Chun-An Cheng

Increased Risk of Cerebral Hemorrhage in Chinese Male Heavy Drinkers with Mild Liver Disorder

Background: Epidemiological evidence suggests that heavy alcohol consumption increases the risk for either stroke or liver disease. The goal of this study was to determine whether heavy drinkers with mild liver disorder (MLD) are at risk of hemorrhagic stroke. Methods:All of the 524 patients recruited were males with a first-ever acute stroke and were consecutively admitted to the Tri-Service General Hospital between January 2000 and December 2001. The risk factors, liver function, stroke subtypes, and hemostatic factors were assessed among 68 patients defined as heavy drinker stroke (HDS) and 456 patients as nonheavy drinker stroke (NHDS). Results: HDS patients had a significantly higher incidence of hemorrhagic stroke than NHDS patients. HDS patients were also associated with significantly higher occurrence of cigarette smoking, hyperuricemia, liver dysfunction, and significantly lower platelet counts. HDS patients with MLD were more likely to have hemorrhagic stroke (76.5%) than HDS patients without MLD (33.3%) and NHDS patients with (40.3%) or without (26.7%) MLD. HDS patients with MLD also exhibited a significantly higher glutamic oxaloacetic transaminase/glutamic pyruvic transaminase ratio (2.0 ± 1.2) and lower platelet number (185,000 ± 85,000 per µl) when compared with HDS patients without MLD (1.4 ± 0.5; 206,000 ± 59,000 per µl) and NHDS patients with (1.1 ± 1.0; 256,000 ± 97,000 per µl) or without (1.4 ± 0.7; 216,000 ± 68,000 per µl) MLD. Conclusions: HDS patients with MLD are at higher risk for hemorrhagic stroke in part due to the changes in hemostatic factors, although other factors may also contribute to hemorrhagic stroke.

99mTc-TRODAT-1 and 123I-IBZM SPECT studies in a patient with extrapontine myelinolysis with parkinsonian features

Osmotic demyelination syndrome can result from the rapid correction of hyponatremia, and is categorized by central pontine myelinolysis and extrapontine myelinolysis (EPM). Magnetic resonance imaging (MRI) is currently the most useful modality for visualizing EPM lesions. However, MRI is unable to delineate the severity of involvement in the nigrostriatal dopaminergic pathway. The authors describe the case of a 48-year-old woman who developed isolated EPM with predominantly right-sided parkinsonian symptoms after rapid correction of hyponatremia. MRI revealed symmetrical demyelinating lesions in the bilateral striatum without central pontine involvement. 99mTc-TRODAT-1 and 123I-iodobenzamide (123I-IBZM) single-photon emission computed tomography (SPECT) images showed unequally decreased uptake in the bilateral striatum. Treatment with carbidopa/levodopa improved the clinical parkinsonian symptoms. 99mTC-TRODAT-1 and 123I-IBZM SPECT images provide presynaptic and postsynaptic molecular information of the nigrostriatal dopaminergic pathway. The lesions demonstrated in the 99mTC-TRODAT-1 and 123I-IBZM SPECT images show higher correlation with the severity of clinical features in EPM than MRI, and the modalities may be useful in the evaluation of patients with parkinsonian symptoms.

Homocysteine induces cerebral endothelial cell death by activating the acid sphingomyelinase ceramide pathway.

Homocysteine (Hcy) levels may rise after a stroke, but the mechanism of Hcy-induced cerebral endothelial cell (CEC) dysfunction has not been explored. In this study we examined the role of the acid sphingomyelinase (Asm)-ceramide pathway in the molecular mechanism of Hcy-induced CEC dysfunction. Murine CECs were prepared from fresh mouse brains. CECs were treated with 50-500 μM Hcy and 30-100 μM C2-ceramide for 48 h. Sphingomyelinase assays were performed to determine Asm activity. Quantitative assessments of cell survival and death by the MTT reduction and LDH release were conducted. Treatment of murine CECs with Hcy and ceramide caused cell death in a dose-dependent manner as determined by LDH and MTT assays. 250 μM Hcy and 50 μM C2-ceramide caused 50% cell death. Hcy induced murine CEC death also occurred in a time-dependant manner with substantial cell death noted as early as 24h after Hcy exposure. C2-ceramide-induced murine CEC death occurred earlier than Hcy-induced cell death by about 18h. Hcy treatment increased Asm activity and intracellular ceramide accumulation. This study demonstrated that Hcy and C2-ceramide can cause murine CEC death. Hcy induces CEC death possibly by activating the Asm-ceramide pathway.

99mTc-TRODAT-1 SPECT as a Potential Neuroimaging Biomarker in Patients With Restless Legs Syndrome.

Background Restless legs syndrome (RLS) is a neurological sensory motor disorder of which pathophysiology remains sketchy. The present study was aimed to determine the diagnostic accuracy and potential of SPECT-TRODAT imaging in discriminating patients with RLS from normal individuals. Patients and Methods A total of 34 subjects, 22 diagnosed with RLS and 12 classified as normal, were enrolled. Brain SPECT images were acquired 180 minutes after IV injection of 740 to 925 MBq (20–25 mCi) 99mTc-TRODAT-1 using a double-headed &ggr;-camera equipped with high-resolution fan-beam collimators. Regions of interest were drawn over the whole striatum, caudate, and putamen nucleus of each hemisphere on composite images of the 9 slices with the highest basal ganglia activity. The brain SPECT 99mTc-TRODAT-1 imaging was compared with early-stage RLS patients and healthy volunteers groups. Result SPECT imaging in RLS patients showed reduced radioactivity accumulation in the striatum profile. The major abnormal result observed is the significantly reduced uptake in striatal dopamine transporter density and activity. The symmetric striatal uptake was observed, and striatum dopamine transporter destiny was more impaired in patients with RLS disease. SPECT images also showed significant differences between patients and volunteers. Conclusions This study supports that symptoms of restless legs resulted from the striatum of the brain dopaminergic system dysfunction.

Acute bilateral hearing loss as a “worsening sign” in a patient with critical basilar artery stenosis

We report a patient who presented with an acute-onset transient vertigo and unsteady gait with bilateral hearing loss. Brain MRI revealed a critical basilar artery (BA) stenosis at the lower pons and infarction in various areas on both sides in the territories of the posterior inferior cerebellar arteries (PICA). Further, we could not visualize the right anterior inferior cerebellar artery (AICA). The bilateral hearing loss may be ascribed to stroke due to the critical BA stenosis, causing hypoperfusion injury extending from the PICA to the AICA on both sides. Local intra-arterial thrombolytic therapy with the administration of 1×10(6) IU of urokinase aided partial recanalization of the BA, after which the right AICA reappeared. The neurological function of the patient recovered to normal, and no hemorrhagic complications were observed. Therefore, practitioners should be alert when treating patients with acute bilateral hearing loss, which may be related to an underlying catastrophic stroke.

An unusual manifestation of systemic lupus erythematosus: hypokalaemic paralysis

Correspondence to: Shankar Raman, MRCS, Department of Surgery, Kent and Canterbury Hospital, Canterbury CT1 3NG, UK Email: shankar.raman@doctors.net.uk References 1 Maounis N, Ellina E, Papadaki T et al. Bilateral primary lymphoma of the breast: a case report initially diagnosed by FNAC. Diagn Cytopathol 2005; 32: 114–8. 2 Pruthi S, Stafyla VK, Phillips SW et al. Primary mammary (non-Hodgkin) lymphoma presenting as locally advanced breast cancer. Mayo Clin Proc 2004; 79: 1310–4. 3 Jackson FI, Lalani ZH. Breast lymphoma: radiologic imaging and clinical appearances. Can Assoc Radiol J 1991; 42: 48–54. 4 Wiseman C, Liao KT. Primary lymphoma of the breast. Cancer 1972; 29: 1705–12. 5 Akbari CM, Welch JP, Pastuszak W. Primary lymphoproliferative disorders of the breast. Conn Med 1995; 59: 651–5. 6 Wahner-Roedler DL, Petersen IA. Risk of breast cancer and breast cancer characteristics in women after treatment for Hodgkin lymphoma. Drugs Today (Barc) 2004; 40: 865–79.

Open-labelled observations of language dysfunction in old ischemic stroke patients with aphasia when given plant and marine-based nutrient supplements for 12 weeks

BACKGROUND AND OBJECTIVES This study aimed to explore the effect of functional foods on aphasia related to a previous ischemic stroke. When stroke-related neurological deficits result in physical dependency and poor selfcare that persists longer than 6 months, full recovery is almost impossible and the patient often requires long-term care. The functional foods, EASE123 and BioBalance#6, include numerous plant and marine-based nutrient supplements that could prove beneficial for such patients. METHODS AND STUDY DESIGN This open-labelled study included 10 patients diagnosed with prior ischemic stroke and aphasia lasting longer than 6 months. Each patient was administered 6 tablets of EASE123 at 10:30 AM and at 90 minutes before sleeping, and 3 tablets of BioBalance# 6 at 2:30 PM. After a treatment period of 12 weeks, the patients were followed during a 4-week withdrawal period. Functional improvement was assessed by scores and subscores on the Concise Chinese Aphasia Test (CCAT) at weeks 4, 8, 12, and 16. RESULTS Average total CCAT scores and matching ability improved significantly at weeks 4, 8, 12, and 16 (p<0.05). Simple response scores improved significantly at weeks 8 and 12 (p<0.05). Auditory comprehension improved significantly at weeks 4 and 12 (p<0.05), and reading comprehension, at week 12 (p<0.05). Repetition ability improved significantly at weeks 8, 12, and 16 (p<0.05), and spontaneous writing, at weeks 4, 12, and 16 (p<0.05). CONCLUSIONS Matching, repetition, and average total CCAT scores improved over the course of the study. Therefore, 6 months after ischemic stroke, EASE123 and BioBalance# 6 administration may improve stroke-related aphasia.

Modifications of Autonomic Activity and Baroreceptor Response on Posture Challenge in Patients with Vasovagal Syncope

Background: Vasovagal syncope (VVS) is diagnosed by medical history and confi rmed by a head-up tilt (HUT) test. The pathophysiology of VVS is controversial. Methods: In this study, we enrolled 30 VVS patients and compared normal study patients in Tri-Service General Hospital. We attempted to examine this controversy by evaluating heart rate variability and baroreceptor sensitivity of VVS in the upright posture. Results: The VVS patients had lower total peripheral vascular resistance, increased LF/HF (low frequency power / high frequency power) ratio, and decreased baroreceptor sensitivity in the HUT position. Conclusion: The VVS patients demonstrated postural vascular sympathetic dysfunction and cardiac sympathetic hyperactivity before syncope. The decreased baroreceptor sensitivity might be partly explained by the failure of the usual compensatory heart rate increase during orthostatic challenge.