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 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The postconcussion syndrome refers to a large number of symptoms and signs that may occur alone or in combination following usually mild head injury. The most common complaints are headaches, dizziness, fatigue, irritability, anxiety, insomnia, loss of consciousness and memory, and noise sensitivity. Mild head injury is a major public health concern because the annual incidence is about 150 per 100,000 population, accounting for 75% or more of all head injuries. The postconcussion syndrome has been recognized for at least the last few hundred years and has been the subject of intense controversy for more than 100 years. The Hollywood head injury myth has been an important contributor to persisting skepticism and might be countered by educational efforts and counter-examples from boxing. The organicity of the postconcussion syndrome has now become well documented. Abnormalities following mild head injury have been reported in neuropathologic, neurophysiologic, neuroimaging, and neuropsychologic studies. There are multiple sequelae of mild head injury, including headaches of multiple types, cranial nerve symptoms and signs, psychologic and somatic complaints, and cognitive impairment. Rare sequelae include hematomas, seizures, transient global amnesia, tremor, and dystonia. Neuroimaging and physiologic and psychologic testing should be used judiciously based on the problems of the particular patient rather than in a cookbook fashion. Prognostic studies clearly substantiate the existence of a postconcussion syndrome. Manifestations of the postconcussion syndrome are common, with resolution in most patients by 3 to 6 months after the injury. Persistent symptoms and cognitive deficits are present in a distinct minority of patients for additional months or years. Risk factors for persisting sequelae include age over 40 years; lower educational, intellectual, and socioeconomic level; female gender; alcohol abuse; prior head injury; and multiple trauma. Although a small minority are malingerers, frauds, or have compensation neurosis, most patients have genuine complaints. Contrary to a popular perception, most patients with litigation or compensation claims are not cured by a verdict. Treatment is individualized depending on the specific complaints of the patient. Although a variety of medication and psychologic treatments are currently available, ongoing basic and clinical research of all aspects of mild head injury are crucial to provide more efficacious treatment in the future.
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PMID:The postconcussion syndrome and the sequelae of mild head injury. 143 59

Anxiety is the fifth most common clinical diagnosis in the primary care setting. Panic disorder, a severe episodic form of anxiety, has been found to occur in approximately 6% of primary care patients. These patients often selectively focus on one of the frightening autonomic symptoms and are frequently misdiagnosed. The three most common presentations of panic disorder in the medical setting are cardiac symptoms (chest pain, tachycardia), neurologic symptoms (headache, dizziness/vertigo, syncope), and gastrointestinal symptoms, especially epigastric distress. The presentation of cardiac symptoms by patients with panic disorder is especially likely to lead to expensive and potentially iatrogenic medical testing. Hypertension and peptic ulcer are the most commonly associated medical diagnoses in patients with panic disorder. Major depression, alcohol abuse, simple phobias, and posttraumatic stress disorder are the most frequently associated psychiatric diagnoses. Psychopharmacologic treatment of panic disorder has been demonstrated to be highly effective in double-blind, placebo-controlled studies. Effective psychopharmacologic agents include the tricyclic antidepressants (notably imipramine and desipramine), the monoamine oxidase inhibitors (phenelzine), and the high-potency benzodiazepines (alprazolam).
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PMID:Panic disorder: epidemiology, diagnosis, and treatment in primary care. 353 Nov 89

A panic attack is characterized by the abrupt onset of apprehension or fear, accompanied by symptoms such as dyspnea, palpitations, chest pain, dizziness, sweating, the feeling of going mad or the fear of dying. The feeling of anxiety often recedes into the background and such patients present to nonpsychiatric physicians with mainly somatic symptoms. The consequences of frequent panic attacks, named panic disorder, are agoraphobia with impairment of psychic and social functioning, increased prevalence of alcohol abuse, depression and, in particular, suicidal attempts. It is of the utmost importance that physicians recognize the somatic symptoms of panic anxiety and plan integrated treatment. The main therapeutic resources at present include antidepressants, selected benzodiazepines and behavioral treatments and are very successful in improving panic attacks and their consequences, which may long go undiagnosed.
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PMID:[Panic attacks]. 809 64

We studied 23 consecutive patients with acute hyperventilation presenting to an inner-city emergency department, diagnosed on clinical grounds by the attending physician and confirmed by arterial blood gas values in 5 patients. An organic basis for the presenting complaints was excluded and chest radiograph, serum biochemistry, blood cell count, and thyroid function test results were normal. The male to female ratio was 12:11. Presenting complaints were dyspnea (61%), paresthesia (35%), chest pain or tightness (43%), muscle spasm (9%), dizziness (13%), palpitations (13%), and panic (30%). Similar previous episodes were reported in 74%. Misattribution of the presenting complaints to a cardiac or other life-threatening disorder was reported in 20 patients (87%) and was the main reason for their presentation to the hospital. Although no patients presented with clinical features of asthma, 7 (30%) were known asthmatics receiving treatment and another 10 (44%) had a history and investigation results suggestive of asthma. Only 2 had a history of anxiety or depression, but 17 (78%) patients exceeded the threshold for anxiety or panic on Clinical Interview Schedule (CIS-R) interview (score > or = 12). Marihuana or alcohol abuse were involved in 17% with a history of past abuse in 26%. When assessed 2 months after the attack, 13 (57%) had resting or stressor-induced hyperventilation with a significant (p < 0.05) association with asthma but not with a positive CIS-R score. These results illustrate the multifactorial basis of acute hyperventilation, the importance of misattribution, and the danger of using the term "hyperventilation syndrome" in the emergency department.
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PMID:Patients with acute hyperventilation presenting to an inner-city emergency department. 922 1

The authors prospectively assessed symptoms induced by the interruption of antidepressants in 16 patients (11 women and 5 men), aged from 33 to 85 years (mean = 52.4 +/- 16.4), treated with antidepressants since at least two weeks. All patients were free of alcohol abuse or dependence disorder and of other dependence to psychoactive substances. None of them presented medical illness. Diagnosis were made by separate evaluations by two authors and confirmed with a semistructered assessment instrument: the Schedule for Affective Disorders and Schizophrenia (Lifetime Version). All patients were submitted to a brutal discontinuation of their antidepressant agent. Patients were assessed twice, before the interruption of the antidepressant, and 72 hours later. Effects of antidepressant interruption were assessed by several means. Modification of anxiety and depression were evaluated using the Montgomery Asberg Depression Rating Scale (MADRS) and the Hamilton Anxiety Scale. Symptoms of withdrawal were assessed with Cassano and al.'s scale SESSH including an evaluation of anxiety, agitation, irritability, anergy, difficulty on concentrating, depersonalization, sleep and appetite disorders, muscle pains, nausea, tremor, sweating, altered taste, hyperosmia, paresthesias, photophobia, motor incoordination, dizziness, hyperacousia pain, delirium. Fourteen of the 16 patients (87.5%) presented modifications of their somatic or psychic state 3 days after the interruption of the antidepressant treatment. Most frequent symptoms were: increase in anxiety (31%), increase in irritability (25%), sleep disorders (19%), decrease of anergia and fatigue (19%). Mean scores of anxiety and depression were not significantly modified by the withdrawal. Following TCAs interruption (7 patients) most frequent symptoms were sleep disorders; increase in anxiety, nausea. Among patients withdrawn from SSRIs (6 patients), most frequent symptoms were increase in anxiety, increase in irritability, headache. Patients also presented a decrease of nausea, and of anorexia.
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PMID:[Prospective evaluation of antidepressant discontinuation]. 969 14

Although there is general agreement that chronic ingestion of alcohol poses great risks for normal cardiovascular functions and peripheral-vascular homeostasis, a direct cause and effect between the real phenomena of alcohol-induced headache and risk of brain injury and stroke is not appreciated. "Binge drinking" of alcohol is associated with an ever-growing number of strokes and sudden death. It is becoming clear that alcohol ingestion can result in profoundly different actions on the cerebral circulation (e.g., vasodilation, vasoconstriction-spasm, vessel rupture), depending upon dose and physiologic state of host. Using rats, it has been demonstrated that acute, high doses of ethanol can result in stroke-like events concomitant with alterations in brain bioenergetics. We review recent in vivo findings obtained with 31P-NMR spectroscopy, optical reflectance spectroscopy, and direct in vivo microcirculatory studies on the intact brain. Alcohol-induced hemorrhagic stroke is preceded by a rapid fall in brain intracellular free magnesium ions ([Mg2+]i) followed by cerebrovasospasm and reductions in phosphocreatine (PCr)/ATP ratio, intracellular pH, and the cytosolic phosphorylation potential (CPP) with concomitant rises in deoxyhemoglobin (DH), mitochondrial reduced cytochrome oxidase aa3 (rCOaa3), blood volume, and intracellular inorganic phosphate (Pi). Using osmotic mini-pumps implanted in the third cerebral ventricle, containing 30% ethanol, it was found that brain [Mg2+]i is reduced 30% after 14 days; brain PCr fell 15%, whereas the CPP fell 40%. Such animals became susceptible to stroke from nonlethal doses of ethanol. Human subjects with mild head injury have been found to exhibit early deficits in serum ionized Mg (IMg2+); the greater the degree of early head injury (30 min-8 h), the greater and more profound the deficit in serum IMg2+ and the greater the ionized Ca (ICa2+) to IMg2+ ratio. Patients with histories of alcohol abuse or ingestion of alcohol prior to head injury exhibited greater deficits in IMg2+ (and higher ICa2+/IMg2+ ratios) and, unlike the subjects without alcohol, did not leave the hospital for at least several days. Women, for some unknown reason, exhibit a much higher incidence of morbidity and mortality from subarachnoid hemorrhage (SAH) than men. Data on 105 men and women with different types of stroke indicate that, on the average, a 20% deficit in serum IMg2+ is seen; total Mg (TMg) or blood pH is usually near normal. Women with SAH, however, exhibit much lower IMg2+ and higher ICa2+/IMg2+ ratios; the presence of ethanol in the blood is associated with even more depression in IMg2+ in SAH in women. It is possible that prior alcohol ingestion is, in large measure, responsible for a great deal of this unexplained higher incidence of SAH in women. It has recently been reported that the cyclical changes in estrogenic hormones appear to control the serum IMg2+ level in young women. A surge in estrogenic levels prior to SAH could thus precipitate, in part, the SAH. In other human studies, it has been shown that migraines and headache, dizziness, and hangover, which accompany ethanol ingestion, are associated with rapid deficits in serum IMg2+ but not in TMg. The former, and the alcohol-associated headache, can be ameliorated with IV administration of MgSO4. Premenstrual tension-headache (PTH) and its exacerbation by alcohol in women is also accompanied by deficits in IMg2+, and elevation in serum ICa2+/IMg2+; IV MgSO4 corrects the PTH and the serum deficit in IMg2+. Animal experiments show that IV Mg2+ can prevent alcohol-induced hemorrhagic stroke and the subsequent fall in brain [Mg2+]i, [PCr], pHi, and CPP. Other recent data indicate that alcohol-induced cellular loss of [Mg2+]i is associated with cellular Ca2+ overload and generation of oxygen-derived free radicals; chronic pretreatment with vitamin E prevents alcohol-induced vascular injury and pathology in the brain. (ABSTRACT TRUNCATED)
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PMID:Association of alcohol in brain injury, headaches, and stroke with brain-tissue and serum levels of ionized magnesium: a review of recent findings and mechanisms of action. 1054 55

Liver alcohol dehydrogenase oxidizes ethanol to acetaldehyde, which is further oxidized to acetate by aldehyde dehydrogenase-2 (ALDH2*1). Individuals who carry a low-activity ALDH2 (ALDH2*2) display high blood acetaldehyde levels after ethanol consumption, which leads to dysphoric effects, such as facial flushing, nausea, dizziness, and headache ("Asian alcohol phenotype"), which result in an aversion to alcohol and protection against alcohol abuse and alcoholism. Mimicking this phenotype may reduce alcohol consumption in alcoholics. RNA interference (RNAi) is a cell process in which a short interfering RNA (siRNA) of 21-25 bp guides the degradation of a complementary target mRNA. Thus, siRNAs may be useful in mimicking the Asian phenotype by inhibiting ALDH2 gene expression. We determined the inhibitory effect of three chemically synthesized siRNAs targeted against rat ALDH2 mRNA in human embryonic kidney cells (HEK-293 cell lines) transfected with a plasmid carrying the rat ALDH2 cDNA. Two of the three siRNAs were active, yielding a 65-75% reduction of ALDH2 activity. Based on the most promising siRNA sequence, three short hairpin RNA (shRNA) genes driven by the human U6 RNA promoter were designed and cloned in a plasmid. After transfection of HEK-293 cells, one of the genes was shown to be active, yielding a 50% reduction of ALDH2 activity. This effect is consistent with a 50% reduction in ALDH2 mRNA, whereas neither beta-actin mRNA nor the interferon-inducible transmembrane protein-1 mRNA levels were affected. This study describes chemically synthesized siRNAs and an endogenously synthesized shRNA, which reduce ALDH2 activity and constitute tools that should be of value for further alcohol research.
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PMID:RNA interference against aldehyde dehydrogenase-2: development of tools for alcohol research. 1925 Nov 11

Quetiapine is regarded as an effective and safe treatment for delirium. An 82-year-old man presented with a 1-week history of violent behavior and dizziness accompanied by weakness on the left side of his body. He was diagnosed with acute cerebral cortical infarction and delirium associated with alcohol abuse. After quetiapine treatment, he complained of fever and coughed up sputum, whereas his aggressive behavior improved. His symptoms persisted despite empirical antibiotic treatment. All diagnostic tests for infectious causes were negative. High-resolution computed tomography revealed bilateral consolidations and ground-glass opacities with predominantly peribronchial and subpleural distributions. The primary differential diagnosis was drug-associated interstitial lung disease, and therefore, we discontinued quetiapine and began methylprednisolone treatment. His symptoms and radiologic findings significantly improved after receiving steroid therapy. We propose that clinicians need to be aware of the possibility that quetiapine is associated with lung injury.
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PMID:A case of drug-induced interstitial pneumonia potentially related to quetiapine (seroquel) therapy for behavioral and psychological symptoms. 2478 51

Background: Because of the shortcomings of traditional pharmacotherapy for major depressive disorder and post-traumatic stress disorder (PTSD), there has been growing interest in the rapid mood-enhancing effect of ketamine. Objectives: To analyze what has been posted about ketamine use for dealing with self-reported depression and/or PTSD on one of the biggest international message boards on the internet. Methods: Qualitative study with online observation of threaded discussions on Bluelight. In-depth online searches were conducted in 2018. Twenty-nine threads, with a total of 708 units of analysis, were selected and subjected to content analysis, where, via a coding process, the units of analysis were organized into nodes. Results: Despite having several negative effects (e.g. dizziness, nausea and inability to talk), the examined discourses suggested that the use of ketamine to elevate mood was both efficient and worthwhile. Intranasal use was the most common route of administration mentioned. We traced how the mood enhancement caused by ketamine is perceived: the loss of pleasure disappears, as well as the depressed mood; the markedly diminished interest in activities vanishes and motivation comes back. From all the posts analyzed, only two reported negative outcomes (i.e. no mood-enhancing effect). The most mentioned adverse event was damage to the urinary bladder and the kidneys in cases of misuse. Conclusion: Although online research of user-generated content has its limitations in terms of reliability and validity, the present study adds relevant information on the use of ketamine for managing depression and PTSD, whether this use is done legally or not.
Am J Drug Alcohol Abuse 2020 Sep 02
PMID:The use of ketamine to cope with depression and post-traumatic stress disorder: A qualitative analysis of the discourses posted on a popular online forum. 3252 53