We performed a revisionary open reduction and internal fixation for treating nonunion of the mid-shaft of the left clavicle with an autogenous cancellous bone graft. On postoperative day 4, the patient presented with neurologic deficits in the left upper extremity. We removed the implant and made a superior angulation to decompress the brachial plexus. At 6 months postoperatively, callus bridging and consolidation were visible and all hand and elbow functions were fully recovered. Our case suggests that brachial plexus neuropathy may be caused by stretching and compression after reduction and straightening of the nonunion site around adhesions or scar tissue. Therefore, care should be taken whether there are the risk factors that can cause brachial plexus neuropathy when revision surgery is performed for treating nonunion of a clavicle shaft fracture.
Bony Callus ; Brachial Plexus Neuropathies ; Brachial Plexus ; Cicatrix ; Clavicle ; Elbow ; Hand ; Humans ; Neurologic Manifestations ; Risk Factors ; Transplants ; Upper Extremity

Lying on the side while falling asleep deeply after drinking or taking a sleeping pill can cause compressive neuropathy. We report a 70-year-old male patient of medial cord of left brachial plexus injury (BPI) after deep sleep. The mechanism of the injury might be compression and stretching of brachial plexus. The electrodiagnostic study was performed and the medial cord lesion of BPI was suggested. The ultrasonography image of compression site revealed the nerve swelling of medial cord of brachial plexus and median nerve at the mid-arm level. Pharmacologic treatment including oral prednisolone and exercise training were prescribed. On 6 months after initial visit, neurologic symptom and pain were improved but mild sequelae was remained.
Accidental Falls ; Aged ; Brachial Plexus ; Deception ; Drinking ; Electrodiagnosis ; Humans ; Male ; Median Nerve ; Neurologic Manifestations ; Prednisolone ; Ultrasonography

OBJECTIVE: There is a lack of knowledge regarding whether decompression is necessary in treating patients with epidural spinal cord compression (ESCC) grade 2. The purpose of this study was to compare the outcomes of minimally invasive surgery (MIS) without decompression and conventional open surgery (palliative laminectomy) for patients with hepatocellular carcinoma (HCC) spinal metastasis of ESCC grade 2.METHODS: Patients with HCC spinal metastasis requiring surgery were retrospectively reviewed. Patients with ESCC grade 2, medically intractable mechanical back pain, a Nurick grade better than 3, 3–6 months of life expectancy, Tomita score ≥5, and Spinal Instability Neoplastic Score ≥7 were included. Patients with neurological deficits, other systemic illnesses and less than 1 month of life expectancy were excluded. Thirty patients were included in the study, including 17 in the open surgery group (until 2008) and 13 in the MIS group (since 2009).RESULTS: The MIS group had a significantly shorter operative time (94.2±48.2 minutes vs. 162.9±52.3 minutes, p=0.001), less blood loss (140.0±182.9 mL vs. 1534.4±1484.2 mL, p=0.002), and less post-operative intensive care unit transfer (one patient vs. eight patients, p=0.042) than the open surgery group. The visual analogue scale for back pain at 3 months post-operation was significantly improved in the MIS group than in the open surgery group (3.0±1.2 vs. 4.3±1.2, p=0.042). The MIS group had longer ambulation time (183±33 days vs. 166±36 days) and survival time (216±38 days vs. 204±43 days) than the open surgery group without significant difference (p=0.814 and 0.959, respectively).CONCLUSION: MIS without decompression would be a good choice for patients with HCC spinal metastasis of ESCC grade 2, especially those with limited prognosis, mechanical instability and no neurologic deficit.
Back Pain ; Carcinoma, Hepatocellular ; Decompression ; Decompression, Surgical ; Humans ; Intensive Care Units ; Life Expectancy ; Minimally Invasive Surgical Procedures ; Neoplasm Metastasis ; Neurologic Manifestations ; Operative Time ; Prognosis ; Retrospective Studies ; Spinal Cord Compression ; Spinal Cord ; Spine ; Walking

Torticollis is an abnormal, asymmetric head or neck position which usually caused by imbalance of paracervical muscles. The traumatic torticollis can be caused by following events; atlantoaxial rotatory subluxation, atlantoaxial dislocation, cervical vertebral fractures, and injury to the cervical musculature. Especially, acute traumatic atlantoaxial rotatory subluxation usually presents limitation of cervical range of motion without pain or neurologic deficit. We report a case of a 58 year-old man who developed the acute atlantoaxial rotatory subluxation right after the chiropractic therapy, which induced the limitation of cervical range of motion to 52.5% of normal range. The magnetic resonance image revealed the facture of the odontoid process and the partial injury in transverse ligaments of the atlas. He underwent intramuscular botulinum toxin injection and 10 days of continuous cervical traction 15 hours a day using a 5 kg weight. The range of the cervical motion restored up to 90.2% of normal range.
Atlanto-Axial Joint ; Botulinum Toxins ; Chiropractic ; Dislocations ; Head ; Ligaments ; Muscles ; Neck ; Neurologic Manifestations ; Odontoid Process ; Range of Motion, Articular ; Reference Values ; Torticollis ; Traction

BACKGROUND: Although kidney transplantation outcomes have improved dramatically after using calcineurin inhibitors (CNIs), CNI toxicity continues to be reported and the mechanism remains uncertain. Here, we investigated the neurotoxicity of CNIs by focusing on the viability of glioma cells.METHODS: Glioma cells were treated with several concentrations of CNIs for 24 hours at 37℃ and their cell viability was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.RESULTS: Exposure to 0, 0.25, 0.5, 2.5, 5.0, and 10.0 mM concentrations respectively showed 100%, 64.3%, 61.3%, 68.1%, 62.4%, and 68.6% cell viability for cyclosporine and 100%, 38.6%, 40.8%, 43.7%, 37.8%, and 43.0% for tacrolimus. The direct toxic effect of tacrolimus on glioma cell viability was stronger than that of cyclosporine at the same concentration.CONCLUSION: CNIs can cause neurological side effects by directly exerting cytotoxic effects on brain cells. Therefore, we should carefully monitor the neurologic symptoms and level of CNIs in kidney transplant patients.
Animals ; Brain ; Calcineurin Inhibitors ; Calcineurin ; Cell Survival ; Cyclosporine ; Glioma ; Humans ; Kidney ; Kidney Transplantation ; Neurologic Manifestations ; Rats ; Tacrolimus

STUDY DESIGN: Prospective cohort study. PURPOSE: The study was aimed at evaluating clinicoradiological factors affecting recovery of neurological deficits in cases of lumbar disc herniation (LDH) treated by lumbar microdiscectomy. OVERVIEW OF LITERATURE: The majority of the available literature on neurological recovery following neurodeficit is limited to retrospective series. The literature is currently limited regarding variables that can help predict the recovery of neurodeficits following LDH. METHODS: A prospective analysis was performed on 70 consecutive patients who underwent lumbar microdiscectomy (L1–2 to L5–S1) owing to neurological deficits due to LDH. Patients with motor power ≤3/5 in L2–S1 myotomes were considered for analysis. Follow-up was performed at 2, 6, and 12 months to note recovery of motor deficits. Clinicoradiological parameters were compared between the recovered and nonrecovered groups. RESULTS: A total of 65 patients were available at the final follow-up: 41 (63%) had completely recovered by 2 months; four showed delayed recovery at the 6-month follow-up; and 20 (30.7%) showed no recovery at 1 year. Clinicoradiological factors, including diabetes, complete initial deficit, areflexia, multilevel disc prolapse, longer duration since initial symptoms, and ≥2 previous symptomatic episodes were associated with a significant risk of poorer recovery (p < 0.05 for all). Age, sex, occupation, smoking, level/type or location of disc herniation, primary canal stenosis, disc fragment dimensions, precipitating factors, bladder involvement, bilaterality of symptoms, and the presence or absence of anal reflex did not affect neurological recovery (p>0.05 for all). Diabetes mellitus (p=0.033) and complete initial motor deficit (p=0.028) were significantly associated with delayed recovery in the multivariate analysis. CONCLUSIONS: The overall neurological recovery rate in our study was 69%. Diabetes mellitus (p=0.033) and complete initial motor deficit were associated with delayed motor recovery.
Cohort Studies ; Constriction, Pathologic ; Diabetes Mellitus ; Follow-Up Studies ; Humans ; Intervertebral Disc Displacement ; Multivariate Analysis ; Neurologic Manifestations ; Occupations ; Precipitating Factors ; Prognosis ; Prolapse ; Prospective Studies ; Reflex ; Retrospective Studies ; Smoke ; Smoking ; Urinary Bladder

Decompressive craniectomy (DC) is commonly performed in patients with intracranial hypertension or brain edema due to traumatic brain injury. Infrequently, neurologic deteriorations accompanied by sunken scalp may occur after DC. We report two patients with traumatic subdural hemorrhage who had neurologic deteriorations accompanied by sunken scalp after DC. Neurologic function improved dramatically in both patients after cranioplasty. Monitoring for neurologic deterioration after craniectomy is advised. For patients showing neurologic deficit with a sunken scalp, early cranioplasty should be considered.
Brain Edema ; Brain Injuries ; Decompressive Craniectomy ; Hematoma, Subdural ; Humans ; Intracranial Hypertension ; Neurologic Manifestations ; Scalp ; Skin

Herein, we report a case of lung transplantation in a patient with profound preoperative hypercapnia, focusing on the cardiopulmonary bypass strategy used for brain perfusion during the operation. We applied the pH-stat method for acid-base regulation, and thereby achieved the desired outcome without any neurologic deficit.
Brain ; Cardiopulmonary Bypass ; Cerebrovascular Circulation ; Humans ; Hypercapnia ; Lung Transplantation ; Lung ; Methods ; Neurologic Manifestations ; Perfusion

The syndrome of the trephined is a neurologic phenomenon that manifests as sudden decline in cognition, behavior, and sensorimotor function due to loss of intracranial domain. This scenario typically occurs in the setting of large craniectomy defects, resulting from trauma, infection, and/or oncologic extirpation. Cranioplasty has been shown to reverse these symptoms by normalizing cerebral hemodynamics and metabolism. However, successful reconstruction may be difficult in patients with complex and/or hostile calvarial defects. We present the case of a 48-year-old male with a large cranial bone defect, who failed autologous cranioplasty secondary to infection, and developed rapid neurologic deterioration leading to a near-vegetative state. Following debridement and antibiotic therapy, delayed cranioplasty was accomplished using a polyetheretherketone (PEEK) implant with free chimeric latissimus dorsi/serratus anterior myocutaneous flap transfer for vascularized resurfacing. Significant improvements in cognition and motor skill were noted in the early postoperative period. At 6-month follow-up, the patient had regained the ability to speak, ambulate and self-feed—correlating with evidence of cerebral/ventricular re-expansion on computed tomography. Based on our findings, we advocate delayed alloplastic implantation with total vascularized soft tissue coverage as a viable alternative for reconstructing extensive, hostile calvarial defects in patients with the syndrome of the trephined.
Cognition ; Craniocerebral Trauma ; Debridement ; Follow-Up Studies ; Free Tissue Flaps ; Hemodynamics ; Humans ; Male ; Metabolism ; Middle Aged ; Motor Skills ; Myocutaneous Flap ; Neurologic Manifestations ; Postoperative Period ; Reconstructive Surgical Procedures

Type 2 diabetes (T2D) increases the risk for cerebrovascular disease (CVD) and dementia. The underlying molecular mechanisms remain elusive, which hampers the development of treatment or/and effective prevention strategies. Recent studies suggest that dyshomeostasis of amylin, a satiety hormone that forms pancreatic amyloid in patients with T2D, promotes accumulation of amylin in cerebral small blood vessels and interaction with Alzheimer's disease (AD) pathology. Overexpression of human amylin in rodents (rodent amylin does not form amyloid) leads to late-life onset T2D and neurologic deficits. In this Review, we discuss clinical evidence of amylin pathology in CVD and AD and identify critical characteristics of animal models that could help to better understand molecular mechanisms underlying the increased risk of CVD and AD in patients with prediabetes or T2D.
Alzheimer Disease ; Amyloid ; Blood Vessels ; Cerebrovascular Disorders ; Dementia ; Diabetes Complications ; Diabetes Mellitus, Type 2 ; Humans ; Islet Amyloid Polypeptide ; Models, Animal ; Neurologic Manifestations ; Pathology ; Prediabetic State ; Rodentia