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A 45 year old office clerk with a two year history of intermittent tension like headache presented with difficulties of walking heel to toe and of exchanging sensorimotor information between both hemispheres (alternating bilateral tapping, contralateral mirroring of finger position, cross localisation of tactile stimuli, finger sequence repetition, and bilateral coordinated arm rotations). There were no complaints about limitations in activities of daily life. The family history was unremarkable regarding motor disabilities, mental retardation, or epilepsy. MRI (A, C-F: TR 25 ms, TE 6.9 ms; B: TR 4000 ms, TE 90 ms) disclosed an absence of the corpus callosum, massa intermedia, posterior commissure (figure A) and septum pellucidum (figure C-F) and a hypoplastic anterior commissure (figure A). On the basis of the history and the anatomic findings, the patient can be classified as having an “asymptomatic” acallosal brain or a complete agenesis of the corpus callosum.1
The convolutional pattern on the medial surface of the hemisphere was abnormal with gyri radiating in a fan-like fashion and without a visible callosomarginal sulcus (figure A). On the axial and coronal slices an anteroposteriorly running fibre tract (arrow head, figure B-F) was visible which could clearly be distinguished from the medially situated cingulate gyrus (arrow in figure D). This fibre tract has been named after Probst (Balkenlängsbündel of Probst, callosal longitudinal bundle) who saw it as a typical sign of agenesis of the corpus callosum.2 Pathoanatomical investigations of the origin and course of the fibre tract led to the conclusion that it consists of heterotopic myelinated callosal fibres and results from a migration disorder of callosal fibres.2 3 During embryogenesis the fibres are thought to arrive at the midplane where they are hindered in their further migration across the midline and then change their direction of growth into an anteroposterior direction and by this form the Probst’s bundles in each hemisphere.3 This hypothesis about the development of the Probst’s bundles is supported by recent investigations in acallosal mice.4
The absence of the corpus callosum and the volume of the Probst’s bundles influence the shape of the ventricles. The posterotemporal parts of the lateral ventricles and the third and fourth ventricle are enlarged. Frontally, the Probst’s bundles are thickest and become smaller on their frontooccipital course (figure B). Frontally they are comma shaped, bulge into the medial wall of the lateral ventricles, and cause a narrowing and dorsolateral transposition of them (bull horn formation of the ventricles in figure D, E).2 3Posteriorly, the Probst’s bundle forms a thin layer on the upper medial wall of the lateral ventricles which are consecutively dilated (figure F). Additionally, a completely separated fornix could vaguely be identified at the lower medial wall of the lateral ventricles directly ventral to the longitudinal callosal bundle (figure D, short arrow in E).
This case illustrates that MRI allows a precise in vivo examination of the anatomical situation in patients with accidentally detected acallosal brains. Especially, the detailed characteristics of Probst’s bundle were to our knowledge previously only defined pathoanatomically, which is somewhat limited by shrinkage artifacts. The detection of Probst’s bundle during life might be useful to further elucidate the function of this fibre tract by evoked potential studies using transcranial magnetic or electric brain stimulation similar to the approach described for an activation of interhemispheric fibres in humans.5
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