Dr. Bernice Grafstein’s paper on the mechanism of spreading depression

2005 ◽  
Vol 94 (1) ◽  
pp. 5-7 ◽  
Author(s):  
Anthony J. Strong

This essay looks at the historical significance of one APS classic paper that is freely available online: Grafstein B. Mechanism of spreading cortical depression. J Neurophysiol 19: 154–171, 1956 ( http://jn.physiology.org/cgi/reprint/19/2/154 ).

1958 ◽  
Vol 195 (1) ◽  
pp. 28-32 ◽  
Author(s):  
Peter Gouras

Microelectrode studies on excised amphibian retina have uncovered a phenomenon of spreading retinal depression which in many respects resembles Leão's spreading cortical depression. The phenomenon is characterized by a spontaneous ‘milky’ wave that periodically marches across the surface of the retina and lasts for 2–3 minutes at any one point. There is a concomitant and sudden negative shift in the resting retinal potential of 1–2 mv which gradually returns to its previous level in 3–6 minutes. As the wave front approaches a microelectrode recording ganglion cell activity, there is a marked increase in its spontaneous firing climaxing in an intense discharge as the wave engulfs the electrode. A profound depression follows so that even the most intense photic stimulation becomes unable to elicit a local response. As the color change disappears and the d.c. level returns, the local area of retina becomes reexcitable. Similar changes occur in the local electroretinogram, which always returns slightly before the ganglion cell activity. The process occurs spontaneously but can also be induced by trauma, electrical current, or the application of KCl. It happens less often in bright light or with oxygenation, although neither of these factors can prevent its occurrence. It appears to be entirely reversible.


Cephalalgia ◽  
1985 ◽  
Vol 5 (2_suppl) ◽  
pp. 47-51 ◽  
Author(s):  
Martin Lauritzen

During the first 1 to 2 h of the classical migraine attack a hypoperfusion develops which starts in the posterior part of the brain and progresses anteriorly at a rate of 2-3mm/min. The hypoperfusion stops at primary sulci outlining major cortical macro-and microstructural changes, but seems not to be inhibited by other changes of the cortical architecture. The low flow regions are cortical and the low flow persists for 4–6 h, until the attack abates. Regions of hyperperfusion are either minor or non-existent. A similar behavior characterizes the velocity and mode of evolution of a cortical spreading depression, a transient perturbation of cortical neuronal function which has profound and long-lasting influence on the cortical blood flow. This paper briefly summarizes the arguments which have been put forward in recent years suggesting that spreading depression is a pathogenetic mechanism of migraine.


1957 ◽  
Vol 190 (3) ◽  
pp. 557-562 ◽  
Author(s):  
Robert D. Tschirgi ◽  
Kazutoyo Inanaga ◽  
J. Langdon Taylor ◽  
Robert M. Walker ◽  
Ralph R. Sonnenschein

Local changes in cerebral cortex hydrogen ion concentration of as much as 0.5 ph units were observed to accompany the waves of cortical spreading depression or convulsion in cats and rabbits. A diphasic wave consisting of an initial alkaline followed by a more prolonged acid shift was observed in most cases. No significant differences were found between the ph changes accompanying spreading depression and those accompanying spreading convulsion. These ph shifts, like the abnormal ECG activity and the slowly changing potential wave which accompanied them, spread over the surface of the cerebral cortex with a velocity of 1–3 mm/min. The curve of cortical ph change is coincident with, and similar in shape to, the slowly changing potential difference measured between a point on the cortical surface and the jugular blood. For every unit change in ph, the cortex-blood P.D. is shifted approximately 30 mv. It is suggested that the slowly changing potential difference arises across the blood-brain barrier rather than as a result of depolarization of neuronal membranes. A significant but variable change in local blood flow accompanied the spreading depression.


2006 ◽  
Vol 291 (6) ◽  
pp. C1104-C1106 ◽  
Author(s):  
Juan A. Rosado

This essay examines the historical significance of an APS classic paper that is freely available online: Kwan CY, Takemura H, Obie JF, Thastrup O, and Putney JW Jr. Effects of MeCh, thapsigargin, and La3+ on plasmalemmal and intracellular Ca2+ transport in lacrimal acinar cells. Am J Physiol Cell Physiol 258: C1006–C1015, 1990. ( http://ajpcell.physiology.org/cgi/reprint/258/6/C1006 )


1995 ◽  
Vol 8 (2) ◽  
pp. 109-114 ◽  
Author(s):  
A. O. Ogunyemi

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.


2004 ◽  
Vol 97 (5) ◽  
pp. 1595-1596 ◽  
Author(s):  
Judith A. Neubauer

This essay looks at the historical significance of an APS classic paper that is freely available online Comroe JH Jr. The location and function of the chemoreceptors of the aorta. Am J Physiol 127: 176—191, 1939 ( http://ajplegacy.physiology.org/cgi/reprint/127/1/176 ).


2004 ◽  
Vol 287 (5) ◽  
pp. H1885-H1886 ◽  
Author(s):  
David R. Harder

This essay looks at the historical significance of an APS classic paper that is freely available online: Fabiato A. Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum. Am J Physiol Cell Physiol 245: C1–C14, 1983 ( http://ajpcell.physiology.org/cgi/reprint/245/1/C1 ).


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

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