Limbic System and Psychoneuroendocrinology: an Animal Analogue of the Neuroendocrine Strategy for Investigating Psychiatric Disturbances

2015 ◽  
pp. 85-98 ◽  
Author(s):  
Jo Seggie
Keyword(s):  
Limbic System ◽  
Psychiatric Disturbances

A Case of Personality Change and Seizure

2018 ◽  
pp. 83-88
Author(s):  
Aaron E. Miller ◽  
Tracy M. DeAngelis ◽  
Michelle Fabian ◽  
Ilana Katz Sand
Keyword(s):  
Cell Membrane ◽  
Limbic System ◽  
Clinical Manifestations ◽  
Personality Change ◽  
T Cell Infiltration ◽  
Psychiatric Disturbances ◽  
Immune Mediated ◽  
Elevated Protein ◽  
Autoimmune Phenomenon ◽  
Immunomodulatory Therapies

The limbic encephalitides comprise a group of immune-mediated conditions that preferentially affect the limbic system, resulting in clinical manifestations such as memory deficits, seizures, and psychiatric disturbances. Limbic encephalitis (LE) may occur as a paraneoplastic syndrome related to underlying tumor, or as a primary autoimmune phenomenon. MRI often shows T2/FLAIR hyperintensities in the temporal lobe. CSF may be normal or may demonstrate mild lymphocytic pleocytosis and/or elevated protein. As the number of identifiable autoantibodies has rapidly increased in recent years, frequently one of these will be noted in the serum or spinal fluid. Antibodies to “classic paraneoplastic” intracellular antigens may only be markers of disease, given pathology studies demonstrating T cell infiltration, whereas antibodies to extracellular/cell membrane-associated antigens seem to be pathogenic and thus these tend to exhibit superior responses to immunotherapies. Treatment involves removal of the tumor if one is present, as well as various immunomodulatory therapies.

Stimulation of Limbic System of Brain in Waking Animals

Science ◽  
1955 ◽  
Vol 122 (3180) ◽  
pp. 1139-1139 ◽  
Author(s):  
B. K. ANAND ◽  
S. DUA
Keyword(s):  
Limbic System ◽  
Stimulation Of

scholarly journals Prolonged ketamine infusion modulates limbic connectivity and induces sustained remission of treatment-resistant depression

2021 ◽  
Author(s):  
Joshua S. Siegel ◽  
Ben J. A. Palanca ◽  
Beau M. Ances ◽  
Evan D. Kharasch ◽  
Julie A. Schweiger ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Limbic System ◽  
Anterior Cingulate ◽  
Sustained Remission ◽  
Treatment Resistant Depression ◽  
Treatment Resistant ◽  
Open Label ◽  
Subgenual Anterior Cingulate Cortex ◽  
Post Infusion ◽  
Resistant Depression

AbstractKetamine produces a rapid antidepressant response in over 50% of adults with treatment-resistant depression. A long infusion of ketamine may provide durable remission of depressive symptoms, but the safety, efficacy, and neurobiological correlates are unknown. In this open-label, proof-of-principle study, adults with treatment-resistant depression (N = 23) underwent a 96-h infusion of intravenous ketamine (0.15 mg/kg/h titrated toward 0.6 mg/kg/h). Clonidine was co-administered to reduce psychotomimetic effects. We measured clinical response for 8 weeks post-infusion. Resting-state functional magnetic resonance imaging was used to assess functional connectivity in patients pre- and 2 weeks post-infusion and in matched non-depressed controls (N = 27). We hypothesized that responders to therapy would demonstrate response-dependent connectivity changes while all subjects would show treatment-dependent connectivity changes. Most participants completed infusion (21/23; mean final dose 0.54 mg/kg/h, SD 0.13). The infusion was well tolerated with minimal cognitive and psychotomimetic side effects. Depressive symptoms were markedly reduced (MADRS 29 ± 4 at baseline to 9 ± 8 one day post-infusion), which was sustained at 2 weeks (13 ± 8) and 8 weeks (15 ± 8). Imaging demonstrated a response-dependent decrease in hyperconnectivity of the subgenual anterior cingulate cortex to the default mode network, and a treatment-dependent decrease in hyperconnectivity within the limbic system (hippocampus, amygdala, medial thalamus, nucleus accumbens). In exploratory analyses, connectivity was increased between the limbic system and frontal areas, and smaller right hippocampus volume at baseline predicted larger MADRS change. A single prolonged infusion of ketamine provides a tolerated, rapid, and sustained response in treatment-resistant depression and normalizes depression-related hyperconnectivity in the limbic system and frontal lobe.ClinicalTrials.gov: Treatment Resistant Depression (Pilot), NCT01179009.

scholarly journals Expanding the genetic spectrum of primary familial brain calcification due to SLC2OA2 mutations: a case series

Neurogenetics ◽  
2021 ◽  
Author(s):  
Luca Magistrelli ◽  
Roberta Croce ◽  
Fabiola De Marchi ◽  
Chiara Basagni ◽  
Miryam Carecchio ◽  
...  
Keyword(s):  
Autosomal Dominant ◽  
Case Series ◽  
Dominant Trait ◽  
Autosomal Dominant Trait ◽  
Phenotypic Spectrum ◽  
Primary Familial Brain Calcification ◽  
Psychiatric Disturbances ◽  
Brain Calcification ◽  
Uncertain Significance ◽  
Six Genes

AbstractPrimary familial brain calcification (PFBC) is a neurological condition characterized by the presence of intracranial calcifications, mainly involving basal ganglia, thalamus, and dentate nuclei. So far, six genes have been linked to this condition: SLC20A2, PDGFRB, PDGFB, and XPR1 inherited as autosomal-dominant trait, while MYORG and JAM2 present a recessive pattern of inheritance. Patients mainly present with movement disorders, psychiatric disturbances, and cognitive decline or are completely asymptomatic and calcifications may represent an occasional finding. Here we present three variants in SLC20A2, two exonic and one intronic, which we found in patients with PFBC associated to three different clinical phenotypes. One variant is novel and two were already described as variants of uncertain significance. We confirm the pathogenicity of these three variants and suggest a broadening of the phenotypic spectrum associated with mutations in SLC20A2.

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