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S J Schreiber, F Doepp, R Klingebiel, J M Valdueza
Internal jugular vein valve incompetence and intracranial venous anatomy in transient global amnesia
J Neurol Neurosurg Psychiatry 2005; 76: 509-513 [Abstract] [Full text] [PDF]
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[Read eLetter] Transient global amnesia: consequent to brain hypoperfusion or hyperperfusion?
Vinod K Gupta   (16 May 2005)

Transient global amnesia: consequent to brain hypoperfusion or hyperperfusion? 16 May 2005
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Vinod K Gupta,
Physician
Dubai Police Medical Services, Dubai, United Arab Emirates

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Re: Transient global amnesia: consequent to brain hypoperfusion or hyperperfusion?

docgupta{at}emirates.net.ae Vinod K Gupta

Dear Editor,

Schreiber and colleagues detected a significantly higher prevalence of internal jugular vein valve incompetence (IJVVI) in patients with transient global amnesia (TGA).[1] No intracranial venous drainage pattern specifically related to IJVVI was, however, found. The relatively late age of onset of TGA and the low rate of recurrence (3-4%) are also features that are not consistent with a persistent anatomic venous predisposition. The pathophysiological role of any aberration that is also found in unaffected controls is always uncertain, particularly if the overall incidence of the illness is low and the ætiopathology of the entity is poorly defined. IJVVI was seen in one-third of controls [1] -- and up to 47% in other studies -- suggesting the recording of a normal anatomic variation rather than a potentially pathogenetic alteration. To produce TGA through venous congestion, sustained cerebral stasis -- and not simply transient venous congestion as might be produced by the Valsalva manœuvre (VM) or coughing -- is required to cause cerebral ischaemia. Nevertheless, there is but little evidence for a critical pathological role for ischaemia – venous or arterial – in the genesis of TGA.[2,3]

The proportion of “spontaneous” TGA unrelated to VM is substantial. The link between hypertension and TGA is striking.[4,5] Also, TGA is frequently associated with migraine.[1] Hypertensive encephalopathy is associated with hyperperfusion of the brain and breakdown of the blood- brain barrier.[6] Diffuse and prolonged hyperperfusion of the cerebral cortex, thalamus and basal ganglia prevails in migraine.[7] States of brain hyperperfusion are associated with white mater hyperintensities (WMH).[6,8,9] Medial temporal WMH has been recently seen in MRI performed within an hour after onset of TGA.[10] White matter abnormalities observed on MR images are associated with attenuated performance on tasks of processing speed, immediate and delayed memory, executive functions, and indices of global cognitive functioning.[11] Temporal lobe WMH are particularly associated with memory impairment.[12] Although WMHs are common in middle adult life, it is only when the medial temporal aspect is affected that development of TGA could be expected.

Both TGA and lacunar infarction might represent the outcome of a non- ischaemic breakdown of the blood-brain barrier that occurs randomly in patients susceptible to episodic brain hyperperfusion.

References

1. Schreiber SJ, Doepp F, Klingebiel R, Valdueza JM. Internal jugular vein valve incompetence and intracranial venous anatomy in transient global amnesia. J Neurol Neurosurg Psychiatry 2005;76:509-513.

2. Hirabayashi H, Shimizu M, Kohara S, Shinohara Y. Activated platelets in transient global amnesia and TIA. Neurology 2004;63:736-738.

3. Huber R, Aschoff AJ, Ludolph AC, Riepe MW. Transient Global Amnesia. Evidence against vascular ischemic etiology from diffusion weighted imaging. J Neurol 2002;249:1520-1524.

4. Santos S, Lopez del Val J, Tejero C, Iniguez C, Lalana JM, Morales F. Transient global amnesia: a review of 58 cases. Rev Neurol 2000;30:1113-1117.

5. Melo TP, Ferro JM, Ferro H. Transient global amnesia. A case control study. Brain 1992 ;115:261-270.

6. Donnan GA. Posterior leucoencephalopathy syndrome. Lancet. 1996;347:988.

7. Kobari M, Meyer JS, Ichijo M, Imai A, Oravez WT. Hyperperfusion of cerebral cortex, thalamus and basal ganglia during spontaneously occurring migraine headaches. Headache 1989;29:282-289.

8. Gupta VK. White matter hyperintensities: pearls and pitfalls in interpretation of MRI abnormalities. Stroke 2004 35: 2756-7; published online before print November 4 2004, doi:10.1161/01.STR.0000147158.89251.5b

9. Gupta VK. Lacunar stroke: on the threshold of a paradigm shift? J Neurol Neurosurg Psychiatry 2005. Available at: http://jnnp.bmjjournals.com/cgi/eletters/76/5/617

10. Inamura T, Nakazaki K, Yasuda O, Oi K, Morioka T, Nakamura Y, Nakamizo A, Inoha S, Amano T, Fukui M. A lesion diagnosed by MRI in a case of transient global amnesia. No To Shinkei 2002;54:419-422.

11. Gunning-Dixon FM, Raz N. The cognitive correlates of white matter abnormalities in normal aging: a quantitative review. Neuropsychology 2000;14:224-232.

12. Burton EJ, Kenny RA, O'Brien J, Stephens S, Bradbury M, Rowan E, Kalaria R, Firbank M, Wesnes K, Ballard C. White matter hyperintensities are associated with impairment of memory, attention, and global cognitive performance in older stroke patients. Stroke 2004;35:1270-1275.

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