Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several hereditary conditions affecting cerebral, retinal and systemic microvessels have recently been described. They include CADASIL, CRV, and HERNS. We here report on a variant form of a hereditary systemic angiopathy (HSA) affecting two generations of a Caucasian family. Clinical symptoms of HSA appear in the mid-forties and are characterized by visual impairment, migraine-like headache, skin rash, epileptic seizures, progressive motor paresis and cognitive decline. Late symptoms include hepatic and renal failure. Retinal capillary microaneurysms and arteriolar tortuosity are associated with marked optic disc atrophy. Radiological hallmarks consist of multiple cerebral calcifications and tumor-like subcortical white matter lesions. Brain, peripheral nerve, muscle, kidney and colon biopsies have revealed a multi organ small vessel involvement with partly altered endothelium, perivascular inflammation and thrombotic microangiopathy. No curative therapeutic options are known for hereditary cerebral vasculopathies. The use of cyclophosphamide, azathioprine and methotrexate was of no benefit in our cases of HSA. Early diagnosis of hereditary systemic angiopathies is important in order to prevent patients from repetitive invasive diagnostic measures and to avoid the use of inappropriate and potentially harmful drugs.
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PMID:Hereditary systemic angiopathy (HSA) with cerebral calcifications, retinopathy, progressive nephropathy, and hepatopathy. 1820 7

The understanding of migraine pathophysiology has evolved from the belief that migraine is a vascular disorder, to evidence that better defines migraine as a neurogenic disorder associated with secondary changes in brain perfusion. There is evidence to suggest that the early phase of migraine pain results from neurogenic inflammation affecting cranial blood vessels and dura. Allodynia, hyperalgesia, and expansion of nociceptive fields occur during most well-established migraine attacks. These clinical features of migraine are evocative of those traditionally associated with neuropathic pain. A hypothesis that defines migraine pain as a unique neuropathic pain disorder can imply the potential for neural plasticity and may provide insight into the mechanisms that underlie the transformation of episodic to chronic forms of migraine. The neuropathic pain model of migraine pathophysiology not only paves the way for mechanism-based treatment strategies that can improve the acute and preventive management of migraine attacks, but also opens the door for the discovery of novel therapeutic targets. It also lends momentum to an understanding of clinically intriguing topics such as opiate-induced hyperalgesia and medication-overuse headache (rebound headache), opioid resistance in the treatment of chronic headache, and disease modification in defending against the potential for migraine transformation.
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PMID:Is migraine a neuropathic pain syndrome? 1877 70

A 48-year-old female presented to an emergency room with symptoms of episodic hemianopsia, dysphasia, and facial numbness. She had no obvious risk factors for cerebral vascular disease but was admitted into the hospital with a diagnosis of transient ischemic attack (TIA). A neurologist reviewed her history and discovered the additional history of bilateral head pressure accompanying her symptoms. The additional diagnosis of complex migraine with aura was added to the differential diagnosis. Migraine with aura is associated with many neurologic symptoms and can mimic stroke and TIA. Migraine-induced stroke is also described in the literature. The complex presentation of some episodes of migraine makes attention to a detailed history paramount for assessing the patient for diagnosis and for risk selection. Recent studies have demonstrated an association between migraine headaches and cardiovascular morbidity and mortality. The attributable mortality risk for migraine-induced stroke is very low.
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PMID:"TIA" or migraine in a woman with no risk factors for cerebral vascular disease. 1931 33

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) is clinically characterized by migraines with aura, recurrent ischemic strokes, cognitive and behaviour impairments and dementia and shows typical histological lesions in the muscular arteries. The disease is linked to mutations in NOTCH3, a gene located in chromosome 19. On the other hand, cerebral autosomal recessive arteriopathy with subcortical infarcts and leucoencephalopathy (CARASIL) is a poorly understood disease mainly described in the Japanese literature. This is also a hereditary vascular disease but the affected gene still is not identified. The disease clinically associates recurrent ischemic strokes with bone lesions and alopecia. None of these conditions are related with hypertension. This paper reviews the genetic, clinical, and pathological aspects of both diseases.
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PMID:[CADASIL and CARASIL]. 1932 91

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a systemic vascular disease characterized by impairment of vascular smooth muscle cell (VSMC) structure and function related to NOTCH 3 mutations. Clinically the syndrome is manifested as recurrent ischaemic strokes, migraine with aura, dementia and psychiatric symptoms. In spite of intensive investigations, there is relatively little insight into the underlying pathomechanisms that link VSMC with the Notch 3 signalling pathway, morphological changes and clinical symptoms. The introduction into neuropathology of novel immunohistochemical and molecular techniques opened new research and diagnostic perspectives in CADASIL studies. We present a review of current concepts regarding CADASIL pathogenesis, clinical picture and diagnosis in which neuropathological examinations played a key role.
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PMID:Mysteries of CADASIL - the contribution of neuropathology to understanding of the disease. 1935 29

Migraine, especially migraine with aura (MA), is an established risk factor for ischemic lesions of the brain. Recent evidence has also linked migraine to a broader range of ischemic vascular disorders including angina, myocardial infarction, coronary revascularization, claudication, and cardiovascular mortality. The mechanisms which link migraine to ischemic vascular disease remain uncertain and are likely to be complex. Cortical spreading depression, the presumed substrate of aura, may directly predispose to brain lesions and that would explain why MA is consistently demonstrated as a risk factor for cerebral ischemia, while for migraine without aura (MO), the evidence is less consistent. Additionally, individuals with migraine have a higher prevalence of risk factors known to be associated with cardiovascular disease (CVD), including hypertension, diabetes, and hyperlipidemia. The increased prevalence of CVD risk factors is also higher for MA than for MO. Since the evidence linking migraine and CVD is getting robust, neurologists should be aware of this association. Individuals with MO seem to be at little increased risk of CVD. MA is associated with an increased risk of ischemic stroke and likely also for other ischemic CVD events. Accordingly, heightened vigilance is recommended for modifiable cardiovascular risk factors in migraineurs, especially with MA. Ultimately, it will be important to determine whether MA is a modifiable risk factor for CVD and if preventive medications for migraine or antiplatelet therapy might reduce the risk of CVD in patients with MA.
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PMID:Migraine and cardiovascular disease: possible mechanisms of interaction. 1947 Sep 70

Epidemiological studies suggests that migraine is associated with disorders of the cerebral, coronary, retinal, dermal and peripheral vasculature. There is evidence that migraine is associated with endothelial dysfunction, both as a cause and a consequence. Endothelial dysfunction, a vascular risk factor, is characterized by endothelial activation and impaired vascular reactivity. Plasma and genetic biomarkers for these conditions have been identified. The clinical significance lies in the potential for the rapid identification of migraineurs at increased risk of ischaemic stroke and vascular disease through ascertainment of endothelial dysfunction biomarkers. It is uncertain whether stroke, myocardial infarction and other vasculopathies can be prevented by migraine prophylaxis, endothelial repair, platelet inhibition or a combination of these strategies.
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PMID:Migraine as a systemic vasculopathy. 1968 7

Migraine is a debilitating disorder of the CNS. Although therapeutic options for migraine attacks have tremendously advanced with the development of triptans more than a decade ago, several conditions (such as vascular disease) restrict their use. Moreover, some patients do not respond to triptans and other currently available medications. Therefore, treatment alternatives are needed. Study data show that 5-HT(1F) receptor agonists successfully abort migraine attacks. These data also suggest a favorable vascular side-effect profile of these substances, which could be beneficial for migraine treatment in subjects with cardiac or vascular disease. We discuss the current knowledge of 5-HT(1F) receptor-mediated effects, in part by comparing them to triptans, and we also summarize data from basic research and clinical trials.
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PMID:5-HT(1F) Receptor agonists: a new treatment option for migraine attacks? 2043 Mar 16

Previous reports of comorbid conditions in poliomyelitis survivors mainly focused on some disease categories, such as respiratory diseases, gastrointestinal diseases, psychiatric diseases, neurological diseases and cancer. Data regarding a wide spectrum of medical comorbidities in patients with poliomyelitis is still sparse. This study aimed to investigate and profile the wide range of comorbidities among the survivors of paralytic poliomyelitis in a Chinese population. In total, 2,032 paralytic poliomyelitis patients were selected as the study group and the comparison group consisted of 10,160 randomly selected enrollees. The comorbidities for analysis were based on a modified version of the Elixhauser Comorbidity Index. Conditional logistic regression analyses were computed to investigate the risk of comorbidities for these two groups. As compared to controls, patients with paralytic poliomyelitis had significantly higher prevalence of hypertension, ischemic heart disease, hyperlipidemia, congestive heart failure, cardiac arrhythmias, peripheral vascular disorder, stroke, paralysis, migraines, Parkinson's disease, rheumatoid arthritis, ankylosing spondylitis, pulmonary circulation disorders, chronic pulmonary disease, liver disease, peptic ulcers, hepatitis B or C, deficiency anemias, depression, and lymphoma. Most of the differences are of clinical interest, ORs often being between 2 and 3. No significant difference between poliomyelitis patients and controls was observed in the prevalence of SLE, tuberculosis, alcohol abuse and drug abuse. Our findings demonstrate that survivors of paralytic poliomyelitis in Taiwan are at higher risk of having multiple medical comorbidities although some potential confounding factors including educational level, marital status, obesity and physical activity are not available in our database. The pattern is generally consistent with previous observations from Western populations. Nevertheless, we found several novel associations which have rarely, if ever, been reported previously.
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PMID:Comorbidity profile of poliomyelitis survivors in a Chinese population: a population-based study. 2127 17

Migraine headache is a common and potentially debilitating disorder often treated by family physicians. Before diagnosing migraine, serious intracranial pathology must be ruled out. Treating acute migraine is challenging because of substantial rates of nonresponse to medications and difficulty in predicting individual response to a specific agent or dose. Data comparing different drug classes are relatively scarce. Abortive therapy should be used as early as possible after the onset of symptoms. Effective first-line therapies for mild to moderate migraine are nonprescription nonsteroidal anti-inflammatory drugs and combination analgesics containing acetaminophen, aspirin, and caffeine. Triptans are first-line therapies for moderate to severe migraine, or mild to moderate migraine that has not responded to adequate doses of simple analgesics. Triptans should be avoided in patients with vascular disease, uncontrolled hypertension, or hemiplegic migraine. Intravenous antiemetics, with or without intravenous dihydroergotamine, are effective therapies in an emergency department setting. Dexamethasone may be a useful adjunct to standard therapy in preventing short-term headache recurrence. Intranasal lidocaine may also have a role in relief of acute migraine. Isometheptene-containing compounds and intranasal dihydroergotamine are also reasonable therapeutic options. Medications containing opiates or barbiturates should be avoided for acute migraine. During pregnancy, migraine may be treated with acetaminophen or nonsteroidal anti-inflammatory drugs (prior to third trimester), or opiates in refractory cases. Acetaminophen, ibuprofen, intranasal sumatriptan, and intranasal zolmitriptan seem to be effective in children and adolescents, although data in these age groups are limited.
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PMID:Treatment of acute migraine headache. 2201 Jun 7


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