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Central Modulation of Pain
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The nuclei in the thalamus that receive these projections are located either laterally (ventral posterior lateral and ventral posterior inferior nuclei and medial posterior complex) or medially in the central lateral nucleus and other intralaminar nuclei. Fibres arising from more caudal segments tend to be located laterally, and those entering from more rostral segments tend to be located in the more medial and ventral part of the tract.
Radiofrequency lesioning and treatment of chronic pain
Published in Harald Breivik, William I Campbell, Michael K Nicholas, Clinical Pain Management, 2008
Ben JP Crul, Jan HM Van Zundert, Maarten Van Kleef
The spinothalamic tract, situated in the anterolateral quadrant of the spinal cord, consists of secondary nociceptive neurons conveying nociceptive stimuli from the contralateral body half. Its origin is in the dorsal horn of the spinal cord and its destination is mainly situated in the ventral posterior lateral and the central lateral nucleus of the thalamus. At the level C1–C2, the column of facetal joints is interrupted, allowing an approach to the spinal cord by a laterally introduced needle electrode.
Current challenges in the pathophysiology, diagnosis, and treatment of paroxysmal movement disorders
Published in Expert Review of Neurotherapeutics, 2021
Cécile Delorme, Camille Giron, David Bendetowicz, Aurélie Méneret, Louise-Laure Mariani, Emmanuel Roze
Clinical studies and animal models support the implication of both basal ganglia and cerebellum in the genesis of paroxysmal dyskinesia. Studies in rodents and primates brought evidence for reciprocal routes of communication between the cerebellum and the striatum [41]. In rodent models, a disynaptic pathway was found from the cerebellar nuclei to the striatum via the central lateral nucleus of the thalamus[42]. Likewise, the main output nucleus of the cerebellum, the dentate nucleus, is at the origin of a disynaptic pathway to the striatum in non-human primates[43]. Aberrant cerebellar activity can percolate through this network and influence activity in the basal ganglia. This may reconcile the apparent dilemma of striatal and cerebellar abnormalities converging into similar manifestations. This concept of network disorder is now a major theory in the pathophysiology of dystonia [44]. Paroxysmal dyskinesia could also be seen as a network disorder, in which either primary striatal dysfunction or aberrant cerebellar output conveyed to the striatum results in the phenotype. Future experimental studies combining neurophysiological and neuroimaging investigations in patients with paroxysmal dyskinesia would help us to better understand the subtle interplay between the cerebellum and the basal ganglia.
Ablative brain surgery: an overview
Published in International Journal of Hyperthermia, 2019
Andrea Franzini, Shayan Moosa, Domenico Servello, Isabella Small, Francesco DiMeco, Zhiyuan Xu, William Jeffrey Elias, Angelo Franzini, Francesco Prada
Stereotactic thalamotomy was performed extensively in the early years of human stereotaxis [111] as it provided significantly less surgical and neurological morbidity than procedures performed at the pontine or mesencephalic level [112]. At first, lesions were made in the lateral sensory thalamic nuclei (ventroposterolateral and ventroposteromedial nuclei). Subsequently, due to an excessively high rate of somatosensory sequalae associated with these lesions, many surgeons targeted the medial thalamic nuclei (centralis lateral nucleus, centromedian/parafascicular complex, posterior complex, the medial pulvinar [112–115] and the posterior central lateral nucleus (CLp)) [114], which relieved pain without inducing any clinically detectable sensory loss or central pain [111,115]. Nonspecific medial thalamic nuclei are interconnected with associative and paralimbic areas of the brain, and the stimulation or lesioning of these areas is thought to address predominantly the affective-motivational component of chronic pain. Conversely, surgeries directed in the lateral thalamus directly interrupt the somatotopically arranged ascending pain pathways as they enter the thalamus. Accordingly, the effect of these surgeries is thought to result from an influence on the sensory-discriminative component of pain [116]. Finally, the posterior complex and CLp nuclei are considered to have an intermediate functional role between diffuse and nondiffuse nuclei and project to large cortical domains, including areas mediating discriminative (SI), affective-motivational (anterior cingulate cortex insula), cognitive (prefrontal cortex) and motor (premotor cortex) aspects of pain [114]. Their surgical lesioning is therefore thought to have a multimodal effect. The most recent study targeting the mesial thalamus with SRS showed that >50% pain relief was achieved in 67% of patients, with 20% of patients achieving complete relief [117]. Similar results were observed in the largest trial of centrolateral thalamotomy, which reported that more than 50% of patients had >50% pain relief and 20% had complete pain relief [118]. Despite variable results in terms of pain relief and side effect profiles (Table 2), a high rate of pain recurrence following ablative thalamic lesions has been commonly reported by authors, especially in the management of pain of benign origin [112].