Itch is an unpleasant sensation that provokes the desire to scratch. While acute itch serves as a protective system to warn the body of external irritating agents, chronic itch is a debilitating but poorly-treated clinical disease leading to repetitive scratching and skin lesions. However, the neural mechanisms underlying the pathophysiology of chronic itch remain mysterious. Here, we identified a cell type-dependent role of the anterior cingulate cortex (ACC) in controlling chronic itch-related excessive scratching behaviors in mice. Moreover, we delineated a neural circuit originating from excitatory neurons of the ACC to the ventral tegmental area (VTA) that was critically involved in chronic itch. Furthermore, we demonstrate that the ACC→VTA circuit also selectively modulated histaminergic acute itch. Finally, the ACC neurons were shown to predominantly innervate the non-dopaminergic neurons of the VTA. Taken together, our findings uncover a cortex-midbrain circuit for chronic itch-evoked scratching behaviors and shed novel insights on therapeutic intervention.
Mice ; Animals ; Gyrus Cinguli/physiology* ; Pruritus/pathology* ; Mesencephalon ; Cerebral Cortex/pathology* ; Neurons/pathology*

Humans ; Cerebral Cortex ; Hallucinations/pathology* ; Neurodegenerative Diseases/pathology* ; Atrophy/pathology* ; Magnetic Resonance Imaging

The purpose of this study is to delineate the pattern of reorganization of cortical language areas using functional magnetic resonance imaging (fMRI) after rehabilitation therapy in patients with aphasia. Six right-handed aphasic patients were investigated. Causes of aphasia were intracerebral hemorrhages of the left basal ganglia in 3 patients, cerebral infarction of the left MCA in 2, and surgical resection of the frontotemporal lobes to control intractable epilepsy in 1. An auditory sentence completion task was used to activate brain language areas during the fMRI. Three patients with left frontal lesions showed activation in the right inferior frontal lobes while performing language tasks, whereas the other 3, whose lesions located at subcortical areas, showed activation in the bilateral frontal and temporal lobes. Our results demonstrated the differences in interhemispheric reorganization of the language network depending on the location of the lesion in aphasic patients. While the patients with subcortical lesion showed tendency of bilateral frontal activation, those with cortical lesion showed activation of the right frontal lobe.
Adult ; Aphasia/*pathology/physiopathology ; Cerebral Cortex/*pathology ; Female ; Human ; *Language ; Magnetic Resonance Imaging ; Male ; Middle Age

OBJECTIVETo analyze the clinical manifestations and magnetic resonance imaging (MRI) features of lissencephaly of various types and provide clinical and imaging evidences for the clinical diagnosis of the disease.

METHODSThe clinical symptoms and signs and the findings in neurobehavioral evaluation, laboratory examination and magnetic resonance imaging (MRI) of 11 cases of lissencephaly were investigated retrospectively.

RESULTSThe 11 patients consisted of 4 with isolated lissencephaly sequence, 3 with Miller-Dieker syndrome, 3 with cobblestone lissencephaly, and 1 with lissencephaly with cerebellar hypoplasia. The main clinical manifestations included mental retardation, developmental delay, microcephaly, epilepsy, hearing abnormality and facial malformation. Cobblestone lissencephaly presented with congenital muscular dystrophy and eye malformation, and lissencephaly with cerebellar hypoplasia showed ataxia manifestations. In terms of MRI features, classical lissencephaly displayed absent or broad cerebral gyri, thickened cortex and reduced white matter, smooth border between the gray and white matter, and thin white matter. Cobblestone lissencephaly displayed thick cortex and gyri deficiency with cobblestone surface. Lissencephaly with cerebellar hypoplasia presented with pachygyria, cerebellar hypoplasia and hippocampal dysplasia.

CONCLUSIONLissencephaly is a developmental malformation of the brain with obvious heterogeneity, and the clinical manifestations and MRI features can be the evidences for a clinical diagnosis and classification of the disease.

Cerebral Cortex ; abnormalities ; pathology ; Female ; Humans ; Infant ; Lissencephaly ; diagnosis ; pathology ; Magnetic Resonance Imaging ; Male ; Retrospective Studies

OBJECTIVETo elucidate the volume changes of cortical and subcortical reward circuitry in patients with type 2 diabetes mellitus.

METHODSHigh-resolution three-dimensional T1-weighted fast spoiled gradient recalled echo MRI images were obtained from 16 patients with type 2 diabetes mellitus and 16 normal controls, and 11 type 2 diabetic patients also received the same MRI scans after insulin therapy for 1 year. Volumetric analysis was performed and analysis of covariance and paired t test were applied.

RESULTSA decreased volume was found in the left insular lobe, left nucleus accumbens area, right hippocampus, putamen and amygdala in type 2 diabetic patients compared with normal controls (P<0.05). After insulin therapy for 1 year, an increased volume of bilateral cortical reward structures was observed (left, 33.65∓3.66 ml; right, 33.35∓4.25 ml) compared the baseline level (left, 31.45∓2.90 ml; right, 31.12∓2.97 ml) in diabetic patients (P<0.05). No significant volume change in the bilateral basal ganglia structures was found after insulin therapy for 1 year (P>0.05), and bilateral ventral diencephalon area showed an increased volume after the treatment (left, 3.26∓0.68 ml; right, 3.20∓0.78 ml) compared with the baseline (left, 2.96∓0.76 ml; right, 2.82∓0.90 ml)(P<0.05).

CONCLUSIONType 2 diabetic patients have a decreased volume of the cortical and subcortical reward circuitry, and insulin therapy can reverse such changes and improve the damage of reward circuitry.

Aged ; Cerebral Cortex ; pathology ; Diabetes Mellitus, Type 2 ; drug therapy ; pathology ; Entorhinal Cortex ; pathology ; Female ; Humans ; Insulin ; therapeutic use ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Nucleus Accumbens ; pathology

The clinical features of cerebral infarction (CI) which cause late post-infarct epilepsy (PIE), are not well understood. We tried to identify the clinical signs which might be associated with late PIE development. We analyzed 60 consecutive patients (PIE group) who had recurrent seizures at least a week after the CI. Neuroradiological findings, clinical features during the acute phase of CI, types of seizures, and the interval between CI and first seizure were analyzed. These data were compared with those of randonly sampled nonepikptic patients with CI (60 patients with CI group). In the epikptic patients who had the history of previous CI (46 patients), hemiparesis was frequent symptom during the acute phase of CI (93.5%). Diabetes mellitus and hypertension were frequent underlying illnesses and were not different between the groups. Heart diseaseswere common in PIE group (40% vs. 13.3%) and correspondingly, the cortical CI involving the superior division of the MCA including motor area was frequent brain pathology (46.7%). Seizures usually began with focamotor activity (50%), but generalized seizure ws also common (35%). In 14 patients, silent CI was identified after the first seizure. Their usual site of CI was subcortical (42.9%), whereas the subcortical CI was infrequent in those with history of CI (13.0%). Acute PIE occurred in six patients and persisted thereafter. These findings suggest that the cortical infarct involving the motor cortex is frequent pathology in the late PIE, that acute PIE may remains as late PIE, and that silent infarct may be an important cause in adult-onset epilepsy.
Brain Diseases ; Cerebral Infarction ; Diabetes Mellitus ; Epilepsy* ; Heart ; Humans ; Hypertension ; Motor Cortex ; Paresis ; Pathology ; Seizures

A 63-year-old man presented with a 1.5-year history of progressive personality changes. Clinical evaluations revealed severe frontal dysfunction and bilateral frontal atrophy/glucose hypometabolism. He was diagnosed as probable behavioral variant frontotemporal dementia. He continued to decline, and died at the age of 66. At autopsy, numerous tau-positive gilial threads and coiled bodies were observed in the white matter. Tau-positive astrocytic plaques and neuronal cytoplasmic inclusions were also seen in cerebral cortices, which were compatible with corticobasal degeneration.
Autopsy* ; Cerebral Cortex ; Coiled Bodies ; Frontotemporal Dementia* ; Humans ; Inclusion Bodies ; Middle Aged ; Neurons ; Pathology*

A 63-year-old man presented with a 1.5-year history of progressive personality changes. Clinical evaluations revealed severe frontal dysfunction and bilateral frontal atrophy/glucose hypometabolism. He was diagnosed as probable behavioral variant frontotemporal dementia. He continued to decline, and died at the age of 66. At autopsy, numerous tau-positive gilial threads and coiled bodies were observed in the white matter. Tau-positive astrocytic plaques and neuronal cytoplasmic inclusions were also seen in cerebral cortices, which were compatible with corticobasal degeneration.
Autopsy* ; Cerebral Cortex ; Coiled Bodies ; Frontotemporal Dementia* ; Humans ; Inclusion Bodies ; Middle Aged ; Neurons ; Pathology*

von Economo neuron (VEN) is a bipolar neuron characterized by a large spindle-shaped soma. VEN is generally distributed in the layer V of anterior insular lobe and anterior cingulate cortex. Fork neuron is another featured bipolar neuron. In recent years,many studies have illustrated that VEN and fork neurons are correlated with complicated cognition such as self-consciousness and social emotion. Studies in the development and morpholigies of these two neurons as well as their pathological changes in various neurological and psychiatric disorders have found that the abnormal number and functions of VEN can cause corresponding dysfunctions in social recognition and emotions both during the neuro-developmental stages of childhood and during the nerve degeneration in old age stage. Therefore, more attentions should be paid on the research of VEN and fork neurons in neuropsychiatric diseases.
Central Nervous System Diseases ; pathology ; Cerebral Cortex ; Humans ; Mental Disorders ; Neurons

Human functional MRI studies in acute and various chronic pain conditions have revolutionized how we view pain, and have led to a new theory that complex multi-dimensional pain experience (sensory-discriminative, affective/motivational, and cognitive) is represented by concurrent activity in widely-distributed brain regions (termed a network or pain matrix). Despite these breakthrough discoveries, the specific functions proposed for these regions remain elusive, because detailed electrophysiological characterizations of these regions in the primate brain are lacking. To fill in this knowledge gap, we have studied the cortical areas around the central and lateral sulci of the non-human primate brain with combined submillimeter resolution functional imaging (optical imaging and fMRI) and intracranial electrophysiological recording. In this mini-review, I summarize and present data showing that the cortical circuitry engaged in nociceptive processing is much more complex than previously recognized. Electrophysiological evidence supports the engagement of a distinct nociceptive-processing network within SI (i.e., areas 3a, 3b, 1 and 2), SII, and other areas along the lateral sulcus. Deafferentation caused by spinal cord injury profoundly alters the relationships between fMRI and electrophysiological signals. This finding has significant implications for using fMRI to study chronic pain conditions involving deafferentation in humans.
Animals ; Cerebral Cortex ; diagnostic imaging ; physiopathology ; Humans ; Pain ; diagnostic imaging ; pathology ; physiopathology ; Primates ; Touch ; physiology