Objectives: To investigate the clinical outcome of patients treated with chronic deep brain stimulation (DBS) of the centromedian nucleus (CM) for refractory epilepsy and to determine the location of active contacts. Methods: The outcome of CM stimulation was evaluated as percent seizure reduction compared to the baseline 3 months. To establish the location of active contacts, 27 leads were studied in 14 patients with refractory epilepsy. An analysis was conducted to reveal whether any coordinates of the center of the active contacts predicted percent seizure reduction. Results: With an average follow-up of 18.2 ± 5.6 months, the mean percent seizure reduction (n = 14) was 68 ± 22.4% (25-100%). Eleven of the 14 patients (78.6%) achieved >50% improvement in seizure frequency. Specifically, all 4 patients (100%) with generalized epilepsy (Lennox-Gastaut syndrome) and 7 of 10 patients (70%) with multilobar epilepsy showed >50% reduction in seizure frequency. The mean coordinates of the center of the active contact were located in the superior part of the anterior ventrolateral CM. The calculated coordinates of laterality from midline (x), anterior-posterior (y) and height (z) from the posterior commissure did not correlate with seizure outcome measured by percent seizure reduction. However, the locations of active contacts used during chronic CM stimulation in multilobar epilepsy were identified more dorsal to those used in generalized epilepsy. Conclusions: Chronic CM stimulation is a safe and effective means in the treatment of refractory epilepsy.

BACKGROUND AND PURPOSE:Spinal CSF leak syndrome is a unique disorder caused by spinal CSF leak. In this study, we attempted to determine whether MR myelography (MRM) can detect the leakage site in the spine.

Here we report a unique case of chronic occipital neuralgia caused by pathological vascular contact of the left greater occipital nerve. After 12 months of left-sided, unremitting occipital neuralgia, a hypesthesia and facial pain developed in the left hemiface. The decompression of the left greater occipital nerve from pathological contacts with the occipital artery resulted in immediate relief for hemifacial sensory change and facial pain, as well as chronic occipital neuralgia. Although referral of pain from the stimulation of occipital and cervical structures innervated by upper cervical nerves to the frontal head of V1 trigeminal distribution has been reported, the development of hemifacial sensory change associated with referred trigeminal pain from chronic occipital neuralgia is extremely rare. Chronic continuous and strong afferent input of occipital neuralgia caused by pathological vascular contact with the greater occipital nerve seemed to be associated with sensitization and hypersensitivity of the second-order neurons in the trigeminocervical complex, a population of neurons in the C2 dorsal horn characterized by receiving convergent input from dural and cervical structures.

Although pathologic vascular contact between the occipital artery and the greater occipital nerve (GON) at the crossing point in the nuchal subcutaneous layer can cause occipital neuralgia, referred hemifacial trigeminal pain from chronic occipital neuralgia owing to this cause is extremely rare.A 61-year-old female patient with left-sided occipital neuralgia for 4 years presented with a new onset of left-sided hemifacial pain. Decompression of the left GON from pathologic contacts with the occipital artery resulted in immediate relief for hemifacial pain and chronic occipital neuralgia. The present case implies that sensitization and hyperactivity of the trigeminocervical complex that receives the convergent input from trigeminal and high cervical occipital nociceptive pathways can be a pathogenic mechanism in referred hemifacial pain from occipital neuralgia. In the present case, a branching tributary of the occipital artery at the crossing point forming a constricting loop above the course of the GON was found to be the cause of entrapment. Because the occipital artery is reported to be consistently located superficial to the GON at the crossing point, a spatial relationship between the occipital artery and the GON rather than a mere adhesion or contact might have pathologic significance in the development of occipital neuralgia.