scholarly journals Aura Mapping: Where Vision and Somatosensation Meet

Vision ◽  
2021 ◽  
Vol 5 (4) ◽  
pp. 52
Author(s):  
Frances Wilkinson
Keyword(s):  
Temporal Relationship ◽  
Spreading Depression ◽  
Neural Mechanism ◽  
Skin Surface ◽  
Cortical Region ◽  
Migraine Aura ◽  
Timing Pattern ◽  
Migraine Episode ◽  
Neural Event ◽  
Insight Into

While migraine auras are most frequently visual, somatosensory auras are also relatively common. Both are characterized by the spread of activation across a cortical region containing a spatial mapping of the sensory (retinal or skin) surface. When both aura types occur within a single migraine episode, they may offer an insight into the neural mechanism which underlies them. Could they both be initiated by a single neural event, or do the timing and laterality relationships between them demand multiple triggers? The observations reported here were carried out 25 years ago by a group of six individuals with migraine with aura. They timed, described and mapped their visual and somatosensory auras as they were in progress. Twenty-nine episode reports are summarized here. The temporal relationship between the onset of the two auras was quite variable within and across participants. Various forms of the cortical spreading depression hypothesis of migraine aura are evaluated in terms of whether they can account for the timing, pattern of symptom spread and laterality of the recorded auras.

scholarly journals Migraine Aura and Related Phenomena: Beyond Scotomata and Scintillations

Cephalalgia ◽  
2007 ◽  
Vol 27 (12) ◽  
pp. 1368-1377 ◽  
Author(s):  
MB Vincent ◽  
N Hadjikhani
Keyword(s):  
Spreading Depression ◽  
Migraine Aura ◽  
Routine Examination ◽  
Colour Perception ◽  
Cortical Areas ◽  
Alien Hand Syndrome ◽  
Proper Name ◽  
Alien Hand ◽  
Cortical Physiology ◽  
Human Faces

Migraine affects the cortical physiology and may induce dysfunction both ictally and interictally Although visual symptoms predominate during aura, other contiguous cortical areas related to less impressive symptoms are also impaired in migraine. Answers from 72.2% migraine with aura and 48.6% of migraine without aura patients on human faces and objects recognition, colour perception, proper names recalling and memory in general showed dysfunctions suggestive of prosopagnosia, dyschromatopsia, ideational apraxia, alien hand syndrome, proper name anomia or aphasia, varying in duration and severity. Symptoms frequently occurred in a successively building-up pattern fitting with the geographical distribution of the various cortical functions. When specifically inquired, migraineurs reveal less evident symptoms that are not usually considered during routine examination. Spreading depression most likely underlies the aura symptoms progression. Interictal involvement indicates that MWA and MWoA are not completely silent outside attacks, and that both subforms of migraine may share common mechanisms.

Neural correlates of pride and joy recognition in early childhood

2021 ◽  
Vol 49 (9) ◽  
pp. 1-13
Author(s):  
Yue Jiang
Keyword(s):  
Early Childhood ◽  
Neural Mechanism ◽  
Neural Correlates ◽  
Event Related Potential ◽  
Central Component ◽  
Positive Component ◽  
Negative Component ◽  
Late Positive Component ◽  
Three Stages ◽  
Insight Into

I investigated neural processing during the recognition of pride and joy in early childhood using the event-related potential (ERP) technique. Electroencephalography recording was taken of 21 children aged between 4 and 6 years. They were shown photographs of familiar peers and strangers whose facial expressions displayed the emotion of either pride or joy. ERPs were recorded for the children's judgment of the expression of these two emotions when an image was presented. The results demonstrate that the neural dynamics during children's recognition of pride and joy involve three stages: The early negative component is spontaneously responsive to familiar faces, the midlatency negative central component is responsive to expression of familiar faces, and the late positive component marks greater extended processing of an expression of pride. These findings provide new insight into the neural mechanism of pride and joy recognition in children aged 4 to 6 years.

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.

Absence of conduction of spreading depression through cortical region damaged by asphyxiation

1964 ◽  
Vol 207 (4) ◽  
pp. 921-924 ◽  
Author(s):  
C. D. Hull ◽  
A. Van Harreveld
Keyword(s):  
Blood Pressure ◽  
Cerebral Cortex ◽  
Spreading Depression ◽  
Nerve Cells ◽  
Cortical Region ◽  
Pass Through

An area of cerebral cortex was asphyxiated for 30–35 min by application of a weight exerting a pressure on the tissue greater than the blood pressure. Three days later the asphyxiated region showed in most experiments a marked loss of nerve cells. The glia seemed to be better preserved. Spreading depression could not be made to pass through the area when asphyxiation had caused substantial neuronal destruction. These observations do not support a possible involvement of the glia in the propagation of spreading depression.

scholarly journals Unique Profile of Spreading Depression in a Primate Model

2002 ◽  
Vol 22 (7) ◽  
pp. 835-842 ◽  
Author(s):  
Chiaki Yokota ◽  
Yuji Kuge ◽  
Yasuhiro Hasegawa ◽  
Masafumi Tagaya ◽  
Takeo Abumiya ◽  
...  
Keyword(s):  
Direct Current ◽  
Spreading Depression ◽  
Direct Evidence ◽  
Ischemic Brain Injury ◽  
Migraine Aura ◽  
Primate Model ◽  
Ischemic Brain ◽  
Cynomolgus Monkeys ◽  
Positron Emission

Spreading depression (SD) is considered to play a role in pathologic conditions of humans such as in the evolution of ischemic brain injury and migraine aura. Because many studies have demonstrated spreading hypoperfusion in patients with migraine and persistent hypoperfusion in nonprimate animal models of SD, these changes in cerebral blood flow (CBF) were regarded as an epiphenomenon of SD. However, there is no direct evidence of the occurrence of SD in primates. The authors attempted to elicit SD by applying 3.3 mol/L potassium chloride to the cerebral cortex of nine male cynomolgus monkeys. The CBF was monitored by positron emission tomography in five animals. Propagated direct-current shifts were found by the two neighboring microelectrodes only in one animal. The direct-current wave propagated at a speed of 4 mm/min and its amplitude was 20 mV, being consistent with the SD findings. Except in one animal with 6 SD episodes, SD waves were recorded infrequently at the rostral site (none in three animals, once in three, and twice in two). Focal hyperemia accompanied SD. Neither spreading hypoperfusion nor persistent hypoperfusion was found. These unique features of SD in primates raise a doubt as to whether the role of SD in nonprimate animals is the same as that in stroke and migraine in humans.

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.

scholarly journals Aristides Leão: a birth centennial homage with comments on his spreading depression

2015 ◽  
Vol 73 (6) ◽  
pp. 544-546 ◽  
Author(s):  
Eliasz Engelhardt ◽  
Marleide da Mota Gomes
Keyword(s):  
Spreading Depression ◽  
Clinical Evidence ◽  
Epileptic Seizures ◽  
Transient Global Amnesia ◽  
Cerebrovascular Diseases ◽  
Personal Life ◽  
The Novel ◽  
Migraine Aura ◽  
New Concepts ◽  
Global Amnesia

The year of 2014 is the birth centenary of Aristides Azevedo Pacheco Leão (1914-1993), and also marks seventy years of the publication of his discovery of the novel electrophysiological phenomenon, named by him “spreading depression” (SD), soon designated “Leão’s wave” or “Leão’s spreading depression”. This was a remarkable scientific milestone, and the author must be celebrated for this achievement, as the studies he triggered proceeded worldwide, with new concepts, as spreading depolarization, until the present days. Robust experimental and clinical evidence emerged to suggest that these and related electrophysiological phenomena are involved in the mechanisms of migraine aura, acute cerebrovascular diseases, traumatic brain injury, transient global amnesia, epileptic seizures, and their pathophysiological characteristics come to offer new therapeutic perspectives. He was a remarkable and complex personality, and the authors remit the readers to a paper where his personal life is contemplated.

Prolonged Migraine Aura Without Headache Arrested by Sumatriptan. A Case Report with Further Considerations

Cephalalgia ◽  
1999 ◽  
Vol 19 (4) ◽  
pp. 241-242 ◽  
Author(s):  
PA Kowacs ◽  
EJ Piovesan ◽  
CE Tatsui ◽  
MC Lange ◽  
LC Ribas ◽  
...  
Keyword(s):  
Case Report ◽  
Blood Brain Barrier ◽  
Spreading Depression ◽  
Brain Barrier ◽  
Migraine Aura ◽  
Visual Aura ◽  
Blood Brain

The case of a 42-year-old woman with prolonged migraine visual aura without headache, whose long-lasting episodes of visual aura were successfully controlled by oral sumatriptan, is reported. Effectiveness of sumatriptan was unequivocal, since, after taking sumatriptan, duration of aura would drop from 1.5 h to approximately 20 min. This case suggests that sumatriptan may cross the blood-brain barrier and block spreading depression.

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