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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.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 wasor = 12 microM/L whereas group II12 microM/L.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 (p0.01). Serum creatinine level correlated directly to and was an independent predictor for the plasma homocysteine level.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.

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).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 p0.0001). However, CD62p expression declined to a significantly lower level on day 7 and to a substantially lower level thereafter (p0.0001). CD62p expression did not differ on day 90 in the 3 groups (both p0.5). Linear regression analysis showed that BIV and modified Rankin scale score (3) were independently associated with increased CD62p expression (48 h) (both p0.01). 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.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.

3-Nitropropionic acid (3-NP), a mitochondrial toxin, impairs cellular energy generation by inhibiting succinate dehydrogenase. The basis of its neurotoxicity is oxidative stress in the wake of cellular energy failure. alpha-Phenyl-tert-butyl-nitrone (PBN), a spin-trapping agent with free radical-scavenging capability, has shown protective effects in various models of experimental brain insults. The effect of PBN on the 3-NP neurotoxicity paradigm was evaluated in this study.Two groups of adult male mice receiving daily systemic 3-NP administration were pretreated with PBN or normal saline respectively for 5 days. After the treatment course, motor dysfunction and the volume of cerebral lesions were quantitatively evaluated. Cellular apoptosis and expressions of glial fibrillary acidic protein (GFAP) and cyclooxygenase-2 (COX-2) in the brain were compared between the 2 groups.All mice treated with normal saline and 3-NP survived but developed mild motor dysfunction. Apoptosis of striatal cells was noted in the absence of destructive cerebral lesions. In contrast, combined treatment with PBN and 3-NP resulted in more severe motor dysfunction and higher mortality in experimental animals. Destructive lesions with cellular necrosis, and enhanced expressions of GFAP and COX-2 were noted in the striatum.3-NP neurotoxicity was paradoxically accentuated by the combined treatment with PBN and 3-NP. Metabolic clearance of 3-NP is probably impaired by PBN and the increased oxidative stress caused by higher 3-NP levels may exceed the free radical-scavenging ability of PBN. The shift from apoptotic to necrotic changes with increased 3-NP toxicity is in accord with the theory that cellular energy reserves determine the pattern of cellular death.

Catatonia as a clozapine withdrawal syndrome has not been well documented. There is only 1 case of excited catatonia described with the diagnosis made according to strict criteria. The authors report a patient who developed a catatonic stuporous state following abrupt discontinuation of clozapine, associated with features of cholinergic and serotonergic hyperactivity. The catatonic state resolved within 1 week with reinstatement of clozapine. It is suggested that serotonergic hyperactivity was involved, contributed by cholinergic rebound, in the pathogenesis of this patient's clozapine withdrawal catatonic syndrome.

Summary: Purpose: Reversible cerebral vasoconstriction has been hypothesized to be the etiology of seizures due to hypercalcemia, but angiographic studies documenting vasoconstriction have not previously been available. Methods: We present a 43-year-old woman who had frequent seizures that later evolved to status epilepticus with marked hypercalcemia at the time of the seizures. Results: Magnetic resonance imaging (MRI) of the patient's brain revealed high signal changes in T2-weighted imaging, fluorescence-attenuated inversion recovery (FLAIR), and diffusion-weighted imaging (DWI) over the bilateral occipital and thalamic areas. Cerebral angiography showed blood vessels narrowing, disappearing altogether over the right posterior cerebral artery (PCA) branch, which is compatible with vasoconstriction. Vasoconstriction caused the MRI high signal in the occipital area, which was associated with subsequent periodic lateralized epileptic discharges. The patient's clinical condition improved with management of seizures and hypercalcemia. A second brain MRI 2 weeks later revealed complete resolution of the high-signal lesions. Follow-up cerebral angiography study also showed total recovery of vasoconstriction. Conclusions: The sequence of events suggests the hypothesis that reversible cerebral vasoconstriction may play a role in hypercalcemia-induced seizures.

Hypertension is known as a cause of endothelial cell damage and it activates humoral immunity. Therefore, it may modulate the anti-beta2-glycoprotein I antibody (abetaGPI) to commit for thrombosis. To elucidate the relation between abetaGPI and hypertension in cerebral ischemia, the blood abetaGPI level was examined in healthy subjects, hypertensive subjects, and patients with cerebral ischemia with and without hypertension, respectively. The results showed that the blood abetaGPI level increased in cerebral ischemia patients with hypertension rather than hypertensive subjects, and patients without hypertension rather than healthy individuals. However, the blood abetaGPI level showed no difference between healthy individuals and hypertensive subjects, nor cerebral ischemia patients with and without hypertension. The serum globulin level did not change among them. Therefore, abetaGPI displays a vital role for cerebral ischemia in both hypertensive and normotensive subjects. An activation of humoral immunity involving abetaGPI warrants further investigation in cerebral ischemia.

Chondrosarcoma is a malignant disease of cartilage. Systemic embolisation usually arises from cancerous invasion of pulmonary vessels or the left atrium but cerebral embolisation or ischaemia is rarely recognised. We report a man with left leg amputation for tibial myxoid chondrosarcoma who suffered multiple cerebral embolisms one year later. Cerebral angiography and aortogram did not reveal luminal stenosis and a cardiac survey was normal. Lupus anticoagulant (LAC) and a prolonged activated partial thromboplastin time were detected. A molecular mimicry between prothrombin and paracrine hormones may have accounted for his LAC. A procoagulant autoantibody reacting against metastatic cancer cells may contribute to cancerous thrombosis, such as in chondrosarcoma.

Protein C (PC), protein S (PS), and antithrombin III (AT-III) are vital thrombin antagonists in circulation. However, the prevalence of these natural inhibitors for cerebral ischemia is barely mentioned in the Chinese population. The prevalence of PC, PS, and AT-III deficiency in Chinese adults with cerebral ischemia is reported. The study subjects were free of antiphospholipid antibody syndrome or systemic lupus erythrematosus. Cardiac, liver, and renal function were normal. An overall rate of thrombophilia was 27%. PS deficiency was the most common disorder, followed by PC with PS and PC deficiency. There was only one patient with AT-Ill deficiency. No gender was specific for thrombophilia. However, PS deficiency was predilected in young adults. A positive correlation between PC and AT-III was achieved in patients with a normal PC activity but not PC deficiency. There was no correlation between AT-III or PS. The odds ratios of PC and PS were 5.29 and 2.86, respectively. Accordingly, an inability for thrombin antagonization by the PC/PS axis may relate to the occurrence of cerebral ischemia in the Chinese population. AT-III seems to display a minor role only.

The parameters influencing the electrochromatographic separation of aliphatic organic acids in a capillary column with a wall-coated macrocyclic polyamine have been studied. Indirect detection using chromate, pyromellitate, trimellitate, o-phthalate, benzoate and acetate as background electrolytes has been tested. A complete separation of polyprotic acids could be achieved with pyromellitate buffer (7.5 mM, pH 6.5), and satisfactory results for the simultaneous separation of monoprotic acids and polyprotic acids were found using a capillary column of 70 cm (50 cm effective length)x75 microm inner diameter, electrokinetic injection (-10 kV, 10 s), benzoate buffer (6 mM, pH 4.6), separation voltage of -10 kV, and detection at 220 nm. For the separation of the geometric isomers fumarate and maleate, acetate buffer was found the best choice among the background electrolytes tested. The method so established has been applied to the determination of organic acids in soy sauce, brandy, lemon juice, spinach juice and cigarette. From the retention behavior, it was found that the separation mechanism on the bonded phase was influenced by the macrocyclic effect, electrostatic attraction, hydrogen bonding, van der Waals forces, and anion exchange, in addition to the differences in electrophoretic mobility.

Anti-beta -glycoprotein I antibody (abetaGPI) has been recognized in raising the risk of cerebral ischemia in patients with antiphospholipid antibody syndrome (APS), especially by protein C (PC) axis perturbation. Although a high potential is also seen in non-APS patients, the mechanism is substantially unknown. In the present study, we examined the effect of abetaGPI on PC and antithrombin-III (AT-III) activity in non-APS patients with non-cardiac cerebral ischemia (NCCI). A total of 111 NCCI patients and 30 healthy controls were enrolled. They were free of APS manifestation, and their anticardiolipin antibody and lupus anticoagulant tests were within normal range. There were 14.4% patients found to have an abnormal increase of blood abetaGPI. The PC, AT-III, albumin, aminotransferases, creatinine, prothrombin time and activated partial thromboplastin time did not differ between our patients and controls, or patients with or without increased abetaGPI. However, a marked decrease of the PC/AT-III ratio was found in patients with increased abetaGPI. The correlation between PC and AT-III activity was highly significant in patients with an increase of abetaGPI (P = 0.001), only marginal in controls (P = 0.042), and was insignificant in patients with a normal abetaGPI (P = 0.277). The abetaGPI did not correlate to PC or AT-III activity in either patients or controls. These findings suggest that high PC/AT-III coupling may relate to NCCI in non-APS patients associated with an increase of abetaGPI. This coupling effect seems not to be caused by abetaGPI directly.

Reflex sympathetic dystrophy is an excessive or abnormal response of the sympathetic nervous system in an extremity to an injury or other condition. The authors describe a 37-year-old man who experienced constant pain and vasomotor instability in both feet after nontraumatic rhabdomyolysis secondary to smoking heroin. Three-phase bone scintigraphy was performed and revealed significantly increased blood-flow, blood-pool, and delayed-phase radioactivity. The follow-up three-phase bone scinitigram showed less radiotracer uptake that was consistent with a good response to calcitonin therapy. Heroin-induced rhabdomyolysis should be added to the list of precipitating conditions that can induce this syndrome.

An abnormal increase in anti-beta2-glycoprotein I antibodies (aβ2GPI) is capable of producing thrombosis and the vasculopathy-simulating antiphospholipid antibody (aPL). However, it is rarely described in cerebral ischemia without an association with aPL. The authors report a middle-aged man who experienced recurrent cerebral ischemia and diffuse cerebral stenosis without the apparent traditional cardiovascular risk factor. He was free of antiphos pholipid/cofactor syndrome (APCS) and systemic lupus erythematosus (SLE). An increase of blood aβ2GPI was detected in serial measurements. The aPL, Venereal Disease Research Laboratory (VDRL) test, Coombs' test, and antinuclear factor were negative. Activated partial thromboplastin time was normal. This patient is a reminder to consider aβ2GPI in an unex plained recurrent cerebral thrombosis and cerebral artery stenosis even when the typical clinical manifestation or laboratory data of APCS is absent.

Delayed and remote effect of focal cerebral cortical lesion on cerebellum remains unclear. The c-Jun, an inducible transcription factor of cellular immediate early gene, is the predominant transcription factor and consistent marker for neurons that respond to stress or injury. We use a mouse cryogenic injury model to study the spatial and temporal changes of c-jun in the cerebellum after focal neocortical lesion. A transient and moderate expression of c-jun mRNA was found in the cerebellum with central dominance since 3 day postinjury and gradually subsided within 2 weeks. A distinct increment of c-Jun protein expression in Purkinje cells of the bilateral cerebellar hemispheres with focal connotation in the vermis was detected since 1 week postinjury. These findings suggest that the delayed and remote c-jun expression of the cerebellum, functionally connected with the cerebral cortex, indicate transneuronal gene activation.

The use of a macrocyclic polyamine, 28[ane]-N 6 O 2 , as a selective modifier in a bonded-phase capillary column for the electrophoretic separation of 14 aromatic acids is described. Parameters that affect the performance of the separations, such as the type of buffer, the pH and concentration of buffer, the applied potential and the injection mode were studied. By changing the buffer pH (4.0–5.0), buffer concentration (10–50 m M ) and applied potential (−10∼−20 kV), optimum conditions were obtained at −20 kV, using an acetate buffer (20 m M , pH 4.5), hydrodynamic injection with a vacuum at the buffer reservoir on the detector side and detection at 220 nm. The results showed that the separation was effective under these conditions. The plate number was greater than 4·10 4 m −1 . Due to the wide variation in the mobilities of the test compounds, injection studies suggested that a vacuum at the buffer reservoir on the detector side would produce a result that is more representative of the initial sample composition. Benzoic acid in soy sauce, salicylic acid in Salic ointment and Aspirin were sampled and analyzed using the established conditions.

Nummular headache (NH) is a newly categorized headache disorder characterized by a consistent clinicographics in each attack. Currently, it is considered as a primary headache disorder due to epicranial neuralgia but the pathomechanism is still unknown. We report a woman, whose recurrent NH subsided after trans-sphenoidal surgery for her pituitary oncocytoma. The recovery of NH in this patient encourages the central mechanism for NH occurrence. After a review of literature concerning, NH and intracranial secondaries we propose that central NH is a referral pain from pain-sensitive structures, such as meninges, superimposing by pre-existing lower pain threshold or pain modulation.

Typical bilateral cheiro-oral syndrome was encountered in a 74-year-old man who had bilateral subdural hematoma after a minor head injury. The delayed grave neurologic deficits occurred 1 month later without expansion of the hematoma. Removal of the lesions reversed both cheiro-oral syndrome and his late-onset neurological disabilities.

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.

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.

Cortical lesion might elicit restricted acral sensory deficit but a disparity of topographies in cheiro-oral-pedal syndrome is very rare. We report the first case of cheiro-oral-pedal syndrome due to a contralateral parasagittal hemangioma involving the supplement sensory area in parietal lobe. This unusual link between neuroanatomy and neurological feature is discussed.

Two patients sought treatment for bilateral fatigable ptosis; one patient had a hematoma, and the other patient had an intracranial metastasis. Compression of the central caudal nucleus in the dorsal midbrain is proposed as the cause of this ptosis, and an alteration of central acetylcholine neurotransmission may contribute to ocular fatigability. Because symptoms that suggest fatigable ptosis can be similar to those that suggest ocular myasthenia gravis, a careful evaluation is necessary to avoid misinterpretation.