BACKGROUND: Tumors with cysts often correlate with gliomas, metastatic tumors, or hemangioblastomas, which require differentiation. METHODS: Thirty-eight cases of cyst associated-meningioma based on preoperative radiologic studies and histologic confirmations were reviewed from November 1998 to July 2017. RESULTS: A total of 395 cases of meningioma were observed in the 20 years, and surgical treatment of intracranial meningioma was performed in 120 cases. Thirty-eight (9.6%) cases of cyst associated meningiomas were analyzed. Nauta type I was the most common type of cyst (39.5%) and the most frequent histopathological subtype was meningothelial type (36.8%). CONCLUSION: Statistically there were no significant associations between meningioma histopathological type and associated cysts; however, the rate of World Health Organization grade II was higher in cyst associated meningiomas than in unrelated meningiomas. This correlation was weak, in accordance with the meningioma grade.
Glioma ; Hemangioblastoma ; Meningioma* ; Neuropathology ; World Health Organization

The number of death from insulin overdose, including accidental poisoning, suicide and homicide, is increasing these years. The forensic diagnosis of death from insulin overdose is a tough task. Glucose is the main energy source of the brain. Therefore, hypoglycemic brain damage is considered to be the main reason of death from insulin overdose. Recently, research of hypoglycemic brain damage caused by insulin overdose is gradually being paid attention in the field of forensic medicine. This paper summarizes the neuropathologic changes, pathophysiologic process and potential neural molecular markers of hypoglycemic brain damage caused by insulin overdose in terms of forensic neuropathology, providing reference for the research and practice in forensic medicine related fields.
Brain ; Drug Overdose ; Humans ; Hypoglycemic Agents ; Insulin ; Neuropathology

Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron degenerative disease that clinically manifests both upper and lower motor neuron signs. However, it is unknown where and how the motor neuron degeneration begins, and conflicting hypotheses have been suggested. Recent advanced radiological techniques enable us to look into ALS neuropathology in vivo. Herein, we report a case with upper motor neuron-predominant ALS in whom the results of brain magnetic resonance imaging (MRI) and myelin water fraction MRI suggest axonal degeneration.
Amyotrophic Lateral Sclerosis* ; Axons ; Brain ; Magnetic Resonance Imaging* ; Motor Neurons ; Myelin Sheath* ; Neuropathology ; Pathology ; Water*

To obtain an in-depth understanding of brain diseases, including neurodegenerative diseases, psychiatric illnesses, and neoplasms, scientific approach and verification using postmortem human brain tissue with or without disease are essential. Compared to other countries that have run brain banks for decades, South Korea has limited experience with brain banking; nationwide brain banks started only recently. The goal of this study is to provide provisional guidelines for brain autopsy for hospitals and institutes that have not accumulated sufficient expertise. We hope that these provisional guidelines will serve as a useful reference for pathologists and clinicians who are involved and interested in the brain bank system. Also, we anticipate updating the provisional guidelines in the future based on collected data and further experience with the practice of brain autopsy in South Korea.
Academies and Institutes ; Autopsy* ; Brain Diseases ; Brain* ; Dementia ; Hope ; Humans ; Korea* ; Neurodegenerative Diseases ; Neuropathology

It has been reported that cross-frequency interactions may play an important role in local processing within thalamus and neocortex, as well as information transfer between subcortical and cortico-cortical brain regions. Strong commonalities in rhythmic network properties have been observed across recording techniques and task demands, but strong neuroscientific theories to situate such observations within a unified framework with direct relevance to explain neuropathologies remain scarce. Based on a comprehensive review of animal and human literature, we probe and introduce a neurophysiological framework to explain how coordinated cross-frequency and interregional oscillatory cortical dynamics underlie typical and atypical brain activation, and the formation of distributed functional ensembles supporting cortical networks underpinning perception and cognition. We propose that local regional activation by an external stimulus via a sensory pathway entails (1) attenuated alpha (8–14 Hz) and increased theta (4–8 Hz) and gamma (30–50 Hz) oscillatory activity, and (2) increased interactions among theta and gamma rhythms. These local dynamics also mediate the integration of activated neural populations into largescale functional assemblies through neuronal synchronization. This comprehensive perspective into the animal and human literature indicates a further thinking beyond synchrony and connectivity and the readiness for more hypothesis-driven research and modeling toward unified principles of thalamo-cortical processing. We further introduced such a possible framework: “The ATG switch”. We also discussed evidence that alpha-theta-gamma dynamics emerging from thalamocortical interactions may be implicated and disrupted in numerous neurological and neuropsychiatric conditions.
Animals ; Brain ; Cognition ; Gamma Rhythm ; Humans ; Neocortex ; Neurons ; Neuropathology ; Thalamus ; Thinking

Bipolar Disorder ; diagnosis ; pathology ; therapy ; Brain ; pathology ; Gene Expression ; physiology ; Humans ; Neuropathology

Cysticercosis and sparganosis are not uncommon parasitic infections in the developing world. Central nervous system infection by both cestodes can present with neurological signs and symptoms, such as seizure and mass effect, including brain hernia. Early detection and accurate diagnosis can prevent a fatal outcome. Histological examinations of brain tissues can confirm the diagnosis of cerebral cysticercosis, which differs from sparganosis by the presence of a cavitated body. We report here a case of cerebral cysticercosis which has the similar clinical and imaging findings as sparganosis.
Brain ; Central Nervous System Infections ; Cestoda ; Cysticercosis* ; Diagnosis ; Epilepsy ; Fatal Outcome ; Hernia ; Magnetic Resonance Imaging ; Neuropathology ; Seizures ; Sparganosis ; Thailand*

BACKGROUND AND PURPOSE: A thick corpus callosum (TCC) can be associated with a very grave outcome in fetuses, but its clinical presentation in older children seems to be markedly different. METHODS: The corpus callosum (CC) was defined as thick based on observations and impressions. We reviewed cases of children who were diagnosed as TCC based on brain magnetic resonance imaging (MRI) studies. The pertinent clinical data of these children were collected, and their CCs were measured. RESULTS: Out of 2,552 brain MRI images, those of 37 children were initially considered as showing a TCC. Those initial imaging were reviewed by an experienced neuroradiologist, who confirmed the diagnosis in 34 children (1.3%): 13 had neurofibromatosis-1 (NF-1), 9 had epilepsy, 3 had macrocephaly capillary malformation (MCM) syndrome, 3 had autistic spectrum disorder, 1 had a Chiari-1 malformation, and 1 had increased head circumference. No specific neurologic disorder could be defined in seven children. The measured thickness of the CC in these children was comparable to those published in the literature for adults. CONCLUSIONS: A TCC is a rare brain malformation that can be found in neuropathologies with apparently diverse pathognomonic mechanisms, such as NF-1 and MCM. It is not necessarily associated with life-threatening conditions, instead being a relatively benign finding, different in nature from that reported in fetuses.
Adult ; Brain ; Capillaries ; Child* ; Corpus Callosum* ; Diagnosis ; Epilepsy ; Fetus ; Genetics ; Head ; Humans ; Magnetic Resonance Imaging ; Megalencephaly ; Nervous System Diseases ; Neurofibromatoses ; Neuropathology

Primary progressive aphasia (PPA) is a clinical syndrome diagnosed when three core criteria are met. First, there should be a language impairment (i.e., aphasia) that interferes with the usage or comprehension of words. Second, the neurological work-up should determine that the disease is neurodegenerative, and therefore progressive. Third, the aphasia should arise in relative isolation, without equivalent deficits of comportment or episodic memory. The language impairment can be fluent or non-fluent and may or may not interfere with word comprehension. Memory for recent events is preserved although memory scores obtained in verbally mediated tests may be abnormal. This distinctive clinical pattern is most conspicuous in the initial stages of the disease, and reflects a relatively selective atrophy of the language network, usually located in the left hemisphere. There are different clinical variants of PPA, each with a characteristic pattern of atrophy. Clinicoanatomical correlations in patient with these variants have led to new insights on the organization of the large-scale language network in the human brain. For example, the left anterior temporal lobe, which was not part of the classic language network, has been shown to play a critical role in word comprehension and object naming. Furthermore, patients with PPA have shown that fluency can be dissociated from grammaticality. The underlying neuropathological diseases are heterogeneous and can include Alzheimer's disease as well as frontotemporal lobar degeneration. The clinician's task is to recognize PPA and differentiate it from other neurodegenerative phenotypes, use biomarkers to surmise the nature of the underlying neuropathology, and institute the most fitting multimodal interventions.
Alzheimer Disease ; Aphasia ; Aphasia, Primary Progressive* ; Atrophy ; Biomarkers ; Brain ; Comprehension ; Dementia ; Frontotemporal Lobar Degeneration ; Humans ; Memory ; Memory, Episodic ; Neuropathology ; Phenotype ; Temporal Lobe

Synucleinopathies are neurodegenerative disorders characterized by the progressive accumulation of α-synuclein (α-syn) in neurons and glia and include Parkinson's disease (PD) and dementia with Lewy bodies (DLB). In this review, we consolidate our key findings and recent studies concerning the role of Toll-like receptor 2 (TLR2), a pattern recognition innate immune receptor, in the pathogenesis of synucleinopathies. First, we address the pathological interaction of α-syn with microglial TLR2 and its neurotoxic inflammatory effects. Then, we show that neuronal TLR2 activation not only induces abnormal α-syn accumulation by impairing autophagy, but also modulates α-syn transmission. Finally, we demonstrate that administration of a TLR2 functional inhibitor improves the neuropathology and behavioral deficits of a synucleinopathy mouse model. Altogether, we present TLR2 modulation as a promising immunotherapy for synucleinopathies.
Animals ; Autophagy ; Dementia ; Immunotherapy ; Lewy Bodies ; Mice ; Neurodegenerative Diseases ; Neuroglia ; Neurons ; Neuropathology ; Parkinson Disease ; Toll-Like Receptor 2 ; Toll-Like Receptors