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Journal articles on the topic 'Central nervous system; Depression'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Reid, Kenneth H., Roger Marrannes, and Albert Wauquier. "Spreading depression and central nervous system pharmacology." Journal of Pharmacological Methods 19, no. 1 (March 1988): 1–21. http://dx.doi.org/10.1016/0160-5402(88)90040-x.

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2

Krause, Monica, and Sara Hocker. "Toxin-Induced Coma and Central Nervous System Depression." Neurologic Clinics 38, no. 4 (November 2020): 825–41. http://dx.doi.org/10.1016/j.ncl.2020.07.002.

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3

Glassman, Alexander H. "Depression, Cardiac Death, and the Central Nervous System." Neuropsychobiology 37, no. 2 (1998): 80–83. http://dx.doi.org/10.1159/000026482.

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4

Redmond, A. D. "CENTRAL NERVOUS SYSTEM DEPRESSION AND HIGH BLOOD ETHANOL LEVELS." Lancet 327, no. 8484 (April 1986): 805. http://dx.doi.org/10.1016/s0140-6736(86)91818-0.

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5

Davis, AndrewR, and AnthonyH Lipson. "CENTRAL-NERVOUS-SYSTEM DEPRESSION AND HIGH BLOOD ETHANOL LEVELS." Lancet 327, no. 8480 (March 1986): 566. http://dx.doi.org/10.1016/s0140-6736(86)90928-1.

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6

Schuster, Louis. "Central Nervous System Peptide Mechanisms in Stress and Depression." Journal of Clinical Psychopharmacology 11, no. 5 (October 1991): 333. http://dx.doi.org/10.1097/00004714-199110000-00023.

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7

HASKETT, ROGER F. "Central Nervous System Peptide Mechanisms in Stress and Depression." American Journal of Psychiatry 151, no. 1 (January 1994): 139—a—140. http://dx.doi.org/10.1176/ajp.151.1.139-a.

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8

Ross, Bradford A. "Central nervous system depression from ingestion of nonprescription eyedrops." Journal of Emergency Medicine 2, no. 4 (January 1985): 315. http://dx.doi.org/10.1016/0736-4679(85)90133-7.

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9

Chen, Kai, Liu Nan Yang, Chuan Lai, Dan Liu, and Ling-Qiang Zhu. "Role of Grina/Nmdara1 in the Central Nervous System Diseases." Current Neuropharmacology 18, no. 9 (October 6, 2020): 861–67. http://dx.doi.org/10.2174/1570159x18666200303104235.

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Glutamate receptor, ionotropic, N-methyl-D-aspartate associated protein 1 (GRINA) is a member of the NMDA receptors (NMDARs) and is involved in several neurological diseases, which governs the key processes of neuronal cell death or the release of neurotransmitters. Upregulation of GRINA has been reported in multiple diseases in human beings, such as major depressive disorder (MDD) and schizophrenia (SCZ), with which the underlying mechanisms remain elusive. In this review, we provide a general overview of the expression and physiological function of GRINA in the central nervous system (CNS) diseases, including stroke, depression ,epilepsy, SCZ, and Alzheimer’s disease (AD).

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10

Andrieieva, O. G., V. I. Yanchenko, V. S. Vasylyk, P. A. Dyachenko, and L. V. Muravskya. "Anxiety-depressive syndrome in patients with damage to the central nervous system by herpes viruses." Reports of Vinnytsia National Medical University 25, no. 1 (March 27, 2021): 57–61. http://dx.doi.org/10.31393/reports-vnmedical-2021-25(1)-10.

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Annotation. Purpose of work – a study of the prevalence and severity of anxiety-depressive syndrome based on the Hospital Anxiety and Depression Scale (HADS) in patients with damage to the nervous system of hepatic virus etiology. In this study, 2 groups of 30 people took part. The first group (main) is 30 people from a verified diagnosis of herpesviral damage to the nervous system aged 14 to 74 years. Viruses were in the stage of activation and persistence. The second group (control), almost healthy people – 30 people. There were 20 women and 10 men in each group. Diagnoses: Encephalitis, meningoencephalitis, arachnoencephalitis, arachnoiditis, disseminated encephalomyelitis, polyneuropathy, arachnoencephalopolyneuropathy, multiple sclerosis. Etiological factors were: HSV, EBV, VZV, HHV-7 + EBV, EBV + VZV, EBV + HSV, EBV + HHV-6, HSV + VZV, HSV + CMV + EBV + VZV, HSV + VZV + CMV + EBV + Tox.g. In all persons of the first group, a moderate course was observed. All subjects were tested on a hospital anxiety and depression scale (HADS). It was established that patients suffering from lesions of the nervous system of herpes virus etiology have signs of depression and anxiety. The duration in days of subclinically expressed depression in 9 people of the first group was 2.54±0.98, at p=0.04, and in the second group, depression not observed. Anxiety was subliminally expressed in the first group in 7 people, the duration in days was 4.20±1.20, and in the second group in 2 people, which was 1.0±0.69, with p=0.02. Thus, in patients with herpes virus lesions of the nervous system, anxiety-depressive syndrome is more pronounced than in practically healthy persons, perhaps this is due to damage to the limbic-diencephalic system of the brain.

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11

Minocha, Anil, Jeffrey T. Barth, David A. Herold, Deborah A. Gideon, and Daniel A. Spyker. "Modulation of ethanol-induced central nervous system depression by ibuprofen." Clinical Pharmacology and Therapeutics 39, no. 2 (February 1986): 123–27. http://dx.doi.org/10.1038/clpt.1986.22.

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12

Mattucci-Schiavone, Linda, and Andrew P. Ferko. "Effect of muscimol on ethanol-induced central nervous system depression." Pharmacology Biochemistry and Behavior 27, no. 4 (August 1987): 745–48. http://dx.doi.org/10.1016/0091-3057(87)90202-4.

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13

Zubenko, George S. "Neurobiology of Major Depression in Alzheimer's Disease." International Psychogeriatrics 12, S1 (July 2000): 217–30. http://dx.doi.org/10.1017/s1041610200007079.

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The original catecholamine hypothesis of affective disorders focused largely on the role of the noradrenergic components of the central nervous system in the etiology of depression and mania (Bunney & Davis, 1965; Schildkraut, 1965). Additional evidence from clinical, pharmacologic, and physiologic studies has emerged since the original hypothesis was proposed and generally supports the view that clinically significant depression can result from a dysfunction of central nervous system mechanisms employing the catecholamine neurotransmitters norepinephrine and dopamine (Jimerson, 1987; Siever, 1987). Neurochemical studies of serotonin (5-HT) receptors and 5-hydroxyindoleacetic acid (5-HIAA) in spinal fluid or brain tissue also suggest an alteration in serotonergic components of the central nervous system in both idiopathic major depression and suicide (Brikmayer & Riederer, 1975; Crow et al., 1984; Lloyd et al., 1974; Mendlewicz et al., 1981; Stanley & Mann, 1983). In contrast to these hypotheses, which suggest that depression may result from the decreased function of one or more central aminergic systems, the cholinergic hypothesis of affective disorders (Janowsky & Risch, 1987) posits that idiopathic depression is associated with the hyperfunctioning of cholinergic systems. This hypothesis is especially interesting in the context of Alzheimer's disease (AD) because the progression of the central cholinergic deficit that occurs in this disorder may interact with the pathophysiology of depression to limit the prevalence of major depression in later stages of this disorder.

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Maia, L., A. Sofia Coutinho, G. C. Irina, and L. Carneiro. "Psychiatric Presentations of Central Nervous System Tumors." European Psychiatry 33, S1 (March 2016): S499. http://dx.doi.org/10.1016/j.eurpsy.2016.01.1837.

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IntroductionFor the most part, central nervous system (CNS) tumors present themselves with focal neurologic sing or manifestations resulting from increased intracranial pressure. However, in particular cases, these tumors may present exclusively psychiatric symptoms.ObjectiveThis communication explores importance of CNS tumors as differential diagnosis of various psychiatric disorders.AimsHighlight the need of acknowledging this important differential diagnosis (CNS tumors) in current psychiatry practice, while presenting a clinical case as an example of the subject.MethodsIt is exposed a bibliographic review of the topic, followed by the description of a clinical case regarding a patient with pituitary adenoma and simultaneous installation of psychotic symptoms namely delusional paranoid ideation.ResultsThe authors present a case report of a 66-year-old patient admitted compulsively in a Psychiatric ward in the context of behavioral changes associated with delusional ideation of paranoid content. Multidisciplinary assessed by specialties of Psychiatry, Neurology, Neurosurgery, Endocrinology and Psychology, concluded by the presence of nonfunctioning pituitary adenoma associated with cognitive major disturbance.ConclusionsThe tumors of the CNS can be associated with a whole variety of psychiatric symptoms such as psychosis, anxiety, depression or cognitive impairment, even in the absence of organic/neurological symptoms. Its role in the genesis of psychiatric symptomatology makes these neoplasias an important differential diagnosis, whose clinical approach should include different medical specialties integrated as a multidisciplinary team.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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15

Pupo, Andre S., and Kenneth P. Minneman. "Adrenergic Pharmacology: Focus on the Central Nervous System." CNS Spectrums 6, no. 8 (August 2001): 656–62. http://dx.doi.org/10.1017/s1092852900001346.

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ABSTRACTNorepinephrine and epinephrine are involved in the control of several important functions of the central nervous system (CNS), including sleep, arousal, mood, appetite, and autonomic outflow. Catecholamines control these functions through activation of a family of adrenergic receptors (ARs). The ARs are divided into three subfamilies (α1, α2, and β) based on their pharmacologic properties, signaling mechanisms, and structure. ARs in the CNS are targets for several therapeutic agents used in the treatment of depression, obesity, hypertension, and other diseases. Not much is known, however, about the role of specific AR sub-types in the actions of these drugs. In this paper, we provide an overview of adrenergic pharmacology in the CNS, focusing on the pharmacologic properties of subtype-selective AR agonists and antagonists, the accessibility of these drugs to the CNS, and the distribution of ARs in different areas of the brain.

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16

Tsyrlin, V. A. "Central regulation of circulation and arterial hypertension." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 12, no. 1 (February 28, 2006): 66–79. http://dx.doi.org/10.18705/1607-419x-2006-12-1-66-79.

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Modern concepts about role of autonomic nervous system central regulation disturbance in pathogenesis of arterial hypertension are analysed in this article. Also it is examined presented hypothesis. explaining the increase of sympathetic nervous system activity and depression of vagal nerve tonuson experimental pathology at animals and essential hypertension at human.

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17

Bloemer, Jenna, Priyanka D. Pinky, Manoj Govindarajulu, Hao Hong, Robert Judd, Rajesh H. Amin, Timothy Moore, Muralikrishnan Dhanasekaran, Miranda N. Reed, and Vishnu Suppiramaniam. "Role of Adiponectin in Central Nervous System Disorders." Neural Plasticity 2018 (July 29, 2018): 1–15. http://dx.doi.org/10.1155/2018/4593530.

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Adiponectin, the most abundant plasma adipokine, plays an important role in the regulation of glucose and lipid metabolism. Adiponectin also possesses insulin-sensitizing, anti-inflammatory, angiogenic, and vasodilatory properties which may influence central nervous system (CNS) disorders. Although initially not thought to cross the blood-brain barrier, adiponectin enters the brain through peripheral circulation. In the brain, adiponectin signaling through its receptors, AdipoR1 and AdipoR2, directly influences important brain functions such as energy homeostasis, hippocampal neurogenesis, and synaptic plasticity. Overall, based on its central and peripheral actions, recent evidence indicates that adiponectin has neuroprotective, antiatherogenic, and antidepressant effects. However, these findings are not without controversy as human observational studies report differing correlations between plasma adiponectin levels and incidence of CNS disorders. Despite these controversies, adiponectin is gaining attention as a potential therapeutic target for diverse CNS disorders, such as stroke, Alzheimer’s disease, anxiety, and depression. Evidence regarding the emerging role for adiponectin in these disorders is discussed in the current review.

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18

Chandavasu, O., and S. Chatkupt. "Central nervous system depression from chlorpromazine poisoning: Successful treatment with naloxone." Journal of Pediatrics 106, no. 3 (March 1985): 515–16. http://dx.doi.org/10.1016/s0022-3476(85)80695-8.

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19

SAISSY, J. M., M. VITRIS, J. DEMAZIÈRE, M. SECK, L. MARCOUX, and M. GAYE. "Flumazenil Counteracts Intrathecal Baclofen-induced Central Nervous System Depression in Tetanus." Anesthesiology 76, no. 6 (June 1, 1992): 1051–53. http://dx.doi.org/10.1097/00000542-199206000-00027.

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20

Tobias, Joseph D. "Central Nervous System Depression Following Accidental Ingestion of Visine Eye Drops." Clinical Pediatrics 35, no. 10 (October 1996): 539–40. http://dx.doi.org/10.1177/000992289603501010.

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21

Amagasu, S. M., A. A. Mikulec, and M. B. Maclver. "Halothane-induced Depression of Axonal Conduction in Mammalian Central Nervous System Fibers." Anesthesiology 81, SUPPLEMENT (September 1994): A1476. http://dx.doi.org/10.1097/00000542-199409001-01475.

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22

Karatas, Aydin Deniz. "Severe central nervous system depression in a patient with acute imidacloprid poisoning." American Journal of Emergency Medicine 27, no. 9 (November 2009): 1171.e5–1171.e7. http://dx.doi.org/10.1016/j.ajem.2009.01.006.

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23

Li, Li, Huijuan Wu, Jialin Qian, Mingzhen Li, Yue Li, Baoming Li, Yu Han, et al. "Decreased Na+/K+ ATPase α1 (ATP1A1) gene expression in major depression patients’ peripheral blood." Open Life Sciences 8, no. 11 (November 1, 2013): 1077–82. http://dx.doi.org/10.2478/s11535-013-0207-8.

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AbstractMajor depression affects the central nervous system and thereafter the autonomic nervous system, immune system, and endocrine system. Na+/K+ ATPase, as a major mediator of cellular transmembrane ionic gradients, plays an important role in nervous signal transduction. Three types of Na+/K+ ATPase α subunit isoforms (ATP1A1, ATP1A2, and ATP1A3) are found in brain but vary in the type of cell and level of expression. It has been confirmed that reduced expression of ATP1A2 and ATP1A3 are related to depressive disorder. However, there is no reported correlation between ATP1A1 and major depression. This study investigated the potential correlation between ATP1A1 gene expression level and major depression. The expression levels of ATP1A1 gene in the peripheral circulation of both depressive patients and healthy human controls were quantified by using reverse transcripted quantitative polymerase chain reaction. Statistical analysis showed a significant decrease of ATP1A1 expression level in major depression patients when compared to that of healthy controls (P<0.01). The differences of gene nucleotide sequences and protein structures among ATP1A1, ATP1A2, and ATP1A3 were also illustrated. This study demonstrates, for the first time, that ATP1A1 gene expression level is significantly associated with major depression and suggests that ATP1A1 could be a significant molecular marker for diagnosis.

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Drisdale III, John K., Monica G. Thornhill, and Alexandre R. Vieira. "Specific Central Nervous System Medications Are Associated with Temporomandibular Joint Symptoms." International Journal of Dentistry 2017 (2017): 1–5. http://dx.doi.org/10.1155/2017/1026834.

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Aims. There is evidence of association between bruxism and the increasingly common central nervous system stimulants prescribed for attention deficit hyperactivity disorder (ADHD), as well as the selective serotonin reuptake inhibitors (SSRIs) often prescribed for depression or anxiety. However, the evidence is not clear on whether these medications inducing bruxism are directly associated with temporomandibular joint disorder (TMD). The aim of this work is to evaluate whether these medications are associated with TMD symptoms.Methods. Medical history and participant data were obtained for 469 patients from the University of Pittsburgh School of Dental Medicine, Dental Registry and DNA Repository, dating back to 2006. The chi-square test was used to determine any statistically significant associations.Results. There were no statistically significant associations between ADHD stimulant medications or SSRIs and reported TMD symptoms. However, there were significant differences seen between specific brands of medications and reported TMD symptoms. Individuals prescribed methylphenidate (Concerta) were less likely to report temporomandibular joint discomfort (p=0.01). Conversely, individuals prescribed citalopram (Celexa) were more likely to report temporomandibular joint discomfort (p=0.04).Conclusion. Signs and symptoms of temporomandibular joint dysfunction may be influenced by the use of certain medications prescribed for depression or attention deficit hyperactive disorder.

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Murinson, Beth Brianna, and Angela Vincent. "Stiff-Person Syndrome: Autoimmunity and the Central Nervous System." CNS Spectrums 6, no. 5 (November 2001): 427–33. http://dx.doi.org/10.1017/s1092852900021805.

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AbstractStiff-person syndrome (SPS) is a rare disease of severe progressive muscle stiffness in the spine and lower extremities with superimposed muscle spasms triggered by external stimuli. Patients with SPS are often referred for psychiatric evaluation and the psychiatrist may be the first to diagnosis SPS. Psychosocial stressors often precede the first manifestations of the disease; depression, anxiety, and alcohol abuse are comorbid illnesses. The identification of an association with antibodies to glutamic acid decarboxylase (GAD) was invaluable for definitively establishing a pathological basis for the disease; antibodies to amphiphysin and gephyrin are also found in cases of SPS but at much lower frequencies. Whether the antibodies inhibit GAD activity in vivo, target GAD-expressing neurons for immune-mediated destruction, are part of a wider immune process, or are merely a marker for destruction of GAD-expressing neurons by an independent neurodegenerative process is not yet clear. Both electromyography and the detection of GAD antibodies are useful in establishing a diagnosis of SPS. Treatment of SPS includes the use of immunomodulating therapies (plasmapheresis and intravenous immunoglobulins) and symptomatic treatment with benzodiazepines and baclofen. The use of tricyclic antidepressants and rapid withdrawal from therapy should be avoided.

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Ludders, JW, GC Seaman, and HN Erb. "Inhalant anesthetics and inspired oxygen: implications for anesthesia in birds." Journal of the American Animal Hospital Association 31, no. 1 (January 1, 1995): 38–41. http://dx.doi.org/10.5326/15473317-31-1-38.

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A number of factors cause respiratory depression in anesthetized birds. Hypoventilation can be due to anesthetic-induced depression of the central nervous system, muscular relaxation of the muscles of respiration, and effects on central and peripheral chemoreceptors. Compared to mammals, respiratory function in birds may be more sensitive to the effects of inhalant anesthetics because of their effect on unique carbon dioxide (CO2)-sensitive intrapulmonary chemoreceptors located within the avian lung. High fractions of inspired oxygen also contribute to hypoventilation, possibly by depressing oxygen-sensitive chemoreceptors. This article is a review of the factors that cause respiratory depression in anesthetized birds.

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Fontes, H., H. Nzwalo, S. Mendes, S. Fernandes, G. Ponte, and M. Pereira. "Central nervous system vasculitis presenting as acute psychotic disorder." European Psychiatry 26, S2 (March 2011): 745. http://dx.doi.org/10.1016/s0924-9338(11)72450-6.

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IntroductionAcute psychosis can represent a diagnosis challenge. Several disorders can be implicated, and some representing a life threatening condition. We report a rare case of acute psychosis with persistent soft neurological signs as a primary presentation of a central nervous system vasculitis.ResultsA 23 year old man, with antecedent of depression, previous history of cocaine and marijuana abuse, admitted to an acute psychiatric ward with three days evolution of disturbed behavior, mainly isolation and immobility. On the psychiatric ward he appeared vague, with negativism, inattentiveness, and elementary and incoherent speech. He had unsystematised delusions. His neurological examination revealed a slight ataxic gait and discoordination, and signs of frontal lobe release. Initial extensive complementary study, including brain CT, EEG, and urine toxicology were negative. He began treatment with risperidone and clomipramine, with improvement of his mental condition, and by the second week he was able maintain a coherent speech. The neurological signs did not improve, and frequent falls appeared. We performed a brain MRI who revealed lesions compatible with vasculitis. The extensive liquor study was negative, with exception of proteins levels (56 md/dl). He was transferred to an internal medicine ward, treated with corticoesteroid. His condition improved in the following weeks and on discharge from Hospital he had recovered his mental status and was autonomous.ConclusionsPsychosis is an uncommon presentation of central nervous system vasculitis. In cases of persistence or progression of the soft neurological signs, further complementary study is essential to exclude organic pathology.

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Robson, Matthew J., Meagan A. Quinlan, and Randy D. Blakely. "Immune System Activation and Depression: Roles of Serotonin in the Central Nervous System and Periphery." ACS Chemical Neuroscience 8, no. 5 (April 3, 2017): 932–42. http://dx.doi.org/10.1021/acschemneuro.6b00412.

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29

Kook, A. I., A. Mizruchin, N. Odnopozov, H. Gershon, and Y. Segev. "Depression and immunity: The biochemical interrelationship between the central nervous system and the immune system." Biological Psychiatry 37, no. 11 (June 1995): 817–19. http://dx.doi.org/10.1016/0006-3223(95)00038-i.

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Carlsen, Jeffrey O., Norman A. Zabriskie, Young H. Kwon, Maria E. Barbe, and William E. Scott. "Apparent central nervous system depression in infants after the use of topical brimonidine." American Journal of Ophthalmology 128, no. 2 (August 1999): 255–56. http://dx.doi.org/10.1016/s0002-9394(99)00083-5.

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31

Wyszynski, Antoinette Ambrosino, and Bernard Wyszynski. "Treatment of Depression With Fluoxetine in Corticosteroid-Dependent Central Nervous System Sjögren's Syndrome." Psychosomatics 34, no. 2 (March 1993): 173–77. http://dx.doi.org/10.1016/s0033-3182(93)71910-6.

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32

Kiryazov, Kiril, Mariyka Stefova, and Violeta Iotova. "Can Ophthalmic Drops Cause Central Nervous System Depression and Cardiogenic Shock in Infants?" Pediatric Emergency Care 29, no. 11 (November 2013): 1207–9. http://dx.doi.org/10.1097/pec.0b013e3182aa1384.

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33

Wells, Douglas G., and Gerald Davies. "Profound Central Nervous System Depression from Epidural Fentanyl for Extracorporeal Shock Wave Lithotripsy." Anesthesiology 67, no. 6 (December 1, 1987): 991–92. http://dx.doi.org/10.1097/00000542-198712000-00022.

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Shagalov, Devorah R., Drew Taylor, Rachel Schleichert, Jonathan Weiss, and Eduardo Weiss. "Association of Central Nervous System Depression With Topical Brimonidine When Used for Hemostasis." JAMA Dermatology 153, no. 6 (June 1, 2017): 575. http://dx.doi.org/10.1001/jamadermatol.2017.0247.

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Okic, M., T. Johnson, J. A. Crifasi, C. Long, and E. K. Mitchell. "Swift Onset of Central Nervous System Depression and Asystole Followingan Overdose of Guaifenesin." Journal of Analytical Toxicology 37, no. 5 (April 11, 2013): 318–19. http://dx.doi.org/10.1093/jat/bkt030.

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Karabiber, Hamza, M. Ayse Selimoglu, Melek Cetin, Serap Tekin, and Sibel Gurbuz. "Acute Central Nervous System Depression after Subcutaneous Use of Prilocaine in an Infant." Journal of Emergency Medicine 42, no. 4 (April 2012): e95-e96. http://dx.doi.org/10.1016/j.jemermed.2010.05.061.

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Li, Xun, Shifeng Chu, Yinjiao Liu, and Naihong Chen. "Neuroprotective Effects of Anthraquinones from Rhubarb in Central Nervous System Diseases." Evidence-Based Complementary and Alternative Medicine 2019 (May 16, 2019): 1–12. http://dx.doi.org/10.1155/2019/3790728.

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Rhubarb is a well-known traditional Chinese medicine; it has been used in China for thousands of years. Rhubarb anthraquinones are the major medicinal ingredients derived from rhubarb including emodin, aloe-emodin, chrysophanol, rhein, physcion, and danthron. These different anthraquinone derivatives alone or in combination play a therapeutic role in central nervous system diseases (CNSD), such as cerebral ischemic stroke, intracerebral hemorrhage, traumatic brain injury, brain tumor, Alzheimer’s disease, depression, and others. We review the experimental studies on these six anthraquinones in the treatment of CNSD by consulting literature published in the last 20 years in PubMed and then give a future perspective on it. In the end of this paper some deficiencies related to these studies also have been pointed out.

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Aydin, Kürsad, Selim Kurtoglu, M. Hakan Poyrazoglu, Kazim Üzüm, H. Basri Üstünbas, and I. Kurtulus Hallaç. "Amitraz poisoning in children: Clinical and laboratory findings of eight cases." Human & Experimental Toxicology 16, no. 11 (November 1997): 680–82. http://dx.doi.org/10.1177/096032719701601109.

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Amitraz poisoning is a rare disorder characterised by central nervous system and respiratory depression, bradycardia, hypotension, hypothermia, hyperglycemia, vomiting, convulsion and glycosuria. In this study, eight pediatric patients with amitraz poisoning were presented. This study revealed that clinical manifestations of poisoning by oral and dermal route emerged within 30- 120 min and that central nervous system depression which is the most important sign resolved with 8-18 h and others 36-48 h. All cases were discharged as recovered after 48 h. To our knowledge only six cases have been reported in the literature. Because of the limited information in the literature, the cases were reported.

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Gold, Philip W. "The PPARg System in Major Depression: Pathophysiologic and Therapeutic Implications." International Journal of Molecular Sciences 22, no. 17 (August 26, 2021): 9248. http://dx.doi.org/10.3390/ijms22179248.

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To an exceptional degree, and through multiple mechanisms, the PPARg system rapidly senses cellular stress, and functions in the CNS in glial cells, neurons, and cerebrovascular endothelial cell in multiple anti-inflammatory and neuroprotective ways. We now know that depression is associated with neurodegeneration in the subgenual prefrontal cortex and hippocampus, decreased neuroplasticity, and defective neurogenesis. Brain-derived neurotrophic factor (BDNF) is markedly depleted in these areas, and is thought to contribute to the neurodegeneration of the subgenual prefrontal cortex and the hippocampus. The PPARg system strongly increases BDNF levels and activity in these brain areas. The PPARg system promotes both neuroplasticity and neurogenesis, both via effects on BDNF, and through other mechanisms. Ample evidence exists that these brain areas transduce many of the cardinal features of depression, directly or through their projections to sites such as the amygdala and nucleus accumbens. Behaviorally, these include feelings of worthlessness, anxiety, dread of the future, and significant reductions in the capacity to anticipate and experience pleasure. Physiologically, these include activation of the CRH and noradrenergic system in brain and the sympathetic nervous system and hypothalamic–pituitary–adrenal axis in the periphery. Patients with depression are also insulin-resistant. The PPARg system influences each of these behavioral and physiological in ways that would ameliorate the manifestations of depressive illness. In addition to the cognitive and behavioral manifestations of depression, depressive illness is associated with the premature onsets of coronary artery disease, stroke, diabetes, and osteoporosis. As a consequence, patients with depressive illness lose approximately seven years of life. Inflammation and insulin resistance are two of the predominant processes that set into motion these somatic manifestations. PPARg agonists significantly ameliorate both pathological processes. In summary, PPARg augmentation can impact positively on multiple significant pathological processes in depression. These include loss of brain tissue, defective neuroplasticity and neurogenesis, widespread inflammation in the central nervous system and periphery, and insulin resistance. Thus, PPARg agonists could potentially have significant antidepressant effects.

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Asgary, Sedigheh. "Saffron and depression." Bioactive Compounds in Health and Disease 4, no. 5 (May 27, 2021): 90. http://dx.doi.org/10.31989/bchd.v4i5.808.

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Throughout the centuries, people have used the dried stigma of Crocus sativus that is known as "saffron" for medicinal and nutritional purposes [1]. Studies have shown that not only is saffron well worth the money, but also, its bioactive compounds (including crocin, precrocin, and safranal that are responsible for color, taste and fragrance respectively) play a crucial role in the central nervous system to positively affect conditions such as anxiety and depression [2-5]. Saffron compounds are also neuroprotective and anxiolytic and can benefit learning and memory impairments [6].

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Lam, Jessica, Lauren Kelly, Catherine Ciszkowski, Marieke L. A. Landsmeer, Marieke Nauta, Bruce C. Carleton, Michael R. Hayden, Parvaz Madadi, and Gideon Koren. "Central Nervous System Depression of Neonates Breastfed by Mothers Receiving Oxycodone for Postpartum Analgesia." Journal of Pediatrics 160, no. 1 (January 2012): 33–37. http://dx.doi.org/10.1016/j.jpeds.2011.06.050.

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Pöyhiä, Reino, and Eija A. Kalso. "Antinociceptive Effects and Central Nervous System Depression Caused by Oxycodone and Morphine in Rats." Pharmacology & Toxicology 70, no. 2 (February 1992): 125–30. http://dx.doi.org/10.1111/j.1600-0773.1992.tb00441.x.

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Isbister, Geoffrey K., Simon P. Heppell, Colin B. Page, and Nicole M. Ryan. "Adult clonidine overdose: prolonged bradycardia and central nervous system depression, but not severe toxicity." Clinical Toxicology 55, no. 3 (January 20, 2017): 187–92. http://dx.doi.org/10.1080/15563650.2016.1277234.

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Ferko, Andrew P. "Effects of L-ascorbic acid on ethanol-induced central nervous system depression in mice." Pharmacology Biochemistry and Behavior 24, no. 3 (March 1986): 543–47. http://dx.doi.org/10.1016/0091-3057(86)90555-1.

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Wadepuhl, M. "Depression of excitatory motoneurones by a single neurone in the leech central nervous system." Journal of Experimental Biology 143, no. 1 (May 1, 1989): 509–27. http://dx.doi.org/10.1242/jeb.143.1.509.

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Intracellular staining techniques have been used to characterize the morphology of a newly identified neurone, cell 151, in the segmental ganglia of the leech. This neurone ramifies extensively within the neuropile and sends multiple extensions into roots and connectives. Strong dye coupling and non-rectifying electrical coupling were observed between the contralateral homologues. No action potentials were recorded from the cell body, but postsynaptic potentials and slow potential changes (greater than 1 s, greater than 15 mV) were observed. Upon injection of hyperpolarizing currents, the efferent spike activity, recorded extracellularly, was depressed in both the ipsi- and the contralateral roots of the ganglion. The depression was gradual and non-adapting and occurred reliably only within the ganglion where cell 151 is situated. Depolarization of cell 151 was without consequence for the tonic firing of isolated ganglia. Many identified excitatory motoneurones follow the hyperpolarization of cell 151. Currents can be exchanged between cell 151 and motoneurones via rectifying electrical synapses. Spontaneous hyperpolarizations of cell 151 were correlated with depression of spike frequencies, recorded in whole nerves as well as in identified motoneurones. The membrane potential of cell 151 was drastically altered by bursts from mechanosensory cells. The ability of cell 151 to distribute inhibition onto a great number of motoneurones and to curtail excessive neuronal activity is discussed.

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Patel, Rutu M., and Digvijaysinh G. Rana. "ROLE OF INSULIN-LIKE GROWTH FACTOR IN DEPRESSION: A REVIEW." International Research Journal of Pharmacy 12, no. 3 (April 6, 2021): 6–10. http://dx.doi.org/10.7897/2230-8407.1203124.

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Depression is a disorder of unknown origin and it involves disturbance of many physiological processes. There are many mechanisms in depression including alterations in neurotrophic factors. It has been suggested in this review that an impairment of synaptic plasticity in specific areas of central nervous system, specifically in hippocampus can be an important factor in the pathophysiology of depression. Further, an abnormal neural plasticity may be related to alterations in the level of neurotrophic factors. In context with this, it can be suggested that there can be a connection between occurrences of depression with the disturbance of neurotrophic factors, raising great attention in the recent years. In the present review, it has been tried to explain the significance of insulin-like growth factor in depression by presenting the several important topics such as neurotrophic factors in depression, insulin like growth factor in central nervous system, insulin like growth factor receptor in depression, neurotrophic role of insulin like growth factor and correlation between insulin like growth factor and brain serotonin levels.

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Khaitovych, M. V. "THE ROLE OF MAGNESIUM DEFICIENCY AND ITS SUPPLEMATION IN DISEASES OF CENTRAL NERVOUS SYSTEM. REVIEW." Medical Science of Ukraine (MSU) 13, no. 3-4 (November 30, 2018): 70–75. http://dx.doi.org/10.32345/2664-4738.3-4.2017.11.

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Relevance. Anti-depressant effects of NMDA receptor antagonists have been proven, a close association between low levels of magnesium in the blood and depression. Therefore, in recent years, antidepressant properties of magnesium are actively studied in animal experiments. Objective: To review modern literary sources about the role of magnesium deficiency in the pathogenesis of diseases of the central nervous system. Materials and methods. Searching for a depth of 12 years at Scopus, Google Scholar. Results. The results of experimental and clinical researches pointed out on association between low level of magnesium in hair, liquor, brain with higher risk of development dementia, depression and anxiety. An additional supplementation with magnesium in patients associates with decreasing risk of ischemic stroke and dementia, in pregnancy – provides neuroprotection of fetus, in case of depression increases effectiveness of antidepressants, in brain injury associates with faster recovery of cognitive functions, in migraines - with decreasing in the frequency of attacks and improvement of the quality patients’ lives, in case of neuroleptic therapy - with the possibility of delayed appearance or absence of manifestations of drug parkinsonism. These changes are explained by antagonistic effects of magnesium on glutamate receptors, decreasing oxidative stress intensity as well as neural cell apoptosis. Conclusion. Magnesium plays an important neuroprotective role.

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Ríos, E., L. Cholich, J. Silva, and O. Acosta de Pérez. "Histopathological lesions in central nervous system of goats poisoned by Ipomoea carnea." Revista Veterinaria 19, no. 2 (July 1, 2008): 130. http://dx.doi.org/10.30972/vet.1921892.

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<p>Ipomoea carnea var. fistulosa (Convolvulaceae) is a perenne poisonous plant, found throughout the Argentine Northeastern. The intoxication produces a lysosomal storage disease in goats, sheep and cattle. Five goats were fed with 50 g/kgBW/day of fresh leaves, flowers and stems of I. carnea, during 43–60 days. Hirsute coat, depression, difficulty to stand up, ataxia, hypermetria, wide–based stance, incoordination of muscular movements, intense tremors, spastic paresis, abnormal postural reactions, nystagmus, hyperreflexia, hypersensitivity to sound, head tilting and loss of equilibrium were observed in all treated animals. The histopathologic study revealed the presence of cytoplasmatic vacuolation mainly in medulla oblongata and cerebellum. Control animals did not show any alterations. We conclude that this poisoning causes central nervous system damage, being Purkinje cells the most severely affected.</p>

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Nowak, Gabriel, Marta Kubera, and Michael Maes. "Neuroimmunological aspects of the alterations in zinc homeostasis in the pathophysiology and treatment of depression." Acta Neuropsychiatrica 12, no. 2 (June 2000): 49–53. http://dx.doi.org/10.1017/s0924270800035705.

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SUMMARYZinc is a trace element which plays a fundamental role in a wide range of biochemical processes in living organisms. Zinc is an essential component of various proteins and is an important factor for physiological function of the mammalian nervous and immune systems. In the central nervous system (CNS), zinc is found at high concentrations in hippocampal neurons. These neurons possess mechanisms for zinc uptake and storage in synaptic terminals and for the stimulation of zinc release along with neurotransmitters. In the central nervous system, zinc modulates predominantly the excitatory (glutamatergic) and inhibitory (GABAergic) amino acid neurotransmission pathways. In the immune system, zinc is necessary for the physiological activity of the thymus and T-cell-dependent responses. Zinc deficiency impairs the activities of the neuroendocrine and immune systems in mammalian organisms. This paper reviews the alterations in the blood and brain zinc concentrations in relation to the neuroimmune pathophysiology and treatment of depression. Major depression is related to lowered serum zinc concentrations, which may be caused by the acute phase and the inflammatory response in that illness. Repeated administration of antidepressants selectively increases and redistributes brain zinc in the hippocampus. Since zinc is an inhibitor of the glutama-te/NMDA receptor, these data are in accordance with the glutamate hypothesis of antidepressant action.

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Misdrahi, D., G. Vila, I. Funk-Brentano, M. Tardieu, S. Blanche, and M. C. Mouren-Simeoni. "DSM-IV mental disorders and neurological complications in children and adolescents with human immunodeficiency virus type 1 infection (HIV-1)." European Psychiatry 19, no. 3 (May 2004): 182–84. http://dx.doi.org/10.1016/j.eurpsy.2003.06.009.

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AbstractAimTo study the types of psychiatric problem encountered in children infected with the human immunodeficiency virus (HIV) and their relationship to central nervous system disorder and the severity of infection.Methods17 HIV-infected children presenting with psychiatric problems were included. Mental disorders were evaluated according to DSM-IV criteria. Neurological disorders and progressive encephalopathy (presence or absence) diagnosis were evaluated by clinical and radiological examination. The severity of infection was assessed by the percentage of CD4 lymphocytes.ResultsThe most frequent diagnoses were major depression (MDD: 47%) and attention deficit hyperactivity disorder (ADHD: 29%). Major depression diagnosis was significantly associated with neuroimaging or clinical neurological abnormalities (p < 0.01). In contrast, no association was found between hyperactivity diagnosed according to DSM-IV criteria and central nervous system disorder. Percentage of CD4 lymphocytes were close to 0 for more than 80% of children presenting with psychiatric complications.ConclusionThe very low % of CD4 lymphocytes of these children suggest that the appearance of a psychiatric complication should be regarded as a factor indicating severe HIV infection. Depressive disorders may be a clinical form of encephalopathy.

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