Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Headache and sleep have long been recognised as being interdependent due to specific causative factors. Yet, the precise understanding of the roles played by these factors in this interdependency remains elusive. Many observations have suggested a reciprocal relationship between headache and sleep; however, these hypotheses have only been partially substantiated by robust findings. Being so, additional well-designed clinical and laboratory studies are required to confirm these relationships. Nonetheless, sleep and headache are known to be related in several ways: primary headache such as migraine, cluster headache (CH) and hypnic headache (HH) can be triggered by sleep, while chronic morning headaches can be caused by sleep disorders such as sleep apnoea and insomnia. Furthermore, headache and sleep disorders can also be symptoms of other underlying pathologies. Migraine, CH and HH seems to be related to sleep stages suggesting that they may in fact be a chronobiological disorder. Patients suffering from chronic morning or nocturnal headache should be considered for the presence of possible sleep disturbances.
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PMID:Headache and sleep. 1687 51

Migraine and obesity are associated in several ways. First, both are prevalent and disabling disorders influenced by genetic and environmental risk factors. Second, migraine with aura, as obesity, seems to be a risk factor for cardiovascular events. Finally, large population-based studies suggest that obesity is a risk factor for chronic migraine after adjusting for comorbidities. In this article, we discuss plausible mechanisms that may account for this association. Several of the inflammatory mediators that are increased in obese individuals are important in migraine pathophysiology, including interleukins and calcitonin gene-related peptide (CGRP). These mediators may increase the frequency, severity, and duration of migraine attacks per se, which in turn would cause central sensitization. Repeated central sensitization may be associated with permanent neuronal damage close to the periaqueductal gray area, with poor modulation to pain. Obesity is also a state of sympathetic activation, which may contribute to increase in headache frequency. Furthermore, the levels of adiponectin are decreased in obesity. At low but not normal levels, adiponectin is nociceptive. Shared biologic predisposition may also play a major role. Orexins modulate both pain and metabolism. Dysfunction in the orexins pathways seems to be a risk factor for both conditions. Finally, conditions that are comorbid to both states (e.g., depression, sleep apnea) may also make the relationship between both diseases more complex.
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PMID:Obesity, migraine, and chronic migraine: possible mechanisms of interaction. 1751 49

A patent foramen ovale (PFO) is a common finding present in 25% of the population. A relationship between PFO and several clinical conditions such as stroke, migraine, platypnea-orthodeoxia syndrome, neurological decompression illness in divers, high altitude pulmonary edema, sleep apnea, and economy class syndrome have been documented. Observational non-randomized studies have shown percutaneous PFO closure more effective than medical treatment for stroke prevention, in particular in patients with complete closure as well as in patients with more than one cerebrovascular event at baseline. In the case of migraine, PFO closure has been shown to result in a marked reduction in migraine burden or migraine days. PFO anatomy, epidemiological data on associated clinical conditions, comparison between percutaneous closure and medical treatment, as well as the technical aspect of the procedure are described in this review.
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PMID:Percutaneous closure of the patent foramen ovale. 1791 71

Chronic headache is still a frequent problem in old age, affecting about 10% of all women and 5% of all men older than 70 years. The incidence of primary headache decreases with advancing age, while that of secondary headache increases. The clinical characteristics of migraine can also change with age; for example, vegetative symptoms are less prominent, and less intense migrainous pain localized predominantly in the neck is frequently reported. Migraine aura can also be experienced more frequently in isolation, without a headache. Hypnic headache is a rare primary headache syndrome that occurs almost exclusively in the elderly. Most of the secondary headache syndromes that occur more frequently in old age present clinically as tension-type headache. Examples of rather common reasons for secondary headache syndromes in the elderly are intracranial space-occupying lesions, ophthalmological problems and autoimmune diseases such as giant cell arteritis. Elderly patients are especially likely to have a number of illnesses at any one time for which they take various medications each day, so that headaches can also quite often be caused by their medication or by withdrawal of these. As a result of such multimorbidity the homeostasis is disturbed in such patients, leading to various conditions that can entail concomitant headaches (sleep apnoea syndrome, dialysis headache, headache attributed to arterial hypertension or hypothyroidism). Familiar facial neuralgias, such as trigeminal neuralgia or postherpetic neuralgia following manifest herpes zoster affecting the face, become markedly more frequent with age. In general, in the treatment of headaches in the elderly it is essential to pay careful attention to potential interactions with the multiple drugs needed because of other diseases; in addition, the comorbidities themselves have to be taken into account, especially depression, anxiety and cognitive impairment, necessitating multimodal, interdisciplinary therapy plans.
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PMID:[Headache in the elderly]. 1822 47

Patent foramen ovale (PFO) is a remnant of the foetal circulation, found in about a quarter of the population. PFO is an asymptomatic condition and the high prevalence infers that it is in most cases of no or only limited clinical significance. However, recent research has found an increased prevalence of PFO in cryptogenic stroke, decompression illness and migraine. The presence of a PFO has also been associated with oxygen desaturation in conditions such as obstructive pulmonary disease and obstructive sleep apnoea. The rapid evolution and widespread availability of catheter-based closing techniques have further stimulated interest. The seemingly growing significance of PFO will be discussed in this review.
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PMID:The significance of patent foramen ovale: a current review of associated conditions and treatment. 1923 60

The treacherous and deceptive nature of pheochromocytoma makes it crucial to detect and treat it promptly; otherwise it will almost certainly be fatal from cardiovascular complications or metastases. Hypertension occurring in patients with pheochromocytomas is sustained in about 50% and paroxysmal in the remainder; however, many patients remain normotensive. Hypertension attacks may be precipitated by physical activity, postural changes, anxiety, certain foods or wine, some drugs, operative procedures, etc. Cardinal manifestations are paroxysmal hypertension, headache, palpitations +/- tachycardia, inappropriate sweating; anxiety, tremulousness, pallor (rarely flushing), chest and abdominal pains; nausea and vomiting often occur. Hypercatecholaminemia manifestations are more common and pronounced when paroxysmal hypertension occurs, but persons with familial pheochromocytoma may be asymptomatic. Protean manifestations of pheochromocytoma may simulate many conditions, some of which may have elevated plasma and urine catecholamines and their metabolites. Baro-reflex failure, postural tachycardia syndrome, sleep apnea, carcinoid, renal failure, and pseudopheochromocytoma may be diagnostic challenges. The history, physical examination, biochemical testing (after eliminating interfering drugs, when possible) for plasma and urinary metanephrines can usually establish or exclude presence of pheochromocytomas. Occasionally a clonidine suppression test is needed to differentiate neurogenic from pheochromocytic hypertension. Manifestations suggesting hypercatecholaminemia without hypertension are highly atypical of pheochromocytoma. Pheochromocytoma may present as panic attacks, pre-eclampsia, cardiomyopathy, infection with fever and leucocytosis, diabetes, migraine, shock, Cushing's syndrome, multiple organ failure with lactic acidosis, neurological manifestations, transitory electrocardiogram abnormalities, constipation, intestinal obstruction, visual impairment, convulsions, etc. The key to diagnosis is always to think of pheochromocytoma in the differential diagnosis of hypertension.
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PMID:The protean manifestations of pheochromocytoma. 1924 99

Epilepsy is a chronic condition that may be associated with several other diseases. In these cases, we should consider the following points: (1) antiepileptic drug (AED) treatment may positively or negatively affect comorbid disease, (2) drugs used for treatment of co-morbid disease may influence seizure threshold, (3) AED toxicity can be affected by a comorbid condition and (4) co-administration of AEDs with drugs used for treatment of comorbid conditions can be associated with clinically relevant drug-drug interactions. In this article, we discuss problems that are usually encountered when an appropriate AED treatment has to be selected in newly diagnosed epileptic patients who also have (an)other neurological disease(s). Comorbidity of epilepsy with cerebrovascular diseases, dementias, mental retardation, attention deficit and hyperactivity disorder, brain tumours, infections of the CNS, migraine, sleep disturbances (obstructive sleep apnoea syndrome), substance abuse and multiple sclerosis is discussed.
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PMID:Neurological comorbidity and epilepsy: implications for treatment. 1952 25

Hand dominance is defined as a proneness to use one hand rather than another in performing the majority of activities and this is the most obvious example of cerebral lateralization and an exclusive human characteristic. Left-handed people comprise 6-14% of the total population, while in Serbia, this percentage is 5-10%, moving from undeveloped to developed environments, where a socio-cultural pressure is less present. There is no agreement between investigators who in fact may be considered a left-handed person, about the percentage of left-handers in the population and about the etiology of left-handedness. In the scientific literature left-handedness has been related to health disorders (spine deformities, immunological disorders, migraine, neurosis, depressive psychosis, schizophrenia, insomnia, homosexuality, diabetes mellitus, arterial hypertension, sleep apnea, enuresis nocturna and Down Syndrome), developmental disorders (autism, dislexia and sttutering) and traumatism. The most reliable scientific evidences have been published about the relationship between left-handedness and spinal deformities in school children in puberty and with traumatism in general population. The controversy of other results in up-to-now investigations of health aspects of left-handedness may partly be explained by a scientific disagreement whether writing with the left hand is a sufficient criterium for left-handedness, or is it necessary to investigate other parameters for laterality assessment. Explanation of health aspects of left-handedness is dominantly based on Geschwind-Galaburda model about "anomalous" cerebral domination, as a consequence of hormonal disbalance.
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PMID:[Left-handedness and health]. 2060 90

Although the majority of patients with glaucoma have elevated intraocular pressure as the presumed etiology for their resultant neuropathy, it is well known that approximately 25% of patients with glaucoma have intraocular pressure within the normal range for their race. These patients may have conditions that facilitate non-pressure related stress to the retina and optic nerve that might directly contribute to their glaucomatous neuropathy and include chronic or intermittent ischemia (i.e atherosclerosis, heart disease, vasospasm, migraine, sleep apnea), altered scleral/optic nerve head morphology that predisposes to glaucomatous stress (i.e myopia); genetic mutations that predispose to glaucoma damage at normal IOP (OPA-1,optineurin, myocilin) and evidence of aberrant immunity that suggests that their glaucoma might be a form of an autoimmune neuropathy (i.e. presumed autoimmune glaucoma). This review provides a critical assessment of the potential role for autoimmunity as an initiating or exacerbating etiology in some patients with glaucoma.
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PMID:The case for autoimmunity in glaucoma. 2080 Nov 14

Glaucoma is now considered an abnormal physiology in the optic nerve head that interacts with the level of intraocular pressure (IOP), with the degree and rate of damage depending on the IOP and presumably the degree of abnormal physiology. Diagnosis of normal-tension glaucoma (NTG), defined as glaucoma without a clearly abnormal IOP, depends on recognizing symptoms and signs associated with optic nerve vulnerability, in addition to absence of other explanations for disc abnormality and visual field loss. Among the findings are a halo or crescent of absence of retinal pigment epithelium around the disc, bilateral pre-chiasmal visual field defects, splinter hemorrhages at the disc margin, vascular dysregulation (low blood pressure, cold hands and feet, migraine headache with aura, and the like), or a family history of glaucoma. Possibly relevant, is a history of hemodynamic crisis, arterial obstructive disease, or sleep apnea. Neurological evaluation with imaging is needed only for atypical cases or ones that progress unexpectedly. Management follows the same principle of other chronic glaucomas, to lower the IOP by a substantial amount, enough to prevent disabling visual loss. However, many NTG cases are non-progressive. Therefore, it may often be wise in mild cases to determine whether the case is progressive and the rate of progression before deciding on how aggressivene to be with therapy. Efforts at neuroprotection and improvement in blood flow have not yet been shown effective.
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PMID:Normal-tension glaucoma (Low-tension glaucoma). 2115 42


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