Schematic of the same disposition. AICA-PICA balanceAn exceedingly well known variation — a continuum, in fact, where AICA and PICA are, respectively, larger and smaller, depending on the extent to which one can capture the territory of the other. The PICA can be conceptualized as a large radiculopial origin vessel (arising from the lateral spinal artery, a homolog of the posterior spinal system), whereas AICA originates as coronary type vessel off the basilar (homolog of anterior spinal artery).
Schematic of balanced arrangement (left image). Right image shows PICA dominance of the “right” vert and AICA dominance of the “left” vert. Below is an angiographic image of the same arrangement, except for a kind of AICA duplication on the left, and a small basilar fenestration (yellow arrow). Notice how PICA and vert change caliber when they go through the dura above foramen magnum. Not to be confused for atherosclerotic disease, of which there is also a small specimen present just above the AICA.
Superior Cerebellar Artery Duplication — same as AICA, just a balance of transverse arteries.
Another illustration, on opposite sides, in a patient with a complete circle of Willis, displayed to advantage by a generous injection.
Another fenestration, on CTA
Again, a rather large fenestration (brown arrow), in a patient with fetal PCOM. Notice, how on the right, a small AICA (with dominant ipsilateral PICA) is accompanied by a number of basilar perforators between the AICA and SCA (not marked with any arrows)
In this patient, a basilar fenestration is associated with an AVM:
A few years later, the AVM is gone, and the fenestration can be better appreciated thru lack of competing inflow from the right vert.
Very rarely, fenestrations can be associated with aneurysm formation — here treated by stent-coiling following rupture. Case courtesy Dr. Moses Aronov. Instragram @neurointervention_Moscow
While the fenestration might be sporadic, one might also postulate that dual channels persisted secondary to AVM-related flow demand during fetal period. This is a tempting, though likely erroneous assumption. Here is another one, courtesy of Dr. Daniel Sahlein:
An ex vivo specimen, courtesy of Peggy Mason, PhD, Department of Neurobiology, University of Chicago, Chicago, IL. Notice also a nice anterior spinal artery (yellow arrow). Also to be seen are petrosal vein, vein of the lateral recess, and nice pontine perforators.
An anaglyph stereo of basilar fenestration
Good angiographic technique is important — the patient below was thought to have an SCA aneurysm
Poor right vert injection, with admixture of unopacified contrast from a co-dominant left vert is not diagnostic — or shouldn’t be
Rotational angio/ VR reconstructions however suggest that a basilar terminus fenestration might be present instead
This requires confirmation — there can be artifacts due to unopacified flow, etc. Optimal projection, strong injection to transiently overcome left vert inflow, and good magnification with no movement confirm presence of this unusual fenestration. See full case here
Finally, a double fenestration courtesy Drs. Shepherd and Raz
Basilar Nonfusion The extreme form of fusion variation is non-fusion. As the basilar forms by fusion of the longitudinal neural axis vessels, a complete deficiency in fusion is not unreasonable, and very rare cases of it do exist. Longitudinal non-fusion refers to a case of “twin basilars” — two parallel channels, which can also be regarded as the extreme form of a fully “unzipped basilar”. Transverse, or axial non-fusion describes a basilar artery which is disconnected in its mid-portion, usually below the AICAs. It is not so uncommon to see diminished flow in the same segment on MRA, which can be appreciated as a “pseudo-stenosis” of mid-basilar (see below). Lasjaunias felt that this basilar segment is an embryologic boundary of sorts, and therefore non-fusions happened there with at least some frequency. Longitudinal Nonfusion, as seen by MRI, electronically reproduced with kind permission of ASNR and First Author: Hoh BL, Rabinov JD, Pryor JC, Hirsch JA, Dooling EC, Ogilvy CS. AJNR Am J Neuroradiol. Persistent nonfused segments of the basilar artery: longitudinal versus axial nonfusion. Aug;25(7):1194-6. 2004, © by American Society of Neuroradiology
Axial non-fusion from the same source, electronically reproduced with kind permission of ASNR and First Author: Hoh BL, Rabinov JD, Pryor JC, Hirsch JA, Dooling EC, Ogilvy CS. AJNR Am J Neuroradiol. Persistent nonfused segments of the basilar artery: longitudinal versus axial nonfusion. Aug;25(7):1194-6. 2004, © by American Society of Neuroradiology
Pseudostenosis of the basilar artery — in some degree possibly related to embryologic boundary in the mid-basilar, as above.
Pontine Perforators:Fronal projection view of the basilar artery, with several transverse pontine “ziggii” perforators (yellow and brown) between the SCA and the duplicated AICAs (red arrows). A loose correlation exists between the number and size of these perforators and distance between the SCA and the AICAs — the longer the distance, the more and larger the perforators tend to be.
High-riding basilar — the position of the basilar tip (red) in relation to the posterior clinoid (white) and less importantly to the petrous apex (blue) is critical in pre-surgical assessment for those who still clip basilar tip aneurysms. An aneurysm neck below the posterior clinoid tip is difficult or impossible to reach and therefor to adequately clip even with a subtemporal appoach. This is a high-riding basilar. Also notice downward sweep of the PCAs relative to basilar tip — another indication of high basilar positon. The opposite istrue of the low basilar
Upper Basilar Perforators
There is a wealth of very clinically significant perforators arising from basilar bifurcation and proximal P1 segment, usually supplying the mesial thalamic structures. The classic “Percheron” is a common origin of such perforator supplying bilateral thalami. Clinically important as injury / occlusion leads to profound level of consciousness alterations.
As in anything — there is a spectrum. One might have a common lenticulostriate group origin or individual ones. Below is a beautiful set of DYNA VR images by Eytan Raz. Note how the more lateral pair of perforators is also more anterior — as is in balance with anterior thalamic perforators typically arising from proximal PCOMs. Also present is a “duplicated SCA” and bilateral “duplicated” AICAs. All part of the same big spectrum idea
Another Percheron Stereo
Another Percheron DYNA
In addition to percheron (dashed arrows), one sees bilateral paired long collicular arteries (arrows) and PCOMs
The medial / posterior thalamic perforators tend to originate from the basilar even in bilateral fetal PCOM cases. These are rare — at least having no P1 at all is much more uncommon than having no PCOM. I does present a bit of a conundrum from embryologic perspective, since the “fetal” PCOM is supposed to be the early way — having more nonexistent PCOMs than P1s is a bit of a problem with this theory. But that is besides the point. The Clinical issue is that these perforators will come off basilar even when P1s are absent — see below
Basilar Occlusion Syndromes
These span the spectrum between asymptomatic and fatal. Focal mid-basilar atheromatous occlusions are extremely well-tolerated when PCOMs are present to supply what’s above. When absent, result is usually death or major disability.
Long segments of basilar occlusion, without PCOMs, are equally deadly. With PCOMs, the result is usually pontine perforator infracts. Unilateral single perforator infarcts have good to excellent prognosis. Bilateral infarcts of multiple perforators, while sparing top of basilar, produce the dreaded locked-in syndrome. See below. Initial presentation was right-sided weakness, due to larger burden of occlusions on the right side, progressing quickly to full syndrome.
Bilateral vertebral occlusions suggest atheromatous etiology
Focal top of basilar occlusions, when blocking thalamic perforators, result in profound decline in consciousness, often markedly out of proportion to size of embolus. Here is a subocclusive embolus in a comatose patient. Notice lack of thalamic perforators on both images
The perfusion images below are actually the most informative — everything is there. it is one of the most amazing perfusion images we ever came across.
Post thrombectomy — all thalamoperforators are arising from the site of prior occlusion…
Full case of above images is here