More than Just Migraine: Cortical Spreading Depression is Linked to Transient Global Amnesia
ABSTRACT & COMMENTARY
Source: Strupp M, et al. Diffusion-weighted MRI in transient global amnesia: Elevated signal intensity in the left mesial temporal lobe in 7 of 10 patients. Ann Neurol 1998;43: 164-170.
Transient global amnesia (tga) remains one of the striking mysteries of clinical neurology. Hodges and Warlow (Brain 1990;113:639-657) established specific diagnostic criteria that have served to help differentiate TGA from transient epileptic amnesia and transient ischemic attacks. Nonetheless, the pathophysiology of pure TGA is still uncertain. Strupp and colleagues report on diffusion-weighted MRI findings in 10 patients with pure TGA which suggest a mechanism of cortical spreading depression (CSD).
Ten patients with pure TGA were defined by the following Hodges and Warlow criteria: 1) episodes of anterograde amnesia; 2) no clouding of consciousness or loss of personal identity; 3) no focal neurologic signs or symptoms; 4) no epileptic seizures; 5) no recent history of head injury or known history of epilepsy; and 6) complete resolution within 24 hours. Diffusion-weighted MRIs were obtained within 2-144 hours of the attack. Seven of the 10 patients showed an abnormal high signal in the left hippocampal region. Three of these seven had bilateral hippocampal signal abnormalities. Two of the three normal scans were obtained at 120 and 144 hours into the attack. Follow-up scans at two weeks were normal in all 10 patients. Conventional T1- and T2-weighted images were initially normal and remained unchanged at two-week follow-up. The diffusion-weighted abnormalities correlate with a decrease in interstitial water and cellular edema. The resolution of these changes and the lack of T2-weighted abnormalities argues against ischemia as the pathophysiological mechanism. Instead, the authors conclude that these changes are better explained by CSD.
COMMENTARY
CSD is an underappreciated clinical phenomenon because it is transient, reversible, and defies traditional neuroradiologic imaging and standard neurophysiologic tracings. Originally described by Leao (J Neurophysiol 1945;8:33-46), CSD refers to a spreading wave of depolarization across the cortex leaving a wake of prolonged neuronal/glial inactivity and concomitant oligemia. Though it has been recognized as the likely mechanism of migraine aura, its significance in other clinical conditions has not been well studied. Caplan (Neurology 1981;31:1167-1170) and Olesen (Acta Neurol Scand 1986;73:219-220) were among the first to make the association between CSD and TGA on clinical and theoretical grounds. Hodges and Warlow show that the prevalence of migraine in patients with TGA is 25%. The current study adds more evidence to support this notion and to a wider appreciation of CSD as a pathophysiological mechanism in neurological disease. Newer scanning techniques like diffusion-weighted MRI will help shed more light on this phenomenon. -jr
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