Recurrent migraine aura-like symptoms in an elderly woman: symptomatic cortical spreading depression?

2021 ◽  
Vol 14 (7) ◽  
pp. e241479
Author(s):  
Kerstin Glössmann ◽  
Christoph Baumgartner ◽  
Johannes Peter Koren ◽  
Franz Riederer
Keyword(s):  
Subarachnoid Haemorrhage ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Epileptic Activity ◽  
Neurological Deficits ◽  
Amyloid Angiopathy ◽  
Migraine Aura ◽  
Transient Ischaemic Attacks ◽  
Long Term Follow Up ◽  
Mri Scans

Cortical spreading depression (CSD) has been directly observed in humans with malignant stroke, traumatic brain injury and subarachnoid haemorrhage and is also considered to be the correlate of migraine aura. We report on a 76-year-old woman with new-onset episodes of headache, paraesthesia, hemiparesis and dysarthria, in whom a small cortical subarachnoid haemorrhage was diagnosed with MRI. Repeated diffusion-weighted MRI scans shortly after transient focal neurological episodes as well as diagnostic workup were normal, which makes recurrent transient ischaemic attacks unlikely. Ictal electroencephalogram recordings showed no epileptic activity. Long-term follow-up revealed a diagnosis of probable cerebral amyloid angiopathy. We propose that CSD could be a pathophysiological correlate of transient focal neurological deficits in patients with cortical bleeding.

Migraine

2020 ◽  
pp. 213-224
Author(s):  
Julio R Vieira ◽  
Richard B Lipton
Keyword(s):  
Chronic Migraine ◽  
Migraine With Aura ◽  
Cortical Spreading Depression ◽  
Migraine Without Aura ◽  
Spreading Depression ◽  
Headache Frequency ◽  
Motor Symptoms ◽  
Migraine Aura ◽  
Younger Age ◽  
Psychiatric Conditions

This chapter examines migraine. The incidence of migraine varies depending on multiple aspects, including age, sex, and the presence of aura. At an earlier age (younger than age ten), migraine initially affects more boys than girls, with migraine with aura (MA) occurring at a younger age than migraine without aura (MO). Later in life, when puberty starts, this relationship changes and it becomes more common in women than men. Migraine aura are focal neurological symptoms that typically occur prior to the onset of a headache due to a phenomenon called cortical spreading depression. The prevalence of migraine with aura vary between visual, sensory, or motor symptoms. It can also present as diplopia, slurred speech, aphasia, dizziness, vertigo, and hemiparesis. Moreover, the prevalence of migraine varies according to headache frequency. The chapter then looks at chronic migraine and menstrual migraine. It also explores several comorbidities associated with migraine, including many neurologic, medical, and psychiatric conditions.

scholarly journals High-mobility group box 1 is an important mediator of microglial activation induced by cortical spreading depression

2016 ◽  
Vol 37 (3) ◽  
pp. 890-901 ◽  
Author(s):  
Tsubasa Takizawa ◽  
Mamoru Shibata ◽  
Yohei Kayama ◽  
Toshihiko Shimizu ◽  
Haruki Toriumi ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Cortical Spreading Depression ◽  
Microglial Activation ◽  
Spreading Depression ◽  
High Mobility ◽  
High Mobility Group ◽  
Migraine Aura ◽  
Double Knockout ◽  
Activated Microglia ◽  
Important Mediator

Single episodes of cortical spreading depression (CSD) are believed to cause typical migraine aura, whereas clusters of spreading depolarizations have been observed in cerebral ischemia and subarachnoid hemorrhage. We recently demonstrated that the release of high-mobility group box 1 (HMGB1) from cortical neurons after CSD in a rodent model is dependent on the number of CSD episodes, such that only multiple CSD episodes can induce significant HMGB1 release. Here, we report that only multiple CSD inductions caused microglial hypertrophy (activation) accompanied by a greater impact on the transcription activity of the HMGB1 receptor genes, TLR2 and TLR4, while the total number of cortical microglia was not affected. Both an HMGB1-neurtalizing antibody and the HMGB1 inhibitor glycyrrhizin abrogated multiple CSD-induced microglial hypertrophy. Moreover, multiple CSD inductions failed to induce microglial hypertrophy in TLR2/4 double knockout mice. These results strongly implicate the HMGB1–TLR2/4 axis in the activation of microglia following multiple CSD inductions. Increased expression of the lysosomal acid hydrolase cathepsin D was detected in activated microglia by immunostaining, suggesting that lysosomal phagocytic activity may be enhanced in multiple CSD-activated microglia.

Oxcarbazepine does not suppress cortical spreading depression

Cephalalgia ◽  
2010 ◽  
Vol 31 (5) ◽  
pp. 537-542 ◽  
Author(s):  
Ulrike Hoffmann ◽  
Ergin Dileköz ◽  
Chiho Kudo ◽  
Cenk Ayata
Keyword(s):  
Single Dose ◽  
Cortical Spreading Depression ◽  
Chronic Treatment ◽  
Spreading Depression ◽  
Screening Tool ◽  
Positive Control ◽  
Migraine Prophylaxis ◽  
Migraine Aura ◽  
Predictive Utility ◽  
Prophylactic Drugs

Background: Cortical spreading depression is the electrophysiological substrate of migraine aura, and may trigger headache. Recently, chronic treatment with five migraine prophylactic drugs was shown to suppress cortical spreading depression, implicating spreading depression as a common therapeutic target in migraine prophylaxis. Materials and methods: In order to assess the negative predictive value of spreading depression susceptibility as a preclinical drug screening tool, we tested oxcarbazepine, an anti-epileptic ineffective in migraine prophylaxis. Valproate served as the positive control. Cortical spreading depression susceptibility was measured in rats using topical KCl or electrical stimulation. Results: Oxcarbazepine did not suppress spreading depression either after a single dose or after daily treatment for 5 weeks. As previously shown, valproate suppressed spreading depression susceptibility after chronic dosing, while a single dose was ineffective. Conclusions: These data provide further support for spreading depression as a relevant target in migraine prophylaxis, and demonstrate the predictive utility of employed spreading depression models.

Vasodilator Agents and Supracollicular Transection Fail To Inhibit Cortical Spreading Depression in the Cat

Cephalalgia ◽  
1999 ◽  
Vol 19 (6) ◽  
pp. 592-597 ◽  
Author(s):  
H Kaube ◽  
YE Knight ◽  
RJ Storer ◽  
KL Hoskin ◽  
A May ◽  
...  
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Case Reports ◽  
Neurological Deficits ◽  
Visual Aura ◽  
Doppler Flowmetry ◽  
Amyl Nitrite ◽  
Flow Changes ◽  
Speed Of Propagation ◽  
Open Question

It remains an open question as to whether cortical spreading depression (CSD) is the pathophysiological correlate of the neurological symptoms in migraine with aura. In the experimental animal, CSD is an electrophysiological phenomenon mainly mediated via NMDA receptors. However, according to case reports in humans, visual aura in migraine can be alleviated by vasodilator substances, such as amyl nitrite and isoprenaline. There is also circumstantial evidence that brainstem nuclei (dorsal raphe nucleus and locus coeruleus) may play a pivotal role in the initiation of aura. In this study, CSD was elicited in α-chloralose anesthetized cats by cortical needle stab injury and monitored by means of laser Doppler flowmetry. Topical application of isoprenaline (0.1-1%) and amyl nitrite (0.05%) onto the exposed cortex had no effect on the elicitation or propagation of CSD. Also, after supracollicular transection, subsequent CSDs showed no differences in the speed of propagation and associated flow changes. We conclude from these data that—given CSD probably exists in humans during migraine—spreading neurological deficits during migraine aura are independent of brainstem influence and have a primarily neuronal rather than vascular mechanism of generation.

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