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Review
. 2020 Dec 18:10:83.
doi: 10.25259/JCIS_49_2020. eCollection 2020.

An Anatomic, Imaging, and Clinical Review of the Medial Longitudinal Fasciculus

Affiliations
Review

An Anatomic, Imaging, and Clinical Review of the Medial Longitudinal Fasciculus

Peter Fiester et al. J Clin Imaging Sci. .

Abstract

The medial longitudinal fasciculus (MLF) is a paired, highly specialized, and heavily myelinated nerve bundle responsible for extraocular muscle movements, including the oculomotor reflex, saccadic eye movements an smooth pursuit, and the vestibular ocular reflex. Clinically, lesions of the MLF are classically associated with internuclear ophthalmoplegia. However, clinical manifestations of a lesion in the MLF may be more complex and variable. We provide an overview of the neuroanatomy, neurologic manifestations, and correlative examples of the imaging findings on brain MRI of MLF lesions to provide the clinician and radiologist with a more comprehensive understanding of the MLF and potential clinical manifestations for an MLF lesion.

Keywords: Internuclear opthalmoplegia; Medial longitudinal fasciculus; One-and-a-half syndrome; Trochlear syndrome; Wall-eyed bilateral internuclear opthalmoparesis syndrome.

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Conflict of interest statement

There are no conflicts of interest.

Figures

Figure 1:
Figure 1:
The medial longitudinal fasciculus (MLF) carries excitatory and inhibitory axonal nerves between the paramedian pontine retricular formation and cranial nerves III, IV, and VI during activation of the frontal eye fields in the cerebral cortex. Axial T2-weighted sequence (a) of the midbrain demonstrating MLF (magenta circles), oculomotor III (blue circles), and trochlear IV (green circles) nuclei. Axial T2-weighted sequence (b) of the dorsal pons demonstrating abducens VI nuclei (orange circles) and MLF (magenta circles).
Figure 2:
Figure 2:
A lesion isolated within the heavily myelinated white matter tract of the medial longitudinal fasciculus disrupts the signal from the contralateral abducens nucleus (CN VI) transmitted through the paramedian pontine retricular formation. This allows abduction of the contralateral eye with nystagmus, but disrupts the synchronized horizontal gaze of the other eye resulting in weakened or absent adduction of the opposite globe.
Figure 3:
Figure 3:
A lesion located at the level of the caudal midbrain between the superior and inferior colliculi affects both the medial longitudinal fasciculus and ipsilateral trochlear nucleus resulting in internuclear ophthalmoplegia (INO) and trochlear syndrome. Clinically, this presents as INO with a contralateral hyperdeviation of the globe due to loss of innervation of the superior oblique muscle.
Figure 4:
Figure 4:
A lesion located in the dorsal pontine tegmentum affects both the medial longitudinal fasciculus and the ipsilateral abducens nuclei and/or paramedian pontine retricular formation. Clinically, this presents with internuclear ophthalmoplegia with horizontal gaze in one direction and lateral gaze palsy in the other direction.
Figure 5:
Figure 5:
A lesion located in the dorsal brainstem affecting the bilateral medial longitudinal fasciculus with sparing of the extraocular muscle nuclei. Clinically, this presents with divergence, or “wall-eyed” appearance, of the globes in the horizontal plane.
Figure 6:
Figure 6:
A 63-year-old male presented with diplopia, dizziness, and right internuclear ophthalmoplegia. Diffusion-weighted sequence (a) with corresponding attenuation diffusion coefficient map (b) demonstrating focal water restriction in the right dorsal pons of the medial longitudinal fasciculus (arrows) consistent with a small acute infarct.
Figure 7:
Figure 7:
A 57-year-old male presented with multifocal embolic stroke. Diffusion-weighted sequence (a) with corresponding attenuation diffusion coefficient map and (b) demonstrating a small, foci of water restriction in the right inferior midbrain consistent with an acute infarct of the medial longitudinal fasciculus (arrows). Diffusion-weighted sequence at the level of the lateral ventricles (c) demonstrating two additional foci of acute ischemic change in the left caudate and splenium of the corpus callosum (arrows).
Figure 8:
Figure 8:
A 38-year-old female presented with dizziness and weakness, without extraocular muscle dysfunction. Axial T2-weighted (a) and FLAIR sequence (b) demonstrating a small, focal demyelinating plaque in the left dorsal pons (arrows). Sagittal FLAIR sequence (c) demonstrating the characteristic periventricular appearance of whiter matter plaques in a patient with multiple sclerosis (arrows).
Figure 9:
Figure 9:
A 44-year-old female with a known clinical history of multiple sclerosis presented with bilateral internuclear ophthalmoplegia. Axial FLAIR sequence (a) demonstrates a lesion in the dorsal pons in the medial longitudinal fasciculus (arrow). Axial diffusion-weighted imaging sequence (b) demonstrates no restricted diffusion (arrows) to suggest an acute infact. Axial and sagittal post-contrast T1 axial images (c and d) demonstrate solid enhancement in this location (arrows).

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