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      Unilateral thalamic infarction onset with lethargy: A case report and literature review

      research-article
      , MD a , , MD b , , MD a , , MD a , , MD, PhD a , * ,
      Medicine
      Lippincott Williams & Wilkins
      case report, cerebral infarction, lethargy, reticular nucleus of thalamus, review

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          Introduction:

          Infarct-induced lethargy is a common disabling symptom that lacks a consensual definition and a standardized method of care. Identifying the causes of the infarct in the thalamic reticular nucleus (TRN) induced lethargy is crucial in stroke patients.

          Case presentation:

          A 68-year-old female patient was admitted to the hospital with lethargy and weakness in the right limb. A computed tomography (CT) scan performed at the presentation showed no bleeding. She was given intravenous thrombolysis. A head computed tomography (CT) scan clearly showed that the infarct was located in the TRN. After 1 hour of treatment, the weakness in the patient’s limb was relieved. However, she was still lethargic, but her lethargy symptoms improved after 3 days.

          Discussion and conclusions:

          Our case highlights that despite the small size of the infarct, the patient was unconscious, which makes it difficult for physicians to understand and treat the condition, resulting in trouble managing the case. We performed a literature review and proposed that the infarction located in the TRN causes lethargy. However, further clinical and pathophysiological research is still needed to improve patient care.

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          Most cited references31

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          Cholinergic innervation of cortex by the basal forebrain: cytochemistry and cortical connections of the septal area, diagonal band nuclei, nucleus basalis (substantia innominata), and hypothalamus in the rhesus monkey.

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            Control of sleep and wakefulness.

            This review summarizes the brain mechanisms controlling sleep and wakefulness. Wakefulness promoting systems cause low-voltage, fast activity in the electroencephalogram (EEG). Multiple interacting neurotransmitter systems in the brain stem, hypothalamus, and basal forebrain converge onto common effector systems in the thalamus and cortex. Sleep results from the inhibition of wake-promoting systems by homeostatic sleep factors such as adenosine and nitric oxide and GABAergic neurons in the preoptic area of the hypothalamus, resulting in large-amplitude, slow EEG oscillations. Local, activity-dependent factors modulate the amplitude and frequency of cortical slow oscillations. Non-rapid-eye-movement (NREM) sleep results in conservation of brain energy and facilitates memory consolidation through the modulation of synaptic weights. Rapid-eye-movement (REM) sleep results from the interaction of brain stem cholinergic, aminergic, and GABAergic neurons which control the activity of glutamatergic reticular formation neurons leading to REM sleep phenomena such as muscle atonia, REMs, dreaming, and cortical activation. Strong activation of limbic regions during REM sleep suggests a role in regulation of emotion. Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function. Sleep disruption interferes with the normal restorative functions of NREM and REM sleep, resulting in disruptions of breathing and cardiovascular function, changes in emotional reactivity, and cognitive impairments in attention, memory, and decision making.
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              • Article: not found

              The function of the sleep spindle: a physiological index of intelligence and a mechanism for sleep-dependent memory consolidation.

              Until recently, the electrophysiological mechanisms involved in strengthening new memories into a more permanent form during sleep have been largely unknown. The sleep spindle is an event in the electroencephalogram (EEG) characterizing Stage 2 sleep. Sleep spindles may reflect, at the electrophysiological level, an ideal mechanism for inducing long-term synaptic changes in the neocortex. Recent evidence suggests the spindle is highly correlated with tests of intellectual ability (e.g.; IQ tests) and may serve as a physiological index of intelligence. Further, spindles increase in number and duration in sleep following new learning and are correlated with performance improvements. Spindle density and sigma (14-16Hz) spectral power have been found to be positively correlated with performance following a daytime nap, and animal studies suggest the spindle is involved in a hippocampal-neocortical dialogue necessary for memory consolidation. The findings reviewed here collectively provide a compelling body of evidence that the function of the sleep spindle is related to intellectual ability and memory consolidation. Copyright © 2010 Elsevier Ltd. All rights reserved.

                Author and article information

                Contributors
                Journal
                Medicine (Baltimore)
                Medicine (Baltimore)
                MD
                Medicine
                Lippincott Williams & Wilkins (Hagerstown, MD )
                0025-7974
                1536-5964
                02 December 2022
                02 December 2022
                : 101
                : 48
                : e32158
                Affiliations
                [a ] Department of Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China
                [b ] Department of Anaesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.
                Author notes
                * Correspondence: Yanbin Wang, Department of Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, No. 20 Yuhuangding East Road, Yantai 264000, China (e-mail: jietong-5@ 123456163.com ).
                Author information
                https://orcid.org/0000-0002-9519-3014
                Article
                00081
                10.1097/MD.0000000000032158
                9726381
                36482596
                4ca1085a-bb08-43a2-bbc3-92434eabbf43
                Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 28 October 2022
                : 11 November 2022
                : 14 November 2022
                Categories
                5300
                Research Article
                Clinical Case Report
                Custom metadata
                TRUE

                case report,cerebral infarction,lethargy,reticular nucleus of thalamus,review

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