scholarly journals Decompression Illness in Repetitive Breath-Hold Diving: Why Ischemic Lesions Involve the Brain?

2021 ◽  
Vol 12 ◽  
Author(s):  
Kiyotaka Kohshi ◽  
Petar J. Denoble ◽  
Hideki Tamaki ◽  
Yoshitaka Morimatsu ◽  
Tatsuya Ishitake ◽  
...  
Keyword(s):  
Cerebral Arteries ◽  
Clinical Manifestations ◽  
First Aid ◽  
Breath Hold ◽  
Decompression Illness ◽  
Gas Embolism ◽  
Normobaric Oxygen ◽  
Underlying Mechanisms ◽  
The 1960S ◽  
The Brain

Nitrogen (N2) accumulation in the blood and tissues can occur due to breath-hold (BH) diving. Post-dive venous gas emboli have been documented in commercial BH divers (Ama) after repetitive dives with short surface intervals. Hence, BH diving can theoretically cause decompression illness (DCI). “Taravana,” the diving syndrome described in Polynesian pearl divers by Cross in the 1960s, is likely DCI. It manifests mainly with cerebral involvements, especially stroke-like brain attacks with the spinal cord spared. Neuroradiological studies on Ama divers showed symptomatic and asymptomatic ischemic lesions in the cerebral cortex, subcortex, basal ganglia, brainstem, and cerebellum. These lesions localized in the external watershed areas and deep perforating arteries are compatible with cerebral arterial gas embolism. The underlying mechanisms remain to be elucidated. We consider that the most plausible mechanisms are arterialized venous gas bubbles passing through the lungs, bubbles mixed with thrombi occlude cerebral arteries and then expand from N2 influx from the occluded arteries and the brain. The first aid normobaric oxygen appears beneficial. DCI prevention strategy includes avoiding long-lasting repetitive dives for more than several hours, prolonging the surface intervals. This article provides an overview of clinical manifestations of DCI following repetitive BH dives and discusses possible mechanisms based on clinical and neuroimaging studies.

scholarly journals Clinical and neuroimaging analysis of carotid infarction in the acute ischemic stroke

2021 ◽  
Vol 17 (5) ◽  
pp. 36-46
Author(s):  
M.M. Prokopiv
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Cerebral Artery ◽  
Anterior Cerebral Artery ◽  
Cerebral Arteries ◽  
Clinical Manifestations ◽  
Short Term ◽  
Middle Cerebral Arteries ◽  
Proximal Anterior Cerebral Artery ◽  
The Brain

Background. The assessment of clinical manifestations in patients with acute pre-circular infarction is important for verification of the lesion, the choice of the treatment program, prediction of the stroke consequences. The purpose is to investigate the clinical, neurological, and neuroimaging features of lacunar and non-lacunar carotid infarctions in acute ischemic stroke and to assess their short-term consequences. Materials and methods. There was performed a clinical and radiological analysis of carotid infarction in 540 patients with acute ischemic stroke, which were divided into two groups: 155 patients were verified for infarcts in the cortex and white matter of the brain in the vasculature of the anterior and middle cerebral artery; in 385 patients, infarct foci were found in the area of the deep hemispheres of the brain (subcortical-capsular infarcts). Results. Clinical neuroimaging analysis of patients with ischemic stroke in the vasculature of the cortical branches of the anterior and middle cerebral arteries of the anterior circulatory basin showed that acute cerebral circulatory disorders caused the development of small cortical infarctions in 89 (57.4 %) patients and 65 (41 %) — lacunar infarction, in one patient (0.7 %) with occlusion of the proximal anterior cerebral artery — total infarction. The neurological clinical picture of infarcts of varying localization, which was determined by the location and size of the lesion, was described. Conclusions. The obtained results showed that the consequences of anterior circular infarctions depended on the localization of the lesion of the arterial area, the caliber of the infarction of the dependent artery, the size of the infarct locus. For the most part, these factors determined the background severity of neurological deficit after the development of acute ischemic stroke.

MR imaging of the central nervous system in diving-related decompression illness

1997 ◽  
Vol 38 (6) ◽  
pp. 940-944 ◽  
Author(s):  
M. Reuter ◽  
K. Tetzlaff ◽  
A. Hutzelmann ◽  
G. Fritsch ◽  
J.-C. Steffens ◽  
...  
Keyword(s):  
Mr Imaging ◽  
Decompression Sickness ◽  
Clinical Manifestations ◽  
Decompression Illness ◽  
Mr Images ◽  
Cerebrovascular Lesions ◽  
The Central Nervous System ◽  
Low Sensitivity ◽  
Spinal Damage ◽  
The Brain

Purpose: This investigation was conducted to determine whether MR imaging showed cerebral or spinal damage in acute diving-related decompression illness, a term that includes decompression sickness (DCS) and arterial gas embolism (AGE) Material and Methods: A total of 16 divers with dysbaric injuries were examined after the initiation of therapeutic recompression. Their injuries comprised: neurological DCS II n=8; AGE n=7; combined cerebral-AGE/spinal-DCS n=1. T1- and T2-weighted images of the brain were obtained in 2 planes. in addition, the spinal cord was imaged in 7 subjects. the imaging findings were correlated with the neurological symptoms Results: MR images of the head showed ischemic cerebrovascular lesions in 6/8 patients with AGE but showed focal hyperintensities in only 2/8 divers with DCS. Spinalcord involvement was detected in 1/7 examinations, which was the combined cerebral-AGE/spinal-DCS case. There was agreement between the locations of the documented lesions and the clinical manifestations Conclusion: MR readily detects cerebral damage in AGE but yields low sensitivity in DCS. A negative MR investigation cannot rule out AGE or DCS. However, MR is useful in the examination of patients with decompression illness

Diving-related disorders in commercial breath-hold divers (Ama) of Japan

2021 ◽  
Vol 51 (2) ◽  
pp. 199-206
Author(s):  
Kiyotaka Kohshi ◽  
◽  
Hideki Tamaki ◽  
Frédéric Lemaître ◽  
Yoshitaka Morimatsu ◽  
...  
Keyword(s):  
Clinical Manifestations ◽  
Field Studies ◽  
Underlying Mechanism ◽  
Neurological Involvement ◽  
Cerebral White Matter ◽  
Breath Hold ◽  
Decompression Illness ◽  
Oxygen Breathing ◽  
Arterial Insufficiency ◽  
Nitrogen Bubbles

Decompression illness (DCI) is well known in compressed-air diving but has been considered anecdotal in breath-hold divers. Nonetheless, reported cases and field studies of the Japanese Ama, commercial or professional breath-hold divers, support DCI as a clinical entity. Clinical characteristics of DCI in Ama divers mainly suggest neurological involvement, especially stroke-like cerebral events with sparing of the spinal cord. Female Ama divers achieving deep depths have rarely experienced a panic-like neurosis from anxiety disorders. Neuroradiological studies of Ama divers have shown symptomatic and/or asymptomatic ischaemic lesions situated in the basal ganglia, brainstem, and deep and superficial cerebral white matter, suggesting arterial insufficiency. The underlying mechanism(s) of brain damage in breath-hold diving remain to be elucidated; one of the plausible mechanisms is arterialization of venous nitrogen bubbles passing through right to left shunts in the heart or lungs. Although the treatment for DCI in Ama divers has not been specifically established, oxygen breathing should be given as soon as possible for injured divers. The strategy for prevention of diving-related disorders includes reducing extreme diving schedules, prolonging surface intervals and avoiding long periods of repetitive diving. This review discusses the clinical manifestations of diving-related disorders in Ama divers and the controversial mechanisms.

Brain MRI-findings in Ph - negative myeloproliferative disorders

2019 ◽  
Vol 91 (7) ◽  
pp. 29-34 ◽  
Author(s):  
M M Tanashyan ◽  
A L Melikyan ◽  
P I Kuznetsova ◽  
A A Raskurazhev ◽  
A A Shabalina ◽  
...  
Keyword(s):  
Cerebrovascular Disease ◽  
Sinus Thrombosis ◽  
Cerebral Arteries ◽  
Brain Mri ◽  
Myeloproliferative Disorders ◽  
Cerebral Venous Sinus Thrombosis ◽  
Mri Findings ◽  
Cerebral Lesions ◽  
Cerebrovascular Pathology ◽  
Underlying Mechanisms

Myeloproliferative disorders (MPD) are accompanied by a high proportion of thrombotic complications, which may lead to cerebrovascular disease (CVD). Aim. To describe MRI-findings in patients with Ph - negative MPD and evaluate any cerebrovascular disease. Materials and methods. We included 104 patients with Ph - negative MPD (age varied between 20 and 58) with clinical correlates of cerebrovascular pathology. Results. Brain MRI showed post - stroke lesions in 20% of patients (7 hemispheric infarcts due to thrombotic occlusion of one of the large cerebral arteries, 14 - cortical infarcts). 37 patients (36%) had vascular cerebral lesions. Cerebral venous sinus thrombosis occurred in 5 patients - in 7% (n=3) of patients with polycythemia vera and 5% (n=2) - in patients with essential thrombocythemia. The incidence of vascular cerebral lesions was associated with higher levels of the following: erythrocyte, platelet count, fibrinogen, and with the decrease in fibrinolytic activity, as well. Conclusion. The pioneering results of the study include the description and analysis of brain MRI-findings in patients with Ph - negative MPD. The underlying mechanisms of cerebrovascular pathology in these patients are associated with certain blood alterations (particularly, hemorheology) which present a major risk factor.

Minocycline inhibits mTOR signaling activation and alleviates behavioral deficits in the Wistar rats with acute ischemia stroke

2020 ◽  
Vol 19 ◽  
Author(s):  
Shengyuan Wang ◽  
Chuanling Wang ◽  
Lihua Wang ◽  
Zhiyou Cai
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Mammalian Target Of Rapamycin ◽  
Mtor Signaling ◽  
Acute Ischemia ◽  
Intragastric Administration ◽  
Underlying Mechanisms ◽  
Signaling Activation ◽  
The Brain ◽  
Minocycline Therapy

Background: Mammalian target of rapamycin (mTOR) has been evidenced as a multimodal therapy in the path-ophysiological process of acute ischemic stroke (AIS). However, the pathway that minocycline targets mTOR signaling is not fully defined in the AIS pathogenesis. This study is to aim at the effects of minocycline on the mTOR signaling in the AIS process and further discover the underlying mechanisms of minocycline involved in the following change of mTOR signaling-autophagy. Methods: Cerebral ischemia/reperfusion (CIR) rat animal models were established with the transient suture occlusion into middle cerebral artery. Minocycline (50mg/kg) was given by intragastric administration. The Morris water maze was used to test the cognitive function of animals. Immunohistochemistry and immunofluorescence were introduced for testing the lev-els of synaptophysin and PSD-95. Western blot was conducted for investigating the levels of mTOR, p-mTOR (Ser2448), p70S6, p-p70S6 (Thr389), eEF2k, p-eEF2k (Ser366), p-eIF4B (Ser406), LC3, p62, synaptophysin and PSD-95. Results: Minocycline prevents cognitive decline of the MCAO stroke rats. Minocycline limits the expression of p-mTOR (Ser2448) and the downstream targets of mTOR [p70S6, p-p70S6 (Thr389), eEF2k, p-eEF2k (Ser366) and p-eIF4B (Ser406)] (P<0.01), while minocycline has no influence on mTOR. LC3-II abundance and the LC3-II/I ratio were upregu-lated in the hippocampus of the MCAO stroke rats by the minocycline therapy (P<0.01). p62 was downregulated in the hippocampus from the MCAO stroke rats administrated with minocycline therapy(P<0.01). The levels of SYP and PSD-95 were up-regulated in the brain of the MCAO stroke rats administrated with minocycline therapy. Conclusion: Minocycline prevents cognitive deficits via inhibiting mTOR signaling and enhancing autophagy process, and promoting the expression of pre-and postsynaptic proteins (synaptophysin and PSD-95) in the brain of the MCAO stroke rats. The potential neuroprotective role of minocycline in the process of cerebral ischemia may be related to mitigating is-chemia-induced synapse injury via inhibiting activation of mTOR signaling.

Macroscopic Anatomy and Brain Vascularization in the Greater Rhea (Rhea americana americana)

2018 ◽  
Vol 46 (1) ◽  
Author(s):  
Herson Da Silva Costa ◽  
Hélio Norberto De Araújo Júnior ◽  
Ferdinando Vinícius Fernandes Bezerra ◽  
Carlos Eduardo Vale Rebouças ◽  
Danilo José Ayres De Menezes ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Carotid Arteries ◽  
Vascular System ◽  
Cerebral Arteries ◽  
Cervical Region ◽  
Type I ◽  
Macroscopic Anatomy ◽  
Rhea Americana ◽  
Vascular Type ◽  
The Brain

 Background: The Rhea americana americana is a wild bird belonging to the group of Ratites, and is important from the scientific point of view given their adaptability to captivity. Considering that information about its morphology is important for the viability of domesticating the species, the aim of this study was to macroscopically identify the brain regions, as well as the cerebral arteries and the cerebral arterial circuit in order to establish the cerebral vascular pattern and systematization.Materials, Methods & Results: Twenty one brains from young and adult Greater Rheas of both sexes were used from animals that had died due to natural causes and were then kept in a freezer. The specimens were thawed and incised in the cervical region to allow exposure of the left common carotid artery, which was cannulated. The vascular system was rinsed with 0.9% saline solution, then perfused with latex Neoprene 650 stained with red pigment. The animals were subsequently fixed in 3.7% aqueous formaldehyde solution for 72 h, and then they were dissected by removing the bones from the skull cap. The brains were analyzed, and the structures were identified, photographed, schematized and denominated. Morphometric measurements were performed on the basilar and cerebellar ventral caudal arteries, recording the values of length and width in millimeters with the aid of a digital caliper. The brain was divided into: telencephalon, diencephalon, brainstem and cerebellum; while externally, the observed structures are: olfactory bulbs, optical lobes, optic nerves, optic chiasm, pituitary and pineal glands. Vascularization was performed by the following arteries: ventral spinal artery, basilar artery, ventricular cerebellar arteries, medium ventricular cerebellar arteries, caudal branches of the carotid arteries of the brain, ventral mesencephalic artery, cerebral caudal arteries, rostral branches of the carotid arteries of the brain, middle cerebral arteries, cerebroethmoidal arteries, rostral intercerebral anastomosis, rostral cerebral arteries, ethmoidal arteries, internal ophthalmic arteries, inter-hemispheric artery, pituitary arteries, dorsal mesencephalic tectal arteries, dorsal cerebellar arteries, occipital, pineal and dorsal hemispherical branches. The cerebral arterial circuit was both caudally and rostrally closed in 100.0% of the samples, being composed of the arteries: basilar artery, caudal branches of the carotid brain, rostral branches of the brain carotid, cerebroethmoidal arteries and rostral intercerebral anastomosis.Discussion: Encephalon classification regarding the presence or absence of gyri is a characteristic associated to evolution­ary aspects among vertebrates, being respectively considered as lisencephalon or girencecephalus when it presents or does not present convolutions. In Greater Rheas, the telencephalon was quite developed, with a relatively rounded shape and the absence of sulci and convolutions in the cortex, which allowed it to be classified as a lisencephalon. Such findings resemble those described for the ostrich and in a comparative study involving kiwis, emus, owls and pigeons, although different sizes and forms of telencephalon development were observed in the latter. Regarding the cerebral arterial circuit, this structure in Rheas was complete and both caudally and rostrally closed in 100.0% of the specimens. Our findings differ from those ob­served for ostriches, in which a rostrally open behavior has been described, while it is caudally closed in 20.0% of cases and opened in 80.0%. Regarding the vascular type of the brain, in the Rhea it was observed that there was only contribution of the carotid system, similar to that found for birds such as ostriches and turkeys which confer a type I encephalic vascularization.Keywords: arteries, brain, arterial circuit, morphometry, ratites.

Hyperbaric treatment of air or gas embolism: current recommendations

2019 ◽  
pp. 673-683
Author(s):  
Richard E. Moon ◽  
Keyword(s):  
Animal Studies ◽  
Decompression Sickness ◽  
Bubble Formation ◽  
Endothelial Damage ◽  
Neurological Deficits ◽  
Breath Hold ◽  
Gas Embolism ◽  
Hyperbaric Treatment ◽  
Pulmonary Capillaries ◽  
Venous Gas Embolism

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac “vapor lock” and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence-based review of adjunctive therapies is presented.

Leptin Functioning in Eating Disorders

CNS Spectrums ◽  
2004 ◽  
Vol 9 (7) ◽  
pp. 523-529 ◽  
Author(s):  
Palmiero Monteleone ◽  
Antonio DiLieto ◽  
Eloisa Castaldo ◽  
Mario Maj
Keyword(s):  
Physical Activity ◽  
Eating Disorders ◽  
Body Weight ◽  
Eating Behaviors ◽  
Clinical Manifestations ◽  
Immune Functions ◽  
Abnormal Eating ◽  
The Brain

AbstractLeptin is an adipocyte-derived hormone, which is involved predominantly in the long-term regulation of body weight and energy balance by acting as a hunger suppressant signal to the brain. Leptin is also involved in the modulation of reproduction, immune function, physical activity, and some endogenous endocrine axes. Since anorexia nervosa (AN) and bulimia nervosa (BN) are characterized by abnormal eating behaviors, dysregulation of endogenous endocrine axes, alterations of reproductive and immune functions, and increased physical activity, extensive research has been carried out in the last decade in order to ascertain a role of this hormone in the pathophysiology of these syndromes. In this article, we review the available data on leptin physiology in patients with eating disorders. These data support the idea that leptin is not directly involved in the etiology of AN or BN. However, malnutrition-induced alterations in its physiology may contribute to the genesis and/or the maintenance of some clinical manifestations of AN and BN and may have an impact on the prognosis of AN.

Causes and Types of Sensorineural Hearing Loss. Clinical Manifestations and Basic Principles of Treatment

2020 ◽  
pp. 9-16
Author(s):  
Sergey Armakov
Keyword(s):  
Hearing Loss ◽  
Sensorineural Hearing Loss ◽  
Inner Ear ◽  
Clinical Manifestations ◽  
Sensorineural Hearing ◽  
Doppler Imaging ◽  
Comprehensive Treatment ◽  
Impaired Hearing ◽  
Temporal Bones ◽  
The Brain

Sensorineural hearing loss is a disorder associated with the damage to the inner ear structures: the cochlea (cortical organ), dysfunctioning of the vestibule-cochlear nerve or the central part of the auditory analyser (brain stem and cortical representation of the cortical temporal lobe). In recent years, there has been a steady increase in ensorineural hearing loss patients; they account for ca. 70% among the total patients with impaired hearing. The disease has numerous causes and a complex pathogenesis. Among the main factors contributing to hearing loss are genetic predisposition, perinatal pathology, including hypoxia at childbirth, exposure to infectious and toxic agents and metabolic disorders, injuries (mechanical, acoustic and altitude trauma). Vascular-rheological disorders in the vertebro-basilar system play an important part because blood is supplied to the inner ear from the anterior inferior cerebellar artery. There are sudden, acute and chronic sensorineural hearing loss. The ensorineural hearing loss isdiagnosed by examinations that allow to verify the diagnosis and to determine the sound analyser damage level. This complex includes audiometric examinations, including the tuning fork examination, speech audiometry, and acoustic impedancemetry. If necessary, ultrasound Doppler imaging of the main blood vessels of the brain, computed tomography of the temporal bones, and MRI of the brain are prescribed. The pattern of comprehensive treatment should include, first of all, the elimination of the disease cause and anti-hypoxic drugs, anti-oxidants and a number of physiotherapy procedures.

Lateral Medullary Infarction with Contralateral Segmental Dysesthesia and Ipsilateral Headache: A Case Report

2021 ◽  
Vol 17 ◽  
Author(s):  
Renjie Wang ◽  
Yankun Shao ◽  
Lei Xu
Keyword(s):  
Medulla Oblongata ◽  
Clinical Manifestations ◽  
Lateral Medullary Infarction ◽  
Case Presentation ◽  
Specific Sign ◽  
Temperature Sense ◽  
Magnetic Resonance Imaging Mri ◽  
The Right ◽  
The Brain ◽  
Medullary Infarction

Introduction: The medulla oblongata is the lowest segment of the brain stem, located adjacent to the spinal cord, with a complex anatomical structure. Thus, a small injury to the medulla oblongata can show complex clinical manifestations. Case Presentation: A patient experienced dysesthesia, which manifested as numbness in her right lower limb and decreased temperature sense, and dizziness 20 days before admission. The numbness worsened 1 week before admission, reaching the right thoracic (T) 12 dermatomes. Her thermoception below the T12 dermatomes decreased, and the degree of dizziness increased, accompanied by nausea and vomiting. Magnetic resonance imaging (MRI) of the neck, chest, and abdomen performed at a local hospital showed no abnormalities. MRI of the brain was performed after admission. One week after admission, she experienced a severe headache in the upper left periorbital area. The numbness extended to T4, and thermoception decreased below T4. Diagnosis: Lateral medullary infarction. Interventions: Anti-platelet aggregation and mitochondrial nutritional therapies were performed along with treatments for improving circulation and establishing collateral circulation. Outcomes: The intensity of limb numbness decreased, and the symptoms of headache and dizziness resolved. Conclusion: Lesions leading to segmental sensory disorders can occur in the medulla oblongata. Ipsilateral headaches with contralateral segmental paresthesia can be a specific sign of lateral medullary infarction.

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