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Brain Structure & Function Jul 2023The mammillary body (MB) is a component of the extended hippocampal system and many studies have shown that its functions are vital for mnemonic processes. Together with... (Review)
Review
The mammillary body (MB) is a component of the extended hippocampal system and many studies have shown that its functions are vital for mnemonic processes. Together with other subcortical structures, such as the anterior thalamic nuclei and tegmental nuclei of Gudden, the MB plays a crucial role in the processing of spatial and working memory, as well as navigation in rats. The aim of this paper is to review the distribution of various substances in the MB of the rat, with a description of their possible physiological roles. The following groups of substances are reviewed: (1) classical neurotransmitters (glutamate and other excitatory transmitters, gamma-aminobutyric acid, acetylcholine, serotonin, and dopamine), (2) neuropeptides (enkephalins, substance P, cocaine- and amphetamine-regulated transcript, neurotensin, neuropeptide Y, somatostatin, orexins, and galanin), and (3) other substances (calcium-binding proteins and calcium sensor proteins). This detailed description of the chemical parcellation may facilitate a better understanding of the MB functions and its complex relations with other structures of the extended hippocampal system.
Topics: Rats; Animals; Mammillary Bodies; Neurochemistry; Anterior Thalamic Nuclei; Amino Acids; Memory, Short-Term
PubMed: 37378855
DOI: 10.1007/s00429-023-02673-4 -
Cureus Nov 2023Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune condition characterized by recurrent episodes of optic neuritis (ON) and transverse myelitis. This case...
Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune condition characterized by recurrent episodes of optic neuritis (ON) and transverse myelitis. This case report aims to highlight the importance of considering atypical presentations of NMOSD when confronted with MRI-detected Wernicke's encephalopathy. The primary target in NMOSD is the aquaporin-4 (AQP4) protein, predominantly located on astrocyte surfaces. Antibodies binding to AQP4 can lead to astrocyte dysfunction and damage, contributing to NMOSD's distinctive pathology. The associated immune response and inflammation can cause secondary harm to various components of the central nervous system, including oligodendrocytes and neuronal axons. This inflammatory process results in perivascular demyelination and axonal injury, further aggravating neurological deficits in NMOSD. In this case, we present a 39-year-old female with no prior medical or surgical history who sought medical attention due to a three-week history of progressive eyelid heaviness and somnolence. NMOSD is an autoimmune condition primarily targeting the AQP4 protein, resulting in recurrent ON and transverse myelitis. The patient was initially misdiagnosed with myasthenia gravis due to somnolence and ptosis. Due to concerns about myasthenia gravis due to diffuse fatigue and bilateral ptosis, the patient was initially treated with intravenous immunoglobulin (IVIG) and admitted to the neurology service. On the first day of her hospitalization, MRI with and without contrast revealed extensive, non-enhancing T2-weighted-fluid-attenuated inversion recovery (T2-FLAIR) hyperintensities surrounding the third ventricle and affecting the periaqueductal grey, medial thalami, and mammillary bodies. There was also an interval increase in T2-FLAIR hyperintensity within the right medial temporal lobe, extending more posteriorly and inferiorly, abutting the temporal horn. Subsequent CSF encephalitis panel results showed positive West Nile virus (WNV) IgG but negative WNV IgM, and AQP4 antibodies were positive. Given the high specificity of AQP4 antibodies, the patient was diagnosed with neuromyelitis optica (NMO) encephalitis. This case underscores the importance of considering atypical presentations of NMO when confronted with MRI-detected Wernicke's encephalopathy. Since our patient primarily displayed somnolence and eye-related symptoms, neither NMO nor Wernicke's encephalopathy were initially considered in the differential diagnosis. Furthermore, despite MRI findings suggestive of Wernicke's encephalopathy, it was considered less likely due to the absence of thiamine deficiency and consistent denials by family members regarding alcohol use, gastrointestinal issues, or inadequate oral intake. This case underscores the importance of considering NMOSD in patients with atypical symptoms, even when initial presentations suggest other conditions. Timely diagnosis is crucial to prevent mismanagement and improve patient outcomes. Clinicians should maintain a high level of suspicion for NMOSD, especially when MRI findings do not align with the initial diagnosis, as early recognition and treatment can significantly impact patient care and prognosis.
PubMed: 38046734
DOI: 10.7759/cureus.48168 -
The Journal of Neuroscience : the... Sep 2023Stimulation-evoked signals are starting to be used as biomarkers to indicate the state and health of brain networks. The human limbic network, often targeted for brain...
Stimulation-evoked signals are starting to be used as biomarkers to indicate the state and health of brain networks. The human limbic network, often targeted for brain stimulation therapy, is involved in emotion and memory processing. Previous anatomic, neurophysiological, and functional studies suggest distinct subsystems within the limbic network (Rolls, 2015). Studies using intracranial electrical stimulation, however, have emphasized the similarities of the evoked waveforms across the limbic network. We test whether these subsystems have distinct stimulation-driven signatures. In eight patients (four male, four female) with drug-resistant epilepsy, we stimulated the limbic system with single-pulse electrical stimulation. Reliable corticocortical evoked potentials (CCEPs) were measured between hippocampus and the posterior cingulate cortex (PCC) and between the amygdala and the anterior cingulate cortex (ACC). However, the CCEP waveform in the PCC after hippocampal stimulation showed a unique and reliable morphology, which we term the "limbic Hippocampus-Anterior nucleus of the thalamus-Posterior cingulate, HAP-wave." This limbic HAP-wave was visually distinct and separately decoded from the CCEP waveform in ACC after amygdala stimulation. Diffusion MRI data show that the measured end points in the PCC overlap with the end points of the parolfactory cingulum bundle rather than the parahippocampal cingulum, suggesting that the limbic HAP-wave may travel through fornix, mammillary bodies, and the anterior nucleus of the thalamus (ANT). This was further confirmed by stimulating the ANT, which evoked the same limbic HAP-wave but with an earlier latency. Limbic subsystems have unique stimulation-evoked signatures that may be used in the future to help network pathology diagnosis. The limbic system is often compromised in diverse clinical conditions, such as epilepsy or Alzheimer's disease, and characterizing its typical circuit responses may provide diagnostic insight. Stimulation-evoked waveforms have been used in the motor system to diagnose circuit pathology. We translate this framework to limbic subsystems using human intracranial stereo EEG (sEEG) recordings that measure deeper brain areas. Our sEEG recordings describe a stimulation-evoked waveform characteristic to the memory and spatial subsystem of the limbic network that we term the "limbic HAP-wave." The limbic HAP-wave follows anatomic white matter pathways from hippocampus to thalamus to the posterior cingulum and shows promise as a distinct biomarker of signaling in the human brain memory and spatial limbic network.
Topics: Humans; Male; Female; Limbic System; Electroencephalography; Evoked Potentials; Epilepsy; Electric Stimulation; Anterior Thalamic Nuclei
PubMed: 37620159
DOI: 10.1523/JNEUROSCI.2201-22.2023 -
Neuropsychologia Dec 2023To understand the neural basis of episodic memory it is necessary to appreciate the significance of the fornix. This pathway creates a direct link between those temporal...
To understand the neural basis of episodic memory it is necessary to appreciate the significance of the fornix. This pathway creates a direct link between those temporal lobe and medial diencephalic sites responsible for anterograde amnesia. A collaboration with Andrew Mayes made it possible to recruit and scan 38 patients with colloid cysts in the third ventricle, a condition associated with variable fornix damage. Complete fornix loss was seen in three patients, who suffered chronic long-term memory problems. Volumetric analyses involving all 38 patients then revealed a highly consistent relationship between mammillary body volume and the recall of episodic memory. That relationship was not seen for working memory or tests of recognition memory. Three different methods all supported a dissociation between recollective-based recognition (impaired) and familiarity-based recognition (spared). This dissociation helped to show how the mammillary body-anterior thalamic nuclei axis, as well as the hippocampus, is vital for episodic memory yet is not required for familiarity-based recognition. These findings set the scene for a reformulation of temporal lobe and diencephalic amnesia. In this revised model, these two regions converge on overlapping cortical areas, including retrosplenial cortex. The united actions of the hippocampal formation and the anterior thalamic nuclei on these cortical areas enable episodic memory encoding and consolidation, impacting on subsequent recall.
Topics: Humans; Memory, Episodic; Diencephalon; Hippocampus; Amnesia; Mental Recall; Mammillary Bodies
PubMed: 37939875
DOI: 10.1016/j.neuropsychologia.2023.108728