• Journal of Korean Neurosurgical Society
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• v.52 no.4
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• pp.312-319
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• 2012

Objective : In patients with spontaneous intracerebral hemorrhage (ICH), the risk factors for seizure and the effect of prophylactic anticonvulsants are not well known. This study aimed to determine the risk factor for seizures and the role for prophylactic anticonvulsants after spontaneous ICH. Methods : Between 2005 and 2010, 263 consecutive patients with spontaneous ICH were retrospectively assessed with a mean follow-up of 19.5 months using medical records, updated clinical information and, when necessary, direct patient contact. The seizures were classified as early (within 1 week of ICH) or late (more than 1 week after ICH). The outcomes were measured with the Glasgow Outcome Scale at discharge and the modified Rankin Scale (mRS) at both 2 weeks and discharge. Results : Twenty-two patients (8.4%; 9 patients with early seizures and 13 patients with late seizures) developed seizures after spontaneous ICH. Out of 263 patients, prophylactic anticonvulsants were administered in 216 patients. The prophylactic anticonvulsants were not associated with a reduced risk of early (p=0.094) or late seizures (p=0.326). Instead, the factors associated with early seizure were cortical involvement (p<0.001) and younger age (60 years or less) (p=0.046). The risk of late seizure was increased by cortical involvement (p<0.001) and communicating hydrocephalus (p=0.004). The prophylactic anticonvulsants were associated with a worse mRS at 2 weeks (p=0.024) and at last follow-up (p=0.034). Conclusion : Cortical involvement may be a factor for provoked seizures. Although the incidence of early seizures tended to decrease in patients prescribed prophylactic anticonvulsants, no statistical difference was found.

• Korean Journal of Biological Psychiatry
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• v.7 no.1
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• pp.34-45
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• 2000

Pharmacotherapy of bipolar disorder is a rapidly evolving field. Mood stabilizers and anticonvulsants have varying biochemical profiles which may predispose them to different adverse effects and drug-drug interactions. Several of the new anticonvulsants appear less likely to have the problems with drug-drug interaction. To provide more effective combination pharmacotherapies, clinicians should be allowed to anticipate and avoid pharmacokinetic and pharmacodynamic drug-drug interactions. We reviewed the role of cytochrome P450 isozymes in the metabolism of the drugs and their interactions. The drug-drug interactions of several classes of drugs which used as mood stabilizers and new anticonvulsants, some of which may have psychotropic profiles, are discussed mainly in this article. Finally, potential pharmacokinetic interactions between the benzodiazepines and other coadministered drugs are discussed briefly.

• Clinical and Experimental Pediatrics
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• v.48 no.4
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• pp.406-410
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• 2005

Purpose : Anticonvulsants have a number of side effects and some of them may be attributed to a disturbance of serum trace metal homeostasis. Although they are minor building components in tissues, they play important functional roles in the peripheral and central nervous system. We measured serum copper and zinc levels in epileptic children who were treated with anticonvulsants to know the effects of anticonvulsants on serum copper and zinc levels. Methods : Serum copper and zinc levels were determined in 64 epileptic patients receiving anticonvulsant therapy in Chungnam National University Hospital, and in 20 normal controls. Sixty-four epileptic patients were divided into three groups : 16 patients who were treated with valproic acid monotherapy; 26 patients who were treated with valproic acid in addition to other anticonvulsants; and 22 patients who were treated with anticonvulsants except for valporic acid. Results : All patients receiving anticonvulsants had significantly lower serum copper levels($80.21{\pm}19.42{\mu}g/dL$) in comparison to the normal controls($102.12{\pm}32.8{\mu}g/dL$). Serum zinc levels in patients receiving anticonvulsants($79.78{\pm}21.88{\mu}g/dL$) were not statistically different from those of controls ($85.26{\pm}29.81{\mu}g/dL$). There were no significant difference of serum copper and zinc levels among the three groups. Conclusion : In this study, we clearly showed that anticonvulsants decreased serum copper levels. Although we did not observe any clinical findings related to copper deficiency, we should pay attention to potent copper deficiency in patients with anticonvulsant treatment.

• Proceedings of the Korea Contents Association Conference
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• 2016.05a
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• pp.433-434
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• 2016

Cerebellar atrophy was found that a patient was taking oral phenytoin for 3 years. 53 years old female patient with General tonic clonic(GTC) type seizure was prescribed phenytoin. In the process, she developed ataxic gate, dysarthria. Brain magnetic resonance imaging(MRI) finding was revealed differential diagnosis cerebellar atrophy. She was prescribed epileptol instead of phenytoin. But leukopenia, thrombocytopenia occurred. As a result, phenytoin restarted. Development of medical state decreased abuse of anticonvulsants. Considering various convulsive disorders, we must give attention to using anticonvulsants.

• Neonatal Medicine
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• v.16 no.1
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• pp.10-17
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• 2009

The immature neonatal brain is susceptible to the development of seizures. Seizures occur in 1% to 5% of infants during the neonatal period. Neonatal seizures are most commonly associated with serious acute illnesses, such as hypoxic-ischemic encephalopathy, birth trauma, metabolic disturbances, or infections. Thus, newborn infants with seizures are at risk for neonatal death and survivors are at risk for neurologic impairment, developmental delay, and subsequent epilepsy. Experimental data have also raised concerns about the potential adverse effects of the currently used anticonvulsants in neonates on brain development. Therefore, in the management of neonatal seizures, confirmatory diagnosis and optimal, but shorter, duration of anticonvulsant therapy is essential. Nevertheless, there has been substantial progress in understanding the developmental mechanisms that influence seizure generation and responsiveness to anticonvulsants. The currently used therapies have limited efficacy and the treatment of neonatal seizures has not significantly changed in the past several decades, This review includes an overview of current approaches to the treatment of neonatal seizures.

• Sleep Medicine and Psychophysiology
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• v.25 no.1
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• pp.5-8
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• 2018

Restless legs syndrome (RLS) is a sleep disorder characterized by an urge to move the legs or arms and uncomfortable paresthesia in the legs. Treatment of RLS can be various depending on the causes, severity, and frequency of the symptoms. In the case of secondary RLS, it is important to identify and manage the cause of RLS. Dopamine agonists have been used as firstline treatments for primary RLS treatment. However, due to augmentation, which is a common side effect of dopamine agonists, recent treatment guidelines are changing to prefer to anticonvulsants such as pregabalin and gabapentin. Iron, opioid, or benzodiazepine may be used when anticonvulsants or dopamine agonists are not adequately treated. Because RLS is a chronic disease, it is essential to establish a long-term treatment plan considering both efficacy and side effects.

• Journal of Dental Rehabilitation and Applied Science
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• v.19 no.2
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• pp.109-113
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• 2003

The inferior alveolar nerve provides unilateral innervation to the dentition, labial mucosa and skin from about commissure to the mental protuberance. Injury to this nerve resulting in sensory impairment can be a distressing problem to some patients. The causes of this problem include trauma, extraction, implant surgery and any maxillofacial surgery and generally the altered sensation is temporary. The surgical procedure has been the most common treatment for this condition but it has some complications. The antidepressants and anticonvulsants have been effective to the treatment of trigeminal dysesthesia. This case report suggests that the use of antidepressants and anticonvulsants is an alternative method to treat the paresthesia after implant surgery or extraction.

• The Journal of the Korean dental association
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• v.49 no.6
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• pp.327-333
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• 2011

Clinically, treatment goal of neuropathic pain focused on not elimination of etiology but management and control of symptoms because we don't know certain about clear etiology of neuropathic pain yet. The drugs used for the management of neuropathic pain were classified as drugs with strong evidence for benefit(antidepressants, anticonvulsants, opioid analgesics etc.), modest evidence for benefit(mexiletine, carbamazepine, clonidine etc.), preliminary evidence for benefit(NSAIDs, dextromethorphan, topiramate etc.). Finally, the treatment for trigeminal neuralgia was outlined separately since this disorder responds to a different group of drugs than other neuropathic pain conditions.

• The Korean Journal of Pain
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• v.33 no.2
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• pp.108-120
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• 2020

From the perspective of the definition of pain, pain can be divided into emotional and sensory components, which originate from potential and actual tissue damage, respectively. The pharmacologic treatment of the emotional pain component includes antianxiety drugs, antidepressants, and antipsychotics. The anti-anxiety drugs have anti-anxious, sedative, and somnolent effects. The antipsychotics are effective in patients with positive symptoms of psychosis. On the other hand, the sensory pain component can be divided into nociceptive and neuropathic pain. Non-steroidal anti-inflammatory drugs (NSAIDs) and opioids are usually applied for somatic and visceral nociceptive pain, respectively; anticonvulsants and antidepressants are administered for the treatment of neuropathic pain with positive and negative symptoms, respectively. The NSAIDs, which inhibit the cyclo-oxygenase pathway, exhibit anti-inflammatory, antipyretic, and analgesic effects; however, they have a therapeutic ceiling. The adverse reactions (ADRs) of the NSAIDs include gastrointestinal problems, generalized edema, and increased bleeding tendency. The opioids, which bind to the opioid receptors, present an analgesic effect only, without anti-inflammatory, antipyretic, or ceiling effects. The ADRs of the opioids start from itching and nausea/vomiting to cardiovascular and respiratory depression, as well as constipation. The anticonvulsants include carbamazepine, related to sodium channel blockade, and gabapentin and pregabalin, related to calcium blockade. The antidepressants show their analgesic actions mainly through inhibiting the reuptake of serotonin or norepinephrine. Most drugs, except NSAIDs, need an updose titration period. The principle of polypharmacy for analgesia in case of mixed components of pain is increasing therapeutic effects while reducing ADRs, based on the origin of the pain.

• Clinical and Experimental Pediatrics
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• v.48 no.5
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• pp.527-533
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• 2005

Purpose : Long-term administration of anticonvulsants in children with epilepsy may cause short stature, hypocalcemia and low bone mineral density. This study was performed for the early detection of abnormal bone metabolism in children with epilepsy on taking anticonvulsants. Methods : Thirty children aged 5 to 16 years who were diagnosed with epilepsy were enrolled in this study. All had taken anticonvulsants for more than one year. Bone mineral density of lumbar vertebra was measured by dual-energy X-ray absorptiometry. Serum calcium, phosphorous, alkaline phosphatase, 25-hydroxycholecalciferol[$25(OH)D_3$], parathyroid hormone, and urine deoxypyridinoline were measured as biochemical bone markers. Bone age and body mass index were also calculated. Results : Bone minreal density, body mass index, bone age, and height were significantly decreased in two female patients who had taken two antiepileptic drugs for more than four years and they also had chronic diseases such as cerebral palsy with microcephaly, encephalomalacia, and microcephaly with atrial septal defect. Bone mineral density had significant positive correlations with body mass index(P<0.01) and bone age(P<0.01). Conclusion : This study showed chronic medication of anticonvulsants in children may cause low bone mineral density and short stature. Bone age and body mass index could be the important surrogate markers to find the population at risk. More studies, including a large study population and long term cohort study, will be required.