Short report
Midbrain infarction: associations and aetiologies in the New
England Medical Center Posterior Circulation Registry
a Department of Neurology, Walton Centre for Neurology
and Neurosurgery, Rice Lane, Liverpool L9 1AE, UK, b Department of Neurology, New England Medical Center, Boston,
Massachusetts, USA, c Department of Neurology, Johns Hopkins Hospital, Baltimore,
USA
Correspondence to: Dr PJ Martin, Department of Neurology, Walton Centre for Neurology and Neurosurgery, Rice Lane, Liverpool L9 1AE, UK. Telephone 0044 151 525 3611; fax 0044 151 525 3857.
Received 18 June 1997 and in revised form 18 August 1997;
Accepted 22 August 1997
Most reports of midbrain infarction have described
clinicoanatomical correlations rather than associations and
aetiologies. Thirty nine patients with midbrain infarction (9.4%) are
described out of a series of 415 patients with vertebrobasilar
ischaemic lesions in the New England Medical Center Posterior
Circulation Registry. Patients were categorised according to the
rostral-caudal extent of infarction. The "proximal" vertebrobasilar
territory includes the medulla and posterior inferior cerebellar artery territory. The "middle" territory includes the pons and anterior inferior cerebellar artery territory. The "distal" territory
includes the rostral midbrain, thalami, superior cerebellum, and medial temporal and occipital lobes. Midbrain infarction was accompanied by
"proximal" territory infarcts in four patients, and by "middle" territory infarction in 19 patients. Thirteen patients had associated "distal" territory infarcts, three of whom had occipital or
temporal lobe infarcts. Only three patients had isolated midbrain
infarcts. Cardioembolism (n=11), in situ thrombosis (n=9), large artery to artery embolism (n=7), and intrinsic branch penetrator disease (n=5)
were the most common aetiologies. Bilateral infarction and accompanying
pontine infarction were associated with the most extensive
vertebrobasilar occlusive disease. Midbrain infarction was 10-fold more
likely to be accompanied by ischaemia of neighbouring structures than
it was to occur in isolation. Recognition of the different patterns of
infarction may act as a guide to the underlying aetiology and vascular lesions.
© 1998 by Journal of Neurology, Neurosurgery, and Psychiatry
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