No abstract available.
N-Methylaspartate*

A 24-year-old nulligravida who presented with seizures and behavioral changes with prodrome of flu-like symptoms was initially treated as a case of viral encephalitis. Neurologic diagnostic tests including electroencephalogram, cerebrospinal fluid analysis (CSF), and cranial magnetic resonance imaging were done and inconclusive. Patient's seizure attacks persisted and her neurologic status was deteriorating despite giving appropriate anti-epileptic medications, hence an autoimmune disease was highly considered. The CSF was positive for N-methyl-D-aspartate receptor antibodies. This prompted a search for an associated teratoma and revealed a diagnostic dilemma between presence of an ovarian new growth versus a normal enlarged ovary. Laparoscopy which is both diagnostic and therapeutic was utilized. This report highlights prompt recognition of a rare case and prevented its progression to a potentially fatal condition as resection of the tumor dramatically relieved the symptoms. The significance of minimally invasive surgery in managing this case, effect in fertility, and possible association with pelvic inflammatory disease are also discussed.
Laparoscopy ; N-Methylaspartate ; Teratoma

OBJECTIVE: This study examined the efficacy and safety of memantine-an uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist-in the treatment of moderate-to-severe dementia. METHODS: Forty-four patients with moderate-to-severe dementia received 20 mg of memantine daily for 24 weeks. The primary efficacy variable was measured by the Korean version of Severe Impairment Battery(K-SIB), and the secondary efficacy variables were measured using the Seoul-Activites of Daily Living(S-ADL) and Neuropsychiatric Inventory-Questionnaire(NPI-Q). Neuropsychological assessments were administrated at baseline, 12 weeks, and 24 weeks. Safety parameters were monitored. RESULTS: Of 44 patients recruited, 30 completed the study and 14 dropped out. Memantine-treated patients showed a therapeutic benefit in all efficacy variables ; the K-SIB, S-ADL, and NPI-Q total scores were not significantly different from baseline either at the endpoint(in the analysis of intention-to-treat, with the last observation carried forward, ITT-LOCF) or at week 24(in the analysis of observed cases, OC). The response rates, when "response" was defined as improved or unchanged in the K-SIB or the S-ADL scores, were 43.3 and 50%, respectively(in the analysis of OC). The responders showed significant improvement in the cognitive subdomain of memory function, praxis, visuospatial ability, and orienting to name. Memantine was shown to be tolerable and safe. CONCLUSIONS: Memantine treatment reduced or delayed clinical deterioration in cognition, function, and behavior in patients with moderate-to-severe dementia.
Cognition ; Dementia* ; Humans ; Memantine* ; Memory ; N-Methylaspartate

No abstract available.
Early Intervention (Education)* ; N-Methylaspartate* ; Psychotic Disorders*

To providean evidence tosupport thecalcium hypothesis ofcerebral ischemia, we examinedthe effectsoftheextracellular calciumandcalciumchelating agent(Bapta-AM), and magnesiumon in vitro ischemia usingrat hippocampal slices. Loss of the populationspike on thehippocampal CA1 region afterelectrical stimulation was usedas indexof damageon thesynaptictransmission andspike amplitudeof the population spikeas index ofrecovery level.Recovery from theloss of orthodromic responses aftertransient hypoxia in lowcalcium treated sliceswas more rapid than nontreated normal calciumslices, and remained robust for4 hours in slices exposed in lowcalcium, whileresponses inslices madehypoxic in normalcalcium remained depressed or more slowlyrecovered. There were statistical significant differences of amplitude between the two group at 5, 10 15, 30, 60, 90 and 120 minute after 10 minute hypoxia (p<0.05).To thelesserextent, similarresults wasobservedin calcium chelating agent, BAPTA-AM, treatedslices, with statistical significant difference at 10minute afterhypoxia(p<0.05). Butin additionto reducingcalcium, elevating magnesium levelwhich is knownas voltagedependent NMDA receptorblocker, did not improve recoverycompared to reducingcalcium alone. We concludethat recovery from the lossof function afterhypoxia was improved bydecreasing extracellular calcium concentration of neuronsand activation of NMDA receptorsprobably played no part in early neuronal damage.
Anoxia* ; Calcium* ; Ischemia ; Magnesium* ; N-Methylaspartate ; Neurons

The use of magnesium sulphate has recently increased in anesthesiology and pain medicine. The roles of magnesium sulphate are as an analgesic adjuvant, a vasodilator, a calcium channel blocker and reducing the anesthetic requirement. These effect are primarily based on the regulation of calcium influx into the cell and antagonism of the N-methyl-D-aspartate receptor. We discuss here the clinical effects of magnesium sulphate on anesthesiology and pain medicine.
Anesthesiology ; Calcium ; Calcium Channels ; Magnesium ; N-Methylaspartate

Clinical observations and recent experimental studies have suggested that the longer status epilepticus (SE) persists, the more difficult it is to control SE pharmacologically. These findings imply that there are fundamental pathophysiologic processes, which make more resistant to intervene in the refractory SE. Recently, it has been recognized that ketamine, N-methyl-D-aspartate receptor antagonists, are effective agents in the treatment of the late stages of SE in the animal model. However, only one clinical experience has been reported. Here, we report two cases with refractory SE, responsive to ketamine.
Ketamine* ; Models, Animal ; N-Methylaspartate ; Status Epilepticus*

Brain ; N-Methylaspartate ; Neurons ; Patch-Clamp Techniques

BACKGROUND: This study was performed to compare the analgesic effects of the systemic versus local administration of ketamine and observe the effects of an NMDA receptor agonist on its peripheral analgesia using the rat formalin test. METHODS: Rats undergoing peripheral analgesia were divided into three groups; the administration of a subcutaneous (s.c.) injection of 0.1 ml of normal saline (Control), and intraperitoneal (i.p.) (Keta/IP) and s.c. (Keta/LO) injections of 2.5 mg/0.1 ml of ketamine administered 5 min before a s.c. injection of 50 ul of 5% formalin. All s.c. injections were performed at the same site: the right hind paw of the rat. To observe the effects of an NMDA receptor agonist, five groups were compared. In addition to the control and Keta/LO groups described above, following three groups with 1-Aminocyclopropanecarboxylic acid (ACPC), an NMDA receptor agonist, in addition to the Keta/LO group; local infiltration with 0.1 mM/0.1 ml ACPC 10 min before or after the administration of ketamine, and an i.p. injection 10 min before the administration of ketamine followed by a s.c. injection of formalin 5 min later. The pain behavior was compared according to the number of flinches during phase 2. RESULTS: All the ketamine groups showed fewer flinches compared to the control (P < 0.01). The Keta/Lo group showed fewer flinches than that of the Keta/IP group (P < 0.01). The analgesic effect of locally administered ketamine was reversed by pretreatment with either s.c. or i.p. ACPC, but not by post-treatment. CONCLUSIONS: These data suggest that locally administered ketamine has a potent peripheral analgesic effect, but the administration of ACPC prior to ketamine decreases the analgesic effect of ketamine.
Analgesia ; Animals ; Formaldehyde* ; Ketamine* ; N-Methylaspartate ; Pain Measurement* ; Rats*

Several decades of research attempting to explain schizophrenia regarding dopamine hyperactivity hypothesis have produced disappointing results. New hypotheses focusing on serotonin-dopamine interactions and hypofunction of the NMDA glutamate transmitter system have been emerging as potentially more promising concepts. The next generation of treatments for schizophrenia, whether they are based on dopamine, serotonin, or glutamate etc., should be effective on negative symptoms and cognitive deficits as well as positive symptoms. In this article, I review the brief overview of these hypotheses and new drugs based on the hypotheses.
Dopamine ; Glutamic Acid* ; N-Methylaspartate ; Receptors, Glutamate* ; Schizophrenia ; Serotonin