Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Factors responsible for presbyacusis include physiological ageing processes as well as endogenous or exogenous causes. In the industrial countries, two main exogenous causes are exposure to loud noise and obesity. Pathomechanisms contributing to presbyacusis are hypoxia/ischemia, reactive species formation and oxidative stress, apoptotic and necrotic death of hair cells and spiral ganglion cells as well as inherited and acquired mutations in the mitochondrial DNA. Important for the successful treatment of presbyacusis is a timely fitting of hearing aids on both ears to improve communication and provide the auditory system with acoustic information. Using the hearing aids will also elevate the detection threshold of an existing tinnitus signal. At present, several therapeutic strategies based on pharmacological intervention are under discussion. The application of antioxidants or caloric restriction are considered to prevent or reduce oxidative stress-induced damage. Animal experiments evidenced that superoxide dismutase 2 (SOD2) strongly decreases in age; thus, a further approach may be the overexpression or modulation of the SOD2 within the cochlea. Adenoviral-mediated gene transfer technology would be a tempting approach to address this type of therapy. Finally, hair cell regeneration could be a possible treatment of presbyacusis in the future.
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PMID:[Pathogenesis and treatment of presbyacusis. Current status and future perspectives]. 1833 47

The translation of a neurovascular hypothesis for Alzheimer's disease to subjective idiopathic tinnitus (SIT) is presented as a challenge to the predominantly sensorineural view of SIT and its clinical application for tinnitus treatment. The concept of neurovascular dysfunction and neurodegeneration (ND) in SIT patients has been proposed and reported as an etiology in a particular subset of tinnitus patients with a diagnosis of medical-audiological tinnitus, through a medical-audiological tinnitus patient protocol, to be a predominantly central-type, severe, disabling SIT (n = 54 of 96). A medical-audiological ND tinnitus profile was the basis for selection of 18 SIT patients (n = 18 of 54) for nuclear medicine brain imaging (i.e., single-photon emission computed tomography or positron emission tomography, or both). Objective findings were reported in 16 of this cohort of 18 SIT patients selected for nuclear medicine imaging (88.9%). Classification of central nervous system (CNS) ND and tinnitus differentiated between (1) ND, nonspecific and of unknown etiology; (2) ND manifested by perfusion asymmetries in brain associated with ischemia (n = 11 of 18); and (3) ND CNS disease consistent with nuclear medicine criteria for senile dementia Alzheimer's-type disease (n = 5 of 18). The diagnosis was associated with cerebrovascular disease (n = 16 of 18). The identification of pathological processes of inflammation and ischemia, linked to ND, in a particular cohort of SIT patients may provide a basis for establishing the medical significance and treatment of SIT and influence the clinical course of the tinnitus.
Int Tinnitus J 2008
PMID:Central nervous system neurodegeneration and tinnitus: a clinical experience. Part II: translational neurovascular theory of neurodegenerative CNS disease and tinnitus. 1861 86

Spontaneous dissection of the internal carotid artery usually presents with stroke-like symptoms secondary to ischemia in its vascular territory, as well as local signs and symptoms, which may include head, face or neck pain, Horner's syndrome, pulsatile tinnitus, and cranial nerve palsies. We report a case of a 44-year-old healthy white male who presented with tongue swelling mimicking angioedema as an unusual manifestation of spontaneous dissection of the internal carotid artery. Two weeks after the initial presentation, the patient returned with similar symptoms and slurred speech. Upon physical examination, he was noted to have isolated left-sided hypoglossal nerve palsy. Subsequent diagnostic imaging revealed segmental narrowing of the left internal carotid artery. The appearance was consistent with the presence of a spontaneous internal carotid artery dissection with associated pseudoaneurysm formation.
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PMID:Spontaneous dissection of internal carotid artery masquerading as angioedema. 1883 59

It has been widely outlined by our group the possibility that a sufferance of the inner ear can take place as a consequence of hemodynamic imbalance which could affect young and healthy people and recognize a merely functional origin. As reported in previous papers, an altered reaction of the autonomic nervous system could actually jeopardize the labyrinthine perfusion even in absence of other damages. From this standpoint, the hypothesis that a hyperactivity of the vagal response to an acute sympathetic drive may result in an inner ear sufferance deserves to be explored. A mechanism which appears to fit to this model is represented by the Bezold-Jarisch reflex (BJR), which is considered to be responsible for vasovagal syncope and is characterized by a dynamic reasonably compatible with our findings. According to these premises, especially considering that the inner ear has a less active protective mechanism against ischemia as compared to brain, in predisposed subjects tinnitus, when considered as an initial symptom of inner ear hypoperfusion, can represent a warning able to prevent the lack of consciousness related to the syncope.
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PMID:Tinnitus as a warning for preventing vasovagal syncope. 1944 64

The mechanism that produces tinnitus remains poorly understood. This article reviews possible mechanisms of tinnitus. The evaluation of the structure of disease in the presence of hearing reduction was studied among 2820 patients who applied for otolaryngological aid. Sensor neural deafness of different genesis was revealed in 512 cases. Apart from deafness, earlier manifesting symptom of the disease was pathological noise in the ear leading to anxiety of patients. Audiological characters and course of disease under the influence of symptomatic complex therapy has been studied. The author has detected /discovered/ present mechanism of beginning of the noise in the ear real reason of which is ischemia of cochlear apparatus in the presence of sensor neural loss of hearing, necessity of carrying out therapy as well and searching other methods of.
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PMID:[The mechanisms of tinnitus in patients with sensor neural deafness]. 1964 83

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used, but have risks associated with their use, including significant upper gastrointestinal tract bleeding. Older persons, persons taking anticoagulants, and persons with a history of upper gastrointestinal tract bleeding associated with NSAIDs are at especially high risk. Although aspirin is cardioprotective, other NSAIDs can worsen congestive heart failure, can increase blood pressure, and are related to adverse cardiovascular events, such as myocardial infarction and ischemia. Cyclooxygenase-2 inhibitors have been associated with increased risk of myocardial infarction; however, the only cyclooxygenase-2 inhibitor still available in the United States, celecoxib, seems to be safer in this regard. Hepatic damage from NSAIDs is rare, but these medications should not be used in persons with cirrhotic liver diseases because bleeding problems and renal failure are more likely. Care should be used when prescribing NSAIDs in persons taking anticoagulants and in those with platelet dysfunction, as well as immediately before surgery. Potential central nervous system effects include aseptic meningitis, psychosis, and tinnitus. Asthma may be induced or exacerbated by NSAIDs. Although most NSAIDs are likely safe in pregnancy, they should be avoided in the last six to eight weeks of pregnancy to prevent prolonged gestation from inhibition of prostaglandin synthesis, premature closure of the ductus arteriosus, and maternal and fetal complications from antiplatelet activity. Ibuprofen, indomethacin, and naproxen are safe in breastfeeding women. Care should be taken to prevent accidental NSAID overdose in children by educating parents about correct dosing and storage in childproof containers.
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PMID:NSAID prescribing precautions. 2000 Feb 99

Ginseng extract is known to have many beneficial effects, including the reversal of pathological and physiological changes induced by ischemia, stress, and aging. Cisplatin, an effective antineoplastic drug, can cause irreversible sensorineural hearing loss and serious tinnitus in humans; thus cisplatin-induced ototoxicity is a useful experimental model for ototoxicity. This study investigated the protective effects of Korean red ginseng extract on cisplatin-induced ototoxicity in auditory cells. Pretreatment with 2.5 mg/mL of ginseng extract prior to application of 20 microM of cisplatin significantly increased cell viability after 48 h of incubation in auditory cells. Pretreatment with ginseng extract significantly attenuated the cisplatin-induced increase in reactive oxygen species (ROS). Ginseng extract also inhibited the expression of caspase-3 and poly-ADP-ribose polymerase related to cisplatin-induced apoptosis because a major mechanism of cisplatin-induced toxicity involves ROS production. Thus, Korean red ginseng extract can play both an anti-apoptotic and anti-oxidative role on cisplatin-induced ototoxicity in an auditory cell line.
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PMID:Protective effect of Korean red ginseng extract on cisplatin ototoxicity in HEI-OC1 auditory cells. 2002 Apr 38

It is hypothesized that in all traumatic brain injury (TBI) patients with a clinical history of closed or penetrating head injury, the initial head trauma is associated with a vibratory sensation and noise exposure, with resultant alteration in vascular supply to the structures and contents of the fluid compartments of brain and ear (i.e., the fluid dynamics vascular theory of brain-inner-ear function [FDVTBE]). The primary etiology-head trauma-results in an initial fluctuation, interference, or interaction in the normal fluid dynamics between brain and labyrinth of the inner ear, with a resultant clinical diversity of complaints varying in time of onset and severity. Normal function of the brain and ear is a reflection of a normal state of homeostasis between the fluid compartments in the brain of cerebrospinal fluid and perilymph-endolymph in the labyrinth of the ear. The normal homeostasis in the structures and contents between the two fluid compartment systems--intracerebral and intralabyrinthine--is controlled by mechanisms involved in the maintenance of normal pressures, water and electrolyte content, and neurotransmitter activities. The initial pathophysiology (a reflection of an alteration in the vascular supply to the brain-ear) is hypothesized to be an initial acute inflammatory response, persistence of which results in ischemia and an irreversible alteration in the involved neural substrates of brain-ear. Clinically, a chronic multisymptom complex becomes manifest. The multisymptom complex, individual for each TBI patient regardless of the diagnostic TBI category (i.e., mild, moderate, or severe), initially reflects processes of inflammation and ischemia which, in brain, result in brain volume loss identified as neurodegeneration and hydrocephalus ex vacuo or an alteration in cerebrospinal fluid production (i.e., pseudotumor cerebri) and, in ear, secondary endolymphatic hydrops with associated cochleovestibular complaints of hearing loss, tinnitus, vertigo, ear blockage, and hyperacusis. The FDVTBE integrates and translates a neurovascular hypothesis for Alzheimer's disease to TBI. This study presents an FDVTBE hypothesis of TBI to explain the clinical association of head trauma (TBI) and central nervous system neurodegeneration with multisensory complaints, highlighted by and focusing on cochleovestibular complaints. A clinical case report, previously published for demonstration of the cerebrovascular medical significance of a particular type of tinnitus, and evidence-based basic science and clinical medicine are cited to provide objective evidence in support and demonstration of the FDVTBE.
Int Tinnitus J 2009
PMID:Fluid dynamics vascular theory of brain and inner-ear function in traumatic brain injury: a translational hypothesis for diagnosis and treatment. 2042 Mar 35

Carotid artery dissections are potentially disabling, probably underdiagnosed, and mainly affect young-aged and middle-aged people. We present three consecutive cases illustrating different clinical presentations and thereby emphasizing the diagnostic challenge of carotid artery dissections for the emergency physician. Neck and facial pain, headache, unilateral pulsatile tinnitus, partial Horner's syndrome (or oculosympathetic palsy), amaurosis fugax, retinal infarction, and anterior circulation brain ischemia may all occur in isolation or in various combinations. Medical imaging plays a pivotal role in making the right diagnosis. Clinical vigilance is of utmost importance as early diagnosis and timely treatment favor long-term prognosis and even prevent ischemic complications. We review the literature and discuss the pathophysiology, etiology, clinical presentation, diagnosis, imaging techniques, treatment, and prognosis of carotid dissections.
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PMID:Carotid artery dissection: three cases and a review of the literature. 2326 11

Despite the lack of clear evidence for their effectiveness in treating vertigo, tinnitus, hearing loss and aural fullness, diuretics, represent a common treatment for Meniere disease (MD), as they are supposed to decrease volume and pressure in the endolymphatic partition of the labyrinth. Our group have outlined the possibility of an adverse effect on inner ear function derived from an abrupt lowering of blood pressure: a subsequent exaggerated vasomotor response inducing local ischemia could be responsible for more or less permanent damage. The inner ear, owing both to its terminal vascular supply and to the necessity of a steady metabolism, seems a reliable target for any hemodynamic imbalance that acutely affect its perfusion. In our opinion, the complexity of the inner ear anatomy and function argues against the usefulness of diuretics to reduce endolymphatic volume, in analogy to their effect on the volemia: too many active mechanisms and "buffer" systems are involved in the labyrinth. Even considering that the finding of mean low pressure values is relatively common in subjects with MD, an attempt should be to maintain a stable blood perfusion to the labyrinth; in fact, an abrupt decrease in systemic blood pressure can trigger an adverse sympathetic reaction and transmit misleading information to the cochlear vasopressin receptors.
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PMID:Diuretics in Meniere disease: a therapy or a potential cause of harm? 2186 86


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