Geum-Jin Yoon

White Matter Hyperintensity as a Factor Associated with Delayed Mood Disorders in Patients with Acute Ischemic Stroke

Background: Mood disorder is a frequent complication of stroke. Comorbid depressive and anxiety disorders are very common, indicating that it is advisable to assess both disorders at the same time. The aim of the present study was to examine the prevalence of post-stroke depression (PSD) and poststroke anxiety (PSA) at baseline and to evaluate factors related to delayed PSD and PSA at 3 months after stroke onset. Methods: This was a prospectively registered and retrospectively analyzed study of patients with acute ischemic stroke between January 2009 and March 2010. Patients included in this study were interviewed in order to evaluate their Hospital Anxiety and Depression Scale (HADS) scores. In this study, each depression and anxiety score was dichotomized into ‘nondepressive and nonanxious’ (HADS-D and HADS-A ≤7) and ‘depressive and anxious’ (HADS-D and HADS-A >7). Multiple logistic regression analysis was used to evaluate the independent factors of depressive and anxious symptoms 3 months after stroke onset. Results: Of the 133 patients, 47.4% were ‘depressive’ and 56.4% were ‘anxious’ at baseline. The depressive and anxious groups had a significantly higher frequency of severe white matter hyperintensity (WMH) than the nondepressive and nonanxious groups (p < 0.05). The independent factors of PSD and PSA at 3 months were deep white matter hyperintensities (DWMH) and modified Rankin scale 0 to 1 at 3 months. Conclusion: In conclusions, the results of our study demonstrated that delayed depression and anxiety after ischemic stroke were related to the severity of DWMH and unfavorable outcomes at 3 months, regardless of anti-anxiety treatment. Our results suggested that WMH might be associated with pathomechanism of delayed depression and anxiety.

Adenosine deaminase activity in cerebrospinal fluid and serum for the diagnosis of tuberculous meningitis.

OBJECTIVE To evaluate the usefulness of serum and CSF adenosine deaminase (ADA) activity for the diagnosis of tuberculous meningitis (TBM) from other meningitis. METHODS We studied CSF and serum ADA activity for 83 cases of TBM, 148 of bacterial meningitis (BM), and 262 of viral or aseptic meningitis. RESULTS The mean ADA activities (IU/L) in CSF and serum were higher in TBM (11.80 ± 2.50, 30.28 ± 7.30) than in other types of meningitis (8.52 ± 3.60, 17.90 ± 9.20 in BM; 5.26 ± 1.90, 8.56 ± 5.9 in viral or aseptic meningitis). When we accepted a serum ADA activity cut-off value of 15 IU/L for the differential diagnosis of TBM and non-TBM with ROC analysis, the sensitivity was 84% and specificity was 82%. Combining CSF (≥ 10) and serum (≥ 15) ADA activity significantly increased overall specificity from 92% to 97% for the diagnosis of TBM. CONCLUSIONS The determination of CSF and serum ADA activity is a simple and reliable test for differentiating TBM from other types of meningitis.

Right-to-left shunts as a cause of juxtacortical spots in patients with migraine.

Backgrounds:  Juxtacortical spots on fluid‐attenuated inversion recovery (FLAIR) images can be frequently detected in patients with migraine. However, the origins of the cerebral lesions (including juxtacortical spots on FLAIR images) found in the previous studies are not known. We sought to investigate the association between juxtacortical spots on FLAIR images and right‐to‐left shunt (RLS) in migraine patients.

Internal border zone lesions as a predictor of early neurological deterioration in minor stroke patients with severe arterial steno-occlusion.

Background: Early neurological deterioration (END) of acute ischemic stroke may be important because it can predict clinical outcomes. We described several cases with similar clinical findings but different outcomes and analyzed the characteristics of their imaging studies. We retrospectively analyzed minor stroke patients with severe arterial stenosis within 6 hours of stroke onset. We defined END as 4 or more deterioration of the National Institutes of Health Stroke Scale score. Diffusion‐weighted imaging (DWI) lesions were classified as lesions of the pial artery (PI), perforating artery (PAI) and border‐zone (BZ). Results: We consecutively analyzed a total of 12 subjects in this study. The patterns of initial DWI lesions were internal BZ (50%), PI (50%), PAI (25%), and cortical BZ (16.7%). Among them, the number of subjects with END was 5, and the frequency of internal BZ on initial DWI was significantly higher in patients with END than in those without. Conclusions: In conclusion, the results of this study suggest that when internal BZ infarcts are detected in patients with acute minor strokes accompanied by severe arterial stenosis, close observation and careful management should be performed because END can be induced at an early stage.

Lesion Patterns of Small Deep Infarcts Have Different Clinical and Imaging Characteristics

Background: The mechanisms underlying small deep infarcts in the subcortical area are unknown. This study used coronal diffusion-weighted imaging (DWI) to investigate clinical and radiological findings in patients with small deep infarcts. Methods: This was a retrospective study of consecutively admitted patients with small deep infarcts in the subcortical area. We divided the patients into two groups as follows: (1) those with isolated lesion (IL) defined as an IL in the parenchyma by coronal DWI (group A), and (2) those with linear lesion (LL), defined as a LL extending to the basal surface on coronal DWI (group B). Results: A total of 86 patients were included in this study, with 43 patients in each group. Neurological decline and ipsilateral MCA stenosis were observed more frequently in group B than in group A. Fluid-attenuated inversion recovery (FLAIR) signals showed that white-matter hyperintensity was more severe in group A than in group B (p = 0.015). Conclusions: This study suggests that LL patterns of small deep infarcts may result in a higher rate of neurological decline and ipsilateral MCA stenosis than IL patterns.

Myasthenia Gravis Aggravated by Steroid-Induced Isolated Mediastinal Tuberculous Lymphadenitis

Background Myasthenia gravis (MG) is occasionally aggravated by chronic infection, of which there are many kinds. Case Report We report herein the case of a 56-year-old woman with MG aggravated by the activation of isolated mediastinal tuberculous lymphadenitis (MTL) during corticosteroid administration. The possibility of MTL had been disregarded in the differential diagnosis of aggravation of MG weakness, because MTL without pulmonary manifestations is uncommon even in areas where tuberculosis is endemic. Conclusions This case suggests that chronic infections such as tuberculosis should be considered in myasthenic patients with progressive exacerbation if definite evidence for aggravating factors of MG is not obtained.

Cluster-like Headache Secondary to Focal Cervical Myelitis

Background: Cluster headache (CH) is characterized by attacks of severe periorbital pain associated with autonomic symptoms. As with other forms of primary headache, structural lesions should be excluded, particularly if the headache presents with an atypical pattern. Case: We report a 41-year-old woman who had no previous history of primary headache and showed a poor response to medication for CH. The patient was finally diagnosed as secondary headache with CH feature due to focal myelitis at the cervical level of the spinal cord. A strong positive Enzyme-linked Immunosorbent Assay test for Toxocara canis antibodies helped us to make a diagnosis of cervical Toxocara myelitis. After starting treatment with intravenous methylprednisolone and albendazole, her headache gradually improved with abortive and preventive treatment for CH. Conclusions: We suggest that neuroimaging of the upper cervical cord as well as the brain is important when CH is showing an atypical clinical course. Cervical Toxocara myelitis might be a possible cause of secondary headache with CH feature.

The Paroxysmal Disorders

dedicated section), or drop attacks. In addition, despite the ‘updating’ intents, the texts appear at least in part relatively dated. For instance, there is no mention throughout the book about the link between paroxysmal exercise-induced dystonia, glucose transporter (GLUT1) deficiency, and epilepsy (which is known at least since 2008), and the therapeutic role of ketogenic diet. The section on epilepsy treatment does not mention medications marketed since 2006, but reports compounds that are nearly almost forgotten (as tiagabine). Furthermore, one would have expected more emphasis on conditions such as vestibular neuritis, epileptic amnesia, semiology of visual illusions/hallucinations (e.g. the role of color in the differential diagnosis between epileptic and migraine auras, or the superposition on the background for peduncular hallucinosis) and of paresis (e.g. no detailed description of the Hoover sign is found), or epilepsy-induced syncope, which may at times challenge the emergency physician/neurologist. Despite these drawbacks, several book parts are very well written and useful for the clinician, like the headache, the ENT (vertigo), sections of the ophtalmological, and the PNES chapters, while other encompass some details (e.g. epilepsy treatment, stroke diagnosis and treatment) that may go beyond the intent of the editors of this work. In conclusion, despite finding much interesting information, the reader may welcome a truly updated edition of this book, where a general diagnostic overview of paroxysmal conditions (e.g. as a table or flow chart) could also contribute to a more homogeneous and synthetic result, and to an additional usefulness for the clinician. Dr. Andrea O. Rossetti, Lausanne, Switzerland Bettina Schmitz, Barbara Tettenborn, Donald L. Schomer (eds.)