Atorvastatin pretreatment attenuates kainic acid-induced hippocampal neuronal death via regulation of lipocalin-2-associated neuroinflammation

Statins mediate vascular protection and reduce the prevalence of cardiovascular diseases. Recent work indicates that statins have anticonvulsive effects in the brain; however, little is known about the precise mechanism for its protective effect in kainic acid (KA)-induced seizures. Here, we investigated the protective effects of atorvastatin pretreatment on KA-induced neuroinflammation and hippocampal cell death. Mice were treated via intragastric administration of atorvastatin for 7 days, injected with KA, and then sacrificed after 24 h. We observed that atorvastatin pretreatment reduced KA-induced seizure activity, hippocampal cell death, and neuroinflammation. Atorvastatin pretreatment also inhibited KA-induced lipocalin-2 expression in the hippocampus and attenuated KA-induced hippocampal cyclooxygenase-2 expression and glial activation. Moreover, AKT phosphorylation in KA-treated hippocampus was inhibited by atorvastatin pretreatment. These findings suggest that atorvastatin pretreatment may protect hippocampal neurons during seizures by controlling lipocalin-2-associated neuroinflammation.

Unilateral Hypoglossal Neuropathy in Multifocal Acquired Demyelinating Sensory and Motor Neuropathy: Differential Diagnosis of Motor Neuron Disease

Multifocal acquired demyelinating sensory and motor neuropathy (MADSAM) is a peripheral neuropathy characterized by multifocal weakness and associated sensory impairment. MADSAM is associated with multifocal persistent conduction block and other signs of demyelination. The incidence of cranial nerve involvement in MADSAM was recently reported to be approximately 15%. However, reports of hypoglossal neuropathy occurring in MADSAM are rare. Unilateral hypoglossal neuropathy in MADSAM is usually misdiagnosed as motor neuron disease. We report a patient with MADSAM presenting with tongue hemiatrophy.

Two Bleeding Foci in a Mixed Vascular Malformation of the Brain

A cavernous angioma (CA) and a developmental venous anomaly may consist a mixed vascular malformation (MVM). Two bleeding foci were observed in a MVM of a man with epilepsy. The hemodynamic association between the two foci was not clear. An advance of neuroimaging may enhance the susceptibility of detection of MVMs. We should consider a MVM when a daughter bleeding focus occurs near the main bleeding focus associated with a CA.

Primary Aldosteronism Presenting as Hypokalemia and Rhabdomyolysis / 대한임상신경생리학회지

Primary aldosteronism is one of the most common cause of secondary hypertension and can be accompanied with hypokalemia. Rhabdomyolysis with hypokalemia in primary aldosteronism has been rarely reported. We describe a patient of primary aldosteronism who presented with limb-girdle type weakness.

Seizure-induced Cerebral Edema Mimicking Multiple Cerebral Infarction

No abstract available.

Middle Cerebral Artery Territory Infarction Caused by Giant Middle Cerebral Artery Dissecting Aneurysm

Dissecting aneurysm of the intracranial arteries is a rare cause of stroke. This condition may induce both ischemic stroke and hemorrhagic stroke by occlusion of the parent artery via direct distortion and stretching, compression secondary to growth of the aneurism, and distal embolization of any intra-aneurysmal thrombi. A patient with an infarction in the right middle cerebral artery territory and a mass lesion located in the right basal ganglia and temporal lobe was examined in this study. The consequent workup suggested that the mass lesion was a huge dissecting aneurysm that had resulted in a cerebral infarction.

Middle Cerebral Artery Territory Infarction Caused by Giant Middle Cerebral Artery Dissecting Aneurysm

Dissecting aneurysm of the intracranial arteries is a rare cause of stroke. This condition may induce both ischemic stroke and hemorrhagic stroke by occlusion of the parent artery via direct distortion and stretching, compression secondary to growth of the aneurism, and distal embolization of any intra-aneurysmal thrombi. A patient with an infarction in the right middle cerebral artery territory and a mass lesion located in the right basal ganglia and temporal lobe was examined in this study. The consequent workup suggested that the mass lesion was a huge dissecting aneurysm that had resulted in a cerebral infarction.

Cerebral Infarction in a Patient with Suicidal Near Hanging

Hanging is one of the most common causes of suicidal death. Most hanging victims are dead when discovered, and hence there are few reports of near-hanging patients or survivors of a hanging injury. We experienced a patient with motor aphasia who survived a hanging injury. Consecutive workup revealed a cerebral infarction on the left middle cerebral artery territory, which was considered to be the cause of his aphasia.

Parry-Romberg Syndrome with Intermittent Exotropia

Parry-Romberg syndrome, or progressive facial hemiatrophy, is a rare and acquired neurocutaneous disease of unknown etiology that is classically characterized by progressive and self=limited atrophy of the skin, subcutaneous tissues, and underlying bone structures. Ophthalmic involvement is reportedly not uncommon, and the most common ocular finding is enophthalmos. Here we report a 46=year=old woman with Parry=Romberg syndrome who presented with intermittent exotropia of the right eye. To the best of our knowledge, this is the first description of intermittent exotropia in a patient with Parry-Romberg syndrome.

Overdrainage Syndrome: Fatal Complication of Ventriculoperitoneal Shunt

No abstract available.

Tumor of Meckel's Cave Presented With Recurrent Transient Monocular Blindness

No abstract available.

Guillain-Barre Syndrome With Treatment-Related Fluctuations

No abstract available.

A Case of Putaminal Hemorrhage from Arteriovenous Malformation / 대한뇌졸중학회지

The most common etiology of spontaneous, non-traumatic intracerebral hemorrhage is hypertension. One of the most decisive factors for the determination of etiology is location of the hemorrhage. Here, we report on a 53-year-old female patient who was admitted with left putaminal hemorrhage. She did not have prominent vascular risk factors other than fundoscopic signs of hypertensive retinopathy. Magnetic resonance imaging and angiography revealed arteriovenous malformation (AVM) in the basal ganglia, which was fed by the lateral lenticulostriate artery. This case suggests that we should consider an AVM-related hemorrhage in relatively young stroke patients, regardless of hematoma location or presence of accompanying hypertension.

Serial Magnetic Resonance Images of a Right Middle Cerebral Artery Infarction : Persistent Hyperintensity on Diffusion-Weighted MRI Over 8 Months

A lesion that is hyperintense on diffusion-weighted imaging (DWI) and hypointense on the apparent diffusion coefficient (ADC) map is a characteristic magnetic resonance imaging (MRI) finding in acute ischemic infarction. In some cases, however, these findings can persist for a few months after infarct onset. It is thought that these finding reflect the different evolution speeds of the infarcted tissue. We report a patient with a right middle cerebral artery territory infarction with persistent hyperintensity on DWI and hypointensity on the ADC map for over 8 months. To our knowledge, this is the most persistent case of hyperintensity lesion on DWI and the serial MRI images of this patient provide important information on the evolution of infarcted tissue.

Acute Non-Traumatic Cortical Subarachnoid Hemorrhage

Most nontraumatic subarachnoid hemorrhages are induced by the rupture of a saccular aneurysm. Acute nontraumatic cortical subarachnoid hemorrhage at the convexity of a cerebral hemisphere is a relatively rare occurrence with various vascular or nonvascular causes. Furthermore, the clinical manifestation of acute nontraumatic cortical subarachnoid hemorrhage differs from that of aneurysmal rupture. We experienced five cases of acute nontraumatic cortical subarachnoid hemorrhage with diverse neurological symptoms. Consecutive workup revealed the various etiologies of that hemorrhage.

Current-Source Dipole of Anterior Temporal Spikes: Clinical Significance of Orientation

BACKGROUND: The voltage topography of temporal spikes has two distinct patterns, designated type I and type II; the orientation of the current-dipole source (O-CDS) of type I spikes tends to be oblique, while that of type II spikes tends to be horizontal. The purpose of this study was to identify the effects of the O-CDS of anterior temporal spikes on clinical factors including onset age, seizure frequency, secondary generalization, disease duration, intractability, polytherapy, febrile seizure, hippocampal sclerosis, and neocortical-temporal aura. METHODS: We examined the scalp electroencephalograms of 24 patients with temporal lobe epilepsy (TLE) and anterior temporal spikes. A spatiotemporal dipole model was applied to determine the O-CDS of the averaged spikes in each patient. We performed current-source analysis of multiple spatiotemporal dipole models using Brain Electrical Source Analysis software. The patients were divided into two subgroups according to their O-CDS pattern: oblique and horizontal. Clinical factors were compared between the two groups. RESULTS: Sixteen patients were classified into the oblique group, and 8 patients into the horizontal group. A neocortical-temporal aura was more commonly observed in the horizontal group (p<0.05), while drug-resistance tendencies were more commonly observed in the oblique group (p<0.1). CONCLUSIONS: The horizontal O-CDS of anterior temporal spikes may be more frequently associated with a neocortical-temporal aura than the oblique O-CDS in TLE. In addition, the oblique O-CDS pattern suggests a tendency toward drug resistance. The findings of this study imply that the oblique O-CDS pattern of anterior temporal spikes may provide additional electrophysiologic information regarding drug-resistant mesial TLE.

Current Source Distribution of Periodic Lateralized Epileptiform Discharge: Comparison With Diffusion-Wighted MR Imaging in Viral Encephalitis

BACKGROUND: Periodic lateralized epileptiform discharges (PLEDs) are the main electroencephalograph (EEG) findings that imply the existence of acute or subacute structural lesions. The purpose of this study was to investigate the electrophysiologic characteristics of PLEDs by identifying the relationship between the current-source distribution (CSD) of PLEDs and the high signal intensity of diffusion-weighted magnetic resonance imaging (MRI; HSI-DWI) in viral encephalitis. METHODS: Six patients were enrolled. Twenty typical EEG, 1-s epochs, including the negative peak of the PLEDs, were averaged into an averaged-PLED (a-PLED). The CSD at the negative peak point of the a-PLED was located on the Talairach human brain map in each patient. The CSDs of the patients were compared with the anatomic locations of encephalitic lesions observed on diffusion-weighted MRI. RESULTS: In all patients, the locations with HSI-DWI were observed in the cortical areas. In two out of the six patients the locations of CSD and those of HSI-DWI were matched. In the other patients, they were partly matched. The matched areas were observed in the frontal, temporal, and parietal areas. The additional areas of CSD were in both insular areas, and those of HSI-DWI were in the frontal, temporal, parietal, and occipital areas. CONCLUSIONS: This study showed that the CSDs of PLEDs in viral encephalitis were mostly matched with the HSI-DWI in the cortical area of the frontal, temporal, and parietal areas. The cortical lesion itself in viral encephalitis may be part of the neural generator of PLEDs.

Basilar Artery Occlusion With Initial Manifestation as Convulsive-Like Movement

Brainstem infarction secondary to basilar artery occlusion often causes very-severe and life-threatening neurological conditions. For better recovery, early diagnosis is essential; however, this is not always easy because of ambiguous symptoms and limited information in some cases. We experienced two patients with basilar artery occlusion who presented with convulsive-like movements as an initial manifestation.

Acute Disseminated Encephalomyelitis Caused by Scrub Typhus

No abstract available.

Changes in Cerebral Vascular Reserve Capacity after Carotid Artery Stenting: A 6-Month Follow-up Study

BACKGROUND: Assessment of cerebral vascular reserve capacity prior to carotid artery stenting is used for predicting hyperperfusion syndrome. However, the changes in vascular reserve capacity after carotid stenting are not fully understood. In this study we investigated the effects of carotid artery stenting on the restoration of vascular reserve capacity using (99m)TC-hexamethylpropylene amine oxime (HMPAO) single-photon-emission computed tomography (SPECT). METHODS: The study population comprised 29 patients who underwent carotid artery stenting. Patients were divided into groups according to occlusion of the contralateral internal carotid artery (unilateral group vs bilateral group) and according to the presence or absence of symptoms related to carotid stenosis (symptomatic group vs asymptomatic group). Pre- and postacetazolamide-activated (99m)TC-HMPAO SPECT were performed prior to stent insertion and at 1 and 6 months postoperatively. Vascular reserve capacity was assessed based on pre-, and 1- and 6-month postacetazolamide gamma count ratio (Post0, Post1, and Post6, respectively) and cerebrovascular reactivity (CVR0, CRV1, and CRV6, respectively). RESULTS: The postacetazolamide gamma count ratio and cerebrovascular reactivity tended to improve at 1 month after stenting, but tended to deteriorate at 6 months after stenting in the unilateral group compared with the bilateral group [Post0-Post1=0.045+/-0.078 (mean+/-SD), p=0.014; Post0-Post6=0.025+/-0.063, p=0.042; Post1-Post6=-0.020+/-0.047, p=0.102; CVR0-CVR1=0.043+/-0.071, p=0.008, CVR0-CVR6=0.019+/-0.063, p=0.097; CVR1-CVR6=-0.024+/-0.047, p=0.008] and in the symptomatic group compared with the asymptomatic group (Post0-Post1=0.058+/-0.106, p=0.038; Post0-Post6=0.048+/-0.103, p=0.061; Post1-Post6=-0.010+/-0.048, p=0.700; CVR0-CVR1=0.037+/-0.083, p=0.074; CVR0-CVR6=0.014+/-0.073, p=0.344; CVR1-CVR6=-0.023+/-0.054, p=0.055). CONCLUSIONS: The observed increases in postacetazolamide gamma count ratio and cerebrovascular reactivity at 1 month followed by decreases at 6 months may reflect the restoration of vascular reserve capacity. Carotid artery stenting can improve vascular reserve capacity, especially in patients with unilateral stenosis and with symptomatic stenosis.