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Case Reports
. 2012 Jul;13(5):425-9.
doi: 10.1007/s10194-012-0449-2. Epub 2012 Apr 28.

Cluster-tic syndrome as the initial manifestation of multiple sclerosis

Affiliations
Case Reports

Cluster-tic syndrome as the initial manifestation of multiple sclerosis

V González-Quintanilla et al. J Headache Pain. 2012 Jul.

Abstract

We report the case of a patient diagnosed as having cluster-tic syndrome as the initial manifestation of multiple sclerosis (MS). The patient's headache bouts improved after treatment with antiepileptic drugs, steroids, and beta-interferon. Magnetic resonance imaging (MRI) scans showed a pontine demyelinating lesion involving the area of the trigeminal root inlet and main sensory nucleus. Neurophysiological studies correlated well with MRI lesions. The association between cluster-tic syndrome and MS is an exception, and the mechanism of the pain is still unknown; therefore, this case might suggest a pathophysiological relationship between the trigeminal main sensory nucleus and cluster-tic syndrome.

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Figures

Fig. 1
Fig. 1
This figure represents the first MRI (without gadolinium) study performed on the patient: axial T2 (a) and coronal T1-weighted images (b) showing T2 hyperintense signals located at the territory of the left trigeminal root inlet and main sensory nucleus in the brainstem, which is hypointense in T1-weighted image coronal section (b)
Fig. 2
Fig. 2
This MRI study was performed 2 years after that of Fig. 1 and showed new T2-weighted lesions, which are hypointense in T1 gadolinium-enhanced images in the pons and cerebellum (arrows). Hyperintense T2 lesions give a mirror image of the trigeminal root inlet and main sensory nucleus. a T2-weighted images; b T1 gadolinium-enhanced image
Fig. 3
Fig. 3
These supratentorial MRI images correspond to the same study as Fig. 2. Both T2-weighted image (a) and FLAIR (b) discovered new periventricular lesions
Fig. 4
Fig. 4
This figure represents the first blink-reflex performed on the patient. After stimulation with superficial electrodes, both R1 components were absent (a, left; b, right), while both R2 components were normal (asterisks; latencies ranged from 35.4 to 41.0 ms). The second study (c, d) was performed 5 years after the first. There was no variation in shape or latencies of R2 components obtained after stimulation of both supra-orbital nerves, but a small and delayed R1 component is visible after stimulation on the right supra-orbital nerve (d, arrow)

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