NMC case report journal最新文献

Dysphagia involving the occipital bone is a critical complication after posterior fusion surgery. However, to our knowledge, dysphagia after posterior fixation of the cervical spine C1-2 has not been reported. Herein, we report a patient with dysphagia after posterior fusion of the cervical spine C1-2. The patient was a man in his 80s. He was referred to our department with a chief complaint of dexterity difficulty. After a thorough examination, we diagnosed subluxation of the atlantoaxial vertebrae and performed C1-2 posterior fusion surgery. Dysphagia appeared the day after surgery, which was thought to be caused by the change in cervical spine alignment after fixation surgery. The patient's dysphagia improved with continued rehabilitation without surgical treatment. The narrowest oropharyngeal airway space, occipital and external acoustic meatus to axis angle, pharyngeal inlet angle, and S-line were examined. We found that our patient had a low range of motion of the O-C1 joint and that compensation via mobility of the O-C1 joint was insufficient to compensate for the decrease in the O-C2 angle after C1-2 fixation. Preoperative evaluation of the O-C1 joint range of motion and increasing O-C2a from preoperative levels may be important for preventing dysphagia onset after posterior fixation of the cervical spine C1-2.

One of the most serious complications of cranial radiotherapy is the development of radiation-induced glioma, which is estimated to occur in 1%-4% of patients who have received cranial irradiation and has a worse prognosis than sporadic glioblastoma. Although comprehensive genetic analysis has recently uncovered the molecular characteristics of radiation-induced glioma, the full picture remains unclear due to its rarity. A 45-year-old man presented with generalized seizures caused by multiple brain tumors involving the right frontal lobe, thalamus, and brainstem. The patient had a history of whole-brain radiotherapy for recurrent Burkitt's lymphoma at the age of 12. He underwent craniotomy, and the histological diagnosis revealed a high-grade glioma with isocitrate dehydrogenase-wildtype, which was presumed to be a radiation-induced glioma that developed 33 years after whole-brain irradiation. Next-generation sequencing identified a CDKN2A/B deletion, as well as coamplification of several receptor tyrosine kinases-encoding genes, including PDGFRA, KIT, and KDR, all of which are located at 4q12. Amplification of this region is broadly observed across cancers and is associated with poor prognosis in sporadic glioblastoma. Nevertheless, the patient received chemoradiotherapy with temozolomide, followed by temozolomide maintenance therapy, resulting in a complete response of all lesions. Although radiation-induced gliomas are generally difficult to treat, our patient unexpectedly responded well to conventional chemoradiotherapy despite the coamplification of multiple receptor tyrosine kinases-encoding genes, which is typically suggestive of an aggressive phenotype. Our case indicates that some radiation-induced gliomas may have distinct molecular characteristics influencing the therapeutic response, which differ from those of sporadic glioblastomas.

We report a case of adult-onset gangliocytoma in the parietal lobe. A 54-year-old woman presented with sensory disturbance in her right upper limb. A computed tomography scan revealed a cystic and calcified lesion in the left parietal lobe. She underwent a left parietal craniotomy with gross total resection, and the pathological diagnosis was confirmed as gangliocytoma. Gangliocytomas are very rare tumors of the central nervous system, predominantly affecting children and young adults, and are often located in the temporal lobe. Reports of gangliocytomas developing after middle age are uncommon. To assess the epidemiology of gangliocytoma, we utilized data from the Surveillance, Epidemiology, and End Results database. From January 1, 2000, to December 31, 2021, a total of 74 cases were identified, 18 of which were in patients over 50 years of age. While 27 patients had tumors in the temporal lobe, the most frequent site, others had tumors in different locations. Notably, there were no patients over 50 with gangliocytoma in the parietal lobe in the Surveillance, Epidemiology, and End Results registry. These findings suggest that in older patients, although gangliocytomas located outside the temporal lobe are rare, they are kept in mind as one of the differential diagnoses.

Surgical treatment of thoracic disc herniation is challenging for spinal surgeons because of the kyphotic structure of the thoracic spine and the obstruction caused by the ribs and lungs during the lateral approach. In particular, highly migrating thoracic disc herniation requires the removal of surrounding structures, including the ribs, pedicles, and vertebral body. We present a case in which an upward-migrating T11/12 thoracic disc herniation was safely removed using full-endoscopic spine surgery. The patient was a 63-year-old man with sudden-onset leg pain and muscle weakness. A physical examination revealed thoracic myelopathy. Magnetic resonance imaging and computed tomography showed an upward-migrating T11/12 thoracic disc herniation without ossification or calcification. Given the severe compression of the spinal cord, a full endoscopic discectomy was performed via the posterolateral approach to relieve his myelopathy. In this study, we demonstrate surgical techniques for removing upward-migrating thoracic disc herniation using full-endoscopic spine surgery. Two important surgical techniques are emphasized: 1) Removal of the inferior and superior articular processes using a high-speed drill along the articular surface at an early stage of surgery. 2) Removal of a small caudal part of the upper vertebral body to insert forceps between the vertebral body and the posterior longitudinal ligament at a later stage of surgery. Our technique is a rapid and minimally invasive method for managing upward-migrating thoracic disc herniation without ossification.

A 24-year-old woman, who was diagnosed with cardiac sarcoidosis as an adolescent, was brought to the emergency room with right hemiparesis and impaired consciousness 21 days after giving birth to her second child by cesarean section. Brain magnetic resonance imaging revealed high diffusion-weighted signal changes in the left insular cortex and temporal lobe. Magnetic resonance angiography revealed occlusion of the left internal carotid artery. She was treated with alteplase administration and mechanical thrombectomy, resulting in the improvement of neurological symptoms. Subsequent examination revealed a ventricular aneurysm caused by cardiac sarcoidosis, leading to the diagnosis of cardioembolic stroke. It was also assumed that the patient's postpartum period caused increased coagulability, which contributed to the ischemic stroke. It is important to recognize that abnormal cardiac function and morphology due to cardiac sarcoidosis and increased coagulability during the postpartum period may contribute to ischemic stroke.

The aim of this single-center, single-arm study was to evaluate the safety of adenosine-assisted clipping surgery for unruptured cerebral aneurysms. Five patients underwent aneurysmal clipping during adenosine-induced hypotension at ≤60 mmHg. The mean age of patients was 63.4±8.5 years, and the mean aneurysm size was 5.3±1.1 mm. The prevalence of patients with modified Rankin Scale scores of zero 30 days after surgery was 100%. The degree of aneurysm obliteration was complete in 4 patients and residual dome in 1 patient. The mean total dosage of adenosine was 37.4±18.8 mg. The mean duration of systolic blood pressure at ≤60 mmHg was 64.2±28.3 secs. No patients exhibited paroxysmal atrial fibrillation within 24 hours after adenosine administration or elevation of high-sensitivity cardiac troponin T on postoperative day 1. There was no reduction in either motor-evoked or somatosensory-evoked potential amplitude during surgery. Adenosine-induced hypotension is a safe procedure in clipping surgery for unruptured cerebral aneurysms.

Wilson's disease is an autosomal recessive disorder of copper metabolism. A current unresolved issue is the worsening of neurological symptoms during the initial treatment phase, particularly with chelation therapy. This phenomenon, termed "early neurological worsening," is attributed to the rapid mobilization and redistribution of copper during treatment initiation. We report the case of a 10-year-old boy, with neuro-hepatic Wilson's disease who developed treatment-refractory generalized dystonia, which improved with intrathecal baclofen therapy. The patient experienced walking discomfort 5 months before referral to our hospital, with rapid progression to dysphagia and a 3 kg weight loss. Initially, he presented with dystonia, including foot inversion. Wilson's disease was diagnosed based on physiological, clinical, and imaging findings, with confirmation of a homozygous mutation in the ATP7B gene. The patient was treated with trientine hydrochloride, followed by zinc monotherapy. Despite appropriate chelation therapy, dystonia progressed to severe axial torsion involving the trunk. His condition deteriorated to status dystonicus, with high-grade fever, elevated creatine phosphokinase levels, and dehydration, requiring midazolam sedation. These symptoms were attributed to "early neurological worsening." A trial of intrathecal baclofen injection provided symptom relief, leading to the implantation of a baclofen pump, which significantly reduced the status dystonicus. At discharge, the patient had a modified Rankin Scale score of 5. Three years later, although wheelchair-dependent, his oral intake and speech are progressively improving with training. This is the first reported case of status dystonicus in Wilson's disease successfully treated with intrathecal baclofen, highlighting its potential as a viable treatment option for Wilson's disease-associated debilitating dystonia.

Sacroiliac joint dysfunction is one of the causes of lower back pain, and although it has characteristic pain locations and aggravating factors, it is difficult to diagnose and is often overlooked. A case of relief of typical pain symptoms due to sacroiliac joint dysfunction by spinal cord stimulation is presented. A 60-year-old woman presented with severe chronic pain in the left lumbar, lower buttock, iliac, and groin areas that worsened even when sitting for short periods, as well as numbness in the right lower extremity. The patient had chronic lower back pain since experiencing acute lumbosacral sprains in her 20s and 40s, and her symptoms worsened without any trigger in her 60s. Standard imaging examinations showed no lesions that could be causing the pain, and blood tests showed no inflammation or other abnormalities. Although pharmacological treatment did not provide sufficient analgesia, sacroiliac joint block provided a significant analgesic effect, leading to a definitive diagnosis of sacroiliac joint dysfunction. A spinal cord stimulation trial was performed using percutaneous 8-contact leads placed at the thoracic vertebra 8-11 level, and pain relief was confirmed. One month later, 2 new percutaneous 16-contact leads and an implantable pulse generator were implanted simultaneously. One month after implantation, the visual analog scale and the quick inventory of depression symptomatology scores decreased dramatically from 83 to 8 and from 16 to 4, respectively. In addition, the numbness of the right lower extremity disappeared. These analgesic effects were sustained for 12 months.

A male patient in his 50s had a head-on collision while driving. Prehospital emergency services recorded pulseless electrical activity on an electrocardiogram, and chest compressions were initiated. Before hospital arrival, return of spontaneous circulation was achieved after 17-min resuscitation during transport. His Glasgow Coma Scale score was 6, with unequal-size pupils unresponsive to light stimuli. A head computed tomography scan revealed a left acute subdural hematoma with a marked midline shift, and computed tomography of the cervical spine showed that the atlanto-occipital and atlanto-axial joint spaces were significantly widened. Initially, an emergency decompressive craniectomy for hematoma evacuation was performed, followed by posterior cervical fixation surgery in the subacute phase. After brain surgery, neurocritical care management was implemented for brain protection. Cervical spine magnetic resonance imaging revealed multiple ligament injuries at the craniovertebral junction, which confirmed the diagnosis of atlanto-occipital and atlanto-axial dislocation. On day 9, posterior fixation from the occiput to the fourth cervical vertebrae was performed. Subsequently, he was transferred to a rehabilitation hospital on day 45. No neurological sequelae were noted except for the neck rotation limitations due to the fixation surgery, and he could return to his previous job. Although craniovertebral junction ligamentous injuries are rare, they may coexist with severe traumatic brain injury. A careful reading of preoperative images focusing on the inter-joint space is important to detect craniovertebral junction ligamentous injuries in patients with traumatic brain injury inflicted with high-energy trauma.

Cavernous malformation, also known as cavernoma or cavernous hemangioma, is a benign vascular malformation characterized by abnormal proliferation of capillaries that lack intervening neural tissue. Spinal intradural extramedullary cavernous malformations are exceedingly rare and, therefore, are often misdiagnosed. Here, we report a rare case of thoracic intradural extramedullary cavernous malformation that mimicked meningioma on preoperative imaging. A 77-year-old male patient presented with a two-month history of myelopathy, progressive paresthesia in the lower extremities, and difficulty walking, noted during an outpatient clinic visit. Spinal magnetic resonance imaging detected an intradural extramedullary mass lesion on the dorsal side at the Thoracic (Th) 10 vertebral level, compressing the thoracic cord. Preoperative imaging revealed a uniform T1- and T2-weighted intensity signal, suggesting meningioma. Intraoperatively, the mass appeared reddish with multiple abnormal vessels and adhered firmly to the thoracic cord. The lesion was completely resected, and postoperative pathological examination confirmed the diagnosis of cavernous malformation. The patient's preoperative symptoms improved postoperatively. Thoracic intradural extramedullary cavernous malformations are extremely rare and typically present with heterogeneous intensity signals on magnetic resonance imaging. Additionally, they can cause subarachnoid hemorrhage, emphasizing the importance of considering them in the preoperative differential diagnosis, even though imaging characteristics may be atypical. Surgical gross total resection should be considered to prevent future hemorrhage and neurological deterioration.