Control of memory by spreading cortical depression: A case for stimulus control.

1967 ◽  
Vol 74 (3) ◽  
pp. 201-215 ◽  
Author(s):  
Allen M. Schneider
Keyword(s):  
Stimulus Control ◽  
Spreading Cortical Depression ◽  
Cortical Depression

scholarly journals Migraine with Prolonged Aura: Correlation of Clinical and EEG Features

1995 ◽  
Vol 8 (2) ◽  
pp. 109-114 ◽  
Author(s):  
A. O. Ogunyemi
Keyword(s):  
Cerebral Cortex ◽  
Migraine With Aura ◽  
Slow Waves ◽  
Spreading Cortical Depression ◽  
Eeg Abnormalities ◽  
Cortical Depression ◽  
Eeg Changes ◽  
Eeg Recordings ◽  
The Brain

Migraine with prolonged aura has rarely been examined with regard to the sequence of the neurological symptoms and the associated EEG changes. This report describes five patients who underwent clinical assessment and EEG recordings during attacks of migraine with prolonged aura. CT scan of the brain was obtained in four of them. Follow-up EEG was also obtained. The aura symptoms either preceded the headache or were coincident with it. The aura symptoms evolved in a manner consistent with posterior-to-anterior dysfunction of the cerebral cortex. The EEG abnormalities were non-epileptiform and consisted of focal delta slow waves or theta slow waves. The EEG abnormalities showed good correlation with the patients' aura symptoms and resolved when the patients became symptom free. The posterior-to-anterior sequence of the aura symptoms is in accord with the findings during cerebral blood flow studies in patients having migraine with aura. Also the symptoms and EEG changes in our patients indicate dysfunction of the cerebral cortex, consistent with the notion that spreading cortical depression may be the underlying pathophysiological event in migraine with aura.

Analysis of MEG signals of spreading cortical depression with propagation constrained to a rectangular cortical strip

1999 ◽  
Vol 843 (1-2) ◽  
pp. 79-86 ◽  
Author(s):  
S.M. Bowyer ◽  
N. Tepley ◽  
N. Papuashvili ◽  
S. Kato ◽  
G.L. Barkley ◽  
...  
Keyword(s):  
Spreading Cortical Depression ◽  
Cortical Depression

Lamotrigine versus Placebo in the Prophylaxis of Migraine with and Without aura

Cephalalgia ◽  
1997 ◽  
Vol 17 (2) ◽  
pp. 109-112 ◽  
Author(s):  
TJ Steiner ◽  
LJ Findley ◽  
AWC Yuen
Keyword(s):  
Adverse Events ◽  
Sodium Channels ◽  
Dose Escalation ◽  
Glutamate Release ◽  
Migraine Prophylaxis ◽  
Double Blind ◽  
Treatment Groups ◽  
Spreading Cortical Depression ◽  
High Incidence ◽  
Cortical Depression

Lamotrigine blocks voltage-sensitive sodium channels, leading to inhibition of neuronal release of glutamate. Release of glutamate may be essential in the propagation of spreading cortical depression, which some believe is central to the genesis of migraine attacks. This study compared safety and efficacy of lamotrigine and placebo in migraine prophylaxis in a double-blind randomized parallel-groups trial. A total of 110 patients entered; after a 1-month placebo run-in period, placebo-responders and non-compliers were excluded, leaving 77 to be treated with lamotrigine ( n=37) or placebo ( n=40) for up to 3 months. Initially lamotrigine therapy was commenced at the full dose of 200 mg/day, but, following a high incidence of skin rashes, a slow dose-escalation was introduced: 25 mg/day for 2 weeks, 50 mg/day for 2 weeks, then 200 mg/day. Attack rates were reduced from baseline means of 3.6 per month on lamotrigine and 4.4 on placebo to 3.2 and 3.0 respectively during the last month of treatment. Improvements were greater on placebo and these changes, not statistically significant, indicate that lamotrigine is ineffective for migraine prophylaxis. There were more adverse events on lamotrigine than on placebo, most commonly rash. With slow dose-escalation their frequency was reduced and the rate of withdrawal for adverse events was similar in both treatment groups.

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