Acute mountain sickness occurring with corpus callosum, globus pallidus and cerebellar peduncle involvement: MRI findings (original) (raw)
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No evidence of cerebral oedema in severe acute mountain sickness
Cephalalgia, 2004
In a randomized, double-blind cross-over study 10 subjects were exposed to a simulated altitude of 4500 m for 10 h after administration of placebo, acetozolamide (250 mg bid) or theophylline (250 mg bid). T2-weighted magnetic resonances images (MRI) and diffusion weighted MRI were obtained directly after exposure to altitude under hypoxic conditions. Although eight of 10 subjects had moderate to severe acute mountain sickness (AMS), we found no evidence of cerebral oedema, irrespective of the medication taken. Almost all subjects showed a decrease in inner cerebrospinal fluid (iCSF) volumes (placebo -10.3%, P = 0.02; acetazolamide -13.2%, P = 0.008, theophylline -12.2%, n.s.). There was no correlation between AMS symptoms and fluid shift. However, we found a significantly positive correlation of large ( > 10 ml) iCSF volume and more severe AMS after administration of placebo ( r = 0.76, P = 0.01). Moderate to severe AMS after high altitude exposure for 10 h is associated with a decreased iCSF-volume independent of AMS severity or medication without signs of cerebral oedema. ᎠHigh altitude, acute mountain sickness, cerebral oedema, diffusion weighted imaging
Cerebral Edema in Chronic Mountain Sickness: a New Finding
Scientific reports, 2017
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 ...
PLoS ONE, 2012
Acute mountain sickness (AMS) is a common condition among non-acclimatized individuals ascending to high altitude. However, the underlying mechanisms causing the symptoms of AMS are still unknown. It has been suggested that AMS is a mild form of high-altitude cerebral edema both sharing a common pathophysiological mechanism. We hypothesized that brain swelling and consequently AMS development is more pronounced when subjects exercise in hypoxia compared to resting conditions. Twenty males were studied before and after an eight hour passive (PHE) and active (plus exercise) hypoxic exposure (AHE) (F i O 2 = 11.0%, P i O 2 ,80 mmHg). Cerebral edema formation was investigated with a 1.5 Tesla magnetic resonance scanner and analyzed by voxel based morphometry (VBM), AMS was assessed using the Lake Louise Score. During PHE and AHE AMS was diagnosed in 50% and 70% of participants, respectively (p.0.05). While PHE slightly increased gray and white matter volume and the apparent diffusion coefficient, these changes were clearly more pronounced during AHE but were unrelated to AMS. In conclusion, our findings indicate that rest and especially exercise in normobaric hypoxia are associated with accumulation of water in the extracellular space, however independent of AMS development. Thus, it is suggested that AMS and HACE do not share a common pathophysiological mechanism.
High-altitude cerebral edema: its own entity or end-stage acute mountain sickness?
Journal of Applied Physiology
High-altitude cerebral edema (HACE) and acute mountain sickness (AMS) are neuropathologies associated with rapid exposure to hypoxia. However, speculation remains regarding the exact etiology of both HACE and AMS and whether they share a common mechanistic pathology. This review outlines the basic principles of HACE development, highlighting how edema could develop from 1) a progression from cytotoxic swelling to ionic edema or 2) permeation of the blood brain barrier (BBB) with or without ionic edema. Thereafter, discussion turns to the available neuroimaging literature in the context of cytotoxic, ionic, or vasogenic edema in both HACE and AMS. Although HACE is clearly caused by an increase in brain water of ionic and/or vasogenic origin, there is very little evidence that this type of edema is present when AMS develops. However, cerebral vasodilation, increased intracranial blood volume, and concomitant intracranial fluid shifts from the extracellular to the intracellular space, ...
Acute Mountain Sickness: Pathophysiology, Prevention, and Treatment
Progress in Cardiovascular Diseases, 2010
Barometric pressure falls with increasing altitude and consequently there is a reduction in the partial pressure of oxygen resulting in a hypoxic challenge to any individual ascending to altitude. A spectrum of high altitude illnesses can occur when the hypoxic stress outstrips the subject's ability to acclimatize. Acute altitude-related problems consist of the common syndrome of acute mountain sickness, which is relatively benign and usually self-limiting, and the rarer, more serious syndromes of high-altitude cerebral edema and high-altitude pulmonary edema. A common feature of acute altitude illness is rapid ascent by otherwise fit individuals to altitudes above 3000 m without sufficient time to acclimatize. The susceptibility of an individual to highaltitude syndromes is variable but generally reproducible. Prevention of altitude-related illness by slow ascent is the best approach, but this is not always practical. The immediate management of serious illness requires oxygen (if available) and descent of more than 300 m as soon as possible. In this article, we describe the setting and clinical features of acute mountain sickness and highaltitude cerebral edema, including an overview of the known pathophysiology, and explain contemporary practices for both prevention and treatment exploring the comprehensive evidence base for the various interventions. (Prog Cardiovasc Dis 2010;52:467-484) An additional clinical assessment scoring is sometimes used. GI indicates gastrointestinal.
Reviews on Environmental Health
Traveling to high altitudes for entertainment or work is sometimes associated with acute high altitude pathologies. In the past, scientific literature from the lowlander point of view was primarily based on mountain climbing. Sea level scientists developed all guidelines, but they need modifications for medical care in high altitude cities. Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema are medical conditions that some travelers can face. We present how to diagnose and treat acute high altitude pathologies, based on 51 years of high altitude physiology research and medical practice in hypobaric hypoxic diseases in La Paz, Bolivia (3,600 m; 11,811 ft), at the High Altitude Pulmonary and Pathology Institute (HAPPI â IPPA). These can occasionally present after flights to high altitude cities, both in lowlanders or high-altitude residents during re-entry. Acute high altitude ascent diseases can be adequately diagnosed and treated in high altitud...
High-Altitude Cerebral Edema With Absence of Headache
Wilderness & Environmental Medicine, 2007
Headache is the cardinal symptom of acute mountain sickness (AMS). The headache normally worsens, with increased cerebral affection and the development of high-altitude cerebral edema (HACE). A Norwegian expedition aimed to climb Baruntse (7129 m) in Nepal in 2003. At 5400 m a 35-yearold man felt exhausted. The next day he aborted his attempt at further climbing as a result of extreme fatigue. Over the next 24 hours he developed cough, dyspnea, and severe hypoxia before progressing to ataxia and blurred vision. At no point did he experience headache or nausea. The patient was evacuated by helicopter. He improved immediately after descent and recovered completely within a week. The speed of progression from AMS to HACE varies. Abrupt onset of HACE is occasionally reported. High-altitude pulmonary edema (HAPE) may induce severe hypoxia that can lead to rapid development of HACE. High-altitude cerebral edema in the setting of HAPE was the most likely diagnosis despite the unusual lack of headache. Rapid onset of HAPE with subsequent severe desaturation should raise awareness of the development of HACE, even in the absence of headache.