BACKGROUND: Atrial fibrillation (AF), commonly considered as a cardiac embolic source, can itself be induced by stroke. We therefore tried to find and analyze this 'stroke-induced' AF. METHODS: From the Inha University Stroke Registry of the past 2 years, 143 middle cerebral artery (MCA) territorial infarct patients who had been admitted within 48 hours after stroke onset were recruited to participate in the study. Electrocardiograms (EKG) on admission and follow-up during hospitalization were analyzed. Also, MCA infarct was subdivided according to insular involvement by brain imaging. RESULTS: Among 143 MCA territorial infarcts, 38 patients had AF on admission (Rt:21; Lt:17). Of those, insular involvements of the MCA infarct was noted in 32 patients. All the patients had a follow-up EKG and AF disappeared in 3 patients (Rt:2; Lt:1). In the remaining 105 patients, 10 patients subsequently developed new AF within 1 week after hospitalization. All those 10 patients had right-sided MCA infarcts and insular involvements were present in 9 patients. In summary, among the 48 MCA infarct associated with AF, 13 AF (Rt:12; Lt:1) were presumed to be the consequence and not the cause of stroke. CONCLUSIONS: Though human insular stimulation and inactivation studies have suggested that AF would be more common in left insular destructive lesions, it was not always supported in clinical series. From our study, presumed 'stroke-induced' AF was highly associated with right insular lesions. The mechanism of arrhythmogenesis by ischemic stroke might be more complicated than previously expected and, not merely the simple inactivation of an anatomical substrate, the insular cortex.
Atrial Fibrillation* ; Electrocardiography ; Follow-Up Studies ; Hospitalization ; Humans ; Middle Cerebral Artery* ; Neuroimaging ; Stroke

Transcranial direct current stimulation (tDCS) is non-invasive brain stimulation technique increasingly used for modulation of central nervous system excitability in humans. The use of non-invasive brain stimulation has significant advantages, such as not involving surgical procedures and having relatively mild adverse effects. In recent years there has been an exponential rise in the number of studies employing tDCS as a means of gaining an improvement on motor and cognitive function in patients with neurological diseases. In the present review, we will first introduce a brief background on the basic principles of tDCS. We also summarize recent studies with tDCS that aimed at enhancing behavioral outcome or disease-specific symptoms in patients suffering from stroke, movement disorders, Alzheimer disease, and epilepsy. Although outcomes of tDCS trials include some conflicting results, the evidence supports that tDCS might have a therapeutic value in different neurological conditions.
Alzheimer Disease ; Brain ; Central Nervous System ; Cognition ; Epilepsy ; Humans ; Movement Disorders ; Nervous System Diseases* ; Stroke ; Transcranial Direct Current Stimulation*

The recent identification of the transactive response DNA binding protein with a molecular weight of 43 kDa (TDP-43) as the major pathological protein, in both amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin positive inclusions (FTLD-U), provides the new insight into understanding disease processes. The pathogenesis of both diseases is unclear, although they are related by having some overlap of symptoms and now by the shared histopathology of TDP-43 deposition. The number of degenerative diseases associated with TDP-43 has increased, leading to the new designation "TDP-43 proteinopathy". TDP-43 is a highly conserved protein ubiquitously expressed in many tissues including the central nervous system where it is present in neuronal and glial nuclei and to a lesser extent in the cytoplasm. Currently, TDP-43 has been implicated in regulating gene transcription and alternative splicing, in addition to maintaining mRNA stability. However, we still need to investigate the effects of posttranslational modifications of TDP-43, including phosphorylation, ubiquitination, and cleavage, on its regulation of various cellular processes. We review recently published studies of TDP-43 and its relationship to human disease with a special focus on ALS and FTLD-U. We conclude that the TDP-43 proteinopathies represent a novel class of neurodegenerative disorders and both ALS and FTLD-U are closely related conditions linked to similar mechanism of neurodegeneration.
Alternative Splicing ; Amyotrophic Lateral Sclerosis ; Central Nervous System ; Cytoplasm ; DNA ; DNA-Binding Proteins ; Frontotemporal Dementia ; Frontotemporal Lobar Degeneration ; Humans ; Molecular Weight ; Neurodegenerative Diseases ; Neurons ; Phosphorylation ; Protein Processing, Post-Translational ; RNA Stability ; TDP-43 Proteinopathies ; Ubiquitin ; Ubiquitination

A 26-year-old woman presented with skin pigmentation and numbness on the upper arm. More than six café au lait spots over 15 mm diameter could be seen throughout her skin. Neurofibromatosis (NF) type 1 was diagnosed based on genetic study. The brain magnetic resonance imaging (MRI) showed Chiari type 1 malformation and syringomyelia was noted in the C2 to T7 level in the spinal MRI. We suggest Chiari malformation and syringomyelia could be a rare manifestation in a patient with NF type 1.

Antibodies to myelin oligodendrocyte glycoprotein (MOG) are associated with central nervous system demyelination inclusive of optic neuritis and transverse myelitis. MOG antibody may rarely be associated with peripheral nervous system involvement. A 48-year-old woman presented with demyelinating polyneuropathy. She previously suffered from myelitis and optic neuritis and had diagnosed with MOG antibody-associated disease (MOGAD). Polyneuropathies, combined central and inflammatory neuropathies may be associated with MOGAD and may be immunotherapy responsive. Further studies were needed to elucidate the utility of MOG antibody testing in polyneuropathy.

Antibodies to myelin oligodendrocyte glycoprotein (MOG) are associated with central nervous system demyelination inclusive of optic neuritis and transverse myelitis. MOG antibody may rarely be associated with peripheral nervous system involvement. A 48-year-old woman presented with demyelinating polyneuropathy. She previously suffered from myelitis and optic neuritis and had diagnosed with MOG antibody-associated disease (MOGAD). Polyneuropathies, combined central and inflammatory neuropathies may be associated with MOGAD and may be immunotherapy responsive. Further studies were needed to elucidate the utility of MOG antibody testing in polyneuropathy.

Antibodies to myelin oligodendrocyte glycoprotein (MOG) are associated with central nervous system demyelination inclusive of optic neuritis and transverse myelitis. MOG antibody may rarely be associated with peripheral nervous system involvement. A 48-year-old woman presented with demyelinating polyneuropathy. She previously suffered from myelitis and optic neuritis and had diagnosed with MOG antibody-associated disease (MOGAD). Polyneuropathies, combined central and inflammatory neuropathies may be associated with MOGAD and may be immunotherapy responsive. Further studies were needed to elucidate the utility of MOG antibody testing in polyneuropathy.

Pancreatic encephalopathy is a rare complication of acute pancreatitis. We report a 80-year-old woman who, after an acute episode of pancreatitis, developed a fluctuating confusion and clouded consciousness. She experienced two relapses with alternating encephalopathic features. Serum amylase was highly increased and symptoms were relieved in accord with normalized amylase value. We suggest that this encephalopathic features may be related with pancreatitis.
Aged, 80 and over ; Amylases ; Consciousness ; Female ; Humans ; Pancreatitis* ; Recurrence

There is an increasing number of reports that the lesion site in isolated cranial neuropathies may be the brainstem. The authors describe a diabetic patient with peripheral type facial palsy and concurrent trochlear palsy. Magnetic resonance imaging showed only a small pontine infarction responsible for the facial palsy. Multiple cranial nerve palsies seen in this patient might be a manifestation of multiple acute small infarcts involving both the brainstem and its cranial nerve root simultaneously.
Brain Stem ; Brain Stem Infarctions ; Cranial Nerve Diseases ; Cranial Nerves ; Diabetes Mellitus* ; Facial Paralysis ; Humans ; Infarction ; Magnetic Resonance Imaging ; Paralysis ; Trochlear Nerve Diseases* ; Trochlear Nerve*

Hypertensive encephalopathy is a medical emergency whose clinical manifestations are usually associated with bilateral parieto-occipital lesions. Predominant brainstem edema without accompanying occipital lesions is rare in hypertensive encephalopathy and usually occurs in patients with secondary hypertension. We describe the clinical and radiological features of two patients with reversible hypertensive brainstem encephalopathy. Both patients had chronic renal failure, but the extensive neuroimaging abnormalities revealed few clinical features of brainstem involvement. The clinical findings and neuroimaging abnormalities resolved once the hypertension was treated.
Brain Stem* ; Edema ; Emergencies ; Humans ; Hypertension ; Hypertensive Encephalopathy* ; Kidney Failure, Chronic ; Neuroimaging