Hak-cheol Ko

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

OBJECTIVESnTo 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.nnnMETHODSnPreoperative 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.nnnRESULTSnThe 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.nnnCONCLUSIONSnSignificant 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.

Intraoperative monitoring of Z-L response (ZLR) and abnormal muscle response (AMR) during microvascular decompression for hemifacial spasm. Interpreting the role of ZLR

BackgroundZ-L response (ZLR) has been suggested to a new electromyographic (EMG) potential recorded from the facial muscle of patient with hemifacial spasm (HFS) during microvascular decompression (MVD). Although ZLR has been suggested to be useful, experience of ZLR monitoring is limited and its significance during MVD is still unclear.MethodsTo investigate the significance of ZLR, both ZLR and abnormal muscle response (AMR) were simultaneously recorded before and after decompression of root exit zone (REZ) in 20 consecutive patients with HFS.ResultsAll 19 AMRs elicited before REZ decompression disappeared immediately after decompression of REZ. ZLRs were also observed before decompression of REZ in 19 (95%) of 20 patients. Despite negative conversion of AMR after decompression in 19 patients, ZLR disappeared in only 13 (68.4%) of 19 patients. Among six sustained ZLRs, three showed reduction in the intensity of ZLRs while the other three remained unchanged. There were nine cases featuring attachment of the distal, non-offending portion of offending vessels to the distal course of the facial nerve in addition to attachment to REZ. Negative ZLR conversion and presence of peripheral contact of offending vessels to distal facial nerves showed significant correlations (pu2009<u20090.05). ZLR could be elicited by electrical stimulation at non-REZ-offending portion of the offending arterial wall, attached to the distal course of the facial nerve. HFS disappeared immediately in all 20 patients.ConclusionsAlthough ZLR might be helpful in cases with multiple offenders, interpretation of ZLR needs caution for non-specific transmission of electric current through vessel wall to facial nerve.

Globus Pallidus Internus Deep Brain Stimulation for Disabling Diabetic Hemiballism/Hemichorea

Unilateral hemichorea/hemiballism (HH) associated with contralateral neuroimaging abnormalities of the basal ganglia, which is characterized by T1 hyperintensity on magnetic resonance imaging (MRI) and is secondary to diabetic nonketotic hyperglycemia, is a rare and unique complication of poorly controlled diabetes mellitus (DM). Although almost all prior reports have documented rapid resolution of HH within days after normalization of blood glucose levels, medically refractory persistent HH has been noted. The experience of surgical intervention for persistent HH is limited. A 46-year-old, right-handed female patient with type 2 DM presented with refractory diabetic HH on the left side of 6 months duration despite DM control and neuroleptic medication usage. Image-guided deep brain stimulation (DBS) on the right globus pallidus internus (GPi) was performed. A mechanical micropallidotomy effect was observed and chronic stimulation of GPi was quite effective in symptomatic control of diabetic HH until a 16-month follow-up visit. DBS of the GPi can be an effective treatment for medically refractory diabetic HH.