Explore chapters and articles related to this topic
Anterior thalamic nucleus stimulation: issues in study design
Published in Hans O Lüders, Deep Brain Stimulation and Epilepsy, 2020
Animal studies on the role of anterior thalamic stimulation on models for epilepsy were very limited, in contrast to more extensive animal studies of cerebellar stimulation for epilepsy.13 Furthermore, animal studies of thalamic stimulation lagged behind clinical trials. Initial studies derived from metabolic mapping of pentylenetetrazol (PTZ) induced seizures in rats and guinea pigs.14Figure 25.1 demonstrates increased metabolism in posterior hypothalamus: mammillary bodies, anterior thalamus, and the connecting tract, the mammillothalamic tract. Lesions of the mam-millothalamic tract increased the threshold for induction of seizures by PTZ.
Conclusion
Published in Jay A. Goldstein, Chronic Fatigue Syndromes, 2020
Since cells that secrete IL-1 may be co-localized with glutamatergic neurons, a multifactorial functional abnormality of dentate gyms cells could be involved in CFS. The activity of the dorsolateral prefrontal cortex could be altered by modulation of the well-known pathway from the hippocampus → fornix → mammillary body → mammillothalamic tract → anterior thalamus → prefrontal cortex → paralimbic areas, especially insula and cingulate gyrus → hippocampus.
Neuroendocrine Morphology
Published in Paul V. Malven, Mammalian Neuroendocrinology, 2019
The following three tracts connect the hypothalamus with the midbrain and lower areas: mammillopeduncular tract (labeled H in Figure 2-3), mammillotegmental tract (G), dorsal longitudinal fasciculus (F). The mammillopeduncular tract and mammillotegmental tract both connect the mammillary bodies of the hypothalamus with the midbrain and lower regions. The hippocampus inputs into the hypothalamus pass by way of the fornix (E) to the preoptic area, arcuate nucleus and mammillary bodies of the hypothalamus. The thalamus connection with the mammillary bodies involves the mammillothalamic tract (I). The amygdala connections with the hypothalamus consist of (1) stria terminalis (C) which curves around in parallel with the fornix and (2) the shorter route from amygdala to hypothalamus called the direct amygdalohypothalamic tract (D). A major fiber tract passing through the hypothalamus is the medial forebrain bundle (B) which connects hypothalamus with the septum, rostral structures such as the olfactory gray, and structures caudal to the hypothalamus. The epithalamus sends input to the preoptic area of the hypothalamus via the stria medullaris (A).
Thalamic neuromodulation in epilepsy: A primer for emerging circuit-based therapies
Published in Expert Review of Neurotherapeutics, 2023
Bryan Zheng, David D. Liu, Brian B Theyel, Hael Abdulrazeq, Anna R. Kimata, Peter M Lauro, Wael F. Asaad
Robust anatomical and neurophysiological data support the involvement of the ANT, which closes the medial limbic circuit via the mammillothalamic tract (Figure 4), in TLE. Indeed, among the earliest clues suggesting a link between the thalamus and epilepsy was the observation that lesions of the mammillothalamic tract protected guinea pigs from pentylenetetrazol(PTZ)-induced temporal lobe seizures[122,123]. A rodent model of electrical stimulation-induced focal limbic seizures demonstrated that the ANT may exhibit seizure activity prior to cortex with a high degree of accuracy and consistency[124]. Such an observation, if generalizable to human TLE, may motivate a more primary role for thalamic seizure detection and modulation in at least this form of epilepsy[125]. Other thalamic nuclei that connect with broader regions of the temporal lobe, particularly the PuM nucleus (Figure 5), have also been shown to be electrographically recruited by seizures, following initiation in cortex[126–129].
Neuromodulation beyond neurostimulation for epilepsy: scope for focused ultrasound
Published in Expert Review of Neurotherapeutics, 2019
Manish Ranjan, Alexandre Boutet, Sanjiv Bhatia, Angus Wilfong, Walter Hader, Mark R Lee, Ali R Rezai, P. David Adelson
One of the potential advantages of MRgFUS is to not only to create an ablation zone but potentially to also modulate neurological functions without tissue damage. By utilizing low-frequency sonication similar to DBS/neurostimulation, MRgFUS has the advantages of not requiring hardware such as depth electrodes and pulse generator. Re-treatment can presumably be done safely if needed. Studies have shown that a single treatment with focused-ultrasound can block nerve conduction [19–21] and may be utilized in neurological disorders with pathological networks. Given that epilepsy is generally considered a disease with pathological/disorganized neural networks, this technique would have the potential to interrupt or modulate these networks. This seems a reasonable approach in future, once more experiences and validation of methods such as rs-fMRI to identify epileptic networks have been validated. The subcortical components have been recognized as a potential significant contributor to the cortical-subcortical networks in epilepsy; however, the overall seizure generation and propagation is a complex overlay of cortical–subcortical network interactions [22,23]. The role of the thalamus in epilepsy is well known [24,25]. In one of the study of AN stimulation for epilepsy, stimulation of the lateroventral AN in close proximity to the mammillothalamic tract was found to be most efficacious in seizure control [26]. This could be a potential site for MRgFUS neuromodulation for epilepsy. One of the advantages of low-frequency sonication, unlike the high-frequency sonication, is that it is non-destructive and a potential cause a reversible neurophysiological alteration. Prior studies using low-frequency sonication (non-ablative) demonstrated alteration of primary sensory functions in humans [27]. Min et al. successfully aborted an acute seizure following the application of low-frequency sonication to the thalamus in an epilepsy animal model with concurrent EEG changes [28]. This study preliminarily supports the potential role of non-ablative neuromodulation using FUS in epilepsy.