Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

EEG abnormalities in migraine have been reported by a number of authors during the last 50 years. Prevalences vary considerably in the older literature. A number of unspecific rhythms related to drowsiness or hyperventilation have probably been counted as "abnormal", and the reported numbers of definitely abnormal EEG rhythms have been consistently low. In a few controlled and blinded studies, however, slight excess of various EEG rhythms has been found in migraine patients. Similar prevalences of interictal EEG abnormalities have generally been found in patients with classic and common migraine, but the diagnostic classification may not have been precise enough in some studies. During visual aura, either slow waves, depression of background activity amplitude or normal EEG have been reported. The most definitely abnormal EEGs with unilateral or bilateral delta activity have been recorded during attacks of hemiplegic migraine, and during attacks of migraine with disturbed consciousness. The relationship between migraine and epilepsy has still not been adequately clarified. The connection seems to exist in several small entities (e.g. migraine-like headache as an epileptic manifestation, epileptic seizures triggered by epileptic attacks, and possibly in epilepsies with occipital spike waves), but it is seemingly not "fundamental". Newer methods, i.e. EEG frequency analysis and topographic brain mapping, are promising tools in this field. So far, mostly small studies have been published with somewhat inconsistent results. A pattern of increased alpha rhythm variability (and/or asymmetry) in the headache-free phase seems to emerge, however. Significant asymmetry of alpha and theta during headache has been reported in one topographic brain mapping study. Magnetoencephalographic studies of migraine patients have demonstrated slow wave-shifts (similar to those observed in animals with spreading depression). The EEG patterns observed in migraine patients seem to suggest a possible physiological connection between sleep, hyperventilation and migraine. The study of such relationship may shed new light on migraine pathophysiology.
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PMID:EEG in migraine: a review of the literature. 205 54

We reviewed the medical records of 283 cocaine users consecutively admitted to a municipal hospital and identified 37 patients (13.1%) complaining of headaches. These patients were divided into three groups. Three patients had migraine-like headaches and transient hemiparesis associated with cocaine use. Five patients had headaches associated with cocaine withdrawal. In 29 patients headaches were not clearly associated with cocaine. Twenty-two of the 29 had chronic daily headaches; nine of these patients were depressed. Three had focal brain lesions with chronic daily headache or acute onset global headache. The four remaining patients had other headaches. Based on these findings, we conclude that: (1) Headache is a common complaint in hospitalized cocaine users; (2) Cocaine may occasionally trigger a syndrome which resembles hemiplegic migraine. The potential mechanisms of this syndrome will be discussed; (3) Hospitalized cocaine users who present with headaches most frequently have depression with suicidal ideation, often associated with cocaine withdrawal; and (4) Structural brain disease in these patients may result from a variety of causes.
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PMID:Headaches in hospitalized cocaine users. 271 72

The authors report the case of a 26 year old non-migrainous man who presented over a 5 week period with a cluster of classical migrainous attacks associated with CSF lymphocytosis. The association of this type of CSF response with attacks of migraine is unusual; in migraine the CSF is normal or may show an isolated increase in protein content (with the exception of the very rare familial hemiplegic migraine). In the reported case, other conditions liable to give rise to migraine and CSF lymphocytosis having been excluded (acute DLE, brucellosis...), this association corresponded to a benign and spontaneously regressive condition, possibly a migraine symptomatic of benign acute lymphocytic meningitis. The authors suggest that a primary meningeal inflammation may have been the cause of the cluster of migraine attacks which in this case were more accompanied perhaps because they induced a wave of depression of cortical activity.
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PMID:[Migraine manifestations and lymphocyte pleocytosis of the cerebrospinal fluid]. 363 29

Following the exemplification of the clinical symptoms the EEG findings of 10 attacks of hemiplegic migraine in 6 children are reported on. Characteristically most of these are severe unilateral or focal disturbances. Five times these appeared as delta-activity, two times as theta-delta-activity, and in one case as theta-activity or alpha-reduction. Only once, a diffuse slowing of the background-activity over both hemispheres could be shown. With one exception in addition to the foci simultaneous diffuse changes were recorded in all children, (four times slight, twice slight to moderate and three times moderate to severe). A predominance of one hemisphere was not recognizable. The foci were not localized to one particular region of the brain. Most of the changes had subsided after a few days. In one case a slight focal voltage depression was apparent even after three month of a year.
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PMID:[The EEG during the hemiplegic migraine attack of children]. 678 Mar 1

The pathophysiology of migraine is not yet fully understood. The most important structures involved seem to be the central nervous system (cortex and brain stem), the trigeminovascular system and related cranial arteries, other autonomic fibres innervating such vessels, and various local vasoactive agents, including SP, CGRP, NO, VIP, NPY, ACh, NA, NKA, among others. The spreading depression phenomenon may explain clinical as well experimental findings in migraine. Its propagation velocity mirrors what is found in clinical aura, it may activate the spinal trigeminal nucleus and may induce CGRP and NO release. Circulatory changes detected with various imaging procedures during migraine also support the pathophysiological role of spreading depression. Three abnormal loci (chromosomes 1 and 19) have been recently found in familial hemiplegic migraine. This produces abnormalities in the voltage-dependent P/Q Ca channel, specific for the central nervous system, which regulates the release of various neurotransmitters, probably including serotonin. It is possible that a channelopathy underlies the pathophysiology of migraine, as in other paroxysmal neurological disorders secondary to membrane hyperexcitability.
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PMID:[Physiopathology of migraine]. 1002 93

Migraine is an inheritable disease, and the mutation causing a rare variant of migraine (familial hemiplegic migraine) has now been demonstrated. The mutated gene encodes a subunit of a brain-specific calcium channel in cell membranes. Brains of patients with recurrent migraine attacks seem to behave differently from other brains, also when examined outside attacks, in that they commonly demonstrate lack of habituation when exposed to serial stimuli. The patho-physiological process of the attack might well consist of a spreading cortical depression starting in the occipital region and gradually involving other parts of the cortex. It is primarily a cerebral process secondarily accompanied by reduced cerebral blood flow, later converting into increased flow. The pain of migraine probably is mediated by way of the trigeminal nerve which releases vasoactive peptides leading to dilatation of the greater blood vessels. During an attack there is increased metabolism in cranial parts of the brain stem, demonstrated as areas of increased blood flow in PET studies. This increased metabolism persists even when the symptoms of migraine have disappeared after drug treatment, perhaps because the migraine attacks may be generated in this region. The primary dysfunction in migraine probably is located in the brain rather than in blood vessels.
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PMID:[Current viewpoints on etiology and physiopathology of migraine]. 1035 52

Migraine aura is probably caused by cortical-spreading depression. No treatment for acute and severe migraine aura has been described previously. The effect of ketamine (25 mg intranasally) was studied in 11 patients with severe, disabling auras resulting from familial hemiplegic migraine. In five patients ketamine reproducibly reduced the severity and duration of the neurologic deficits, whereas in the remaining six patients no beneficial effect was seen. Ketamine offers, for the first time, a possible treatment option for severe and prolonged aura.
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PMID:Aura in some patients with familial hemiplegic migraine can be stopped by intranasal ketamine. 1089 26

The pathophysiology of the neurological deficits in hemiplegic migraine remains unclear. Both neurogenic and vascular etiologies have been proposed to explain this phenomenon. We present the case of a patient with hemiplegic migraine in whom there was no diffusion weighted magnetic resonance imaging evidence of cerebral ischemia, despite persistent left hemiplegia and diffuse vasospasm on cerebral angiography, there was no diffusion weighted magnetic resonance imaging evidence of cerebral ischemia. In addition, hypoperfusional changes were seen diffusely, more so on the less symptomatic hemisphere, whereas depression of cortical electrical activity was seen for several days on the right side. These findings support the notion that although both neurogenic and vascular changes occur in hemiplegic migraine, the former seems to be a more likely explanation for the neurological deficits.
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PMID:Prolonged cortical electrical depression and diffuse vasospasm without ischemia in a case of severe hemiplegic migraine during pregnancy. 1286 63

The field of migraine genetics has seen an explosion of information over the last year. In a recent breakthrough, missense mutations in a chromosome 1q23 gene, ATP1A2, encoding a Na+, K+-ATPase, have been identified in four distinct pedigrees with a rare form of familial hemiplegic migraine (FHM). ATP1A2 is expressed in the brain, like the voltage gated calcium channel gene, CACNA1A, previously identified as the first hemiplegic migraine gene (FHM1). The shared hemiplegic migraine phenotype of mutations in ATP1A2 and CACNA1A raises the possibility that they coordinately regulate ion homeostasis that determines susceptibility to the initiation of both migraine aura and the pain phase of migraine. For the more common and genetically complex forms of migraine, genome-wide screens have identified several new loci on 4q24, 6p12.2-21.1, 11q24, and 14q21.2-q22.3, suggesting additional migraine genes in these regions. In addition, a recent large case-control association study has linked single nucleotide polymorphisms in the insulin receptor/INSR gene with migraine. However, these polymorphisms do not result in detectable changes in receptor function. The continuing genetic identification of key proteins involved in migraine will refine our understanding of this common and sometimes debilitating disorder, which can strike during the most productive years of a person's life. Given the co-morbidity of migraine with depression and bipolar disorder, our knowledge of the causes of migraine may also contribute to our understanding of these disorders.
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PMID:Update on the genetics of migraine. 1462 54

Our knowledge about migraine pathogenesis has increased exponentially over the last decade and this greatly due to the advances in genetics. In familial hemiplegic migraine (FHM), the findings of mutations in the CACNA1A gene (19p13), coding for the pore-forming subunit (alpha1A) of neuronal voltage-dependent P/Q-type calcium channels (FHM1), and in the ATP1A2 gene (1q21-23), encoding the alpha2-subunit of the Na+, K+ ATPase ionic pump (FHM2) have focused attention on central nervous system ionic channels and helped to better understand FHM pathophysiology. A dysfunction of these channels modifies neuronal excitability (favouring spreading depression), chemical neurotransmission and, indirectly, neuronal metabolism. These channels may represent targets for novel anti-migraine drugs, which underscores their importance for the frequent forms of migraine (without or with aura). Studies of gene associations, neuromuscular transmission, cerebellar functions, neuronal excitability and metabolism and certain drug effects suggest indeed that ionic channels play a pathogenic role in migraine with aura patients. However, in the majority of patients they are probably not the sole culprit, since most of the frequent forms of migraine seem to have a more complex genetic predisposition based on a number of single nucleotide polymorphisms. The challenge for the next decade is to establish correlations between the geno- and the phenotype of migraine patients which needs more frequent and focused genetic studies and a more precise phenotype, based on clinical as well as on neurophysiologic and metabolic data.
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PMID:[Genetics of migraines: from ionic channels to single nucleotide polymorphisms?]. 1534 75


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