Changes in cerebral blood flow and vasoreactivity in response to acetazolamide in patients with transient global amnesia

Abstract

Objective-Previousreports about changes in cerebral blood flow (CBF) in transient global amnesia disclosed decreased flow in some parts of the brain. However, CBF analyses in most reports were qualitative but not quantitative. The purpose of this study was to determine changes in CBF in transient global amnesia. Methods-The CBF was measured and the vasoreactive response to acetazolamide was evaluated in six patients with transient global amnesia using technetium-99m hexamethylpropylene amine oxime singlephoton emission computed tomography (SPECT). The CBF was measured during an attack in two patients and soon after an attack in the other four. About one month later, CBF was re-evaluated in each patient. Results-Two patients examined during an attack and one patient examined five hours after an attack had increased blood flow in the occipital cortex and cerebellum. Three patients examined at six to 10 hours after an attack had decreased blood flow in the thalamus, cerebellum, or putamen. These abnormalities of blood flow almost disappeared in all patients one month after onset. The vasodilatory response to acetazolamide, which was evaluated initially using SPECT, was poor in areas of increased blood flow. By the second evaluation of CBF with acetazolamide, the vasodilatory response had returned to normal. Conclusions-In a patient with transient global amnesia, CBF increased in the vertebrobasilar territory during the attack and decreased afterwards. The vasodilatory response to acetazolamide may be impaired in the parts of the brain with increased blood flow. It is suggested that transient global amnesia is distinct from migraine but may share the same underlying mechanism.

Cerebrovascular Risk Factors and Triggers in Transient Global Amnesia Patients with and without Jugular Valve Incompetence: Results from a Sample of 243 Patients

“…Different results and interpretations of DWI lesions were given: DWI abnormalities in TGA did not resemble DWI findings in TIA in terms of time course delay, size of lesion and diffusion coefficient values [5,6,7,8,9,10,14]. Moreover, studies supported the hypothesis that vasospasms due to impaired vasoreactivity may trigger TGA [12,13]. …”

“…Different neuroimaging findings have been conducted to elucidate the different pathogentic mechanisms in patients with TGA. Several studies suggested that arterial-inflow changes as related to venous incompetence trigger a vasoreactive arterial response [11,12,13]. …”

A Tc-99m SPECT study of regional cerebral blood flow in patients with transient global amnesia

“…Findings from previous functional imaging studies of TGA patients have been inconsistent and include abnormalities in perfusion of the temporal lobes (Asada et al, 2000; Evans et al, 1993; Jung et al, 1996; Matsuda et al, 1993; Schmidtke et al, 2002; Stillhard et al, 1990; Strupp et al, 1998; Tanabe et al, 1991; Warren et al, 2000), thalamus (Goldenberg et al,1991; Sakashita et al,1997; Schmidtke et al, 2002), and striatum (Baron et al, 1994; Schmidtke et al, 2002). Although most studies of TGA have reported decreased perfusion, hyperperfusion in persons with TGA has also been reported in a handful of studies, particularly in the hippocampus, amygdala, and thalamus of the left hemisphere (Asada et al, 2000; Jung et al, 1996; Matsuda et al, 1993).…”

P2–087: Reflections of two parallel pathways between the hippocampus and neocortex in transient global amnesia: A cross‐sectional study using DWI and SPECT

“…Therefore, the head of the hippocampus may be more susceptible to venous congestion due to the limited outflow tracts available. Although most patients with TGA showed regional hypoperfusion [4][5][6][7][8][9][10][11][12][13][14], in a few patients in whom SPECT was performed during or immediately after the episode of TGA, there was transient hyperperfusion of the medial temporal or occipitocerebellar areas [10,36,37]. This discrepancy between the results of previous SPECT studies may be due to different timings of the SPECT scans with respect to the chronology of each individual attack [37].…”

“…Most studies investigating regional cerebral blood flow in TGA via single photon emission computed tomography (SPECT) have noted mesiotemporal hypoperfusion with or without the concomitant involvement of various cortical, subcortical and cerebellar structures [4][5][6][7][8][9][10][11][12][13][14].…”