Prevalence and Characteristics of Symptomatic Intracranial Atherosclerotic Plaques in People Residing at Middle and High Altitudes: A Preliminary Study.

BACKGROUND: This study aims to determine how atherosclerotic plaque prevalence and characteristics vary between individuals residing year-round at middle and high altitudes who have intracranial atherosclerotic disease. METHODS: We conducted a retrospective analysis of patient data from our hospital, focusing on individuals with cerebrovascular symptoms who underwent high-resolution vessel wall imaging (HR-VWI). Patients who had lived at an altitude of <2500 meters for an extended period were classified in group A (n = 91), while those residing at an altitude of ≥2500 meters were placed in group B (n = 75). We examined the differences in plaque prevalence and characteristics between these two groups. RESULTS: The detection rate of basilar artery plaque was higher in group A compared to group B (16% vs. 7.6%, p = 0.036). Conversely, the detection rate of anterior cerebral artery plaque was significantly lower in group A than in group B (4% vs. 11.8%, p = 0.016). The eccentricity index (EI) was greater in group B than in group A (0.72 ± 0.11 vs. 0.68 ± 0.12, p = 0.012). The prevalence of intraplaque hemorrhage (IPH) was lower in group B than in group A (39.5% vs. 58.7%, p = 0.002). CONCLUSIONS: IPH prevalence was lower in patients residing at high altitudes than in those residing at middle altitudes. However, patients living at high altitudes had a higher EI compared to those residing at middle altitudes. These findings underscore the presence of disparities in the prevalence and characteristics of intracranial atherosclerotic plaques between individuals residing at medium and high altitudes. It is essential to account for these distinctions when diagnosing plaques.

Cerebral Edema in Chronic Mountain Sickness: a New Finding.

We observed patients with chronic mountain sickness (CMS) in our clinic who developed progressive neurological deterioration (encephalopathy) and we wished to investigate this. We studied nine such CMS patients, and compared them to 21 CMS patients without encephalopathy, and to 15 healthy control subjects without CMS. All 45 subjects lived permanently at 3200-4000 m. Measurements at 2260 m included CMS symptom score, multi-slice CT, perfusion CT, pulse oximetry (SpO2%), and hemoglobin concentration (Hb). One patient had MRI imaging but not CT; 5 had CSF pressure measurements. CMS subjects had lower SpO2, higher Hb, higher brain blood density, lower mean cerebral blood flow (CBF), and significant cerebral circulatory delay compared to controls. The nine CMS subjects with neurological deterioration showed diffuse cerebral edema on imaging and more deranged cerebral hemodynamics. CSF pressure was elevated in those with edema. We conclude that cerebral edema, a previously unrecognized complication, may develop in CMS patients and cause encephalopathy. Contributing factors appear to be exaggerated polycythemia and hypoxemia, and lower and sluggish CBF compared to CMS patients without cerebral edema; but what triggers this complication is unknown. Recognition and treatment of this serious complication will help reduce morbidity and mortality from CMS.