ABSTRACT
Inner ear decompression sickness (IEDCS) is an uncommon diving-related injury affecting the vestibulocochlear system, with symptoms typically including vertigo, tinnitus, and hearing loss, either in isolation or combination. Classically associated with deep, mixed-gas diving, more recent case series have shown that IEDCS is indeed possible after seemingly innocuous recreational dives, and there has been one previous report of IEDCS following routine hyperbaric chamber operations. The presence of right-to-left shunt (RLS), dehydration, and increases in intrathoracic pressure have been identified as risk factors for IEDCS, and previous studies have shown a predominance of vestibular rather than cochlear symptoms, with a preference for lateralization to the right side. Most importantly, rapid identification and initiation of recompression treatment are critical to preventing long-term or permanent inner ear deficits. This case of a U.S. Navy (USN) diver with previously unidentified RLS reemphasizes the potential for IEDCS following uncomplicated diving and recompression chamber operations - only the second reported instance of the latter.
Subject(s)
Decompression Sickness , Diving , Hyperbaric Oxygenation , Decompression Sickness/etiology , Humans , Diving/adverse effects , Male , Ear, Inner/injuries , Military Personnel , Adult , Vertigo/etiology , Tinnitus/etiology , Atmosphere Exposure ChambersABSTRACT
Cluster headaches (CHs) are one of the most debilitating of all the identified headache syndromes. Their pathogenesis is poorly understood, which has made their treatment challenging. Various medicines and modalities have been put forth in an effort to minimize the symptoms, but none have proven to be consistently reliable. For the active duty military aviator with CHs, this is further compounded by the administrative restrictions to use many of those medications secondary to their unwanted and potentially dangerous side effects. We present a case of refractory CH in an active duty air crewman, treated with fluticasone, which resulted in a remarkable reduction in symptoms allowing him to resume his primary flight duties. We propose that fluticasone's effectiveness in improving his CH symptoms stems from its anti-inflammatory properties.
Subject(s)
Cluster Headache/drug therapy , Fluticasone/administration & dosage , Military Personnel , Adult , Anti-Inflammatory Agents/administration & dosage , Humans , Male , Nasal SpraysABSTRACT
BACKGROUND: Adverse radiation effects are a known complication after the use of SRS for AVMs, although it is difficult to predict which patients will manifest with these side effects. Treatment of swelling due to ARE is usually medical, but refractory cases may require surgical decompression. CASE DESCRIPTION: This report presents a case of a patient who experienced AREs after SRS (edema, headaches, and nausea) that failed to respond to steroid treatment but was successfully treated with HBO. The treatment characteristics of this and of 5 other cases of radiation injury after SRS for AVM managed with HBO therapy are reviewed, and the pathophysiology is discussed. CONCLUSION: Hyperbaric oxygen therapy provides a therapeutic option to treat AREs following SRS of cerebral AVMs.
Subject(s)
Brain/radiation effects , Hyperbaric Oxygenation , Intracranial Arteriovenous Malformations/surgery , Radiation Injuries/etiology , Radiation Injuries/therapy , Radiosurgery/adverse effects , Adolescent , Brain/pathology , Brain Edema/etiology , Humans , Intracranial Arteriovenous Malformations/diagnosis , Intracranial Pressure , Magnetic Resonance Angiography , Magnetic Resonance Imaging , Male , Nausea/etiology , Necrosis/etiology , Radiation Injuries/diagnosis , Radiation Injuries/physiopathology , Tomography, X-Ray Computed , Treatment Outcome , Vomiting/etiologyABSTRACT
BACKGROUND: Inducible NO synthase (NOS)-derived peroxynitrite (ONOO-) during ischemia/reperfusion contributes to ischemic brain injury. However, inducible NOS (iNOS) regulation in ischemic stroke remains unknown. Tetrahydrobiopterin (BH4) is an essential cofactor for NOS activity. The present study tested the hypothesis that inhibition of endogenous BH4 rate-limiting enzyme GTP cyclohydrolase I (GTPCH I), and thus BH4 synthesis, reduces cerebral infarction via inhibiting iNOS and ONOO- in transient focal ischemia. METHODS: Focal ischemia (2 hours) was created in adult male Sprague-Dawley rats (250 to 300 g) by middle cerebral artery occlusion (MCAO). Rats were treated 12 hours before MCAO with vehicle or diamino-6-hydroxypyrimidine (DAHP; 0.5 g/kg IP), a selective GTPCH I inhibitor. Brains were harvested 24 hours after reperfusion for assays of infarct volume, blood-brain barrier (BBB) permeability, GTPCH I activity, BH4 levels, GTPCH I and NOS mRNA, protein expression, and superoxide anion (O2*-) and ONOO- levels. RESULTS: Endogenous GTPCH I activity, BH4 levels, iNOS activity, and (O2*- and ONOO- levels were all augmented after ischemia/reperfusion. DAHP treatment significantly reduced GTPCH I activity, resulting in decreased BH4 levels, iNOS activity, and ONOO- levels. Consequently, DAHP treatment significantly reduced the infarct size compared with the nontreated group (22.3+/-5.6 versus 38.3+/-7.4%; n=6; P<0.05). Similarly, BBB permeability was significantly reduced after DAHP pretreatment compared with the control group (4.11+/-0.22 versus 7.78+/-0.44 microg/g tissue; n=5; P<0.05). CONCLUSIONS: These results demonstrate that blockade of endogenous brain BH4 synthesis attenuates cerebral infarction via inhibiting iNOS and ONOO-, which may provide a mechanistic basis of novel therapeutic strategies for ischemic stroke.
