Transient Global Amnesia by A. J. Larner

Author:A. J. Larner
Language: eng
Format: epub
ISBN: 9783030989392
Publisher: Springer International Publishing

5.1.2.6 Pathogenesis of MR-DWI Changes

What is the pathogenesis of the punctate lesions seen on MR-DWI in TGA patients? Many early studies interpreted the appearances as indicative of ischaemia (e.g. [10, 11, 15, 23]), but their time course is not that of a classic ischaemic lesion nor do they resemble venous congestion or infarcts.

As discussed (Sect. 5.1.2.5), the typical MR-DWI appearances seen in TGA are not specific for ischaemia, although very occasional cases of acute stroke may mimic the phenotype of TGA (Sect. 3.​1.​2; Table 3.​4). Certainly, the CA1 region of the hippocampus is known to be particularly vulnerable to hypoxia and selective injury may be associated with amnesia (e.g. [54–56]). Other investigational modalities (MRS; Sect. 5.2.4) suggest that some form of acute metabolic stress occurs [57], but the exact pathogenesis currently remains uncertain (see Sect. 9.​7.​5 and 9.​7.​6 for further discussion).

Although finding MR-DWI changes may be helpful in differential diagnosis (Chap. 3) in the appropriate clinical circumstances [30], the suggestion that these changes indicate that TGA is a disease process localised or in some way restricted to CA1 may be challenged, both empirically and conceptually . Empirically, CA1 lesions may not be seen in some TGA cases, and extrahippocampal lesions without CA1 involvement may occur (Sect. 5.1.2.2); moreover, the imaging changes become increasingly apparent with time after the clinical event (Sect. 5.1.2.3) suggesting they are downstream events. Conceptually, damage to a specific area associated with a specific functional consequence does not necessarily indicate that that particular location is responsible for that particular function. Whilst the method of lesion observation may assist in clinico-anatomical or clinico-radiological correlation, the observed lesion may have simply interrupted fibres of passage, abolished tonic “permissive” inputs or interfered with blood supply to tissue elsewhere (transient diaschisis) ([58], p.15–16).

Thus, to describe TGA as a “natural lesion model of hippocampal CA1 neurons” ([39], p.737) appears to be an oversimplification, and data interpretation which “critically relies on the selectivity of CA1 lesions” ([39], p.745) must be vulnerable to critique. Attempts to model TGA pathogenesis should rightly be predicated on hippocampal anatomy but need to take account of more than simply CA1 (Sect. 9.​7).

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