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jueves, 14 de abril de 2011

MIGRAÑA Y RESONANCIA MAGNETICA

Apreciados compañeros:

les envio una revisión de Migraña y resonancia magnética, los artículos son de acceso a texto completo, libres.

Muy cordiales saludos a la comunidad del AMEINNN


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PubMed Results
Items 1 - 20 of 1112

1. Magn Reson Med Sci. 2011;10(1):49-52.

Susceptibility-weighted Imaging and Magnetic Resonance Angiography during Migraine Attack: A Case Report.

Shimoda Y, Kudo K, Kuroda S, Zaitsu Y, Fujima N, Terae S, Sasaki M, Houkin K.

Department of Neurosurgery, Hokkaido University Graduate School of Medicine.

Abstract

We performed magnetic resonance angiography (MRA) and susceptibility-weighted imaging (SWI) to observe cerebral changes during a migraine attack in a 28-year-old man. MRA revealed regional arterial spasm, and findings of SWI were consistent with decreased blood flow and/or venous dilatation. Because these noninvasive techniques can be performed repeatedly at short intervals, they can be useful for evaluating hemodynamic changes during and after migraine attacks.

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PMID: 21441728 [PubMed - in process]

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2. BMJ. 2011 Jan 18;342:c7357. doi: 10.1136/bmj.c7357.

Headache, migraine, and structural brain lesions and function: population based Epidemiology of Vascular Ageing-MRI study.

Kurth T, Mohamed S, Maillard P, Zhu YC, Chabriat H, Mazoyer B, Bousser MG, Dufouil C, Tzourio C.

INSERM Unit 708--Neuroepidemiology, Paris, France. tobias.kurth@upmc.fr

Abstract

OBJECTIVE: To evaluate the association of overall and specific headaches with volume of white matter hyperintensities, brain infarcts, and cognition.

DESIGN: Population based, cross sectional study.

SETTING: Epidemiology of Vascular Ageing study, Nantes, France.

PARTICIPANTS: 780 participants (mean age 69, 58.5% women) with detailed headache assessment.

MAIN OUTCOME MEASURES: Brain scans were evaluated for volume of white matter hyperintensities (by fully automated imaging processing) and for classification of infarcts (by visual reading with a standardised assessment grid). Cognitive function was assessed by a battery of tests including the mini-mental state examination.

RESULTS: 163 (20.9%) participants reported a history of severe headache and 116 had migraine, of whom 17 (14.7%) reported aura symptoms. An association was found between any history of severe headache and increasing volume of white matter hyperintensities. The adjusted odds ratio of being in the highest third for total volume of white matter hyperintensities was 2.0 (95% confidence interval 1.3 to 3.1, P for trend 0.002) for participants with any history of severe headache when compared with participants without severe headache being in the lowest third. The association pattern was similar for all headache types. Migraine with aura was the only headache type strongly associated with volume of deep white matter hyperintensities (highest third odds ratio 12.4, 1.6 to 99.4, P for trend 0.005) and with brain infarcts (3.4, 1.2 to 9.3). The location of infarcts was predominantly outside the cerebellum and brain stem. Evidence was lacking for cognitive impairment for any headache type with or without brain lesions.

CONCLUSIONS: In this population based study, any history of severe headache was associated with an increased volume of white matter hyperintensities. Migraine with aura was the only headache type associated with brain infarcts. Evidence that headache of any type by itself or in combination with brain lesions was associated with cognitive impairment was lacking.

PMCID: PMC3022913 Free PMC Article

PMID: 21245119 [PubMed - indexed for MEDLINE]

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3. Acta Neurol Taiwan. 2010 Dec;19(4):275-80.

Vertebral artery dissection presented as lateral medullary syndrome in a patient with migraine: a case report.

Yen JC, Chan L, Lai YJ.

Section of Neurology, Department of Internal Medicine Far-Eastern Memorial Hospital, Taipei, Taiwan.

Abstract

PURPOSE: Migraine and artery dissection are both rare causes of ischemic stroke. The mechanism of migraine-related intracranial artery dissection is still unknown. It is proposed that the repeated attack of migraine would make the involved artery more vulnerable to tearing and lead to dissection.

CASE REPORT: We describe a 42-year-old female suffering from basilar-type migraine for more than 20 years. The patient complained severe dizziness with hyperventilation while watching television. Initially anxiety and migraine attack were impressed in the emergency room, but dizziness accompanied with dysarthria and dysphagia was noted later. After admission, lateral medullary syndrome was suspected after a detailed neurological examination, and a brain magnetic resonance image (MRI) revealed an acute infarction on the left lateral medulla oblongata, confirming the clinical diagnosis Furthermore, cerebral angiography revealed the left distal vertebral artery dissection. The patient was reluctant to use an anticoagulant; therefore aspirin was given for secondary stroke prevention and topiramate for migraine prophylaxis.

CONCLUSION: The exact mechanism of migraine-related intracranial artery dissection has yet to be proven, we propose that this may be caused by vessel wall edematous changes with repeated migraine attacks resulting in sudden or unusual stretching.

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PMID: 21210329 [PubMed - indexed for MEDLINE]

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4. Acta Neurol Taiwan. 2010 Jun;19(2):137-44.

[Neuroimaging guidelines in nonacute headaches].

[Article in Chinese]

Treatment Guideline Subcommittee of the Taiwan Headache Society.

Collaborators: Chen YY, Chen HM, Chen WH, Chen WT, Fuh JL, Juang KD, Lee LH, Liao YC, Lin KC, Tseng HP, Tsai JJ, Wang PJ, Wang SJ, Yang CP, Yiu CH, Wu ZA.

Department of Neurology, Taipei Veterans General Hospital, Taiwan.

Abstract

The Treatment Guideline Subcommittee of the Taiwan Headache Society evaluated the indication of neuroimaging for nonacute headache according to the principles of evidence-based medicine. We have assessed the qualities of studies, levels of evidence, and referred to other guidelines proposed by Western countries. After several panel discussions, we merged opinions from the subcommittee members and proposed a Taiwan consensus. Neuroimaging is not necessary for patients with nonacute and recurrent migraine or tension-type headache when there is no recent change of headache characteristics and neurological examinations are normal. Neuroimaging is suggested for patients who have headaches with abnormal neurological examinations. For patients who are diagnosed as having cluster headache and have never received neuroimaging studies, or patients whose headache characteristics are atypical for cluster headaches, neuroimaging studies should be considered. Neuroimaging is also recommended for patients with cough headache, exertional headache and headache associated with sexual activity. Although the resolution of MRI is superior to CT, evidence is insufficient to make recommendation regarding the choice of MRI or CT for the evaluation of nonacute headache patient. Clinicians should make a judgment by themselves according to the patient's specific conditions.

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PMID: 20714966 [PubMed - indexed for MEDLINE]

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5. Turk Neurosurg. 2010 Jul;20(3):406-8. doi: 10.5137/1019-5149.JTN.1891-09.1.

Pure sensory stroke due to bilateral basal ganglion hemorrhage: a case report.

Terzi M, Akkaya O, Onar M.

Ondokuz Mayis University, Faculty of Medicine, Department of Neurology, Samsun, Turkey. mterzi@omu.edu.tr

Abstract

Bilateral simultaneous hypertensive intracerebral hemorrhages are extremely rare. The predisposing factors and pathophysiological mechanisms leading to the development of this picture are not well known. Possible mechanisms of simultaneous multiple hemorrhages include concomitant primary hemorrhages in two or more regions, or development of a second hemorrhage in another region shortly after the primary hemorrhage. The etiology of the cases presenting with bilateral simultaneous basal ganglion hemorrhage include migraine, lightning stroke, hyperglycemic hyperosmolar coma, hypertension and diabetic ketoacidosis coma. Bilateral simultaneous hemorrhage has a poor prognosis. The case of bilateral simultaneous intracerebral hemorrhage presented here had a good clinical course similar to a pure sensorial stroke.

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PMID: 20669117 [PubMed - indexed for MEDLINE]

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6. Neurol Neurochir Pol. 2010 Mar-Apr;44(2):118-22.

Stroke in patients with migraine.

De Reuck J, Paemeleire K, Van Maele G.

Department of Neurology, Ghent University Hospital, Belgium. dereuck.j@gmail.com

Abstract

BACKGROUND AND PURPOSE: Migraine with aura (MA) is considered as a risk factor for ischaemic stroke. The present observational retrospective study compares migraine patients admitted for a documented stroke with those presenting focal neurological symptoms and headache without a demonstrable lesion and in which the final diagnosis was a migraine attack with aura.

MATERIAL AND METHODS: The study included 14 migraine patients with a stroke and 37 without a stroke. The clinical characteristics, the vascular risk factors and the results of the technical examinations were compared.

RESULTS: Stroke occurred in migraine patients with aura as well as without aura. Classical vascular risk factors were rather rare. Patent foramen ovale (PFO) with or without atrial septum aneurysm appeared to be the main risk factor for stroke in patients with a history of migraine. Infarcts were mainly located in the supratentorial territory of the posterior cerebral circulation. Also some lobar haematomas were observed, but their aetiology remained uncertain. The strokes were generally mildly severe with good outcome. Hyperintense signals in the cerebral white matter and cerebellum, on T2-weighted magnetic resonance imaging, were more frequent in the migraine patients with stroke.

CONCLUSIONS: The presence of PFO, rather than of MA, appeared to be the main risk factor for stroke patients with migraine. No direct relation between migraine and stroke could be demonstrated.

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PMID: 20496281 [PubMed - indexed for MEDLINE]

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7. Intern Med. 2010;49(8):711-2. Epub 2010 Apr 15.

Does high resolution magnetic angiography detect changes in the middle meningeal artery during migraine attacks?

Hirata K, Watanabe Y, Tanaka H.

Comment on:

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PMID: 20424359 [PubMed - indexed for MEDLINE]

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8. J Clin Neurol. 2010 Mar;6(1):1-9. Epub 2010 Mar 26.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: a genetic cause of cerebral small vessel disease.

Choi JC.

Department of Neurology and Institute of Medical Science, Jeju National University School of Medicine, Jeju, Korea.

Abstract

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a single-gene disorder of the cerebral small blood vessels caused by mutations in the Notch3 gene. The exact prevalence of this disorder was unknown currently, and the number of reported CADASIL families is steadily increasing as the clinical picture and diagnostic examinations are becoming more widely known. The main clinical manifestations are recurrent stroke, migraine, psychiatric symptoms, and progressive cognitive impairment. The clinical course of CADASIL is highly variable, even within families. The involvement of the anterior temporal lobe and the external capsule on brain magnetic resonance imaging was found to have high sensitivity and specificity in differentiating CADASIL from the much more common sporadic cerebral small-vessel disease (SVD). The pathologic hallmark of the disease is the presence of granular osmiophilic material in the walls of affected vessels. CADASIL is a prototype single-gene disorder that has evolved as a unique model for studying the mechanisms underlying cerebral SVD. At present, the incidence and prevalence of CADASIL seem to be underestimated due to limitations in clinical, neuroradiological, and genetic diagnoses of this disorder.

PMCID: PMC2851292 Free PMC Article

PMID: 20386637 [PubMed - in process]

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9. Rev Neurol. 2010 Mar 16;50(6):341-8.

[Mesial temporal sclerosis in paediatrics: its clinical spectrum. Our experience gained over a 19-year period].

[Article in Spanish]

Monge-Galindo L, Pérez-Delgado R, López-Pisón J, Lafuente-Hidalgo M, del Olmo-Izuzquiza IR, Peña-Segura JL.

Unidad de Neuropediatría. Hospital Universitario Miguel Servet. Zaragoza, España.

Abstract

INTRODUCTION: Mesial temporal sclerosis (MTS) is defined as neuron loss and gliosis in the hippocampus and adjacent structures. Here we report on our 19 years' experience in dealing with this condition.

PATIENTS AND METHODS: A retrospective, descriptive study was conducted of patients diagnosed with MTS between May 1990 and January 2009.

RESULTS: A diagnosis of MTS was established in 16 cases (62.5% males). By location these cases were distributed as follows: 12 were unilateral (seven left temporal and five right) and four were bilateral. It was associated to cortical dysplasia in six patients (37.5%) and to hippocampal arachnoid cysts in two other cases. As regards possible causations, in one case herpes simplex encephalitis was suspected; in three cases, a prenatal cerebral vascular pathology; and in three others, prenatal infection by cytomegalovirus. The distribution of the clinical spectrum was as follows: five patients with isolated clinical epilepsy; one with isolated psychomotor retardation or mental retardation (PMR-MR); one with isolated autism spectrum disorder (ASD); three with epilepsy associated to PMR-MR; one with epilepsy associated to ASD; two with PMR-MR and ASD; and two with the triad consisting of epilepsy together with PMR-MR and ASD. In one case, MTS was discovered in migraine studies, without any other symptoms. Crises were controlled with monotherapy in all the patients who received antiepileptic treatment except in three, one of whom required surgery.

CONCLUSIONS: The definitive diagnosis of MTS is pathologic, but the latest neuroimaging techniques have allowed a very reliable approximate diagnosis to be reached. It may be associated to other malformative disorders, such as focal cortical dysplasia or cysts. MTS can be observed in epilepsy (whether refractory or not), but also in ASD, PMR-MR or asymptomatic patients.

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PMID: 20309832 [PubMed - indexed for MEDLINE]

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10. Ann Neurol. 2010 Feb;67(2):221-9.

Microemboli may link spreading depression, migraine aura, and patent foramen ovale.

Nozari A, Dilekoz E, Sukhotinsky I, Stein T, Eikermann-Haerter K, Liu C, Wang Y, Frosch MP, Waeber C, Ayata C, Moskowitz MA.

Stroke and Neurovascular Regulation Laboratory, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.

Abstract

OBJECTIVE: Patent foramen ovale and pulmonary arteriovenous shunts are associated with serious complications such as cerebral emboli, stroke, and migraine with aura. The pathophysiological mechanisms that link these conditions are unknown. We aimed to establish a mechanism linking microembolization to migraine aura in an experimental animal model.

METHODS: We introduced particulate or air microemboli into the carotid circulation in mice to determine whether transient microvascular occlusion, insufficient to cause infarcts, triggered cortical spreading depression (CSD), a propagating slow depolarization that underlies migraine aura.

RESULTS: Air microemboli reliably triggered CSD without causing infarction. Polystyrene microspheres (10 microm) or cholesterol crystals (<70 microm) triggered CSD in 16 of 28 mice, with 60% of the mice (40% of those with CSD) showing no infarcts or inflammation on detailed histological analysis of serial brain sections. No evidence of injury was detected on magnetic resonance imaging examination (9.4T; T2 weighted) in 14 of 15 selected animals. The occurrence of CSD appeared to be related to the magnitude and duration of flow reduction, with a triggering mechanism that depended on decreased brain perfusion but not sustained tissue damage.

INTERPRETATION: In a mouse model, microemboli triggered CSD, often without causing microinfarction. Paradoxical embolization then may link cardiac and extracardiac right-to-left shunts to migraine aura. If translatable to humans, a subset of migraine auras may belong to a spectrum of hypoperfusion disorders along with transient ischemic attacks and silent infarcts.

PMCID: PMC2921919 Free PMC Article

PMID: 20225282 [PubMed - indexed for MEDLINE]

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11. BMC Neurol. 2010 Jan 6;10:2.

A migraine variant with abdominal colic and Alice in Wonderland syndrome: a case report and review.

Hamed SA.

Department of Neurology and Psychiatry, Assiut University Hospital, Assiut, Egypt. hamed_sherifa@yahoo.com

Abstract

BACKGROUND: Abdominal migraine is a commonly described migraine variant in children and young adults, but associations with Alice in Wonderland syndrome and lilliputian hallucinations are exceptional.

CASE PRESENTATION: A 20 years-old male experienced frequent and prolonged attacks of abdominal colic associated with autonomic manifestations started at the age of ten. At the age of 17, he additionally described prolonged attacks (>or= 7 days) of distortions of shape, size or position of objects or subjects. He said "Quite suddenly, objects appear small and distant (teliopsia) or large and close (peliopsia). I feel as I am getting shorter and smaller "shrinking" and also the size of persons are not longer than my index finger (a lilliputian proportion). Sometimes I see the blind in the window or the television getting up and down, or my leg or arm is swinging. I may hear the voices of people quite loud and close or faint and far. Occasionally, I experience attacks of migrainous headache associated with eye redness, flashes of lights and a feeling of giddiness. I am always conscious to the intangible changes in myself and my environment". There is a strong family history of common migraine. Clinical examination, brain-MRI and EEG were normal. Transcranial magnetic stimulation and evoked potentials revealed enhanced cortical excitability in multiple brain regions. Treatment with valproate resulted in marked improvement of all clinical and neurophysiological abnormalities.

CONCLUSIONS: The association between the two migraine variants (abdominal migraine and Alice in Wonderland Syndrome) might have clinical, pathophysiological and management implications. I think this is the first description in the literature.

PMCID: PMC2817660 Free PMC Article

PMID: 20053267 [PubMed - indexed for MEDLINE]

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12. Intern Med. 2009;48(24):2141-4.

Short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA).

Tada Y, Ikuta N, Negoro K.

Department of Neurology, Ube-Kousan Central Hospital, Ube. ytada@orange.ocn.ne.jp

Abstract

Short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA) is a rare primary headache syndrome. The diagnostic criteria include attacks of unilateral orbital, supraorbital or temporal stabbing pain accompanied by one of the following: conjunctival injection and/or tearing, nasal congestion and/or rhinorrhea, and eyelid edema. The duration of pain is 2 seconds to 10 minutes, and the frequency of attacks is described as once a day or more. The etiology and pathology of SUNA has yet to be documented. We report an 18-year-old man with SUNA. Lomerizine hydrochloride which is used as a preventive medicine for migraine, improved his headaches.

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PMID: 20009409 [PubMed - indexed for MEDLINE]

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13. Intern Med. 2009;48(24):2133-5.

The middle meningial artery during a migraine attack: 3T magnetic resonance angiography study.

Nagata E, Moriguchi H, Takizawa S, Horie T, Yanagimachi N, Takagi S.

Department of Neurology, Tokai University School of Medicine, Isehara. enagata@is.icc.u-tokai.ac.jp

Comment in:

Abstract

We performed 3T magnetic resonance angiography (MRA) during a spontaneous migraine attack. The patient was a 42-year-old woman migraineur diagnosed by the IHS criteria. The change of the middle meningial artery (MMA) was measured on the axial brain images using MATLAB for three phases (attack-free period, during an attack, a period after medication). There were no dramatic changes of vasodilation in the MMA during the attack (2.0 mm), attack-free period (diameter 1.9 mm), or period after medication (1.7 mm), resembling extrapolations of observations in experimental animal models. This finding suggests that the dramatic vasomotion might not be associated with migraine pathophysiology.

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PMID: 20009407 [PubMed - indexed for MEDLINE]

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14. Stroke. 2009 Dec;40(12):3725-9. Epub 2009 Nov 5.

Crescendo transient Aura attacks: a transient ischemic attack mimic caused by focal subarachnoid hemorrhage.

Izenberg A, Aviv RI, Demaerschalk BM, Dodick DW, Hopyan J, Black SE, Gladstone DJ.

Dr Thomas and Harriet Black Acute TIA Unit and Regional Stroke Prevention Clinic, Division of Neurology and Brain Sciences Program, Sunnybrook Health Sciences Centre, Department of Medicine, University of Toronto, Toronto, Toronto, Ontario Canada.

Abstract

BACKGROUND AND PURPOSE: Diagnosis of transient ischemic attack can be difficult because many mimics exist. We report the clinical and neuroimaging features of a distinct hemorrhagic transient ischemic attack mimic.

METHODS: Case series.

RESULTS: We describe 4 elderly patients presenting with a cluster of stereotyped somatosensory migraine auras, initially referred for "crescendo transient ischemic attacks". Neuroimaging in each patient revealed an unexpected finding of spontaneous focal subarachnoid hemorrhage conforming to a cortical sulcus in the contralateral hemisphere. We postulate that the episodic aura symptoms corresponded to recurrent cortical spreading depression triggered by the presence of subarachnoid blood, and speculate that such episodes could be a presenting feature of cerebral amyloid angiopathy in the absence of typical cerebral microbleeds or history of cognitive impairment.

CONCLUSIONS: Focal subarachnoid hemorrhage can present clinically with transient repetitive migraine auras. Awareness of this entity is important because misdiagnosis as cerebral ischemic events could lead to incorrect treatment. We recommend that elderly patients presenting with a cluster of new unexplained migraine auras should be investigated ideally with MRI to detect focal subarachnoid hemorrhage.

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PMID: 19893001 [PubMed - indexed for MEDLINE]

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15. Arq Neuropsiquiatr. 2009 Sep;67(3B):906-8.

Migrainous infarction as a complication of sporadic hemiplegic migraine in childhood.

Ribeiro RT, Pinto MM, Villa TR, Gamba LT, Tengan CH, de Souza-Carvalho D. Free Article

PMID: 19838529 [PubMed - indexed for MEDLINE]

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16. Stroke. 2009 Dec;40(12):3740-4. Epub 2009 Oct 15.

Normal cortical energy metabolism in migrainous stroke: A 31P-MR spectroscopy study.

Schulz UG, Blamire AM, Davies P, Styles P, Rothwell PM.

Stroke Prevention Research Unit, University Department of Clinical Neurology, John Radcliffe Hospital, Oxford OX2 9DU, UK. ursula.schulz@clneuro.ox.ac.uk

Abstract

BACKGROUND AND PURPOSE: Previous (31)P-magnetic resonance spectroscopy ((31)P-MRS) studies have shown that cerebral cortical energy metabolism is abnormal in migraine and that cortical energy reserves decrease with increasing severity and duration of aura. Migrainous infarction is a rare complication of migraine with aura, and its pathophysiology is poorly understood. We used (31)P-MRS to determine whether migrainous stroke shows similar interictal abnormalities in cortical energy metabolism as severe, prolonged aura.

METHODS: We used (31)P-MRS to study patients with a diagnosis of either migrainous infarction or migraine with persistent aura without infarction (aura duration >7 days) according to International Headache Society criteria. We compared clinical presentation and metabolite ratios between patient groups. We also studied healthy controls with no history of migraine.

RESULTS: Patients with persistent aura without infarction had lower phosphocreatine-phosphate (PCr/Pi) ratios (mean+/-SD, 1.61+/-0.10) compared with controls (1.94+/-0.35, P=0.011) and with patients with migrainous stroke (1.96+/-0.16, P<0.0001). These differences were present in cortical tissue only. In migrainous stroke patients, the metabolite ratios did not differ significantly from those of controls without migraine.

CONCLUSIONS: The differences in cortical energy reserves between patients with migrainous stroke and in those with migraine with persistent aura suggest that the pathomechanisms of these conditions differ and that migrainous infarction does not simply represent a particularly severe form of migrainous aura. This finding supports the revised International Headache Society criteria, which now distinguish between migrainous infarction and migraine with persistent aura without infarction.

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PMID: 19834021 [PubMed - indexed for MEDLINE]

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17. Arch Soc Esp Oftalmol. 2009 Sep;84(9):473-6.

[Migraineous anterior optic ischemic neuropathy].

[Article in Spanish]

González-Martín-Moro J, Pilo-de-la-Fuente B, Moreno-Martín P.

Servicio de Oftalmología, Hospital de la Princesa, Madrid, España. juliogmm@yahoo.es

Abstract

CASE REPORT: We report the case of a 22-year-old man who presented with headache and blurred vision which had started four days previous. A periventricular lesion was found in the magnetic resonance imaging. The patient was diagnosed with demyelinating neuritis and treated with intravenous methylprednisolone. DISCUSSION: After six months visual function had not improved, so the initial diagnosis was probably erroneous. It is likely that the patient suffered from migraineous optic ischemic neuropathy. In this paper we review the scarce literature about this topic, and the role of migraine as a cardiovascular risk factor.

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PMID: 19809927 [PubMed - indexed for MEDLINE]

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18. Acta Neurol Taiwan. 2009 Jun;18(2):104-12.

Cranial autonomic symptoms in patients with pituitary adenoma presenting with headaches.

Wang SJ, Hung CW, Fuh JL, Lirng JF, Hwu CM.

Department of Neurology, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan. sjwang@vghtpe.gov.tw

Abstract

Different types of symptomatic trigeminal autonomic cephalalgias (TACs) have been reported in patients with pituitary adenoma. We investigated the significance of the presence of cranial autonomic symptoms (CAS) in patients with pituitary adenoma presenting with headaches. The records of patients with pituitary adenoma from 1998 to 2004 in our headache clinic were reviewed including headache profile, presence or absence of CAS, and the characteristics of the pituitary adenoma. CAS were ascertained if one or more autonomic symptoms defined for the diagnosis of TACs in the International Classification of Headache Disorders, 2nd edition (ICHD-2) was identified. Thirty-three patients (24F/9M) with pituitary adenoma presenting with headache were recruited for this study: 18 with CAS (55%) and 15 without. Chronic migraine was the most common headache phenotype (n=16, 48%). Three patients were diagnosed as hemicrania continua-like and three, cluster headache-like. In the group with CAS (CAS+), the sides of the tumor were significantly concordant with the sides of headaches (kappa=0.58, p<0.001) and those of CAS (kappa=0.67, p<0.001). However, this relationship was not demonstrated in those without CAS (CAS-) (kappa=0.07, p=0.61). Compared with the patients in the CAS- group, the patients in the CAS+ group had higher frequencies of macroadenoma (78% vs. 40%, p=0.027) and acromegaly (50% vs. 7%, p=0.009). The presence and absence of CAS in pituitary adenoma-associated headache were associated with different characteristics of the underlying pituitary adenomas including side concordance and incidence of acromegaly and macroadenoma. The pathogeneses for headache might differ between these two groups.

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PMID: 19673362 [PubMed - indexed for MEDLINE]

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19. Acta Neurol Taiwan. 2009 Jun;18(2):81-90.

Notch signaling and CADASIL.

Tang SC, Jeng JS, Lee MJ, Yip PK.

Stroke Center, National Taiwan University Hospital, Taiwan.

Abstract

Notch signaling plays an essential role in vascular development and human vascular diseases. In adults, mutations of the Notch3 gene cause a hereditary vascular degenerative disease known as cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy (CADASIL). CADASIL is characterized by recurrent strokes and cognitive impairment. Over the past decade, the number of CADASIL patients increased significantly with improvements in genetic testing and other diagnostic tools, but the true prevalence of CADASIL is still underestimated, especially in Asia. Basic studies suggest that Notch3 is essential for the development and survival of the vascular smooth muscle cells, but the mechanisms by which Notch3 mutations become pathogenic are still unclear. This article reviews the clinical features and possible pathogenesis of CADASIL. Efforts to improve the diagnostic accuracy and define the role of Notch3 mutation in brain damage and clinical presentations of CADASIL should be continued.

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PMID: 19673359 [PubMed - indexed for MEDLINE]

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20. Mol Pain. 2009 Jun 30;5:34.

Excitatory neurotransmitters in brain regions in interictal migraine patients.

Prescot A, Becerra L, Pendse G, Tully S, Jensen E, Hargreaves R, Renshaw P, Burstein R, Borsook D.

Brain Imaging Center, McLean Hospital, Belmont, MA 02478, USA. andrew.prescot@utah.edu

Abstract

OBJECTIVE: To examine biochemical differences in the anterior cingulate cortex (ACC) and insula during the interictal phase of migraine patients. We hypothesized that there may be differences in levels of excitatory amino acid neurotransmitters and/or their derivatives in migraine group based on their increased sensitivity to pain.

METHODS: 2D J-resolved proton magnetic resonance spectroscopy (1H-MRS) data were acquired at 4.0 Tesla (T) from the ACC and insula in 10 migraine patients (7 women, 3 men, age 43 +/- 11 years) and 8 age gender matched controls (7 women, 3 men, age 41 +/- 9 years).

RESULTS: Standard statistical analyses including analysis of variance (ANOVA) showed no significant metabolite differences between the two subject cohorts in the ACC nor the insula. However, linear discriminant analysis (LDA) introduced a clear separation between subject cohorts based on N-acetyl aspartylglutamate (NAAG) and glutamine (Gln) in the ACC and insula.

CONCLUSION: These results are consistent with glutamatergic abnormalities in the ACC and insula in migraine patients during their interictal period compared to healthy controls. An alteration in excitatory amino acid neurotransmitters and their derivatives may be a contributing factor for migraineurs for a decrease in sensitivity for migraine or a consequence of the chronic migraine state. Such findings, if extrapolated to other regions of the brain would offer new opportunities to modulate central system as interictal or preemptive medications in these patients.

PMCID: PMC2714306 Free PMC Article

PMID: 19566960 [PubMed - indexed for MEDLINE]

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