• Journal of Trauma and Injury
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• v.30 no.2
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• pp.66-69
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• 2017

We introduce a patient who was suffered from isolated traumatic bilateral oculomotor nerve palsy after head trauma. The patient presented with bilateral ptosis and abnormal pupilary responses with slightly drowsy mentality at first. Performed images demonstrated some hematomas along subarachnoid, intraventricular, subdural spaces and multiple small supratentorial contusions. There was no bony abnormality or ligament injury. We assumed that small amount of interpeduncular hematoma might be the proper lesion associated with oculomotor nerve palsies, since the clinical symptom and signs presented bilaterally and the oculomotor neural fascicles run through the interpeduncular fossa.

• Journal of Korean Neurosurgical Society
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• v.51 no.6
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• pp.367-369
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• 2012

Terson syndrome was originally used to describe a vitreous hemorrhage arising from aneurysmal subrarachnoid hemorrhage. Terson syndrome can be caused by intracranial hemorrhage, subdural or epidural hematoma and severe brain injury but is extremely rare in intraventricular hemorrhage associated with moyamoya disease. A 41-year-old man presented with left visual disturbance. He had a history of intraventicular hemorrhage associated with moyamoya disease three months prior to admission. At that time he was in comatose mentality. Ophthalmologic examination at our hospital detected a vitreous hemorrhage in his left eye, with right eye remaining normal. Vitrectomy with epiretinal membrane removal was performed. After operation his left visual acuity was recovered. Careful ophthalmologic examination is mandatory in patients with hemorrhagic moyamoya disease.

• Journal of Korean Neurosurgical Society
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• v.41 no.5
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• pp.314-317
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• 2007

Ventriculoperitoneal [VP] shunt is a common treatment for hydrocephalic patients. However, complications, such as shunt tube occlusion, infection, intracranial hemorrhage, seizure can occur. Of these, intracranial hemorrhage may occur due to intracranial vascular injury or a rapid decrease of intracranial pressure [ICP]. Most of these hemorrhages are subdural hematomas [SDH] while a few are epidural hematomas [EDH]. It is extremely rare for an intracranial hemorrhage to occur due to an extension of the bleeding from an injured extracranial vessel. We report two cases of EDH due to occipital artery injury following VP shunt and extraventricular drainage [EVD].

• The Korean Journal of Pain
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• v.12 no.1
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• pp.157-161
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• 1999

We report a patient with spontaneous intracranial hypotension. In addition to the cardinal feature of a postural headache and a low CSF pressure, the patient also had subdural hematoma demonstrated by brain MRI. Radionuclide cisternography revealed a CSF leakage in the intracranium. CSF leakage from spinal meningeal defects may be the most common cause of this syndrome. The headache is a consequence of the low CSF pressure producing displacement of pain-sensitive structures. Methods of treatment are identical to those for post-dural puncture headaches. We experienced a patient with spontaneous intracranial hypotension developed in the intracranium who was successfully managed with a cervical blood patch.

• Journal of Korean Neurosurgical Society
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• v.39 no.6
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• pp.443-446
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• 2006

Intracranial arachnoid cyst is presumed to be a developmental anomaly and its natural history is not well defined. Often it is detected incidentally in a asymptomatic patient and hemorrhagic events of arachnoid cyst following head injury are rarely reported. We report hemorrhagic complications including two intracystic hemorrhages, two subdural hematomas, and an epidural hematoma in 5 patients with intracranial arachnoid cyst after minor head injury and review pertinent literatures.

• Journal of Korean Neurosurgical Society
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• v.48 no.3
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• pp.244-250
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• 2010

Objective : Adequate management of increased intracranial pressure (ICP) is critical in patients with traumatic brain injury (TBI), and decompressive craniectomy is widely used to treat refractory increased ICP. The authors reviewed and analyzed complications following decompressive craniectomy for the management of TBI. Methods : A total of 89 consecutive patients who underwent decompressive craniectomy for TBI between February 2004 and February 2009 were reviewed retrospectively. Incidence rates of complications secondary to decompressive craniectomy were determined, and analyses were performed to identify clinical factors associated with the development of complications and the poor outcome. Results : Complications secondary to decompressive craniectomy occurred in 48 of the 89 (53.9%) patients. Furthermore, these complications occurred in a sequential fashion at specific times after surgical intervention; cerebral contusion expansion ($2.2{\pm}1.2$ days), newly appearing subdural or epidural hematoma contralateral to the craniectomy defect ($1.5{\pm}0.9$ days), epilepsy ($2.7{\pm}1.5$ days), cerebrospinal fluid leakage through the scalp incision ($7.0{\pm}4.2$ days), and external cerebral herniation ($5.5{\pm}3.3$ days). Subdural effusion ($10.8{\pm}5.2$ days) and postoperative infection ($9.8{\pm}3.1$ days) developed between one and four weeks postoperatively. Trephined and post-traumatic hydrocephalus syndromes developed after one month postoperatively (at $79.5{\pm}23.6$ and $49.2{\pm}14.1$ days, respectively). Conclusion : A poor GCS score ($\leq$ 8) and an age of $\geq$ 65 were found to be related to the occurrence of one of the above-mentioned complications. These results should help neurosurgeons anticipate these complications, to adopt management strategies that reduce the risks of complications, and to improve clinical outcomes.

• Journal of Korean Neurosurgical Society
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• v.65 no.5
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• pp.652-664
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• 2022

The Kernohan-Woltman notch phenomenon (KWNP) refers to an intracranial lesion causing massive side-to-side mass effect which leads to compression of the contralateral cerebral peduncle against the free edge of the cerebellar tentorium. Diagnosis is based on "paradoxical" motor deficit ipsilateral to the lesion associated with radiologic evidence of damage to the contralateral cerebral peduncle. To date, there is scarce evidence regarding KWNP associated neuroimaging patterns and motor function prognostic factors. A systematic review was conducted on Medline database from inception to July 2021 looking for English-language articles concerning KWNP, in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The research yielded 45 articles for a total of 51 patients. The mean age was 40.7 years-old and the male/female sex ratio was 2/1. 63% of the patients (32/51) suffered from head trauma with a majority of acute subdural hematomas (57%, 29/51). 57% (29/51) of the patients were in the coma upon admission and 47% (24/51) presented pupil anomalies. KWNP presented the neuroimaging features of compression ischemic stroke located in the contralateral cerebral peduncle, with edema in the surrounding structures and sometimes compression stroke of the cerebral arteries passing nearby. 45% of the patients (23/51) presented a good motor functional outcome; nevertheless, no predisposing factor was identified. A Glasgow coma scale (GCS) of more than 3 showed a trend (p=0.1065) toward a better motor functional outcome. The KWNP is a regional compression syndrome oftentimes caused by sudden and massive uncal herniation and leading to contralateral cerebral peduncle ischemia. Even though patients suffering from KWNP usually present a good overall recovery, patients with a GCS of 3 may present a worse motor functional outcome. In order to better understand this syndrome, future studies will have to focus on more personalized criteria such as individual variation of tentorial notch width.

• Journal of Korean Neurosurgical Society
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• v.52 no.4
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• pp.396-403
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• 2012

Objective : The predictors of cranioplasty infection after decompressive craniectomy have not yet been fully characterized. The objective of the current study was to compare the long-term incidences of surgical site infection according to the graft material and cranioplasty timing after craniectomy, and to determine the associated factors of cranioplasty infection. Methods : A retrospective cohort study was conducted to assess graft infection in patients who underwent cranioplasty after decompressive craniectomy between 2001 and 2011 at a single-center. From a total of 197 eligible patients, 131 patients undergoing 134 cranioplasties were assessed for event-free survival according to graft material and cranioplasty timing after craniectomy. Kaplan-Meier survival analysis and Cox regression methods were employed, with cranioplasty infection identified as the primary outcome. Secondary outcomes were also evaluated, including autogenous bone resorption, epidural hematoma, subdural hematoma and brain contusion. Results : The median follow-up duration was 454 days (range 10 to 3900 days), during which 14 (10.7%) patients suffered cranioplasty infection. There was no significant difference between the two groups for event-free survival rate for cranioplasty infection with either a cryopreserved or artificial bone graft (p=0.074). Intergroup differences according to cranioplasty time after craniectomy were also not observed (p=0.083). Poor neurologic outcome at cranioplasty significantly affected the development of cranioplasty infection (hazard ratio 5.203, 95% CI 1.075 to 25.193, p=0.04). Conclusion : Neurologic status may influence cranioplasty infection after decompressive craniectomy. A further prospective study about predictors of cranioplasty infection including graft material and cranioplasty timing is necessary.

• Journal of Korean Neurosurgical Society
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• v.29 no.3
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• pp.353-359
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• 2000

Objective : The fracture on the frontal bone in head-injured patients may be commonly encountered in the clinical situations. Biomechanical studies demonstrate that the anterior wall of the frontal sinus is intermediate in its ability to resist fracture on direct impact. If the frontal sinus is large and the anterior table is able to disperse the force of the impact over a greater area, the posterior table and intracranial contents usually can be spared. We analyzed the clinical features of the patients who presented with frontal skull fracture due to frontal blows. Patients and Methods : From January, 1992 to December, 1997, 172 patients with frontal skull fracture were selected among 1911 patients with head injury who were admitted to department of neurosurgery. Clinical records and radiological studies of all patients were reviewed and evaluated retrospectively. Results : The neurobehavioral changes was seen in 34 cases(19.8%) and showed statistical significances in case of facial bone fractures, acute subdural hematoma(SDH), and positive frontal lobe releasing sign(p<0.05). The good glasgow outcome score group(GOS, good recovery & moderate disability) at discharge was revealed in 77.3% of total patient population. The poor GOS group(severe disability & vegetative state & death) at discharge was revealed in 22.7%. The poor GOS group at discharge have statistical significances with acute epidural hematoma(EDH), traumatic intraventricular hemorrhage(t-IVH), traumatic intracranial lesion, poor initial glasgow coma scale(GCS) scores & Revised Trauma Score(RTS)(p<0.05). Conclusion : Because of their anatomical relationships and neurobehavioral patterns due to vulnerability of the frontal lobe, the frontal injury should be considered as complicated facial injuries. Therefore, these patients are more likely to have a cosmetic or neuropsychiatric problems.

• Journal of Korean Neurosurgical Society
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• v.58 no.1
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• pp.76-78
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• 2015

This report details a case of unexpected, severe post-operative cerebral edema following cranioplasty. We discuss the possible pathological mechanisms of this complication. A 50-year-old female was admitted to our department with sudden onset of stuporous consciousness. A brain computed tomography (CT) revealed a subarachnoid hemorrhage with intracranial hemorrhage and subdural hematoma. Emergency decompressive craniectomy and aneurysmal neck clipping were performed. Following recovery, the decision was made to proceed with an autologous cranioplasty. The cranioplasty procedure was free of complications. An epidural drain was placed and connected to a suction system during skin closure to avoid epidural blood accumulation. However, following the procedure, the patient had a seizure in the recovery room. An emergency brain CT scan revealed widespread cerebral edema, and the catheter drain was clamped. The increased intracranial pressure and cerebral edema were controlled with osmotic diuretics, corticosteroids, and antiepileptic drugs. The edema slowly subsided, but new low-density areas were noted in the brain on follow-up CT 1 week later. We speculated that placing the epidural drain on active suction may have caused an acute decrease in intracranial pressure and subsequent rapid expansion of the brain, which impaired autoregulation and led to reperfusion injury.