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Medial medullary infarction with contralateral glossoplegia
  1. D Chang,
  2. S-H Cho
  1. Department of Neurology, College of Medicine, Kyunghee University
  1. Correspondence to:
 Dr Dae-il Chang
 Department of Neurology, College of Medicine, Kyunghee University, 1 Hoegi-dong, Dongdaemun-ku, Seoul, 130-702, South Korea; dichangkhmc.or.kr

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Medial medullary infarction with contralateral glossoplegia

There is a relative lack of information on the course of corticohypoglossal projections in the human brain stem,1,2 especially in the medulla. Using transcranial magnetic stimulation and magnetic resonance imaging (MRI) in 11 patients with ischaemic lesions at different brain stem levels, Urban et al showed that pontine lesions at the ventral paramedian base close to the midline affected the contralateral corticohypoglossal projections, while lateral lesions at the pontine base affected the ipsilateral projections. Lesions of the dorsolateral and mediolateral medulla impaired only ipsilateral corticohypoglossal projections.3

We report a patient with contralateral glossoplegia in the ventromedial lesion of the upper medulla.

Case report

A 52 year old hypertensive man suddenly developed right sided paraesthesiae distal to the elbow and knee. The next day he had right hemiparesis. On neurological examination, he was found to have left beating nystagmus on left lateral gaze. Unilateral tongue paresis was demonstrated by voluntary protrusion, during which the tip of the tongue deviated to the right (fig 1A). When the tongue was not protruded, the right half of the tongue base was seen to bulge. Neither atrophy nor fasciculation was observed in the tongue. There were no abnormalities on tongue electromyography. He had mild right hemiparesis, mildly diminished sensation in all modes, which gradually worsened, and truncal lateropulsion to the right. Brain MRI, done three days after symptom onset, showed an infarct in the ventromedial portion of the left rostral medulla extending deep into the dorsal portion (fig 1B and 1C). The paraesthesiae and sensory deficits disappeared spontaneously in two weeks, and the limb weakness and the glossoplegia gradually improved, with complete resolution two months after stroke onset.

Figure 1

 (A) The protruded tongue deviating to the right about 1.5 cm from the midline. Magnetic resonance imaging (T2 sagittal (B) and diffusion weighted (C)) showed an acute unifocal ischaemic lesion in the left ventromedial part of the upper medulla. The schematic drawing (D) shows the proposed corticohypoglossal decussation at the upper medulla level.

Comment

This patient’s glossoplegia was a supranuclear palsy because the tongue deviated to the contralateral side of the lesion and neither atrophy nor fasciculation was observed. Protrusion of the tongue is accomplished by the unopposed action of the normal contralateral genioglossus. The corticobulbar fibres controlling the genioglossus muscles are crossed; the other tongue muscles appear to have bilateral supranuclear control.2,4 With regard to the supranuclear projections to the hypoglossal nucleus in the brain stem, it is still unclear at what level they decussate over the midline to reach the contralateral nucleus. Urban et al showed that lesions of the ventral pontine base located close to the midline only impair the contralateral corticohypoglossal projections, while lesions extending to the lateral part of the basis pontis and dorsolateral lesions of the upper medulla near the pontine border affect the ipsilateral projections. They suggested that the main decussation of these fibres is located close to the pontomedullary junction.3

In this patient with contralateral supranuclear glossoplegia, the lesion was located on the ventromedial part of the rostral medulla. This finding shows that the corticohypoglossal projections in this patient are decussated at the upper medullary level (fig 1D), more caudally than the pontomedullary junction described by Urban et al.3

References

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Footnotes

  • Competing interests: none declared

  • Consent was obtained for publication of figure 1A

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