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LETTER TO EDITOR
Year : 2016  |  Volume : 64  |  Issue : 5  |  Page : 1055--1057

Wernekink commissure syndrome

S Sheetal, P Byju 
 Department of Neurology, Pushpagiri Institute of Medical Sciences and Research Centre, Thiruvalla, Kerala, India

Correspondence Address:
S Sheetal
Department of Neurology, Pushpagiri Institute of Medical Sciences and Research Centre, Thiruvalla, Kerala
India




How to cite this article:
Sheetal S, Byju P. Wernekink commissure syndrome.Neurol India 2016;64:1055-1057


How to cite this URL:
Sheetal S, Byju P. Wernekink commissure syndrome. Neurol India [serial online] 2016 [cited 2020 Jan 24 ];64:1055-1057
Available from: http://www.neurologyindia.com/text.asp?2016/64/5/1055/190299


Full Text



Sir,

Midbrain infarcts have a wide spectrum of clinical presentations. Wernekink commissure syndrome is a rare midbrain syndrome, which selectively destroys the Wernekink commissure involving the decussation of the superior cerebellar peduncle in the midbrain. It is characterized by bilateral cerebellar ataxia and eye movement disorders, especially internuclear ophthalmoplegia. We, herein, report the case of a 51-year-old male, who developed cerebellar ataxia and internuclear ophthalmoplegia, whose magnetic resonance imaging (MRI) of the brain revealed an unusual ischemic stroke involving the paramedian midbrain on the left side. It has been rarely reported in the literature.

Our patient is a 51-year-old male with history of systemic hypertension, and coronary artery disease and on regular treatment. He presented to our emergency department with acute onset of unsteadiness of gait, slurring of speech, and diplopia when viewing targets on the right side. He was conscious, well-oriented, had a pulse of 66 per minute, regular in rhythm, and a blood pressure of 160/100 mmHg. His speech was dysarthric. Examination of the ocular movement showed that the adduction of the right eye was limited and the left eye had nystagmus on abduction, suggestive of internuclear ophthalmoplegia [Figure 1]. He had normal power of all four limbs. However, he had bilateral finger nose incoordination and truncal ataxia. The sensory system was normal.{Figure 1}

MRI of the brain showed a hyperintensity involving the paramedian midbrain on the left side on fluid-attenuated inversion recovery sequences [Figure 1], with diffusion restriction [Figure 2] and low apparent diffusion coefficient values [Figure 3], indicating an acute infarct. The symptoms of the patient were considered to be due to the disruption of the Wernekink commissure in the midbrain. He was started on dual antiplatelets and statins, and he started improving over the next 2 weeks.s{Figure 2}{Figure 3}

Wernekink commissure syndrome is a rare midbrain syndrome, which selectively destroys the Wernekink commissure involving the decussation of the superior cerebellar peduncle in midbrain.[1] It was first described by Lhermitte in 1958. It is characterized by bilateral cerebellar syndrome and internuclear ophthalmoplegia or ocular signs. Lesions of the medial longitudinal fasciculus cause internuclear ophthalmoplegia. The primary function of the medial longitudinal fasciculus is to coordinate lateral gaze by connecting the sixth nerve nucleus on the one side with the third and fourth nerve nuclei on the opposite side to allow the two eyes to move synchronously.

Midbrain infarction is divided into three groups based on the location of the lesions-infarction of the paramedian, lateral, or posterior area.[2],[3]

The paramedian area is supplied by the branches that diverge from the proximal portion of the posterior cerebral artery (PCA) before the branching of the posterior communicating artery. As Wernekink commissure is located in the paramedian area of the pons and midbrain, Wernekink syndrome, as a result of midbrain infarction, is associated with ischemia of the paramedian area.[4],[5] Limb movements, consciousness, cognition, and oculomotor capacities are the functions mainly involved in midbrain strokes, and their combinations tend to be characteristic. Other neuro-ophthalmological features, including skewed deviations, tonic ocular-tilt reactions, intermittent corectopia, internuclear ophthalmoplegia, and seesaw nystagmus have been reported.

[INLINE:1]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest

References

1Liu H, Qiao L, He Z. Wernekink commissure syndrome: A rare midbrain syndrome. Neurol Sci 2012;33:1419-21.
2Kim JS, Kim J. Pure midbrain infarction: Clinical, radiologic, and pathophysiologic findings. Neurology 2005;64:1227-32.
3Bogousslavsky J, Maeder P, Regli F, Meuli R. Pure midbrain infarction: Clinical syndromes, MRI, and etiologic patterns. Neurology 1994;44:2032-40.
4Dai AI, Wasay M. Wernekink comissure syndrome: A rare midbrain syndrome secondary to stroke. J Pak Med Assoc 2006;56:289-90.
5Krespi Y, Aykutlu E, Coban O, Tunçay R, Bahar S. Internuclear ophthalmoplegia and cerebellar ataxia: Report of one case. Cerebrovasc Dis 2001;12:346-8.