Complex Migraine (vascular related ?)

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Complex Migraine (vascular related ?)

Postby pairOdime » Sat Feb 19, 2011 11:31 am

Complex migraine symptoms are similar to stroke
http://www.king5.com/health/Symptoms-of ... 08003.html

Along with garbled speech during her live report, Branson remembers losing feeling in her hands and face. She was eventually diagnosed with a complex migraine which can can mimic a stroke.


The last few seconds of the video report this list is provided.

Stroke and Complex Migraine Similar Symptoms
>Numbness, Loss of Balance
>Trouble Speaking
>Sudden Trouble Seeing
>Sudden Severe Headache
It's a paradigm shift
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Postby Stayfit » Sat Feb 19, 2011 5:55 pm

Do you have any references connecting migraines and vascular issues?
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Postby pairOdime » Sat Feb 19, 2011 6:08 pm

http://www.ncbi.nlm.nih.gov/pubmed/20189084
J Stroke Cerebrovasc Dis. 2010 Mar;19(2):92-103.
Vascular risk factors, endothelial function, and carotid thickness in patients with migraine: relationship to atherosclerosis.
Hamed SA, Hamed EA, Ezz Eldin AM, Mahmoud NM.
Department of Neurology, Assiut University Hospital, Egypt. hamed_sherifa@yahoo.com

Recent studies indicated that migraine is associated with specific vascular risk profile. However, the functional and structural vascular abnormalities in migraine are rarely addressed. We evaluated the vascular risk factors, endothelial function, and carotid artery (CA)-intima-media thickness (IMT), segregators of preclinical atherosclerosis, in migraineurs. This preliminary study included 63 adults with headache (migraine with aura [n=14], migraine without aura [n=24], transformed migraine [n=6], and tension headache [n=19]) and 35 matched healthy subjects.

The following vascular risks were assessed: body mass index (BMI), systolic blood pressure (SBP) and diastolic blood pressures (DBP), serum levels of C-reactive protein, fasting glucose, fasting insulin, total cholesterol, and triglycerides. Plasma endothelin (ET)-1, a vasoactive peptide produced by vascular smooth muscle cells and marker for endothelial injury and atherosclerosis, was measured. Endothelial-dependent vasoreactivity was assessed using brachial artery flow-mediated dilatation (FMD) in response to hyperemia. CA-IMT, structural marker of early atherosclerosis, was measured. Compared with control subjects, SBP, DBP, glucose, insulin, ET-1, and CA-IMT were elevated with migraine. FMD% was inversely correlated with SBP (P < .001), DBP (P < .01), glucose (P < .001), and insulin levels (P < .01). CA-IMT was correlated with BMI (P < .05), SBP (P < .01), total cholesterol (P < .01), triglycerides (P < .001), glucose (P < .001), insulin (P < .01), and FMD% (P < .05). In multivariate analysis, ET-1 was correlated with duration of illness, SBP, DBP, glucose, insulin, IMT, and FMD%.

We conclude that endothelial injury, impaired endothelial vasoreactivity, and increased CA-IMT occur with migraine and are associated with vascular risk factors that strongly suggest that migraine could be a risk for atherosclerosis.
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http://www.ncbi.nlm.nih.gov/pubmed/21245119
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

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.
It's a paradigm shift
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Postby pairOdime » Sun Feb 20, 2011 6:46 am

http://www.ncbi.nlm.nih.gov/pubmed/21331756
J Headache Pain. 2011 Feb 18. [Epub ahead of print]
Risk factors of migraine-related brain white matter hyperintensities: an investigation of 186 patients.
Trauninger A, Leél-Őssy E, Kamson DO, Pótó L, Aradi M, Kövér F, Imre M, Komáromy H, Erdélyi-Botor S, Patzkó A, Pfund Z.
Department of Neurology, University of Pécs, 7623 Pécs, Rét u. 2, Pecs, Hungary.

Brain white matter hyperintensities are more prevalent in migraine patients than in the general population, but the pathogenesis and the risk factors of these hyperintensities are not fully elucidated. The authors analyzed the routine clinical data of 186 migraine patients who were referred to the Outpatient Headache Department of the Department of Neurology, Medical School, University of Pécs, Hungary between 2007 and 2009: 58 patients with white matter hyperintensities and 128 patients without white matter hyperintensities on 3 T MRI.

Significant associations between the presence of white matter hyperintensities and longer disease duration (14.4 vs. 19.9 years, p = 0.004), higher headache frequency (4.1 vs. 5.5 attacks/month, p = 0.017), hyperhomocysteinemia (incidence of hyperintensity is 9/9 = 100%, p = 0.009) and thyroid gland dysfunction (incidence of hyperintensity is 8/14 = 57.1%, p = 0.038) were found.

These data support the theory that both the disease duration and the attack frequency have a key role in the formation of migraine-related brain white matter hyperintensities, but the effects of comorbid diseases may also contribute to the development of the hyperintensities.
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Postby jimmylegs » Sun Feb 20, 2011 7:08 am

Arterial Stenosis in Migraine: Spasm or Arteriopathy?†
http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract
Segmental arterial narrowing has rarely been angiographically demonstrated in patients with migraine. One new case is reported and 12 previous cases are reviewed. Though often referred to as vasospasm, arteriographic stenosis may result from edema of the vessel wall, arterial dissection, the effects of puerperium or arteritis.

A biphasic course of spasm, similar to the pattern noted with subarachnoid hemorrhage, has been recorded in some migraineurs. The current neurogenic and biochemical concepts of “spasm” developed for subarachnoid hemorrhage are reviewed.

Arterial narrowing may be important in several phenomena associated with migraine. It may account for migrainous cerebral infarction or hemorrhage. Vasoconstriction has also been invoked to explain the aura and other features of migraine. But the site of stenosis does not always correlate with the headache or focal neurologic features in location or timing. The angiographic changes are probably an epiphenomena rather than a primary mechanism of migraine. These changes may result from altered sympathetic neuronal activity; factors supporting that concept are reviewed.
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Postby pairOdime » Sun Feb 20, 2011 7:30 am

Thanks jimmylegs....nice find. I found this also.

http://www.americanheadachesociety.org/

The American Headache Society
53rd Annual Scientific Meeting
June 2 – 5, 2011 Washington, DC
New Discoveries in Headache Medicine


http://www.ahsevents.org/annual/

About the Meeting
Who Should Attend?
The 53rd Annual Scientific Meeting is designed for physicians, psychologists, physician assistants, nurse practitioners, and other health professionals involved in the care of patients with head, neck, and orofacial pain.

Education Mission Statement
The provision of quality CME is a primary mission of the The American Headache Society® . The Society’s educational objectives are to continue to improve the knowledge, skills, and professional performance of physicians, psychologists, and other health professionals in the care of patients with head, neck, and orofacial pain by:
• Providing a forum for presentation of free scientific communication on research and clinical practice.
• Providing educational symposia.
• Improving education in medical schools and residency programs.
• Identifying and developing new educational initiatives.
• Supporting educational programs directed to people with head, neck, and orofacial pain.
• Maintaining strict adherence to ACCME guidelines.
• Developing education activities and tools that are designed, and then evaluated, for their role in improving the learners’ competence, performance, and the overall quality and safety of the care they give to individuals suffering from head, neck, and orofacial pain.
It's a paradigm shift
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Postby jimmylegs » Sun Feb 20, 2011 8:31 am

and one more...

Prolonged Vasospasm in Migraine Detected by Noninvasive Transcranial Doppler Ultrasound
http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract
We describe three patients with different forms of migraine in whom transcranial Doppler (TCD)showed prolonged diffuse vasospasm in the basal cerebral arteries when patients were asymptomatic. Vasospasm was more severe in one patient during her attack. These findings demonstrate the usefulness of TCD in evaluating vascular changes in patients with migraine.
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Postby jimmylegs » Sun Feb 20, 2011 8:42 am

and for a subset of migraine sufferers...

Deficiency In Serum Ionized Magnesium But Not Total Magnesium In Patients With Migraines. Possible Role Of Ica2+/IMg2+ Ratio
http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract
It has been suggested that magnesium (Mg) may play a role in the pathogenesis of headaches. Serum and intracellular measurements of Mg in headache patients have produced inconsistent results. The recent development of an ion-selective electrode for Mg2+ allowed precise measurement of serum ionized magnesium (IMg2+) in patients with various headache syndromes. Low serum Img2+ and a high ICa2+/IMg2+ ratio were found in 42% of patients having an attack of migraine, but only in 23% of patients with e severe continuous headache. Total serum Mg was normal in both groups of patients. However, in patients with low serum IMg2+ total serum Mg was lower than in patients with normal serum IMg2+. These results are compatible with the serotonin and vascular concepts of migraine pathogenesis. Low IMg2+ and a high ICa2+/Img2+ would result in cerebral vasospasm and reduced blood flow in the brain. The activity of serotonin receptors can also be affected by changes in IMg2+ levels. The finding of a difference in IMg2+ levels in two different headache types suggests a possible novel classification of headaches and that migraine patients with a low serum IMg2+ or a high ICa2+/IMg2+ ratio may benefit from Mg supplementation.
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Postby bluesky63 » Sun Feb 20, 2011 9:36 am

Dr. Oliver Sacks has said that a migraine can be like a slow-motion seizure.

Sometimes the very meds that people are given induce vitamin deficiencies, which in turn create create additional symptoms -- and then the doctors assume the disease has taken a turn for the worse. So, more meds, more deficiences, vicious cycle.


Migraines are extremely common among people with MS.

An interesting article that mentions magnesium, zinc, vitamin B and their effects on seizures as well as the association between anti-seizure meds and vitamin deficiencies.

Anti-seizure meds are often prescribed for migraine patients.

http://www.worldwidehealthcenter.net/articles-115.html
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Postby cheerleader » Sun Feb 20, 2011 9:56 am

Great thread...migraines are most certainly related to circulatory issues. Women tend to suffer more than men (3 to 1), due to estrogen fluctuations. It creates a vasospasm. (Women have all the fun.)

Attacks of migraine usually occur during the late luteal and menstrual phases of the menstrual cycle, when serum estrogen levels have decreased. Estrogen may increase vasomotor tone independent of serum progesterone levels. When estrogen is withdrawn or reduced, rebound vasodilation occurs. This is clinically demonstrated among patients using oral contraceptives, in whom the frequency of migraine attacks is higher overall and related temporally to cyclic discontinuation of estrogen-containing pills.

http://www.encognitive.com/node/6925
http://womenshealth.about.com/cs/headac ... ranes1.htm

Although I don't have MS, I used to get the migraine with aura, jagged vision, vomiting. They were terrible. Started when I was a girl and beginning menstruation. My Mom read Prevention Magazine (in the 1970s, she was a hippy) and learned about magnesium and kelp (iodine) supplements to reduce hormonal migraines...put me on them, and the migraines were greatly reduced. I don't get them anymore, I used to have an occasional ocular migraine from stress (stress enduces vasoconstriction), but since I started the endothelial health program with Jeff, I haven't had one. Knock wood. They blow.
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migraine tips

Postby hwebb » Sun Feb 20, 2011 1:03 pm

used to suffer from migraines...but they are under control. I avoid my triggers - chocolate, coffee, red wine and lack of sleep. If I have the warning signs of a migraine (such as sudden light sensitivity, or jagged silver lines obscuring my vision) I take two "Aspro clear". This easily dissolved asprin stops migraine developing. Haven't had a fully fledged migraine in twenty years following this management plan.
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Postby pairOdime » Mon Feb 21, 2011 8:25 am

http://www.ncbi.nlm.nih.gov/pubmed/20666172
J La State Med Soc. 2010 May-Jun;162(3):174.
CADASIL can mimic multiple sclerosis.
Phillips CD, Zuckerman SJ; Medical Education Commission.
Phillips Neurological Institute Baton Rouge, Louisiana, USA.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) can be confused with multiple sclerosis (MS). We report a man with a father diagnosed with MS via magnetic resonance imaging (MRI). The index patient was subsequently diagnosed with MS after MRI for evaluation of migraine headaches. Genetic testing confirmed the CADASIL diagnosis. CADASIL is characterized by a history of migraine headaches, mid-adult onset of progressive cerebrovascular disease, diffuse white matter changes, and dementia. The mutation involves the Notch3 gene which changes a codon for arginine to cysteine at amino acid position 90.
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http://www.ncbi.nlm.nih.gov/pubmed/15631641
Neurologist. 2005 Jan;11(1):19-29.
Migraine and cerebral white matter lesions: when to suspect cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).
Gladstone JP, Dodick DW.
Mayo Clinic College of Medicine, Department of Neurology, 13400 E. Shea Blvd., Scottsdale, AZ 85259, USA. jon.gladstone@utoronto.ca

BACKGROUND: Patients with migraine are at an increased risk for white matter lesions, typically multiple, small, punctate hyperintensities in the deep or periventricular white matter, best observed on magnetic resonance imaging utilizing T2-weighted or FLAIR sequences. The underlying pathogenesis of white matter lesions in migraineurs is unknown, and the lesions are usually nonspecific and of unclear clinical significance.

REVIEW SUMMARY: Often the presence of white matter lesions causes uncertainty for physicians and anxiety for patients and may lead to a variety of diagnostic tests and treatments. Occasionally, white matter lesions may represent a secondary cause for headaches such as CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy). CADASIL is underrecognized and underdiagnosed; it should be suggested by (i) 1 or more of recurrent subcortical ischemic strokes (especially before age 60 and in the absence of vascular risk factors), migraine (especially with aura, including atypical or prolonged auras) and/or early cognitive decline or subcortical dementia; (ii) bilateral, multifocal, T2/FLAIR hyperintensities in the deep white matter and periventricular white matter with lesions involving the anterior temporal pole, external capsule, basal ganglia, and/or pons; and (iii) an autosomal-dominant family history of migraine, early-onset stroke, or dementia. The clinical spectrum of CADASIL is broad, and there is a poor genotype-phenotype correlation. In certain individuals or families, migraine may be the only clinical manifestation.

CONCLUSIONS: While the prevalence of nonspecific white matter lesions in migraineurs is increased, the white matter lesions may occasionally represent a secondary cause for headache such as CADASIL. Greater awareness of the unique clinical, neuroimaging, and pathologic features, as well as the availability of diagnostic genetic testing, should enhance the recognition and diagnosis of this fascinating condition.
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Postby bluesky63 » Thu Feb 24, 2011 4:15 pm

Interesting -- mentions SPECT imagine that shows slowed cerebral perfusion in people experiencing "prolonged migraine aura," which sounds awfully hard to distinguish from MS symptoms.

http://www.migraine-aura.org/content/e2 ... ex_en.html

(It starts out talking about visual symptoms but also goes into other symptoms like numbness, confusion, dizziness, etc., and mentions they can last for weeks, months, or years.)
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Postby bluesky63 » Tue Mar 01, 2011 3:12 pm

Here's another one about CADASIL -- very interesting in light of it being an MS mimic. This abstract mentions slowed cerebral blood flow.

http://stroke.ahajournals.org/cgi/content/full/33/2/509
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Postby 1eye » Tue Mar 01, 2011 4:28 pm

"Try - Just A Little Bit Harder" - Janis Joplin
CCSVI procedure Albany Aug 2010
'MS' is over - if you want it
Patients sans/without patience
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