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Physiology of the Pain System
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
The brain does not merely witness the nociceptive signal. It actively participates in constructing the nociceptive signal. The spinothalamic tract ultimately communicates with higher nociception processing centers within the brain. The lateral thalamic nuclei, SI, and SII somatosensory cortices play a sensory discriminative role. The medial thalamic nuclei, and anterior and medial cingulate cortices interpret the emotional significance of the stimuli via the limbic system. The insula, cerebellum, and prefrontal cortex contribute to memory and fear avoidance behaviors. The lentiform nucleus, and cerebellum are involved in reflexive motor responsiveness.2
Anatomy for neurotrauma
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Anesthesia for Neurotrauma, 2018
Vasudha Singhal, Sarabpreet Singh
The basal ganglia include clusters of neurons located deep beneath the cerebral cortex, associated with the modulation of motor activities in the brain. It comprises of the corpus striatum, divided by the fibers of the internal capsule into a medial caudate nucleus, and a lateral lentiform nucleus; the claustrum; and the amygdaloid body. The lentiform nucleus is further subdivided into putamen and globus pallidus. The caudate nucleus and the putamen are together referred to as the striatum, while the globus pallidus is called the pallidum. Recent researches indicate the subthalamic nucleus (part of the diencephalon) and the substantia nigra (part of the midbrain) to be functionally related to the basal ganglia.
Head
Published in Harold Ellis, Adrian Kendal Dixon, Bari M. Logan, David J. Bowden, Human Sectional Anatomy, 2017
Harold Ellis, Adrian Kendal Dixon, Bari M. Logan, David J. Bowden
The posterior limb of the internal capsule (25) is transected in this section and can be seen descending into the pons (35). Medial to the internal capsule can be seen the tail of the caudate nucleus (21) and the thalamus (20), while laterally lies the lentiform nucleus, made up of the putamen (23) and, more medially, the globus pallidus (24). Lateral to the lentiform nucleus lies the claustrum (22), sandwiching the narrow external capsule between the two.
Deep brain stimulation for the treatment of severe intractable anorexia nervosa
Published in British Journal of Neurosurgery, 2019
Michał Sobstyl, Angelika Stapińska-Syniec, Marlena Sokół-Szawłowska, Anna Kupryjaniuk
Zhang et al.18 performed a pre/post experimental design study looking at changes in brain glucose metabolism following DBS of NAc. Given the overlap in symptomatology of OCD and AN, they theorized that a common abnormal brain region may contribute to the symptoms of both disorders. The study included 6 AN patients (only four underwent bilateral DBS of NAc) and 12 healthy controls. The primary outcomes measured included brain glucose metabolism, BMI, and the need for drugs after DBS in NAc. Four AN patients had a follow-up scan three to six months after the surgery to assess for changes. Findings in the 4 AN patients who had DBS included decreased glucose metabolism in the frontal lobe, bilateral lentiform nucleus, and hippocampus, which were identified as those areas differing most from the healthy controls. In addition, BMI increased in all the four subjects from a mean of 12.13–15.65 kg/m2, and no drugs were required after bilateral DBS of NAc at the last follow-up.18
Aplasia Cutis Congenita with Ischemic Cortical Change and Normal Array Cytogenetic Analysis with a Fetus Papyraceus Twin
Published in Fetal and Pediatric Pathology, 2018
Laura A. Skillen, Damien Gates, Julie-Ann Collins, Nivedita Saxena, Daniel Hurrell, Kevin McKenna, Patrick J. Morrison
There were no organ anomalies other than a small inguinal hernia. There were no dysmorphic features and zygodactyly of both feet was apparent. Cranial imaging (on day 2) with magnetic resonance scan (MR) showed enhancement of the left lentiform nucleus, external capsule and within the adjacent frontal lobe gyri consistent with cortical laminar necrosis and ischemia. Follow-up MR scan (at day 9) post-gadolinium enhancement, confirmed the continued evidence of ischemic change and cortical laminar necrosis of the left frontal lobe and lentiform nucleus. No vascular malformations or other abnormalities were noted in the remainder of the brain and radiology of the abdomen and limbs was normal. Array cytogenetic analysis (a-CGH) was normal in the surviving twin but genetic testing of skin on the fetus papyraceus was unsuccessful. At follow-up of 3 months, the areas of aplasia had healed (Fig. 5) with scarring and regrowth of hair follicles. Development appeared normal for age and growth was proceeding along the second centiles for height and weight.
Methylenedioxymethamphetamine (MDMA)-induced toxic leukoencephalopathy: a case report
Published in Psychiatry and Clinical Psychopharmacology, 2018
Haitham Salem, Travis Barton, Taha Ali, Ashley Anderson, Antonio L Teixeira
The attending clinicians considered hypotheses of delirium and/or puerperal psychosis and conducted a comprehensive workup in the inpatient setting. Her lab results, which included a complete blood count, metabolic panel, lipid profile, thyroid function tests, and serum toxicological screen, were all unrevealing. A magnetic resonance imaging (MRI) of the brain (Figure 1) showed diffuse, extensive confluent T2 hyper-intensity of the periventricular deep and subcortical white matter. There was sparing of subcortical U-fibres with associated patchy areas of abnormal restricted diffusion/cytotoxic oedema, predominantly along the deep and subcortical white matter. There was also signal abnormality that involved the bilateral caudate heads and lentiform nucleus. To a lesser extent, there was also involvement of the bilateral thalami. Subtle T2 hyper-intensity involving the left insular cortex and left amygdala was noted. Based on these findings, the diagnosis of delirium due to toxic leukoencephalopathy was strongly suspected. The patient was sent to an inpatient neurology setting for further investigation and management.