(Stroke. 2001;32:2725-a.)
© 2001 American Heart Association, Inc.
Letters to the Editor |
Re: Molecular Anatomy of an Intracranial Aneurysm
Departments of Anatomy, and Diagnostic and Therapeutic Neuroradiology, University Hopital Bicetre, Paris, France
Department of Interventional Neuroradiology, Toronto Western Hospital, Toronto, Canada
To the Editor:
I read with great interest the recent Stroke article by David Peters and collaborators.1 This paper illustrates the passage of aneurysms as diseases of the lumen to the evidence that aneurysms are diseases of the arterial wall and sometimes even of the extravascular space. A few remarks need to be made concerning the case and its relevance in the approach to aneurysmal diseases.
The case occurs in a young child, where aneurysms are rare2; it is seated on the distal middle cerebral artery (MCA), which is not a frequent location in general, even in children. It ruptures and gives rise to intracerebral hematoma and not subarachnoid hemorrhage. Such differences are significant if one wants to extrapolate such a case to subarachnoid aneurysmal rupture in adults.
The authors themselves mention that this was far from constituting an ideal model. I certainly agree with them, in particular because the diseases in children compared with adults are so different that the underlying genetic problems can probably be hardly compared.
In this particular case, we would certainly not describe the lesion as multiple aneurysms, since within a hematoma some of the pockets will necessarily correspond to a communication between the intravascular lumen and the hematoma cavity. Assimilating the case to berry aneurysm of the distal branches of the MCA may certainly correspond to a misnomer; this meaningless denomination is traditionally used for subarachnoid aneurysms, and the one involved is likely to be subpial. The extravascular space is therefore significantly different. The age of the lesion (the length of time that the aneurysm has been present and unruptured) and the age of rupture point to the exposure of the biological system to various signals during an undetermined amount of time. Stressing the role played by the extravascular space certainly points to the fact that the subpial environment is significantly different from the subarachnoid in the generation of the aneurysm, its rupture, and the reaction to that rupture.
The various changes that have been observed, as pointed out by the authors, cannot be assessed. Using the superficial temporal artery (STA) for comparison is probably the most difficult problem of the study. It certainly maintains the idea that the arterial system is homogenous enough that vessels as different as the MCA and STA can be successfully compared. The segmental vulnerability3 shows that this vessel has significant differences: phylogenetic, embryological, and hemodynamic. In addition, the STA does not develop aneurysms; these are characteristic of the external carotid biological evolution rather than that of the internal carotid branches. The hemodynamics and shear stresses in both systems are different, and the few aneurysms described in the STA are seen following trauma or MCA-STA anastomoses. This certainly emphasizes again the role played by the surroundings and that of the signals coming from the distal territory and the surrounding tissue in the regulation and expression of the various genes.
The epidemiological references quoted certainly do not apply to children, even though they carry a genetic predisposition to the development of aneurysms (eg, polycystic kidney disease). The arterial immune reactions and their potential constitutional weakness (AIDS, familial candidosis) demonstrate the specificity of some targets and responses with regard to triggers.4
Finally, damaged repair systems in some hereditary diseases such as hereditary hemorrhagic telangiectasia type 1 with endoglin and transforming growth factor-ß1 do not produce arterial aneurysms but rather different types of vascular alterations. One can also question the maturation over time of some genetic programs of modeling and remodeling of the brain vessels. The cell turnover and repair capacities are unlikely to be continuous and spread over an equal period throughout life. Postnatal maturation represents additional challenges that one should foresee in interpreting gene-expression disorders.
All these remarks are not meant to be restrictive for this extremely interesting paper but rather should stress the need to establish links between clinical observations and biological or genetic ones to ensure a rapid benefit in the treatment of patients.
References
1.
Peters DG, Kassam AB, Feingold E, Heidrich-O’Hare E, Yonas H, Ferrell RE, Brufsky A. Molecular anatomy of an intracranial aneurysm: coordinated expression of genes involved in would healing and tissue remodeling. Stroke. 2001; 32: 1036–1042.
2. Lasjaunias P. Segmental identity and vulnerability in cerebral arteries. Intervent Neuroradiol. 2000; 6: 113–124.
3. Lasjaunias P. From aneurysms to aneurysmal vasculopathies. Intervent Neuroradiol. 1999; 5: 105–108.
4. Lasjaunias P. Vascular Diseases in Neonates, Infants, and Children. Berlin, Germany: Springer-Verlag; 1997.
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