Jin-gyu Choi

Clinical Outcome of Patients with Deep Brain Stimulation of the Centromedian Thalamic Nucleus for Refractory Epilepsy and Location of the Active Contacts.

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.

Relationship between Postoperative EEG Driving Response and Lead Location in Deep Brain Stimulation of the Anterior Nucleus of the Thalamus for Refractory Epilepsy

Objectives: Interpreting the postoperative electroencephalographic (EEG) driving response (DR) as an indicator of electrode placement within the thalamic nucleus in deep brain stimulation (DBS) of the anterior nucleus of the thalamus (ANT) for refractory epilepsy is controversial. Materials and Methods: We retrospectively investigated the relationship between postoperative EEG DR and the location of 11 electrodes in 6 patients who underwent ANT DBS for refractory epilepsy. Results: Cerebral synchronizing EEG DR was observed in 10 electrodes. However, 9 of the 11 electrodes were located within the ANT. For the 2 electrodes that missed the ANT, DR was observed in 1 misplaced electrode facing the anterior surface of the ANT within the third ventricle. The other misplaced electrode without DR elicitation showed a DR after electrode repositioning. Conclusions: The diagnostic significance of DR as indirect evidence of electrodes being within thalamic nuclei is limited. If DR is not elicited, it should be regarded as a misplacement. Even if DR is elicited, it may not be interpreted as a sound indicator of proper electrode placement within the thalamus. A sophisticated, postoperative imaging study is warranted in every case of ANT DBS.

Multimodal, Intraoperative Monitoring during Paddle Lead Placement for Cervicothoracic Spinal Cord Stimulation.

Background and Objective: We investigated the efficacy of combined somatosensory evoked potentials (SSEP) and electromyography monitoring during paddle lead placement through cervicothoracic laminectomy under general anesthesia in a retrospective review of data from 25 patients. Methods: Muscle motor evoked potentials (MEP) recordings and SSEP monitoring were used for surveillance of the spinal cord. Collision testing of SSEP and threshold amplitudes of compound muscle action potentials (CMAP) in the bilateral upper and lower extremities evoked by electrode contacts of the paddle lead were checked to determine the laterality of the lead in the mediolateral direction. Results: A significant decrease in amplitudes of muscle MEP in spite of stable SSEP occurred in 2 patients: 1 patient with a retrograde C1-C2 insertion and another patient with an anterograde C4/C5 insertion. Repositioning of leads based on significantly asymmetrical collision testing of SSEP and thresholds of CMAP in bilateral extremities was needed in 6 and 8 patients, respectively. In 22 patients, paresthesia coverage of the painful area was consistently located in the painful side, either unilaterally or bilaterally. There was no episode of revision for suboptimal lead placement. Conclusions: Intraoperative neurophysiological guidance using SSEP and muscle MEP was useful for the safe and accurate placement of paddle leads for cervicothoracic SCS.

Hemifacial Pain and Hemisensory Disturbance Referred from Occipital Neuralgia Caused by Pathological Vascular Contact of the Greater Occipital Nerve

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.

Long-Term Migration of a Deep Brain Stimulation (DBS) Lead in the Third Ventricle Caused by Cerebral Atrophy in a Patient with Anterior Thalamic Nucleus DBS

The long-term (5-years) antiepileptic effect of deep brain stimulation (DBS) of the anterior nucleus of the thalamus (ANT) against refractory epilepsy has been reported. However, experience with ANT DBS for epilepsy is limited, and so hardware complications and technical problems related to ANT DBS are unclear. We report the case of a 57-year-old male who underwent re-implantation of a DBS lead in the left ANT because of lead migration into the third ventricle detected 8 years after the first DBS, and which was caused by the significant enlargement of the lateral and third ventricles. After re-implantation, the patient showed a mechanically-related antiepileptic effect and a prominent driving response of the electroencephalography was verified. We speculate that progressive dilatation of the ventricle and shallow, insufficient implantation of the lead during the initial ANT DBS may have caused migration of the DBS lead. Because dilatation of the ventricle could progress years after DBS in a patient with chronic epilepsy, regular follow-up imaging is warranted in ANT DBS patients with an injured, atrophied brain.

The Relief of Unilateral Painful Thoracic Radiculopathy without Headache from Remote Spontaneous Spinal Cerebrospinal Fluid Leak

Spontaneous intracranial hypotension (SIH) caused by spontaneous spinal cerebrospinal fluid (CSF) leaks produces orthostatic headaches. Although upper arm pain or paresthesia is reportedly associated with SIH from spontaneous spinal CSF leak in the presence of orthostatic headache, low thoracic radicular pain due to spontaneous spinal CSF leak unassociated with postural headache is extremely rare. We report a 67-year-old female who presented with chronic, positional radicular right T11 pain. Computed tomography myelography showed a spontaneous lumbar spinal CSF leak at L2-3 and repeated lumbar epidural blood patches significantly alleviated chronic, positional, and lower thoracic radiculopathic pain. The authors speculate that a chronic spontaneous spinal CSF leak not severe enough to cause typical orthostatic headache or epidural CSF collection may cause local symptoms such as irritation of a remote nerve root. There might be considerable variabilities in the clinical features of SIH which can present a diagnostic challenge.

Compression of Thoracic Spinal Cord with Decreased Cerebrospinal Fluid Space After Implantation of Paddle Lead Spinal Cord Stimulation at T9: A Three-Dimensional Myelographic Computed Tomography Study

OBJECTIVES To investigate the extent of spinal cord compression and cerebrospinal fluid (CSF) space after T9 paddle lead spinal cord stimulation (SCS) using three-dimensional myelographic computed tomography scans. METHODS Preoperative and postoperative three-dimensional myelographic computed tomography scans were performed in 15 patients with paddle lead SCS at T9 for neuropathic back and leg pain. Four axial levels between each row of the electrodes were selected and the cross-sectional areas of thecal sac and spinal cord, the width of anterior and posterior CSF space, and contact angle of the lead within T9 spinal canal were measured with 12-month pain relief assessment. RESULTS The cross-sectional areas of thecal sac and spinal cord under each contact of paddle leads decreased significantly (23.89 ± 11.48% and 9.45 ± 4.80%; P < 0.05, respectively). The width of posterior CSF space decreased by 38.65 ± 20.97% and that of anterior CSF space showed a greater reduction by 59.09 ± 18.39% (P < 0.05). We achieved a mean pain relief of 45.49 ± 13.73% at 12-month follow-up and found a significant correlation with percentage reduction in the area of the spinal cord. CONCLUSIONS Significant reduction in the cross-sectional area of spinal cord and anterior CSF space as well as thecal sac and posterior CSF space resulted in deformation of the spinal cord under paddle leads at T9 within 7 postoperative days. Close approximation to the dorsal column and the mass effect of paddle leads may determine the clinical outcome of paddle lead SCS and also raise safety concerns.

Technical Implications in Revision Surgery for Deep Brain Stimulation (DBS) of the Thalamus for Refractory Epilepsy.

Background and Purpose Implantation of deep brain stimulation (DBS) electrodes in the anterior nucleus of the thalamus (ANT) or the centromedian nucleus (CM), for the treatment of refractory epilepsy, is technically demanding. To enhance the accuracy of electrode placement within the ANT and CM, we analyzed our experience with electrode revision surgery in ANT and CM DBS and investigated the cause of misplacement and verifying methods for accurate placement. Methods A retrospective analysis of the medical records of 23 patients who underwent DBS for refractory epilepsy during the period from 2013 to 2016 was performed. Results Misplacement of the electrode occurred in 1 (25%) of 4 ANT DBS and 2 (14.3%) of 14 patients with CM DBS performed in our institute, and revision surgery was performed in three patients. During this period, we performed three revision surgeries for misplaced electrodes in ANT DBS that were performed at another hospital. Therefore, we performed six revision surgeries (four in ANT, two in CM) for mistargeted DBS electrodes for thalamic DBS. Transventricular lead placement and an anatomical targeting of the ANT was the cause of misplacement in the ANT and intraoperative brain shift was found to be the cause in the CM. For verification of the location of lead placement, magnetic resonance imaging (MRI) was superior to computed tomography and electroencephalography (EEG). Conclusions To reduce the rate of electrode misplacement for refractory epilepsy, image-based targeting of the ANT according to individual anatomical variation, and efforts to minimize intraoperative brain shift are essential. To verify the location of the electrode, MRI examination is mandatory in DBS for refractory epilepsy.

Hemifacial Trigeminal Pain Referred from Occipital Neuralgia Due to Compression of the Greater Occipital Nerve by the Occipital Artery

Abstract 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.

A Case of Diffuse Leptomeningeal Glioneuronal Tumor Misdiagnosed as Chronic Tuberculous Meningitis without Brain Biopsy

Here we report a rare case of diffuse leptomeningeal glioneuronal tumor (DLGNT) in a 62-year-old male patient misdiagnosed as having tuberculous meningitis. Due to its rarity and radiologic findings of leptomeningeal enhancement in the basal cisterns on magnetic resonance imaging (MRI) similar to tuberculous meningitis, DLGNT in this patient was initially diagnosed as communicating hydrocephalus from tuberculous meningitis despite absence of laboratory findings of tuberculosis. The patients symptoms and signs promptly improved after a ventriculoperitoneal shunting surgery followed by empirical treatment against tuberculosis. Five years later, mental confusion and ataxic gait developed in this patient again despite well-functioning ventriculoperitoneal shunt. Aggravation of leptomeningeal enhancement in the basal cisterns was noted in MRI. An additional course of antituberculosis medication with steroid was started without biopsy of the brain. Laboratory examinations for tuberculosis were negative again. After four months of improvement, his mental confusion, memory impairment, dysphasia, and ataxia gradually worsened. A repeated MRI of the brain showed further aggravation of leptomeningeal enhancement in the basal cisterns. Biopsy of the brain surface and leptomeninges revealed a very rare occurrence of DLGNT. His delayed diagnosis of DLGNT might be due to prevalence of tuberculosis in our country, similarity in MRI finding of prominent leptomeningeal enhancement in the basal cisterns, and extreme rarity of DLGNT in the elderly. DLGLT should be considered in differential diagnosis of medical conditions presenting as communicating hydrocephalus with prominent leptomeningeal enhancement. A timely histologic diagnosis through a leptomeningeal biopsy of the brain and spinal cord in case of unusual leptomeningeal enhancement with uncertain laboratory findings is essential because cytologic examination of the cerebrospinal fluid in DLGNT is known to be negative.