standard for assessing recovery, HRQoL offers a broader perspective by integrating physical, emotional, and social aspects often overlooked in clinical practice. The objective of this review is to synthesize current evidence on the tools used to assess HRQoL in patients with GBS and to analyze demographic, clinical, and paraclinical factors associated with outcomes. Longitudinal studies indicate that HRQoL is most impaired during hospitalization and early recovery, with gradual improvement over time. Worse HRQoL is associated with advanced age, prolonged mechanical ventilation, dysautonomia, sensory deficits, high disability scores, axonal variants, urinary dysfunction, depression, and post-traumatic stress disorder. Overall, the evidence highlights the need for a disease-specific HRQoL instrument and longitudinal studies to enable accurate evaluation and guide targeted interventions that improve long-term outcomes in GBS patients.
Objective: To describe clinical features, diagnostic challenges, and therapeutic response of diabetic striatopathy in Latin American patients, an underrepresented population in current literature, and to highlight the importance of early recognition and interdisciplinary collaboration in improving diagnosis and management. Methods: Case series of two Latin American women with poorly controlled type 2 diabetes mellitus who developed hyperkinetic movement disorders. Clinical presentation, neuroimaging findings, diagnostic approach, and clinical outcomes following metabolic and symptomatic treatment were analyzed. Results: One patient presented with acute-onset chorea accompanied by pain and hypoesthesia, with striatal hyperdensity on computed tomography and T1 hyperintensity on magnetic resonance imaging, achieving complete symptom resolution within 48 hours after intensive insulin therapy. The second patient developed progressive choreiform movements, initially misdiagnosed as epilepsy, without response to antiepileptic drugs. Neuroimaging confirmed diabetic striatopathy; insulin therapy produced partial improvement, and adjunctive haloperidol reduced movement severity, with residual symptoms at discharge. Both cases demonstrated characteristic imaging findings despite distinct clinical phenotypes. Conclusions: Diabetic striatopathy shows heterogeneous clinical presentations and may mimic other neurological disorders, leading to diagnostic delays. Early recognition and prompt glycemic control are essential, although treatment response varies and may require individualized management strategies.
The determination of brain death or death by neurological criteria (BD/DNC) typically relies on clinical assessment: coma, absence of brainstem reflexes, and apnea. However, in cases with primary posterior fossa lesions, clinical criteria alone may be insufficient. Unlike supratentorial injuries, these lesions can selectively impair brainstem function without causing global cerebral circulatory arrest or significantly increasing intracranial pressure. As a result, patients may retain cerebral blood flow (CBF) and electroencephalogram (EEG) activity despite meeting clinical BD/DNC criteria. In such cases, confirmatory tests are not discretionary but diagnostically essential. Evaluations of bioelectrical activity (e.g., EEG and evoked potentials) and CBF (e.g., transcranial Doppler, computed tomography angiography, and radionuclide imaging) provide critical confirmation, reducing diagnostic errors and supporting ethical and legal standards. Clinical cases, including the widely known case of Jahi McMath, highlight the risks of declaring brain death without confirmatory confirmation in posterior fossa injuries. Therefore, BD/DNC protocols must be updated to require confirmatory testing when posterior fossa pathology is present, when clinical findings are unclear, or when a comprehensive examination is not feasible. This clinical viewpoint, accompanied by a literature synthesis, calls for an urgent revision of protocols, enhanced clinician education, and institutional preparedness to ensure that brain death determinations remain accurate, ethical, and credible.
