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Studies of the neurobiological causes of anxiety disorders have suggested that the γ-aminobutyric acid (GABA) system increases synaptic concentrations and enhances the affinity of GABA A (type A) receptors for benzodiazepine ligands. Flumazenil antagonizes the benzodiazepine-binding site of the GABA/benzodiazepine receptor (BZR) complex in the central nervous system (CNS). The investigation of flumazenil metabolites using liquid chromatography (LC)-tandem mass spectrometry will provide a complete understanding of the in vivo metabolism of flumazenil and accelerate radiopharmaceutical inspection and registration. The main goal of this study was to investigate the use of reversed-phase high performance liquid chromatography (PR-HPLC), coupled with electrospray ionization triple-quadrupole tandem mass spectrometry (ESI-QqQ MS), to identify flumazenil and its metabolites in the hepatic matrix. Carrier-free nucleophilic fluorination with an automatic synthesizer for [ 18 F]flumazenil, combined with nano-positron emission tomography (NanoPET)/computed tomography (CT) imaging, was used to predict the biodistribution in normal rats. The study showed that 50% of the flumazenil was biotransformed by the rat liver homogenate in 60 min, whereas one metabolite (M1) was a methyl transesterification product of flumazenil. In the rat liver microsomal system, two metabolites were identified (M2 and M3), as their carboxylic acid and hydroxylated ethyl ester forms between 10 and 120 min, respectively. A total of 10-30 min post-injection of [ 18 F]flumazenil showed an immediate decreased in the distribution ratio observed in the plasma. Nevertheless, a higher ratio of the complete [ 18 F]flumazenil compound could be used for subsequent animal studies. [ 18 F] According to in vivo nanoPET/CT imaging and ex vivo biodistribution assays, flumazenil also showed significant effects on GABA A receptor availability in the amygdala, prefrontal cortex, cortex, and hippocampus in the rat brain, indicating the formation of metabolites. We reported the completion of the biotransformation of flumazenil by the hepatic system, as well as [ 18 F]flumazenil's potential as an ideal ligand and PET agent for the determination of the GABA A /BZR complex for multiplex neurological syndromes at the clinical stage.

Objectives: In contrast to previous concept that tinnitus is confined to an otologic disorder, current evidence supports it as a phantom sensory phenomenon of vestibulocochlear damage with cortical reorganization. It is a common problem worldwide, but the treatment response is always unsatisfactory., Patients and Methods: In this study, we report 10 patients who described their staccato tinnitus as simulating the ticking sound of a pendulum or quartz clock (or termed clocking tinnitus). The tinnitus characteristics, laboratory tests, and treatment response were recorded., Results: Clocking tinnitus was unilateral in three patients, bilateral in one patient, and at midline in another six patients. It usually subsided within 15 min. Neither patient experienced vertigo, hemifacial spasm, focal neurological deficit or otic disorder in association with tinnitus. Pre-existing migraine was present in seven patients. During tinnitus attack, a few migraine symptoms concurrently occurred in six patients. Pure-tone audiometry showed symmetric sloping pattern of hearing impairment in half patients whereas brainstem auditory evoked potentials revealed a prolonged wave I-III latency in 30% of patients. The p300 and electroencephalogram were normal in all of them. Neuroimaging study did not disclose structural change. All patients responded poorly to conventional treatments but favorably to flunarizine or topiramate., Conclusion: Clocking tinnitus may be an audiology manifestation of migraine in some individuals. Antimigraine treatment can be considered in this specific group of staccato tinnitus. Audiogenic classification of tinnitus may provide diagnostic and treatment clues in tinnitus patients., (Copyright © 2019 Elsevier B.V. All rights reserved.)

The headache associated with intercourse or masturbatory activity is a well-recognized clinical entity but pornography headache is barely mentioned. We report a young man who suffered preorgasmic headache pertaining only to pornography of specific erotic contents but not to other sexual or nonsexual act. An antecedent activation of sexual arousal and vasoconstriction during pain were found. Finally, oral indomethacin favorably prevented the pain. Therefore, pornography headache is a distinguished headache disorder distinct from other sexual-related headache disorders. Sexual arousal-mediated cerebrovascular dysregulation consequence to visuoneural uncoupling in response to erotic stimulus is proposed. Pornography headache may be underestimated in population as pain-killer overuse may mask the actual incidence in real world., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Objectives: Spontaneous orgasm is characterized by a spontaneous onset of orgasm without any preceding sexual or nonsexual trigger. It sheds insight on the mechanisms underlying orgasms and the sexual response cycle in humans., Methods: We report a male patient of repetitive spontaneous orgasm under trazodone treatment and systematically review the literature on drug-associated spontaneous orgasm (DASO)., Results: A total of 25 patients (18 women and 7 men), including our reported case, experienced 27 DASO events. Over half of them were under 50 years of age during the DASO event. Depression was the leading morbidity for these patients, and a limited list of antidepressants and antipsychotics were involved in 92.5% of all DASO events. Although offending drugs possess variable pharmacological properties, their common effect is an augmentation of serotonin-1A (5HT1A) neurotransmission. Offending drugs seemingly increase personal susceptibility to DASO. Over half of the patients, especially men, did not concurrently experience sexual arousal or desire during the DASO event. In the remaining patients, the orgasm was accompanied by or ensued with arousal or desire. A reduction of dose or discontinuation of the offending drug usually abolished DASO., Conclusions: It appears that 5HT1A has a key role in generating orgasm. Orgasms may be activated through arousal-independent or arousal-dependent pathways, and both orgasms and sexual arousal are bidirectionally activated. This double-bidirectional model of sexual response cycle may promote the success of sexual procreation and recreation, and further research on this pathway could offer an innovative method to manage anorgasmia in the future.

Objective: Cheiro-pedal syndrome (CPS) is an incomplete sensory disorder confined to hand and foot and is generally considered a benign entity. However, knowledge comes from case report or case series only. The aim of this study is to clarify the etiology, localization and outcome of CPS., Patient and Method: A total of 21 CPS patients from our database and another 9 patients from literature were reviewed. CPS was classified into 4 types, namely unilateral and ipsilateral (Type I), bilateral (Type II), incomplete bilateral (Type III), and crossed (Type IV)., Results: They were 20 men and 10 women; including 20 Type I patients, 9 Type II patients, 1 Type III patients, and 0 Type IV patient. Vascular disorders, non-vascular cervical disorder and polyneuropathy were the responsible causes in 18 patients, 7 patients, and 2 patients, respectively. Etiology was unknown in another 3 patients. Lesions were located at brain parenchyma in 16 patients, and cervical cord above C5 level in 9 patients. Disable motoroparesis occurred between 4days to 2 months in two-third of deteriorated patients. In three patients, their lesions were detected only on recurrence or exacerbation of CPS 4 months to 2 years later. Recovery, residual deficit and deterioration ensued in 44%, 28% and 28% patients, respectively. A 33.3% of brain involvement patients and 100.0% of spinal involvement patients terminated to residual deficit or deterioration. The sensitivity and specificity of prediction for deterioration was 77.8% and 100%, respectively, by type II or III CPS., Conclusion: CPS is actually not a benign neurological disorder but a sensory alarm sign. A thorough examination of brain parenchyma and cervical spinal cord is urgent for identifying any treatable or preventable pathological lesions to reduce harmful consequence, especially in case of type II or III CPS., (Copyright © 2017. Published by Elsevier B.V.)

Crossed cheiro-oral syndrome (CCOS) is characterized by crossed sensory disturbance confined to the unilateral perioral area and contralateral hand/finger(s). Although a few classical crossed sensory syndromes accurately predict brainstem or spinal involvement, the clinical significance of CCOS remains unclear. In this study, we analyzed the etiology, localization and outcome of CCOS patients. The results showed that ischemic stroke is the exclusive cause of CCOS. The location of responsible stroke is pertinent to the middle or upper level of the lateral medulla oblongata medial to the lateral sulcus. The vascular supply is from the vertebral artery or the posterior inferior cerebellar artery. Half of the CCOS patients progressed to Wallenberg's syndrome and complicated with disabled daily living. However, no patient died during the follow-up period. A larger size and dorsal extension of the infarction correlated with neurological deterioration. Therefore, CCOS is an independent clinical sign of medullary involvement. It strongly predicts involvement at the lateral medulla oblongata, especially the ischemic stroke, and neurological deterioration. A rapid evaluation of the infarction location and vascular status is suggested in cases of CCOS., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Endothelial dysfunction leads to worse cognitive performance in Alzheimer's dementia (AD). While both cerebrovascular risk factors and endothelial dysfunction lead to activation of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and E-selectin, it is not known whether these biomarkers extend the diagnostic repertoire in reflecting intracerebral structural damage or cognitive performance. A total of 110 AD patients and 50 age-matched controls were enrolled. Plasma levels of VCAM-1, ICAM-1 and E-selectin were measured and correlated with the cognitive performance, white matter macro-structural changes, and major tract-specific fractional anisotropy quantification. The AD patients were further stratified by clinical dementia rating score (mild dementia, n=60; moderate-to-severe dementia, n=50). Compared with the controls, plasma levels of VCAM-1 (p< 0.001), ICAM-1 (p=0.028) and E-selectin (p=0.016) were significantly higher in the patients, but only VCAM-1 levels significantly reflected the severity of dementia (p< 0.001). In addition, only VCAM-1 levels showed an association with macro- and micro- white matter changes especially in the superior longitudinal fasciculus (p< 0.001), posterior thalamic radiation (p=0.002), stria terminalis (p=0.002) and corpus callosum (p=0.009), and were independent of, age and cortical volume. These tracts show significant association with MMSE, short term memory and visuospatial function. Meanwhile, while VCAM-1 level correlated significantly with short-term memory (p=0.026) and drawing (p=0.025) scores in the AD patients after adjusting for age and education, the significance disappeared after adjusting for global FA. Endothelial activation, especially VCAM-1, was of clinical significance in AD that reflects macro- and micro-structural changes and poor short term memory and visuospatial function.

Objective: To report an unusual involvement of focal distal muscles but not proximal muscles in a patient with hypokalemic periodic paralysis (hypoPP)., Clinical Presentation and Intervention: A middle-aged woman presented with episodic weakness of the bilateral thumbs lasting for 2 years. Hypokalemia and a left adrenal mass were subsequently found. Her weakness subsided after surgical removal of the adrenal mass, which was pathologically proven to be an adrenal adenoma., Conclusion: The findings for this patient should alert physicians to consider focal distal motor paresis due to hypoPP. A preexisting occult trauma may predispose to paralysis at an atypical location in secondary hypoPP., (Copyright © 2013 S. Karger AG, Basel.)

Background: Although it has been established that antiphospholipid antibodies (APAbs) bind to and modulate the signaling of cerebellar neurons in vitro, the clinical correlation between increased APAbs and cerebellar ataxia has rarely been investigated., Methods: We reviewed 10 patients presenting with cerebellar ataxia with increased blood APAbs from our database along with 3 APAb-associated cerebellar ataxia patients in the literature., Results: Of these 10 patients, 4 exhibited a subacute onset of progressive ataxia, and there were no significant structural changes in their brains that appeared to be responsible for the symptoms. Another 6 showed a chronic course of ataxia, and shared similar morphological changes that included symmetrical lesions in bilateral hemispheres, periventricular lucency and central and temporal atrophy of varying severity; the cerebellum was spared. The predominant APAbs for subacute and chronic ataxia were the anti-beta2-glycoprotein I antibody and anticardiolipin antibody, respectively. Cancer was found in 1 patient with subacute ataxia and in 4 with chronic ataxia. The removal of the cancer, the plasmapheresis and immunosuppressive therapy successfully abolished the ataxia and increased APAb levels in all 5 patients., Conclusions: The relation between APAbs and nonvascular neurological disorders, such as cerebellar ataxia, should be further studied. APAbs may mediate neurological deficits via different mechanisms such as structural damage or functional neurotoxicity. Clinically, the examination of blood APAb levels is recommended for patients with cerebellar ataxia without a determined cause, and the further survey of systemic cancers in the case of APAb positivity is also recommended. Finally, plasmapheresis is a reasonable and effective treatment for APAb-associated cerebellar ataxia.

The radio-isotope rhenium-labeled N-[2-(triphenylmethyl)thioethyl]-3-aza-19-ethyloxycarbonyl-3-[2-(triphenylmethyl)thioethyl] octadecanoate) ligand (188Re-MN-16ET) is a novel therapeutic agent under preclinical evaluation for hepatoma. A reversed-phase high performance liquid chromatography coupled with a tandem mass spectrometric analysis method and diode array detector (DAD) involving a T type splitter was developed to characterize this pharmaceutical in rat liver tissue solution and determine its biotransformation rate. The separation was accomplished on a C18 column (chromolith silica, 4.6 mm x 100 mm) using an acetonitrile-ammonium acetate buffer gradient as the mobile phase. The detection was achieved by DAD set at 250nm and tandem mass spectrometry using electrospray ionization in the positive ion mode. Re-MN-16ET displayed a retention time of 23.2 min and a transition ion pair corresponding to m/z677 --> 631 for multiple reaction monitoring. Its biotransformation reaction in rat liver homogenate proceeded for 90 min in a 37°C water bath. The characterization was conducted using aliquots that were extracted and concentrated from the reaction mixture for various incubation times. Re-MN-16ET exhibited a biotransformation half-life (t1/2) of 8-9 min in liver tissue solution and was almost completely exhausted after 90 min. Two of its metabolites, consisting of the Re-labeled carboxylic acid derivative, predominately, and its corresponding demetallized disulfide ligand were found in the liver homogenate, providing a metabolism pathway for the radio-pharmaceutical.

Inhibition of human serotonin transporter (hSERT) has been reported to be a potent strategy for the treatment for depression. To discover novel selective serotonin reuptake inhibitors (SSRIs), a structure-based pharmacophore model (SBPM) was developed using the docked conformations of six highly active SSRIs. The best SBPM, consisting of four chemical features: two ring aromatics (RAs), one hydrophobic (HY), and one positive ionizable (PI), was further validated using Gunner-Henry (GH) scoring and receiver operating characteristic (ROC) curve methods. This well-validated SBPM was then used as a 3D-query in virtual screening to identify potential hits from National Cancer Institute (NCI) database. These hits were subsequently filtered by absorption, distribution, metabolism, excretion, and toxicity (ADMET) prediction and molecular docking, and their binding stabilities were validated by 20-ns MD simulations. Finally, only two compounds (NSC175176 and NSC705841) were identified as potential leads, which exhibited higher binding affinities in comparison with the paroxetine. Our results also suggest that cation-π interaction plays a crucial role in stabilizing the hSERT-inhibitor complex. To our knowledge, the present work is the first structure-based virtual screening study for new SSRI discovery, which should be a useful guide for the rapid identification of novel therapeutic agents from chemical database., (© 2013 John Wiley & Sons A/S.)

Although a previous or recent history of varicella-zoster virus (VZV) infection is known to increase the risk of stroke in both children and adults, the influence of zoster sine herpetic remains unclear. We report an immunocompetent man with common cold symptoms and conjunctivitis, followed by an acute onset of bulbar weakness and hemihypesthesia without preceding skin rash. Acute medullary infarction and left vertebral artery stenosis were detected. VZV infection was finally identified. Zoster sine herpetic interferes with accurate diagnosis of infectious stroke, and vertebral artery involvement is unusual in ischemic stroke in this situation. An unexplained course of ischemic stroke event should be suspected in patients with VZV cerebrovasculopathy, especially in those without conventional stroke risk factors and those exhibiting concomitant infectious complications., (Copyright © 2013 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Atherosclerosis is a chronic inflammatory disorder. Macrophage migration inhibitory factor (MIF) is a potent cytokine that plays an important role in the regulation of immune responses. Polymorphisms including five- to eight-repeat CATT variants ((CATT)(5-8)) and G-173C in the promoter region of the MIF gene are associated with altered levels of MIF gene transcription. The purpose of the study is to investigate the relationship between promoter polymorphisms of the MIF gene and the severity of carotid artery atherosclerosis (CAA). The severity of CAA was assessed in 593 individuals with a history of ischemic stroke by using sonographic examination, and the MIF promoter polymorphisms of these individuals were genotyped. The carriage of (CATT)7 (compared to genotypes composed of (CATT)5, (CATT)6, or both), carriage of C allele (compared to GG), and carriage of the haplotype (CATT)7-C (compared to genotypes composed of (CATT)5-G, (CATT)6-G, or both) were significantly associated with an increase in the severity of CAA. We conclude that polymorphisms in the MIF gene promoter are associated with CAA severity in ischemic stroke patients. These genetic variants may serve as markers for individual susceptibility to CAA., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Understanding the nature of the recognition between amyloid protofibrils and dye molecules at the molecular level is essential to improving instructive guides for designing novel molecular probes or new inhibitors. However, the atomic details of the binding between dyes and amyloid fibrils are still not fully understood. In this study, molecular docking, consensus scoring, molecular dynamics (MD), and molecular mechanics Poisson-Boltzmann surface area (MM-PBSA) analyses were integrated to investigate the binding between Congo red (CR) and the GNNQQNY protofibril from yeast prion protein Sup35 and to further evaluate their binding stabilities and affinities. Our results reveal that there are four CR binding sites located on GNNQQNY protofibril surface. These four CR binding sites adopt dual binding modes by which CR binding with its long axis parallel and perpendicular to the long axis of the protofibril. In addition, CR was also found to bind to the edge of the protofibril via hydrophobic/aromatic and hydrogen-bonding interactions, which is inferred as the possible inhibition mechanism to prevent the elongation of the protofibril from the addition of incoming peptides. Virtual screening from National Cancer Institute (NCI) database obtained three hit compounds with higher binding affinity than CR to the edge of the protofibril due to the fact that the central parts of these compounds are able to form additional hydrogen bonds with the protofibril. The results of the study could be useful for the development of new molecular probes or inhibitors for clinical applications.

Oligonucleotide (T30695) modified gold nanoparticles (T30695-Au NPs) have been prepared and employed for quantification of lead ions (Pb(2+)) in blood. The detection of Pb(2+) ions is through the formation of Au-Pb alloys and oligonucleotide-Pb(2+) complexes that catalyze the H(2)O(2)-mediated oxidation of non-fluorescent Amplex UltraRed (AUR) to form a highly fluorescent oxidized AUR product. Surface-assisted laser desorption/ionization time-of-flight mass spectrometry (SALDI-TOF MS) and inductively coupled plasma mass spectrometry (ICP-MS) revealed the formation of Au-Pb alloys on the surfaces of the 40T30695-Au NPs (i.e., the system featuring 40 molecules of T30695 per Au NP) in the presence of Pb(2+) ions, leading to increased catalytic activity for the H(2)O(2)-mediated oxidation of AUR. The fluorescence intensity (excitation/emission maxima: ca. 540/584 nm) of the oxidized AUR product is proportional to the concentration of Pb(2+) ions over the range 0.1-100 nM, with a linear correlation (R(2) = 0.99). The 40T30695-Au NP/AUR probe is highly selective toward Pb(2+) ions (by at least 200-fold over other tested metal ions). The 40T30695-Au NPs/AUR probe provided limits of detection (LOD, at a signal-to-noise ratio 3) for Pb(2+) ions of 0.05 and 0.1 nM, in Tris-acetate solution (5 mM, pH 8.0) without and with salt (150 mM NaCl, 5 mM KCl, 1 mM MgCl(2), and 1 mM CaCl(2)), respectively. Without conducting tedious sample pretreatment, the approach allows detection of Pb(2+) ions in blood samples, showing the potential of the 40T30695-Au NPs/AUR assay for on-site and real-time detection of Pb(2+) ions in biological samples.

Electric injury is a common physical injury in daily life. Because of the low resistance of vascular tissue, vascular injury and thrombosis are frequently found in cases of high-voltage electric injury but are rarely reported in low-voltage conditions. We present the case of a diabetic woman who suffered symptomatic brainstem stroke after a short duration of 60 Hz/110 V alternate current electric contact with a home washer socket. A stroke risk factor survey did not reveal remarkable cardiac or vascular abnormality, except increased glycohemoglobin levels and decreased protein C activity. In contrast to a direct and adequate energy transfer in high-voltage electric injury, a pre-existing vasculohemostatic deficit, such as coagulopathy, has been proposed to provide a predisposition to thrombosis in low-voltage electric injury. Nevertheless, the findings in this patient remind the possibility of physical triggering factor for stroke occurrence in our environment as new technology and product generates rapidly enough for understanding their safety and biologic effect., (Copyright © 2012 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Bilaterally progressive tinnitus and hearing impairment occurred in a hypertensive patient shortly after an episode of right ganglionic hemorrhage. Audiometric tests showed a mixed sensorineural and conduction hearing loss. When low-dose gabapentin was administrated for the pre-existing postherpetic thoracic neuralgia, the tinnitus dramatically improved but recurred after discontinuation of the drug. Hearing function did not change. In view of a controversy of gabapentin and tinnitus in previous trials, the findings in this patient support that low-dose gabapentin benefits the subgroup of tinnitus patients with secondary contributing factors, such as stroke., (Copyright © 2012 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Backgrounds: Nummular headache (NH) is currently considered a form of peripheral neuralgia originating from the terminal branch in epicranial tissue but its etiopathogenesis is still unknown. Since autoimmune disorders often involve the trigeminosensory nerve to provoke craniofacial pain, we hypothesize that autoimmunity aberration may play a role with regard to NH., Methods: We examined the antibodies to antinuclear factor, ds-DNA, extracted nuclear antigens, rheumatoid factor, as well as antiphospholipid antibodies, in 23 primary NH patients., Results: Among them were 16 patients (69.6%) found as having at least one abnormal autoimmune index, namely, antibodies to antinuclear factor in 8 patients, SSA/La in 6 patients, rheumatoid factor in 4 patients, SSB/Ro in 2 patients, and ds-DNA in 1 patient. An abnormal increase of blood anti-beta2-glycoprotein I antibody was noted in 4 patients and lupus anticoagulant in 1 patient, whereas HLA-B27 seropositivity was detected in 1 patient. Except for 2 patients positive for antinuclear factor without other associated features, 15 patients (65%) were finally diagnosed as having Sjogren/sicca syndrome, rheumatoid arthritis or antiphospholipid antibody syndrome., Conclusions: A high prevalence of abnormal autoimmune indices and disorders is present in primary NH patients, suggesting a probable relationship between autoimmunity aberration and epicranial neuralgia in NH., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Background and Purpose: The salt-and-pepper pain is a characteristic sensory disturbance confined to the eyes and regional facial structures. Although a poor prognosis has been mentioned in previously reported patients, the precise pathomechanism and clinical significance are still unknown., Patients and Methods: We report four patients with ocular salt-and-pepper pain, and review the clinical course, neuroimaging and prognosis in another eight patients reported in the literature., Results: In our series, they were three men and one woman, and their underlying cause was pontine hemorrhage; hypertensive hemorrhage in three and cavernous hemangioma in one patient, respectively. In these 12 salt-and-pepper patients, the identifiable etiology was exclusively brainstem stroke. Life-threatening or disable neurological deterioration ensued within 24 h after pain onset in all patients. Their ocular pain subsided rapidly after neurological deterioration occurred. A dual excitation of nociceptive quinothalamic pain fiber and disinhibition of trigeminosensory system from pontine reticular formation and cerulotrigeminospinal circuit may be responsible for this pain., Conclusion: In clinical practice, ocular salt-and-pepper pain in quiet eyes should be alerted for intracranial pathology and neurological deterioration until underlying cause is identified., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Cheiro-pedal syndrome (CPS) is an incomplete pure sensory disorder confined strictly to simultaneous hand/finger and ipsilateral foot/toe symptoms. However, its clinical significance and pathogenesis are unclear. We present nine patients with typical CPS, and review another seven previously reported patients. Ischemic stroke is the leading cause of CPS in these 16 patients. In 13 patients, the lesions responsible were distributed widely in the brain from the corona radiata to the medulla oblongata whereas in three patients the lesions were found in the cervical spinal cord or peripheral nerves. All patients had a favorable outcome. The close proximity of the cheiral and pedal sensory fibers in the pons, thalamus, internal capsule and the caudal thalamocortical projection increases the vulnerability for CPS. Therefore, the underlying cause of CPS should be investigated rapidly despite it causing only minor symptoms. The pathogenesis of CPS may consist of several interacting factors including preconditioned neuronal damage and proximity of the acral sensory fibers., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

A nummular headache (NH) is a type of primary headache that results from cranial neuralgia without a known cause. We herein report the case of a woman who suffered two episodes of focal headache in the left parietal area with identical characteristics that were compatible with NH. During the recovery phase of the second NH episode, the pain resurged with shingles coinciding with the painful area. The patient's NH subsided in parallel with resolution of the shingles. These findings support a diagnosis of peripheral neuralgia with NH. Latent virus infections, such as Varicella-zoster virus, that frequently cause distal nerve damage in patients with zoster sine herpete may be associated with epicranial neuralgia and NH.

Paramethoxymethamphetamine (PMMA) is an emerging and prevalent psychoactive drug with a structure analogous to amphetamine and related psychostimulants. However, the neurobehavioral effect is only studied in experimental animals and is barely mentioned in human. The authors report the antemortem neurobehavioral manifestations in 8 patients with PMMA use. There were 2 different antemortem presentations. The first group of patients showed delirium, hypertalkativity, and incoherence speech and then turned into convulsion and death. They did not exhibit the typical hyperdopaminergic movement disorder. The second group of patients gradually fell asleep and then suffered respiratory or cardiovascular collapse. The heart blood PMMA level was higher in the second group than in the first group of patients. Forensic autopsy showed variable findings, ranging from no remarkable change to significant pathological damage similar to serotonin syndrome in both groups of patients. PMMA seems to enhance serotoninergism than dopaminergism, and exerts a concentration-related dual effect on human.

Background and Purpose: Cheiro-oral syndrome (COS) is an established neurological entity characterized by a sensory impairment confined to the mouth angle and ipsilateral finger(s)/ hand. The current understanding of localization is a concomitant involvement of the spinothalamic and trigeminothalamic tract between the cortex and pons. The cervical spinal cord has not been mentioned in this situation yet, and this unusual location may heretofore increase the risk of misdiagnosis., Material and Methods: Six patients who presented with unilateral COS due to cervical cord disorder are reported., Results: All patients were women and their age ranged between 42 and 70 years. Their neurological deficits included unilateral paraesthesiae restricted to cheirooral distribution, positive radicular sign, and mild change of tendon reflex. Cervical spinal stenosis at middle/lower cervical spine with variable magnitude of cord compression and intrinsic cord damage was found. A diagnostic dilemma obviously arises from the lack of tangible neurological signs or typical pattern of myelopathy, in addition to the previous concept of cerebral involvement. A benign course ensued in all reported patients., Conclusions: Cheiro-oral syndrome can be an early neurological sign for cervical cord disorder; it further suggests that it is a strong neurological but weak localizing sign. A reciprocal influence of multiple factors is considered to generate COS at the cervical cord. Therefore, an absence of brain pathology should lead to a thorough examination of the cervical cord in case of COS.

Purpose: Tissue plasminogen activator (tPA) was approved by the Food and Drug Administration for ischemic stroke treatment since 1996 at the United States of America and also 2002 at Taiwan. Since after it is strongly advertised for a promising benefit to early thrombolysis that is further echoed by a recommendation in clinical guidelines from multiple medical associations in worldwide. Because of an overwhelming data of positive benefit collected in the evidence-based medicine database, legal dispute subsequently occurs when tPA is failed to be administrated in appropriate time., Methods: In order to elucidate the legal viewpoint for tPA used in ischemic stroke, a review of the domestic judiciary decrees regarding this issue was conducted. Cases in Taiwan were executed from the open access database of the Judicial Yuan, Taiwan. The background, legal dispute and judgment of each case were analyzed., Results: Till August, 2010, there were 6 cases in Taiwan. All cases occurred after 2003. The causes of disputes were a loss of chance for thrombolysis due to a delay of diagnosis (4 cases, 67%) and a failure of thrombolytic treatment after a diagnosis of ischemic stroke (2 cases, 23%). All cases were presented to non-neurologists at initial. Five cases expired or terminated into vegetation before litigation., Conclusion: A failure of early diagnosis or treatment after a diagnosis of ischemic stroke are important for medicolegal dispute in tPA usage, which is expected to become prevalent in Taiwan in future. A fatal or poor outcome may be a triggering factor for litigation. Therefore, an improvement of the knowledge and practice to increase early diagnosis of ischemic stroke is the key factor for reducing medicolegal issue regarding tPA use in ischemic stroke. This is particularly true for non-neurologist physicians.

Ankylosing spondylitis (AS) is an autoimmune spondyloarthropathy involving principally the sacroiliac joint and axial skeleton. Spinal cord involvement is an infrequent and late complication. It mostly results from compressive myelopathy due to skeletal osteopathy and usually presents with radiculomyelopathic sensory and motor deficits. To report three patients who suffered a progressive paraparesis/tetraparesis compatible with motor myelopathy without typical skeletal symptom. Myelopathy of unknown origin was initially interpreted in these patients. Radiography did not show typical change at sacroiliac joint or vertebrate. Spinal magnetic resonance image revealed cord atrophy at cervical and thoracic segment. A positivity of B27 antigen was found afterward. Their spondyloarthropathic symptoms developed within six months later with radiographic sacroiliitis. Seropositive AS with noncompressive myelopathy was finally established. Patients showed a reverse of motor impairment when their pain was well undercontrolled. Motor myelopathy may be neglected or underestimated in AS, in especially when typical skeletal symptom is absent or minimal. It may progress surreptitiously to harm spinal function or superimpose to crippling disability in compressive spinal cord injury. Therefore, a careful evaluation and monitor of spinal cord function is important for AS patient despite spinal deformity is not observed.

Although the somatosensory afferent of the tip of the tongue runs proximal and parallel along the spinothalamocortical and trigeminothalamocortical pathway up to the sensory cortex, central involvement has been rarely described in cases of nongustatory sensory disturbance at the tip of the tongue. In a hypertensive woman who experienced an acute onset of an isolated numbness at the tip of her tongue, recent small infarctions were found at the postcentral gyrus of the right parietal lobe. Thus, central involvement should not be neglected in the case of sensory disturbance at the tip of tongue., (Copyright © 2011 Mosby, Inc. All rights reserved.)

Pure motor hemiparesis is a vascular syndrome that is occasionally mimicked by central or spinal pathologies. However, metabolic neuromuscular disorders have not been reported to mimic this condition. We present a 52-year-old male patient with hypokalemic paralysis who presented with the early symptoms of acute-onset pure motor hemiparesis. Neurological examinations revealed right-sided weakness without bulbar, extraocular, or respiratory involvement. Ischemic stroke was initially diagnosed on the basis of the acute-onset unilateral motor deficit and the patient's history of hypertension, stroke, and previous cerebral infarctions. The right hemiparesis and weakness of the left limbs worsened on the day after admission. The patient's weakness rapidly reversed after correction of hypokalemia, and a diagnosis of hypokalemic paralysis was finally established. This unusual hemineurological presentation should alert medical personnel to the possibility of reversible metabolic neuromuscular disorders, thereby avoiding delayed diagnosis., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

Purpose: To report the experience of carotid artery angioplasty with stenting (CAS) by cardiologists (CV) and neuroradiologists (NR) in an area with less incidence of extracranial artery stenosis., Methods: From 1999 to 2008, 210 patients with 231 stents were collected by claim records from the administrative office and reviewed by one independent neurologist. Outcome measures were peri-procedural adverse events (AE), restenosis and recurrent ipsilateral stroke (RS) rate, categorized into treatment groups by either CV or NR., Results: The average age was 69.0 years and 82.9 % of the patients were men. 63.8% of the patients with 62.8% stents were treated by CV and the remaining 36.2% of patients with 37.2% stents were done by NR. Symptomatic CAS was evident in 70.1% of the CV cases and 83.0% in NR treated patients (P = 0.017). The peri-procedural AE rate was 31.6%; 35.9% in CV group and 24.4% in the NR group (P = 0.071). RS rate was 4.8% in 663.3 days; 4.1% in 920.8 days in the CV group and 5.8% in 354.2 days in the NR group (P = 0.865). The restenosis rate was 10.9% in 630.5 days; 5.4% in the CV group in 224.8 days and 20.6% in the NR group in 817.8 days (P = 0.007)., Conclusions: The restenosis and recurrent stroke rates after carotid artery stenting in Taiwan appears to be consistent with other published and well organized trials. Measures to minimize peri-procedural AR rates are definitely warranted.

Purpose: After a century, cheiro-oral syndrome (COS) was harangued and emphasized for its localizing value and benign course in recent two decades. However, an expanding body of case series challenged when COS may arise from an involvement of ascending sensory pathways between cortex and pons and terminate into poor outcome occasionally., Materials and Methods: To analyze the location, underlying etiologies and prognosis in 76 patients presented with COS collected between 1989 and 2007., Results: Four types of COS were categorized, namely unilateral (71.1%), typically bilateral (14.5%), atypically bilateral (7.9%) and crossed COS (6.5%). The most common site of COS occurrence was at pons (27.6%), following by thalamus (21.1%) and cortex (15.8%). Stroke with small infarctions or hemorrhage was the leading cause. Paroxysmal paresthesia was predicted for cortical involvement and bilateral paresthesia for pontine involvement, whereas crossed paresthesia for medullary involvement. However, the majority of lesions cannot be localized by clinical symptoms alone, and were demonstrated only by neuroimaging. Deterioration was ensued in 12% of patients, whose lesions were large cortical infarction, medullary infarction, and bilateral subdural hemorrhage., Conclusion: COS arises from varied sites between medulla and cortex, and is usually caused by small stroke lesion. Neurological deterioration occurs in 12% of patients and relates to large vessel occlusion, medullary involvement or cortical stroke. Since the location and deterioration of COS cannot be predicted by clinical symptoms alone, COS should be considered an emergent condition for aggressive investigation until fatal cause is substantially excluded.

Although antiphospholipid antibodies (APAbs) are considered to possess neurotoxic property, their relation with non-vascular neurological disorder is still disputed. This dilemma is mainly due to only a cross-sectional analysis or sporadic pictorial description in previous reports. In addition, treatment strategy is unknown in this situation. We encountered a patient who exhibited head-shaking and cerebellar ataxia had an increase of blood anti-beta2-glycoprotein I antibody and anticardiolipin antibody. Her neurological deficits did not respond to corticosteroid pulse therapy but rapidly subsided after plasmapheresis associated with a normalization of APAbs. Accordingly, a causal relation between APAbs and non-vascular neurological disorder is favored. The pathogenesis of APAb-related non-vascular neurotoxicity is warranted for further study to avoid premature conclusion. Plasmapheresis is recommended when movement disorder responds poorly to conventional treatment, especially when APAb is found.

Objectives: Restricted sensory syndrome provides an excellent chance for the understanding of neuroanatomic correlation. The trigeminal nerve has been shown to convey buccal sensory impulse to central compartment. However, the pathway between cortex and the trigeminal sensory nucleus remains largely unknown., Method: A patient presented with cheirobuccopedal syndrome, or objective sensory impairment confined to the left intraoral cheek, hand and foot, was reported., Results: Decrease in pinprick pain and fine touch sensation was detected at the left intraoral cheek, hand and foot. A recent infarction was disclosed at the left paramedian pons. The foregoing hypalgesia and hypesthesia recovered within one month after onset., Discussion: The trigeminobuccal sensory tracts are deemed to run in parallel with other spinothalamic and trigeminothalamic tracts within the brainstem. The rarity of buccal sensory deficit upon brainstem damage may be due to dispersion of the trigeminobuccal sensory tracts on their way of ascending, or their relatively high tolerance to different insults.

Objectives: Cheiro-oral syndrome is characterized by sensory impairment confined to perioral area and ipsilateral fingers/hand. It results from an involvement of the ascending sensory tracts above the pons. However, a crossed pattern of perioral and acral paresthesia was rarely reported before., Patients and Methods: This study reports the neuroanatomic relationship, course and clinical significance of perioral and contralateral acral paresthesia in four patients. We term it the crossed cheiro-oral syndrome., Results: All patients had lateral or dorsolateral medullary infarctions that were ipsilateral to their perioral paresthesia. The contributory origin is considered a diagonal lesion involving the par oralis fibers within the descending trigeminal sensory tract and acral portion of the lateral spinothalamic tract at the lateral portion of medulla oblongata. Despite of a restricted sensory disturbance at initial, progressive neurological disability terminated to Wallenberg's syndrome ensued in three patients and disabling deficits persisted in two of them., Conclusion: The crossed cheiro-oral syndrome seems a mild form of Wallenberg's syndrome. Therefore, it predicts medullary involvement and is also a warning sign for progression.

Purpose: Cutis marmorata is a cutaneous livedoid disorder which can be differentiated from livedo reticularis in both clinical and pathological presentations. Unlike Sneddon syndrome, a detailed immunocoagulation profile has not yet been delineated for cutis marmorata in patients with cerebral ischemia., Methods: To analyze the immunocoagulation profile in cutis marmorata patients associated with cerebral ischemia (CMCI) in a series of 135 cerebral ischemia patients., Results: A total of 32 patients were found to have cutis marmorata. The blood protein C activity, protein S activity, antithrombin III activity, platelet count, fibrinogen and frequency of abnormal antiphospholipid antibody level were similar among 32 CMCI patients, 103 cerebral ischemia patients without cutis marmorata, and 35 healthy subjects. However, uncoupling of protein C and anti-thrombin III was observed in CMCI patients. Serum antinuclear antibody and Venereal Disease Research Laboratory were not detected in these patients., Conclusion: Cutis marmorata is not uncommon in our ischemic stroke patient population, and is characterized by uncoupling of protein C and antithrombin III with altered thrombin hemostasis. Our findings raise the need for a careful cutaneous examination in patients with ischemic stroke. Abnormal immunocoagulating profile should alert physicians to the risk for cerebral ischemia even in the absence of other cardiovascular risk factors.

Pretreatment with dilute sulfuric acid of silvergrass was compared with the pretreatment's effect on other commonly used lignocellulosic materials, namely rice straw and bagasse, in order to evaluate the potential of this feedstock for ethanol production. The highest yield of xylose from silvergrass was between 70% and 75%, which was similar to bagasse. However, silvergrass gave a higher level of fermentability than bagasse using the hydrolysate because less acetic acid was formed. The release of sugars resulted in an about 2.0-fold increase in specific surface area of the pretreated silvergrass. Increasing the specific surface area did not obviously enhance enzymatic digestibility. The hydrophilicity of the acid pretreated silvergrass was characterized using its Fourier transform infrared (FTIR) spectra. The increase in hydrophilicity may enhance enzymatic adsorption onto lignin and increase the accumulation of cellobiose for enzymatic hydrolysis as pretreatment severity increases.

By virtue of an understanding of hemostasis and coagulopathy using modern techniques, the exact role of individual serum protein in vascular thrombosis or hemorrhage becomes more apparent. Cryoglobulin causes vasculitude and thrombosis in various vascular beds, but its role in brain hemorrhage is unknown. We encountered a cryoglobulinemic patient to have cryoglobulinemia, hypocomplementia, and cerebellar hemorrhage during a reactivation of cytomegalovirus infection. Because cryoglobulin is harmful to vessel and hemostasis, and often increases nonspecifically in response to incitement, its weight in vascular syndrome must seriously be reviewed. Coagulopathy in a reactivation of latent virus such as cytomegalovirus should be cautioned in older patients.

Abnormal increases of antiphospholipid antibody and plasma homocysteine levels are recently emerging as nonlipidic risk factors for cerebral atherogenesis and thrombosis. Both antiphospholipid antibody and homocysteine share many similar bioeffects in hemostasis, but their interaction is still inconsistent. In this study, we examined the relation between the plasma homocysteine level and lupus anticoagulant, anticardiolipin antibody, and anti-beta2-glycoprotein I antibody in patients with noncardiac cerebral ischemia. Systemic lupus erythrematosus patients were excluded. The results showed a higher frequency of moderate hyperhomocysteinemia in patients with an abnormal increase of lupus anticoagulant only. Neither the serum folate and cobalamin levels nor methylenetetrahydrofolate reductase allele mutation contributes to this result. Accordingly, homocysteine interacts with lupus anticoagulant to promote cerebral atherosclerosis and ischemia. The role of vasculopathic or prothrombotic autoantibody generation in response to specific pathological change such as hyperhomocysteinemia warrants further investigation.

Purpose: Hyperhomocysteinemia (HHcy) is associated with a higher risk of cerebral ischemia and other vascular thrombosis. Homocysteine is greatly influenced by a broad spectrum of physiological and pathological conditions but the confounding factor for HHcy is unknown in our population, especially in normocreatininemic individuals. It is our aim in this study to elucidate the relation between homocysteine and cardiovascular risk factors, and also describe the distribution of plasma homocysteine level in cerebral ischemia patients with normal serum creatinine level., Methods: A retrospective study was conducted to understand the frequency of HHcy in cerebral ischemia patients, and the confounding cardiovascular risk factors in HHcy. Patients were classified into two groups by their plasma homocysteine levels; group I patients were those whose level was > or = 12 microM/L whereas group II < 12 microM/L., Results: A total of 218 patients were enrolled. Their plasma homocysteine level ranged from 3.57 to 46.37 microM/L (mean: 10.01 +/- 5.03 microM/L). Group I included 45 patients whereas group II 173 patients. The frequency of hypertension, diabetes mellitus and cardiac disease, as well as age, aminotransferases, total cholesterol, triglyceride, albumin, hematocrit, hemoglobin and leucocyte count did not differ between group I and II patients, except serum creatinine level was higher in group I patients (p < 0.01). Serum creatinine level correlated directly to and was an independent predictor for the plasma homocysteine level., Conclusions: HHcy is common in our cerebral ischemia patients. Since renal function is a determinant for HHcy even in normocreatininemic patients, as a cardiovascular risk factor which detriments the renal function, it should be regularly monitored as HHcy is amenable for treatment.

Primary Objective: Nigrostriatal hypodopaminergism is the fundamental basis in parkinsonism. It may arise secondarily from a variety of disorders but is rarely mentioned shortly after surgery., Methods and Procedures: To report the clinical course of five patients who had had symptomatic parkinsonism developed shortly after surgery (lumbar laminectomy, prostatectomy and cholestectomy). Appropriate investigations were done to elucidate their pathogenesis., Main Outcomes and Results: There was no remarkable finding of their anesthetic agents, duration of surgery, type of surgery, medical conditions or preoperative screening test. Extensive investigations did not reveal consistent abnormality. However, an abnormal presence of lupus anticoagulant was detected in four patients; primary antiphospholipid antibody syndrome was fulfilled in two of them. The lupus anticoagulant restored to the reference range in another two patients later. Catastrophic antiphospholipid antibody syndrome was not seen. Initially, their parkinsonian symptoms rapidly progressed but slowed down after six months., Conclusion: Lupus anticoagulant possesses neurotoxic property and has been found in cases of movement disorder involving with the central dopaminergism. Surgery, a form of traumatic stress, has been reported to bring on lupus anticoagulant and catastrophic antiphospholipid antibody syndrome. These relationships remind a generation or an enhancement of pathognomic autoantibody vulnerable for dopaminergic toxicity, such as lupus anticoagulant or other antiphospholipid antibody.

Background: The present study investigated serial changes in platelet activation (expressed by CD62p) and von Willebrand factor (VWF), and the correlation between increased CD62p expression, VWF and brain infarct volume (BIV: measured by magnetic resonance imaging), and prognostic determinants in non-valvular atrial fibrillation (NVAF) patients after acute ischemic stroke (IS)., Methods and Results: CD62p expression and plasma VWF concentrations were serially measured (<48 h, on days 7, 21 and 90) using flow cytometry and enzyme-linked immunosorbent assay, respectively after acute IS in 61 NVAF patients. CD62p expression and VWF concentrations were also examined in 50 NVAF-risk control and 30 healthy individuals. The VWF concentration had no significant changes at 4 intervals among the patients and did not differ among 3 groups at acute stroke phase. CD62p expression was significantly higher in the acute phase after IS than in both control groups (both p<0.0001). However, CD62p expression declined to a significantly lower level on day 7 and to a substantially lower level thereafter (p<0.0001). CD62p expression did not differ on day 90 in the 3 groups (both p>0.5). Linear regression analysis showed that BIV and modified Rankin scale score (>3) were independently associated with increased CD62p expression (<48 h) (both p<0.01). Furthermore, the Cox proportional hazards model showed that BIV was the only independent predictor of intermediate-term (8.8+/-4.4 months) combined recurrent stroke and death., Conclusions: The CD62p expression, which reflected increased BIV, was significantly increased in NVAF patients in acute-phase IS and substantially declined thereafter. The BIV was predictive of unfavorable intermediate-term clinical outcomes.

Introduction: Catastrophic antiphospholipid syndrome (CAPS) is a life-threatening disorder urgent for aggressive treatment, and its characterized systemic thromboses and coagulopathy prompt for a rapid diagnosis., Case Report: A woman fell into unconsciousness two weeks after a stable course of massive cerebral ischemia was identified due to CAPS with Sjogren syndrome. Her thrombocyte count and coagulation times were was normal at initial. A high blood anti-beta(2)-glycoprotein I antibody level was found. Plasmapheresis rapidly reversed her consciousness and coagulation function., Conclusions: A normal hemostatic parameters should not exclude CAPS. A favorable prognosis depends on the rapidity of appropriate treatment.

Background/purpose: Patients with severe strokes may have different associated medical comorbidities from those with mild strokes. This study evaluated the neurologic and non-neurologic medical predictors of mortality in patients with severe cerebral infarction in the acute stage., Methods: Patients admitted to a neurologic intensive care unit (ICU) due to cerebral infarction were included. Neurologic and non-neurologic predictors for in-unit mortality were determined by logistic regression analyses. Two models using (A) neurologic factors and (B) combined neurologic and non-neurologic factors as mortality predictors were developed. The performance of the models in predicting overall, neurologic and non-neurologic mortalities was compared by areas under the receiver-operating characteristic curves (AUC) of the derived regressive equations., Results: Of 231 patients with cerebral infarction admitted to the ICU, 34 (14.7%) died during ICU stay. Conscious state and acute physiologic abnormalities were significant predictors of mortality. The length of ICU stay in patients with non-neurologic mortality was longer than in those with neurologic mortality (p = 0.044). The AUC of Model B was larger than that of Model A in predicting overall (0.768 +/- 0.045 vs. 0.863 +/- 0.033, p = 0.005) and non-neurologic mortalities (0.570 +/- 0.073 vs. 0.707 +/- 0.074, p = 0.009), while there was no difference in predicting death from neurologic causes (0.858 +/- 0.044 vs. 0.880 +/- 0.032, p = 0.217)., Conclusion: Impaired consciousness and acute physiologic abnormalities are independent predictors of mortality for severe ischemic stroke during the acute stage. Neurologic factors predict early mortality from intrinsic cerebral dysfunction, while non-neurologic factors, especially the associated physiologic abnormalities, predict late mortality from medical complications.

Objectives: A restricted neurological deficit is not uncommon in patients with cortical lesions. However, in cheiro-oral syndrome (COS) associated with cortical involvement, the topographic disparity of the cheiral and oral representation area is hardly explained by the restricted sensorium at the homolateral mouth angle/lip and finger/hand, with sparing of the facial structures., Patients and Methods: In order to elucidate the factors of clinical significance and pathogenesis in cortical COS, 11 patients with COS associated with contralateral cortical lesions were analyzed, and the cases of similar patients described in the literature were reviewed., Results: In our patients, the etiologies of COS were infarct, subdural hematoma, meningioma, and vascular malformation. The lesions were sizable enough to involve areas beyond the postcentral gyrus of the parietal lobe. A cortical sensory sign was detected in only six patients. Their paroxysmal sensorium without exacerbation on stimulus was in contrast to the clinical features of COS associated with thalamic lesions. Five patients suffered worsening of their neurological deficits without a parallel expansion of their infarct or hemorrhage. Removal of the hematoma or tumor in four patients rapidly abolished their sensorium., Conclusion: Cortical COS is a warning sign of a potentially life-threatening etiology. Since there is a high frequency of exacerbation, COS should be carefully investigated, as a paucity of associated clinical signs was found in our patients. Paroxysmal sensorium signifies possible cortical involvement. Rapid decompression within the "golden period" is encouraged. It seems that the interaction between previously existing vascular compromise, sensory plasticity, and neuronal vulnerability predisposes patients to this peculiar sensory disorder. Epileptogenesis is unlikely. Thus, a reconsideration of COS in clinical practice is warranted.

Squamous cell carcinoma antigen (SCCA) is traditionally engaged for detecting and following up malignancy from a squamous cell origin. We encountered an unusual increase of blood SCCA but no other cancer markers in a patient associated with an infective lumbar spondylitis due to Pseudomonas aeruginosa. An overshooting of Th1 expression, such as tumor necrosis factor alpha, bumped up by his uremia as a result of P. aeruginosa infection may hasten SCCA. Therefore, SCCA might additionally serve as a serological marker for infection besides squamous cell cancer, and its false-positive increase also highlights the appropriateness of tumor marker screening.

We encountered three patients with hypokalemic paralysis following a convulsion in the early stages of alcohol abstinence. The transtubular potassium gradient was less than 2.0, suggesting intracellular potassium shift. Hypokalaemic paralysis may result from retention of intracellular cationic potassium bound by anionic phosphorylated compounds, precipitated by an acceleration of the (Na+)-(K+) pump in alcohol withdrawal and convulsions. These findings warn of the lethal hypokalemia that may occur after convulsions, particularly soon after alcohol abstinence associated with moderate withdrawal symptoms.

A chemical worker working with urea-formaldehyde resin hazard for 20 years suffered cerebral ischemia in association with an increase of blood beta2-glycoprotein I-dependent anticardiolipin antibody (aCL)-IgG and IgM isotype, and a prolongation of activated partial thromboplastin time (aPTT). Major histocompatibility complex antigen showed DR4 positivity. On follow-up for over 6 years, aCL-IgG and aPTT decreased to reference range but aCL-IgM was still abnormally high despite a cessation of exposure. This patient highlights the induction of antibody-mediated thrombosis in chronic chemical exposure, especially in an individual with subclinical autoimmune disorder. The role of environment for coagulopathic vascular thrombosis is warranted for investigation.

Dengue is a common mosquito-transmitted viral disease prevalent at many undeveloped and developing countries. Although, neurological complication and hemostatic disturbance are common in dengue virus infection, cerebral ischaemia is barely mentioned. A 61-year-old woman experienced an acute onset of right hemiparesis in her early course of dengue virus type II infection. Extensive laboratory investigation revealed an increase of lupus anticoagulant activity and a prolonged activated partial thromboplastin time that were normalized in the convalescent stage. Her human leucocyte antigens were A2, A11, B8, Cw7, DR4 and DR9. This patient highlights the co-operation between transient activation of humoral immunity and preferential immunogenetic for coagulopathic thrombosis in specific viral disease.

Objective: Vascular occlusion is not an uncommon event in malignancy. However, the frequency of ischemic stroke after chemotherapy has been mentioned only occasionally in clinical studies. A large-scale study is lacking., Methods: A retrospective study was conducted at Chang Gung Memorial Hospital, Kaohsiung, Taiwan, to analyze the incidence of ischemic stroke post-chemotherapy, further, to evaluate a possible causative relationship between the ischemic stroke and the chemotherapy regimen, the interval between the latest chemotherapy session and onset of ischemic stroke and the survival of patients with ischemic stroke post-chemotherapy. The data were retrieved from the Cancer Database from 1993 to 2004., Results: During this period, a total of 10,963 patients, with malignancies were followed-up for 1 month after chemotherapy, underwent 45,294 chemotherapy sessions. Among this group, there were 15 patients experiencing 16 ischemic strokes within the first month after the latest chemotherapy. Among them, 14 patients were followed-up until death and one patient was lost in follow-up after discharge against medical advice. The incidence of post-chemotherapy ischemic stroke was 0.137% and the frequency of chemotherapy cycles complicated by ischemic stroke was 0.035%. Adenocarcinoma was the most common histological type not only in ischemic stroke (40%) but also in overall patients (36.7%). The hemispheric stroke with middle cerebral artery territory involvement was the most common image finding. Platinum compounds, especially cisplatin, were the most commonly used chemotherapeutic agents for ischemic stroke patients. Twelve (75%) of these 16 ischemic strokes occurred within 10 days of the latest chemotherapy session and 10 (62.5%) occurred after the first cycle of chemotherapy. The median survival after ischemic stroke was 4 weeks., Conclusion: Our results provide valuable data on the relationship between malignancy, treated with chemotherapy, and ischemic stroke. The risk of ischemic stroke after chemotherapy is predicted by the use of cisplatin-based chemotherapy not cancer histologic type. Infarction usually involves the territorial subtype, causes obvious neurological disabilities and carries a grave prognosis.

Although anticardiolipin antibody (aCL) has been suggested to be a potent risk factor for thrombosis and atherosclerosis in multiple arterial beds, conflicting results exist between aCL and cerebral ischemia in the general stroke population. To elucidate if this discrepancy relates to the heterogeneity of underlying etiologies, the blood beta(2)-glycoprotein I dependent-aCL in 432 Taiwanese adults was examined. The associated cerebral ischemia in these patients was classified into five subtypes according to the cause of cerebral ischemia. The results were compared with those in 100 healthy controls. A definite increase of aCL-IgG isotype was found in 41 patients (9.35%) and four controls (4.0%). The relative risk was 2.52. The frequency of increased aCL-IgG was 12.2%, 12.8%, 8.8%, 3.9%, and 3.5% in patients with large-artery atherosclerotic disease, stroke of unknown etiology, small-artery occlusive disease, cardioembolism, and stroke of other known etiology, respectively. Only patients with large-artery atherosclerotic disease (p<0.025) and stroke of unknown etiology (p<0.05) had higher frequencies of increased aCL than those in control subjects. The frequencies of abnormal results of activated partial thromboplastin time, antinuclear factor, Coombs' test, and venereal disease research laboratory were 2.84%, 1.22%, 1.02%, and 1.34% in these 41 patients, respectively. Accordingly, aCL-IgG selectively increases in patients with large-artery atherosclerosis and stroke of unknown etiology, reflecting selective activation of humoral immunity for aCL in the pathogenesis of cerebral ischemia.