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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Headaches represent one of the most common reasons why children and adolescents seek medical attention and are the primary reason that they are referred to pediatric neurology practices. The most common headache syndromes diagnosed are migraine, tension-type, and chronic daily headache, and the bulk of recent medical literature regarding headache in children has focused on these clinical entities. Children are prone to have unusual headache syndromes, most of which fall under the category of "primary headache," most notably as manifestations of migraine with aura. Included within this group are basilar-type and hemiplegic migraine. The most intriguing subset included in the International Headache Society's classification system is the so-called "periodic syndromes of childhood that are precursors to migraine." These syndromes, quite peculiar to children, present a wide variety of episodic symptoms, including movement disorders, vomiting, ataxia, and vertigo, and may not include headache at all. This article provides an overview of some of the more unusual headache syndromes in children and adolescents.
Curr Pain Headache Rep 2007 Oct
PMID:Unusual headache syndromes in children. 1789 29

The aim of this study was to delineate any dysfunction of neuromuscular transmission (NMT) by single-fibre electromyography (SFEMG) in some rare types of migraine. Recent studies have shown subclinical dysfunction of NMT in migraine with aura and cluster headache by using SFEMG, whereas another recent study has shown NMT to be normal in familial hemiplegic migraine (FHM) with CACNA1A mutations. Thirty patients with rare primary headache syndromes [18 with sporadic hemiplegic migraine (SHM), six with FHM and six with basilar-type migraine (BM)] and 15 healthy control subjects without any headache complaints underwent nerve conduction studies, EMG and SFEMG during voluntary contraction of the extensor digitorum communis muscle. Ten to 20 different potential pairs were recorded and individual jitter values calculated. The results obtained from patient groups were compared with those from the normal subjects. Of 600 individual jitter values of the patients, 27 (4.5%) were abnormally high, whereas only 3/205 (1.5%) jitter values from normal subjects were abnormal. Abnormal NMT was found in 4/30 (13.3%) patients (three SHM and one BM), but in none of the control subjects. Only in SHM patients was the number of individual abnormal jitter values slightly but significantly different from normal controls. The present study demonstrates that subclinical NMT abnormality is slightly present in only SHM and BM patients, but not in FHM patients.
Cephalalgia 2007 Nov
PMID:Investigation of neuromuscular transmission in some rare types of migraine. 1791 7

The comorbidity between epilepsy and migraine has been well known for a century, yet it is still not fully understood; the two disorders also share some risk factors, symptoms, and preventive drug therapy. A series of clinical observations and scientific data support the hypothesis of alteration of cortical excitability as a possible mechanism underlying their pathology, with both disorders characterized by transient paroxysmal neurological disturbance. So far, the numerous pathophysiological mechanisms responsible for neuronal hyperexcitability have only been studied in familial hemiplegic migraine (FHM), but they do suggest a link between migraine and epilepsy. Several studies support the hypothesis of a clinical continuum between some types of migraine and some types of epilepsies, with possibly even a complete overlap, representing, in particular cases, headache as the sole ictal manifestation of seizures. Taking into account the data in the literature, we hypothesize that several aetiopathological noxae (either environmental or genetics), such as Na+-K+ ATPase pump impairment, converging on a common final pathway represented by neuronal membrane hyperexcitability, could manifest as either epilepsy or headache/migraine, or both. The potential implications arising from this point of view include (a) a revision of headache/migraine diagnostic criteria as the sole ictal epileptic manifestation in international classifications of both epilepsies and headache disorders; (b) the careful follow-up of patients with headache/migraine as a residual feature, taking into consideration a revised concept of "complete seizure control" to avoid mistakes due to inopportune withdrawal of antiepileptic treatment. In addition, we suggest that headache is associated with other ictal-sensitive and motor features (more than those reported); these may be highly underestimated due to impairment of consciousness during complex partial seizures with or without secondary generalization.
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PMID:Hypothesis on neurophysiopathological mechanisms linking epilepsy and headache. 1819 8

A possible relation between migraine and epilepsy has been a matter of debate for many decades. Clinical, epidemiological and therapeutic similarities may be coincidental and are no proof of a common aetiological background. However, a genetically determined dysfunction of ion channels seems to point to a common underlying mechanism for both paroxysmal disorders. For example, mutations in the three known genes for familial hemiplegic migraine can cause epilepsy. It is likely that the development of specific drugs aimed at restoring ion-channel function and/or related cellular signalling pathways might benefit patients with epilepsy as well as those with migraine. This review will briefly summarize the clinical, epidemiological, pathophysiological and therapeutic similarities between migraine and epilepsy. Most attention will be paid to the genetic relationship between these two paroxysmal disorders.
Cephalalgia 2008 Feb
PMID:A review of the genetic relation between migraine and epilepsy. 1819 81

Latent class analysis was performed on migraine symptom data collected in a Dutch population sample (N = 12,210, 59% female) in order to obtain empirical groupings of individuals suffering from symptoms of migraine headache. Based on these heritable groupings (h(2) = 0.49, 95% CI: 0.41-0.57) individuals were classified as affected (migrainous headache) or unaffected. Genome-wide linkage analysis was performed using genotype data from 105 families with at least 2 affected siblings. In addition to this primary phenotype, linkage analyses were performed for the individual migraine symptoms. Significance levels, corrected for the analysis of multiple traits, were determined empirically via a novel simulation approach. Suggestive linkage for migrainous headache was found on chromosomes 1 (LOD = 1.63; pointwise P = 0.0031), 13 (LOD = 1.63; P = 0.0031), and 20 (LOD = 1.85; P = 0.0018). Interestingly, the chromosome 1 peak was located close to the ATP1A2 gene, associated with familial hemiplegic migraine type 2 (FHM2). Individual symptom analysis produced a LOD score of 1.97 (P = 0.0013) on chromosome 5 (photo/phonophobia), a LOD score of 2.13 (P = 0.0009) on chromosome 10 (moderate/severe pain intensity) and a near significant LOD score of 3.31 (P = 0.00005) on chromosome 13 (pulsating headache). These peaks were all located near regions previously reported in migraine linkage studies. Our results provide important replication and support for the presence of migraine susceptibility genes within these regions, and further support the utility of an LCA-based phenotyping approach and analysis of individual symptoms in migraine genetic research. Additionally, our novel "2-step" analysis and simulation approach provides a powerful means to investigate linkage to individual trait components.
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PMID:A genome-wide linkage scan provides evidence for both new and previously reported loci influencing common migraine. 1836 23

A 71-year-old woman presented with recurrent episodes of headache accompanied by hemihypoesthesia, fever, aphasia, reduced consciousness and worsening of pre-existing ataxia. Brain imaging revealed atrophy of the cerebellum. The white cell count in the cerebrospinal fluid was slightly increased. The patient had a family history of migraine and cerebellar ataxia. DNA testing revealed a missense mutation in the CACNA1A gene, confirming the diagnosis of familial hemiplegic migraine. Familial hemiplegic migraine is a rare subtype of migraine with aura. It follows an autosomal dominant pattern of inheritance. Patients with familial hemiplegic migraine exhibit a wide spectrum of symptoms, which can hinder the diagnosis. If a patient presents with recurrent coma or encephalitis with or without cerebellar ataxia, familial hemiplegic migraine should be included in the differential diagnosis.
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PMID:[Familial hemiplegic migraine resulting in recurrent coma]. 1838 Mar 88

In children and young adults migraine attacks can be triggered by mild head injury. The literature on this syndrome was surveyed and 50 case reports found to meet the latest criteria of classification requiring at least two similar attacks for diagnosis of migraine (except for common migraine which was excluded from review). 33 subjects had at least one trauma-triggered attack and one identical or similar spontaneous attack, 17 cases at least two similar or identical trauma triggered attacks. An analysis of all cases showed the following features: The symptoms of migraine mostly start with a latency between one and thirty minutes after the injury and dissolve within one day. First attacks without mention of headache were mainly found in children younger than 8 years. Trauma-triggered migraine attacks are well documented for familial hemiplegic migraine, migraine attacks with hemispheric symptoms and attacks with disturbances of consciousness, while the view that posttraumatic transient cortical blindness and transient global amnesia are migraine attacks is insufficiently supported. A hereditary predisposition for a traumatic trigger mechanism seems to be present at least in familial hemiplegic migraine. Nosologic relations to syndromes of secondary neurological deterioration after mild head injury in childhood are discussed.
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PMID:[Trauma-triggered migraine attacks. Review of the literature.]. 1841 97

We studied four members of a family suffering from typical attacks of familial hemiplegic migraine (FHM) caused by a new mutation, R548C, of ATP1A2 gene in exon 12. One individual had also childhood absence epilepsy and generalized tonic-clonic seizures (GTCS). GTCS were followed by a severe attack of hemiplegic migraine at four times. Sodium valproate enabled control of both the epileptic seizures and the most severe FHM attacks. This association of FHM and epileptic seizures and their control with the same treatment suggest similar pathophysiological mechanisms.
Cephalalgia 2008 Jul
PMID:Severe attacks of familial hemiplegic migraine, childhood epilepsy and ATP1A2 mutation. 1849 90

The aim of this study was to investigate the involvement of the CACNA1A and ATP1A2 gene in a population-based sample of sporadic hemiplegic migraine (SHM). Patients with SHM (n = 105) were identified in a nationwide search in the Danish population. We sequenced all exons and promoter regions of the CACNA1A and ATP1A2 genes in 100 patients with SHM to search for possible SHM mutations. Novel DNA variants were discovered in eight SHM patients, four in exons of the CACNA1A gene and four in exons of the ATP1A2 gene. Six of the variants were considered non-pathogenic. The causal role of the two remaining DNA variants is unknown until functional studies have been made or independent genetic evidence is discovered. Only very few DNA variants were identified in 100 SHM patients, and regardless of whether the identified variants are causal the CACNA1A and ATP1A2 genes are not major genes in SHM.
Cephalalgia 2008 Sep
PMID:Screen for CACNA1A and ATP1A2 mutations in sporadic hemiplegic migraine patients. 1851 63

Migraines carry a substantial genetic liability, and in families affected with the typical migraines (migraine with, MA, and without aura, MO) linkage to some chromosomal loci has been reported. As yet however, no genes are known for MA/MO, while the three genes discovered as responsible for familial hemiplegic migraine (FHM) are not involved in the typical migraines. Accordingly, we propose to consider FHM as a syndromic migraine and not as a variety of MA. Moreover, we suggest that epigenetic mechanisms play a role in the determination of the typical migraines, and that the primary headaches represent behavioural responses (sickness behaviour, fight-or-flight responses), having adaptive advantage and having been evolutionary conserved, in which pain represents a signal of homeostatic imbalance. Epigenetic mechanisms and this proposed genetic behavioural model could be usefully incorporated into headache genetic research.
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PMID:Migraine: a genetic disease? 1854 96


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