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Paroxysmal dyskinesia due to a subthalamic lesion is a rare finding. We describe a patient with paroxysmal tonic spasms due to a well-defined lesion in the subthalamic area. In this case, we confirm the nonepileptic nature of the episode and collect with detail the clinical features by means of a video-electroencephalographic recording. We also report an excellent response to carbamazepine in subthalamic paroxysmal dyskinesias.
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A 39-year-old patient developed phantom pain after amputation of both upper arms following a burn injury. The pain did not respond to naproxen, morphine, carbamazepine, amitriptyline, calcitonin or transcutaneous electrical nerve stimulation (TENS). At the 39th post-operative day an axillary catheter was placed on the right side, as well as an interscalene catheter on the left. Ropivacaine 0.2% was infused, starting with a rate of 4 ml/h, that was increased to 6 ml/h during the subsequent 6 days. Within 20 min of catheter placement complete pain relief was achieved. The patient did not need any other analgesics and remained painfree for 7 months. Neither motor block, nor any other side effects occurred during the infusion of ropivacaine 0.2%. Thus, the patient not only received analgesia, but also got an effective treatment of established phantom pain. A similar approach with bupivacaine may not have been feasible, because of the possibility of toxic side effects. Ropivacaine is a long-acting local anaesthetic which is less toxic than bupivacaine and has the additional advantage of producing less motor-blockade in the concentration used, so the patient was able to move actively without experiencing any pain.
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Previously reported data indicated that infants prenatally exposed to PHT, in monotherapy or polytherapy with STP, were at increased risk for hyperexcitability (screeching, refusing to attend to stimuli, lack of visual orientation). This was not the case for infants prenatally exposed to STP monotherapy.
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Application of the findings in this study to patient care may permit selection of an appropriate initial maintenance dosage to achieve target haloperidol serum concentrations, thus enabling the clinician to achieve the desired therapeutic effect.
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At the end of 3 months of treatment, all patients improved compared with their baseline, but there was no difference in mood ratings in subjects with an initial MADRS >15 (ERCC, 18.2 +/- SD 11.9, vs IR, 12.0 +/- 4.5; P = .3) or YMRS >15 (ERCC, 6.5 +/- 6.4, vs IR, 4.7 +/- 3.1; P = .7). When compared with their baseline, patients receiving IR improved earlier than patients receiving ERCC. There were no differences in overall adverse events in patients receiving IR or ERCC (23.1 +/- 13.42 vs 22.3 +/- 13.40; P = .9).
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We based this review on published aggregate data. The main outcomes measured were the proportions of patients achieving a 12-month remission from seizures, reporting adverse effects, and being withdrawn from the treatment they had been randomised to receive.
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Ocular neuromyotonia is a rare ocular motility disorder characterized by involuntary contraction of extraocular muscles resulting in paroxysmal diplopia. Although ocular neuromyotonia is reported as a rare complication after radiation therapy, there are a few cases of ocular neuromyotonia in the absence of irradiation. In the reported cases the possibility of vascular compression has been suggested on radiological imaging. The authors report a case of ocular neuromyotonia treated by microvascular decompression of the third cranial nerve, supporting the hypothesis that neurovascular compression may play a role in its pathogenesis. The usefulness of preoperative 3D imaging for microvascular decompression is also discussed.
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In an attempt to find the key to reducing the excessive morbidity and mortality seen with mood disorders, our laboratory has been extensively investigating lithium's mechanisms of action in an integrated series of clinical and preclinical studies. We have found that the chronic administration of the 2 structurally highly dissimilar agents, lithium and valproate, brings about a strikingly similar reduction in protein kinase C (PKC) alpha and epsilon isozymes in rat frontal cortex and hippocampus. In view of PKC's critical role in regulating neuronal excitability and neurotransmitter release, we have postulated that PKC inhibition may have antimanic efficacy. In a small study, we have found that tamoxifen (which, in addition to its estrogen receptor blockade, is also a PKC inhibitor) has marked antimanic efficacy. These exciting preliminary results suggest that PKC inhibitors may represent a novel class of improved therapeutic agents for bipolar disorder, and this is under further investigation. The beneficial effects of mood stabilizers require a lag period for onset of action and are generally not immediately reversed upon drug discontinuation; such patterns of effects suggest alterations at the genomic level. We have therefore undertaken a series of studies to investigate the effects of these agents on the AP-1 family of transcription factors and have found that both drugs increase AP-1 DNA binding activity in areas of rodent brain ex vivo and in human neuronal cells in culture. Both treatments also increase the expression of a reporter gene driven by an AP-1-containing promoter, and mutations in the AP-1 sites of the reporter gene promoter markedly attenuate these effects. Both treatments also increase the expression of several endogenous proteins, whose genes are known to be regulated by AP-1. Although the precise mechanisms have not been fully elucidated, preliminary results suggest that these effects may be mediated, in part, by mitogen-activating protein kinases and glycogen synthase kinase 3beta. We have also utilized mRNA reverse transcription-polymerase chain reaction (RT-PCR) differential display to identify concordant changes in gene expression induced by the chronic administration of both lithium and valproate. We have identified concordant changes in a number of cDNA bands by both lithium and valproate. Cloning and characterizing of these genes is currently underway. The identification of the functions of these genes offers the potential not only for improved therapeutics for reducing the morbidity and mortality associated with mood disorders, but may also provide important clues about the underlying pathophysiology.
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The objectives of this study were to find the most common branch of trigeminal nerve affected and the most common side involved.
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In 71 schizophrenic patients (age 32.6 +/- 12.1, range 18-63 years; 31 women, 40 men), plasma olanzapine levels were assessed in 377 tests by high-performance liquid chromatography (HPLC) with electrochemical detection. Fifty-six of these plasma levels were assessed while patients were receiving olanzapine as monotherapy; otherwise, the plasma levels were assessed with the patients receiving various co-medications.
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The patients with solitary cysticercus granuloma had favorable seizure-related prognosis when compared with patients having normal neuroimaging. Serial seizures and headache predicted seizure recurrence in patients with solitary cysticercus granuloma. The presence of electroencephalographic abnormality predicted seizure recurrence in patients with normal neuroimaging.
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The underlying mechanisms behind hepatotoxicity induced by AED are not clear. Reactive metabolites from AED can, in some cases, lead to direct cytotoxicity and liver cell necrosis, whereas in other cases this may lead to neoantigen formation inducing immunoallergic mechanisms.
Eribulin was primarily metabolized by CYP3A4, resulting in the formation of at least four monooxygenated metabolites. In human liver microsomal preparations, eribulin suppressed the activities of CYP3A4-mediated testosterone and midazolam hydroxylation with an apparent K (i) of approximately 20 microM. Eribulin competitively inhibited the testosterone 6beta-hydroxylation, nifedipine dehydration, and R-warfarin 10-hydroxylation activities of rCYP3A4, with an average apparent K (i) of approximately 10 microM. These inhibitions were reversible, with no apparent mechanism-based inactivation. Eribulin did not induce the expression or activities of CYP1A and CYP3A enzymes in human primary hepatocytes, and clinically relevant concentrations of eribulin did not inhibit CYP3A4-mediated metabolism of various therapeutic agents, including carbamazepine, diazepam, paclitaxel, midazolam, tamoxifen, or terfenadine.
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VPA exposure resulted in a decrease in estradiol levels and a general downregulation of expression of genes encoding for enzymes early in steroidogenesis. No consistent changes were seen with LEV or CBZ exposure.
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Facial pain is a complex disease with a number of possible etiologies. Trigeminal neuropathic pain (TNP) is defined as pain caused by a lesion or disease of the trigeminal branch of the peripheral nervous system resulting in chronic facial pain over the distribution of the injured nerve. First line treatment of TNP includes management with anticonvulsant medication (carbamazepine, phenytoin, gabapentin, etc.), baclofen, and analgesics. TNP, however, can be a condition difficult to adequately treat with medical management alone. Patients with TNP can suffer from significant morbidity as a result of inadequate treatment or the side effects of pharmacologic therapy. TNP refractory to medical management can be considered for treatment with a growing number of invasive procedures. Peripheral nerve stimulation (PNS) is a minimally invasive option that has been shown to effectively treat medically intractable TNP. We present a case series of common causes of TNP successfully treated with PNS with up to a 2 year follow-up. Only one patient required implantation of new electrode leads secondary to electrode migration. The patients in this case series continue to have significant symptomatic relief, demonstrating PNS as an effective treatment option for intractable TNP. Though there are no randomized trials, peripheral neuromodulation has been shown to be an effective means of treating TNP refractory to medical management in a growing number of case series. PNS is a safe procedure that can be performed even on patients that are not optimal surgical candidates and should be considered for patients suffering from TNP that have failed medical management.
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We enrolled 171 patients and analyzed 168 as the per-protocol (PP) group (3 patients had protocol violations). The mean age of the PP group was 8.4±2.7 years. The maintenance dose of OXC was 24.9±8.0mg/kg/day. Of the 168 patients included in the efficacy analysis, 122 (72.6%) completed the study and 94 (56.0%) became seizure-free after the OXC treatment. Comparing the efficacy of OXC for intellectually normal and intellectually impaired patients, 79 (56.8%) of the 139 intellectually normal patients and 15 (51.7%) of the 29 intellectually impaired patients became seizure-free (P=0.61). After treatment, intelligence scale scores improved in intellectually normal patients compared to the intellectually impaired children (P<0.05). Social problems quantified by behavior scales improved in intellectually impaired patients compared to intellectually normal children (P<0.05).
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To give an overview of epidemiologic data and pharmacological management of epilepsy in the elderly. It is a common and important clinical problem. The increased awareness of this phenomenon has led to better understanding of the etiology of seizures and complexity of the pharmacokinetics in the elderly.
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ESL-QD resulted in 33.3% higher peak plasma concentration (Cmax,ss ) of eslicarbazepine and similar extent of plasma exposure (AUCss,0-τ ) when compared to ESL-BID, which may contribute to the efficacy profile reported with once-daily ESL. In comparison to OXC-BID, administration of ESL-QD resulted in 40.6% increase in the delivery of eslicarbazepine into the plasma as well as a significantly lower systemic exposure to (R)-licarbazepine and oxcarbazepine.
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Th anti-seizure medication carbamazepine is often found in treated sewage effluent and environmental samples. Carbamazepine has been shown to be very persistent in sewage treatment, as well as ground water. Due to environmental persistence, irrigation with sewage effluent could result in carbamazepine contamination of surface and ground water. To determine the potential for leaching of carbamazepine, a series of adsorption and desorption batch equilibrium experiments were conducted on irrigated soils. It was found that carbamazepine adsorption to biosolid-amended (T) soils had a KD of 19.8 vs. 12.6 for unamended soil. Based on adsorption, carbamazepine leaching potential would be categorized as low. During desorption significant hysteresis was observed and KD increased for both soils. Desorption isotherms also indicate a potential for irreversibly bound carbamazepine in the T soil. Results indicate that initial removal of carbamazepine via adsorption from irrigation water is significant and that desorption characteristics would further limit the mobility of carbamazepine through the soil profile indicating that carbamazepine found in sewage effluent used for irrigation has a low leaching potential.
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Dravet syndrome is among the most challenging electroclinical syndromes. There is a high likelihood of recurrent status epilepticus; seizures are medically refractory; and patients have multiple co-morbidities, including intellectual disability, behaviour and sleep problems, and crouch gait. Additionally, they are at significant risk of sudden unexplained death. This review will focus predominantly on the prophylactic medical management of seizures, addressing both first-line therapies (valproate and clobazam) as well as second-line (stiripentol, topiramate, ketogenic diet) or later options (levetiracetam, bromides, vagus nerve stimulation). Sodium channel agents-including carbamazepine, oxcarbazepine, phenytoin and lamotrigine-should be avoided, as they typically exacerbate seizures. Several agents in development may show promise, specifically fenfluramine and cannabidiol, but they need further evaluation in randomized, controlled trials. In addition to prophylactic treatment, all patients need home-rescue medication and a status epilepticus protocol that can be carried out in their local hospital. Families must be counselled on non-pharmacologic strategies to reduce seizure risk, including avoidance of triggers that commonly induce seizures (including hyperthermia, flashing lights and patterns). In addition to addressing seizures, holistic care for a patient with Dravet syndrome must involve a multidisciplinary team that includes specialists in physical, occupational and speech therapy, neuropsychology, social work and physical medicine.
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Retrospective chart review study of 405 veterans with bipolar disorder followed for a mean of 3 years, with month by month review of clinical progress notes, and systematic assessment of current pharmacotherapy and suicide completion, attempt or hospitalization for suicidality. Comparison of suicide event rates (events/100 patient years) between mood stabilizers and during-vs-after discontinuation of mood stabilizers, with linear regression analysis for influence of potential confounding variables, and robust bootstrap confirmation analysis.