Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Familial typical migraine is a common, complex disorder that shows strong familial aggregation. Using latent-class analysis (LCA), we identified subgroups of people with migraine/severe headache in a community sample of 12,245 Australian twins (60% female), drawn from two cohorts of individuals aged 23-90 years who completed an interview based on International Headache Society criteria. We report results from genomewide linkage analyses involving 756 twin families containing a total of 790 independent sib pairs (130 affected concordant, 324 discordant, and 336 unaffected concordant for LCA-derived migraine). Quantitative-trait linkage analysis produced evidence of significant linkage on chromosome 5q21 and suggestive linkage on chromosomes 8, 10, and 13. In addition, we replicated previously reported typical-migraine susceptibility loci on chromosomes 6p12.2-p21.1 and 1q21-q23, the latter being within 3 cM of the rare autosomal dominant familial hemiplegic migraine gene (ATP1A2), a finding which potentially implicates ATP1A2 in familial typical migraine for the first time. Linkage analyses of individual migraine symptoms for our six most interesting chromosomes provide tantalizing hints of the phenotypic and genetic complexity of migraine. Specifically, the chromosome 1 locus is most associated with phonophobia; the chromosome 5 peak is predominantly associated with pulsating headache; the chromosome 6 locus is associated with activity-prohibiting headache and photophobia; the chromosome 8 locus is associated with nausea/vomiting and moderate/severe headache; the chromosome 10 peak is most associated with phonophobia and photophobia; and the chromosome 13 peak is completely due to association with photophobia. These results will prove to be invaluable in the design and analysis of future linkage and linkage disequilibrium studies of migraine.
 ...
PMID:Genomewide significant linkage to migrainous headache on chromosome 5q21. 1608 Jan 25

A 34-year-old man was admitted with his unsteady gait, difficulty in speech and a paroxysmal severe headache accompanied with sensori-motor disturbance of the right extremities and aphasic symptom. His family history was unremarkable. His unsteadiness has progressed very slowly from childhood. He noted to be inarticulate at the age of 18 years. At the age of 33 years, he suddenly had an attack of severe throbbing headache, which was mainly left parietal, with nausea and photophobia. During the headache, his right extremities were paralyzed and he became aphasic. He had lost a partial memory of the event All these symptoms had gone within 24 hours. Thereafter, the same headache occurred about once a month. Neurological examination revealed a mild truncal ataxia and ataxic dysarthria. Electroencephalography (EEG) showed intermittent delta waves restricted over the left fronto-temporal region. Brain MRI showed a moderate atrophy of superior cerebellar vermis and anterior cerebellar lobe. The diagnosis of sporadic hemiplegic migraine (SHM) with cerebellar ataxia was made. Our case was very similar to familial hemiplegic migraine (FHM) 1, of which some families are accompanied with transient amnesia, cerebellar ataxia and EEG abnormality. Although we did not detect any mutations in CACNA1A gene previously reported in FHM1, our case might share same pathogenesis with FHM1.
 ...
PMID:[Case of sporadic hemiplegic migraine with cerebellar ataxia]. 1959 4

Headache associated with moyamoya disease (HAMD) is common in moyamoya disease. However, the characteristics and classification of HAMD are largely unknown. We present a case of a 39-year-old woman with HAMD. To characterize and classify the features of this syndrome, the patient was asked to complete a 4-month diagnostic headache diary. There was a total of 15 ictal days. All episodes were without aura. The headache was more commonly pressing (10/15), mild to moderate in severity (14/15), unchanged by physical activity (11/15), and associated with photophobia (10/15). The International Headache Society Classification was utilized to determine that eight episodes met criteria for probable migraine without aura, while seven episodes met criteria for probable frequent episodic tension-type headache. We identified four other case reports of HAMD with partial descriptions of the characteristics. When combined with our patient, the median age was 34 years old (range 6-49, SD 16). Four were female, while the patient with cluster headache was male. The median time from headache onset to diagnosis with moyamoya disease was 9.5 months (range 0-192, SD 88.0). Headaches were described as migraine with aura in two of five cases, hemiplegic migraine in one of five, and cluster headache in one of five. The highest intensity was described as severe in three of three cases, in which headache intensity was reported. Meanwhile, nausea, vomiting, and photophobia were present in two of three cases, where these features were reported, while nausea without vomiting was seen in one of three cases. In all five cases, patients had other neurological symptoms, such as paresis, seizures, visual disturbances, dysarthria, allodynia, ptosis, and unilateral restless leg syndrome. In conclusion, HAMD can present as migraine without aura. It can be the first presenting symptom of moyamoya disease. The headache features are not diagnostic; hence, early neurovascular imaging should be considered in patients with new onset, refractory migraine-like headache, especially in the setting of other neurological symptoms to exclude underlying moyamoya disease. Further reports using headache diaries are needed to better characterize HAMD as well as to determine whether headache with tension-type features is also part of this condition.
 ...
PMID:Headache associated with moyamoya disease: a case story and literature review. 2001 51

A 39-year-old woman suddenly developed numbness of the left arm following mild weakness of the left upper and lower extremities, blindness in the left visual field, and difficulty finding words. Her symptoms lasted for two hours with no deficit remaining. Six months after the first episode, the first of several more occurred. Two of the episodes were followed by nausea and a non-pulsative headache around the left temporo-parietal regions and the orbit. She had also been suffering recurrent skin eruptions for the previous two years. There was no family history of migraine. Her neurological symptoms fulfilled the criteria of sporadic hemiplegic migraine (SHM). Biopsy of skin eruption revealed lymphocytic infiltration and liquefied degeneration of basal lamina. These findings were compatible with systemic lupus erythematosus (SLE). There were no lesions evident on brain MR. We diagnosed SLE and after administration of aspirin (100 mg/day) and lomerizine hydrochloride (10 mg/day), her neurological symptom completely disappeared. SHM-like headache in patients with SLE is extremely rare. Although an autoimmune or thrombotic mechanism has been suggested for neurological symptoms in SLE, further studies are needed to elucidate the mechanism. We propose that SLE should be considered as one of the differential diagnoses of SHM.
 ...
PMID:[Sporadic hemiplegic migraine-like headache in a patient with systemic lupus erythematosus]. 2053 84

Migraine is amongst the oldest of diseases known to mankind. Migraine is a heterogenous entity, usually characterised by periodic attacks of headache on one or both sides of the head. These may be accompanied by nausea, vomiting, increased sensitivity of the eyes to light (photophobia), increased sensitivity to sound (phonophobia), dizziness, blurred vision, cognitive disturbances, and other symptoms. Migraines are not always preceded by an aura and some migraines may not include headache. If migraine does not manifest itself in the form of headache but in some other form such as paroxysmal episodes of prolonged visual auras, atypical sensory, motor, or visual aura, confusion, dysarthria, focal neurologic deficits with or without a headache, it is labelled a Migraine Variant (MV). MV is therefore diagnosed by the history of paroxysmal symptoms with or without cephalgia and a prior history of migraine with aura, in the absence of other medical disorders that may contribute to the symptoms. Many of the MVs have been included and redefined in the revised edition of The International Classification of Headache Disorders (ICHD-II) 2004 classification. These include hemiplegic migraine, basilar migraine, childhood periodic syndromes, retinal migraine, complicated migraine and ophthalmoplegic migraine. Even though conditions such as vertiginous migraine, acute confusional migraine of childhood and nocturnal migraine are well recognized entities, they have not yet been included in IHCD-II, but will be discussed here in brief because they are relatively common conditions.
 ...
PMID:Migraine variants and beyond. 2104 1

Sporadic hemiplegic migraine (SHM) is a rare form of migraine. I report a 23-year-old Nigerian lady with SHM. She had recurrent attacks characterized by visual aura that progressed to headache, dysphasia, and hemiplegia. Her motor symptom was always followed by development of nausea and photophobia lasting several hours. Computerized tomography of the brain and electroencephalography were normal. She was treated with carbamazepine, aspirin, and codeine. Differential diagnoses of SHM were highlighted.
...
PMID:Sporadic hemiplegic migraine in a Nigerian woman. 2400 93

Migraine is a complex, debilitating neurovascular disorder, typically characterized by recurring, incapacitating attacks of severe headache often accompanied by nausea and neurological disturbances. It has a strong genetic basis demonstrated by rare migraine disorders caused by mutations in single genes (monogenic), as well as familial clustering of common migraine which is associated with polymorphisms in many genes (polygenic). Hemiplegic migraine is a dominantly inherited, severe form of migraine with associated motor weakness. Family studies have found that mutations in three different ion channels genes, CACNA1A, ATP1A2, and SCN1A can be causal. Functional studies of these mutations has shown that they can result in defective regulation of glutamatergic neurotransmission and the excitatory/inhibitory balance in the brain, which lowers the threshold for cortical spreading depression, a wave of cortical depolarization thought to be involved in headache initiation mechanisms. Other putative genes for monogenic migraine include KCKN18, PRRT2, and CSNK1D, which can also be involved with other disorders. There are a number of primarily vascular disorders caused by mutations in single genes, which are often accompanied by migraine symptoms. Mutations in NOTCH3 causes cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a hereditary cerebrovascular disease that leads to ischemic strokes and dementia, but in which migraine is often present, sometimes long before the onset of other symptoms. Mutations in the TREX1 and COL4A1 also cause vascular disorders, but often feature migraine. With respect to common polygenic migraine, genome-wide association studies have now identified single nucleotide polymorphisms at 38 loci significantly associated with migraine risk. Functions assigned to the genes in proximity to these loci suggest that both neuronal and vascular pathways also contribute to the pathophysiology of common migraine. Further studies are required to fully understand these findings and translate them into treatment options for migraine patients.
 ...
PMID:Genetics of Migraine: Insights into the Molecular Basis of Migraine Disorders. 2961 Nov 88

Migraine is a disorder characterized by attacks of monolateral headaches, often accompanied by nausea, vomiting, and photophobia. Around 30% of patients also report aura symptoms. The cause of the aura is believed to be related to the cortical spreading depression (CSD), a wave of neuronal and glial depolarization originating in the occipital cortex, followed by temporary neuronal silencing. During a migraine attack, increased expression of inflammatory mediators, along with a decrease in the expression of anti-inflammatory genes, have been observed. The aim of this study was to evaluate the expression of inflammatory genes, in particular that of IL-1 receptor antagonist (IL-1RN), following CSD in a mouse model of familial hemiplegic migraine type 1 (FHM-1). We show here that the expression of IL-1RN was upregulated after the CSD, suggesting a possible attempt to modulate the inflammatory response. This study allows researchers to better understand the development of the disease and aids in the search for new therapeutic strategies in migraine.
 ...
PMID:Upregulation of IL-1 Receptor Antagonist in a Mouse Model of Migraine. 3133 Nov 9

Objectives: Vestibular migraine (VM) is a common vestibular disorder, and familial aggregation of VM with autosomal-dominant inheritance has been described, which supports a genetic background. This study aimed to describe the clinical phenotype of a family with VM, and identify a candidate gene for VM. Methods: We recruited six individuals (four affected and two unaffected) from three consecutive generations of a Korean family with VM, and performed whole-exome sequencing to search for candidate genes. Results: All affected individuals presented with recurrent vertigo, headache, and nausea/vomiting that fulfilled the diagnostic criteria of VM. Two individuals also experienced transient hemiparesis or dysarthria during the episodes. The symptoms were triggered by physical or emotional stress. Interictal examinations showed uni- or bi-directional horizontal gaze-evoked nystagmus in three of the individuals. They had no causative mutations in genes causing familial hemiplegic migraine or episodic ataxia. Through whole-exome sequencing from three affected individuals, we identified a nonsense mutation c.3526C>T in TRPM7 that encodes a cation channel selective to Ca2+ and Mg2+. Conclusions: Alterations in intracellular Ca2+ and Mg2+ homeostasis by TRPM7 mutation may contribute to the development of the VM phenotype. Our result suggest that TRPM7 is a novel candidate gene for VM.
 ...
PMID:TRPM7 as a Candidate Gene for Vestibular Migraine. 3319 64