scholarly journals Understanding psychosis: treatment and rehabilitation (updates for clinicians)

2022 ◽  
Vol 13 (1) ◽  
pp. 115-121
Author(s):  
Gayane Kirakosyan ◽  
Alina Frolova
Keyword(s):  
Depressive Disorders ◽  
Psychotic Disorders ◽  
Gradual Increase ◽  
Clinical Signs ◽  
Hospital Setting ◽  
Review Article ◽  
Comprehensive Treatment ◽  
Hunger Strike ◽  
The Central Nervous System ◽  
The Brain

Psychosis is a group of psychotic disorders. Its manifestation depends on the specific type of functional violation. However, this is characterized by a gradual increase in clinical signs and a change in behavior. Symptoms of psychosis can be recognized by the following manifestations: hallucinations, delusional ideas, movement disorders, mood disorders including manic and depressive disorders and changes in emotional sphere. Psychosis occurs due to problems in the functioning of neurons. Due to the violation of bonds in the molecules, they do not receive nutrition and they are deficient in oxygen. This leads to the fact that neurons cannot transmit nerve impulses; multiple dysfunctions occur in the central nervous system. The type of psychosis depends on a part of the brain suffered from the hunger strike. The causes of this disorder are of 3 types: endogenous, associated with internal processes, exogenous or external and organic, when the causes of psychosis are changes in the brain such as tumors, trauma or hemorrhage. Psychosis is usually treated in a hospital setting. Such patients require urgent admission as they cannot control their actions, they can harm themselves and others. Psychosis is a relapse-prone disease. With timely and comprehensive treatment, the prognosis will be favorable. This review article is a good educational material for medical and psychological practitioners whose goal is to improve knowledge of treatment and rehabilitation processes of psychosis and its related disorders.

scholarly journals Presence of amastigotes in the central nervous system of hamsters infected with Leishmania sp.

2011 ◽  
Vol 20 (2) ◽  
pp. 97-102 ◽  
Author(s):  
Elisangela de Oliveira ◽  
Elisa Teruya Oshiro ◽  
Rebeca Vieira Pinto ◽  
Bruna Corrêa de Castro ◽  
Karla Borges Daniel ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Signs ◽  
Direct Examination ◽  
Mato Grosso ◽  
The Central Nervous System ◽  
Animal House ◽  
Immunohistochemical Studies ◽  
Negative Controls ◽  
The Brain

Visceral leishmaniasis (VL) is a severe chronic disease caused by Leishmania (Leishmania) infantum chagasi. Better knowledge on the effects caused by this disease can help develop adequate clinical management and treatment. Parasitological and immunohistochemical studies were performed golden hamsters Mesocricetus auratus infected with bone marrow from individuals with VL in the State of Mato Grosso do Sul, central-west Brazil. The effects of parasitism in the spleen, liver, kidneys, lungs, heart and brain of the animals were examined. Eighteen hamsters were inoculated intraperitoneally, and six healthy animals were used as negative controls. The animals were kept in the animal house and checked for clinical signs. Specimens of each organ were examined for the presence of amastigotes. Immunohistochemical technique was performed in all brain specimens and organs negative on the direct examination of parasites. Direct examination of amastigotes was positive in the spleen and liver of all infected animals; 33.3% showed the parasite in the kidneys and lungs, and 16.7% in the heart. Parasitic forms were seen in 83.3% (15/18) of the brain examined. Immunohistochemistry confirmed the results of the direct examination, except in two specimens of lung tissue and in the brain specimens. Other studies are needed to further clarify the effect of the parasite in the central nervous system.

Nanotechnology Approaches for Enhanced CNS Drug Delivery in the Management of Schizophrenia

2021 ◽  
Author(s):  
Rajalakshmi R ◽  
Krishnakumar N Menon ◽  
Sreeja C Nair
Keyword(s):  
Drug Delivery ◽  
Targeted Drug Delivery ◽  
Symptomatic Relief ◽  
Therapeutic Strategies ◽  
Review Article ◽  
Visual Hallucinations ◽  
Cns Drug Delivery ◽  
The Central Nervous System ◽  
The Brain

Schizophrenia is a neuropsychiatric disorder mainly affecting the central nervous system, presented with auditory and visual hallucinations, delusion and withdrawal from society. Abnormal dopamine levels mainly characterise the disease; various theories of neurotransmitters explain the pathophysiology of the disease. The current therapeutic approach deals with the systemic administration of drugs other than the enteral route, altering the neurotransmitter levels within the brain and providing symptomatic relief. Fluid biomarkers help in the early detection of the disease, which would improve the therapeutic efficacy. However, the major challenge faced in CNS drug delivery is the blood-brain barrier. Nanotherapeutic approaches may overcome these limitations, which will improve safety, efficacy, and targeted drug delivery. This review article addresses the main challenges faced in CNS drug delivery and the significance of current therapeutic strategies and nanotherapeutic approaches for a better understanding and enhanced drug delivery to the brain, which improve the quality of life of schizophrenia patients.

Psychoneuroimmunology

2012 ◽  
pp. 205-211
Author(s):  
Robert Dantzer ◽  
Keith W. Kelley
Keyword(s):  
Immune System ◽  
Depressive Disorders ◽  
Clinical Signs ◽  
Essential Elements ◽  
Neural Pathways ◽  
New Information ◽  
Disciplinary Field ◽  
Expression Of Emotions ◽  
Psychological Events ◽  
The Brain

Mind-body literature, in the form of magazines and self-help books on stress and healing, is full of definitive claims for the existence of powerful influences of emotions and psychosocial stressors on the immune system, leading to onset or progression of cancers or infectious diseases. This literature often makes explicit reference to research in psychoneuroimmunology to support these claims. Psychoneuroimmunology is a multi-disciplinary field that has grown rapidly during the last three decades at the crossroads of immunology, behavioural neurosciences, neuroendocrinology, and psychology. It studies mechanisms and functional aspects of bidirectional relationships between the brain and the immune system. Although still controversial, there is evidence that psychological events including emotions can and do influence the outcome of infectious, autoimmune, and neoplastic diseases via modulation of cells of the immune system. A surprising finding has been that immune events occurring in the periphery also affect mood, behaviour, and metabolism by modulating brain functions, thereby providing a biologically important link between the immune system and brain. The original discovery that activation of the innate immune system in the periphery causes clinical signs of sickness that are processed in the brain is now being extended to the involvement of the immune system in depressive disorders. This new information has solidified the idea that neurotransmitters, neuropeptides, neural pathways, and immune-derived signals such as cytokines are the minimal essential elements that permit the immune system and brain to communicate with one another. These new data offer the unexpected conclusion that the immune system is likely to be involved in not only how emotions affect health but also how immune events regulate the development and expression of emotions.

scholarly journals MicroRNAs, Multiple Sclerosis and Depression

2021 ◽  
Vol 22 (15) ◽  
pp. 7802
Author(s):  
Hsiuying Wang
Keyword(s):  
Multiple Sclerosis ◽  
Depressive Disorders ◽  
Nitrosative Stress ◽  
Mirna Regulation ◽  
Oxidative And Nitrosative Stress ◽  
Relapsing Remitting ◽  
The Central Nervous System ◽  
Patients Experience ◽  
Brain And Spinal Cord ◽  
The Brain

Multiple sclerosis (MS) is a chronic disease of the central nervous system that affects the brain and spinal cord. There are several disease courses in MS including relapsing–remitting MS (RRMS), primary progressive MS (PPMS), and secondary progressive MS (SPMS). Up to 50% of MS patients experience depressive disorders. Major depression (MD) is a serious comorbidity of MS. Many dysfunctions including neuroinflammation, peripheral inflammation, gut dysbiosis, chronic oxidative and nitrosative stress, and neuroendocrine and mitochondrial abnormalities may contribute to the comorbidity between MS and MD. In addition to these actions, medical treatment and microRNA (miRNA) regulation may also be involved in the mechanisms of the comorbidity between MS and MD. In the study, I review many common miRNA biomarkers for both diseases. These common miRNA biomarkers may help further explore the association between MS and MD.

Distribution and histopathological changes induced by cysts ofTaenia soliumin the brain of pigs from Tanzania

2014 ◽  
Vol 89 (5) ◽  
pp. 559-564 ◽  
Author(s):  
E.M. Mkupasi ◽  
H.A. Ngowi ◽  
C.S. Sikasunge ◽  
P.S. Leifsson ◽  
M.V. Johansen
Keyword(s):  
Parietal Lobe ◽  
Taenia Solium ◽  
Clinical Signs ◽  
Occipital Lobe ◽  
Loss Of Consciousness ◽  
Parasitic Disease ◽  
Histopathological Changes ◽  
The Central Nervous System ◽  
Spinal Cord Cysts ◽  
The Brain

AbstractNeurocysticercosis (NCC) caused byTaenia soliumcysts is a frequent but neglected parasitic disease of the central nervous system (CNS) worldwide. The aim of this study was to describe anatomical locations of cysts in the CNS and the corresponding inflammation. A total of 17 naturally infected pigs were used to evaluate the distribution of cysts and, of these, seven were used to evaluate the corresponding inflammation further, through histopathology. Clinical signs in the pigs included dullness, sluggishness, somnolence, apathy and loss of consciousness. Cysts were distributed in all cerebral lobes, i.e. 39.7% in the frontal lobe, 20.3% in the parietal lobe, 20.0% in the occipital lobe and 19.7% in the temporal lobe, and only 0.4% in the cerebellum. No cysts were found in the spinal cord. Cysts were localized as follows: 47.9% in the dorsal subarachnoid, 46.9% in the parenchyma, 4.4% in the subarachnoid base and 0.9% in the ventricles. The results of the histopathology revealed lesions in an early inflammatory stage, i.e. stage I, in all anatomical locations except for two, which showed more of an inflammatory reaction, stage III, in one pig. It was concluded that clinical signs in pigs were neither pathognomonic nor consistent. These signs, therefore, cannot be used as a reliable indicator of porcine NCC. Furthermore,T. soliumcysts were found to be in abundance in all cerebral lobes, and only a few were found in the cerebellum. Regarding the inflammatory response, no significant differences were found in the location and total number of cysts. Thus, further studies are needed to explain the determinants of cyst distribution in the CNS and assess in detail clinical signs associated with porcine NCC.

scholarly journals Naphthoquine-induced Central Nervous System and Hepatic Vasculocentric Toxicity in the Beagle Dog

2016 ◽  
Vol 44 (8) ◽  
pp. 1128-1136 ◽  
Author(s):  
Jean-Rene Galarneau ◽  
Emily K. Meseck ◽  
Robert L. Hall ◽  
Wenkui Li ◽  
Margaret L. Weaver
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Signs ◽  
Drug Candidate ◽  
Oral Gavage ◽  
Plasma Exposure ◽  
Toxicology Study ◽  
The Central Nervous System ◽  
The Brain ◽  
Microscopic Findings

Naphthoquine phosphate (NP) was considered as a partner drug with a promising antimalarial drug candidate. Here we report unexpected adverse clinical signs and microscopic findings in a canine pilot toxicology study with NP. Male and female dogs were dosed daily by oral gavage with NP at 2, 10, or 50 mg/kg/day for a maximum of 14 days. NP was not tolerated at ≥10 mg/kg/day; several animals were sacrificed in moribund condition and marked neurological clinical signs were noted at 50 mg/kg/day. The main microscopic observation was central nervous system vasculocentric inflammation (mainly lymphocytes and macrophages) in the white and gray matter of various regions of the brain at ≥2 mg/kg/day and at lower incidence in the spinal cord at ≥10 mg/kg/day. Vasculocentric microscopic changes predominantly centered on the centrilobular vein were also observed in the liver at ≥2 mg/kg/day. Females were more sensitive than males with comparable NP plasma exposure. In conclusion, under the conditions of this study, the administration of NP to dogs via daily oral gavage for up to 2 weeks was not tolerated causing moribundity, marked neurological clinical signs, and vasculocentric microscopic changes in the central nervous system and the liver.

The role of IgG hypersensitivity and changes in gut microbiota in the pathogenesis and therapy of depressive disorders

2016 ◽  
Vol 33 (S1) ◽  
pp. S24-S25 ◽  
Author(s):  
H. Karakula-Juchnowicz ◽  
P. Szachta ◽  
D. Juchnowicz ◽  
S. Grochowski ◽  
M. Gałęcka
Keyword(s):  
Gut Microbiota ◽  
Structural Changes ◽  
Depressive Disorders ◽  
Immunological Mechanisms ◽  
Study Results ◽  
Important Addition ◽  
The Central Nervous System ◽  
Competing Interest ◽  
Depressive Episodes ◽  
The Brain

Depression is a complex, heterogeneous psychiatric disorder with multifactorial aetiology. Substantial evidence indicates that depressive episodes are associated not only with changes in neurotransmission in the central nervous system (CNS), but also may lead to structural changes in the brain through neuroendocrine, inflammatory, and immunological mechanisms. Among the factors deserving special attention connected with developing systematic inflammation are altered intestinal permeability, IgG food intolerance, and changes in gut microbiota.We present a possible scenario of the development of depression, linking elevated zonulin production, loosening of the tight junction barrier, an increase in permeability of the gut wall, and the passage of macromolecules, normally staying the gut, into the bloodstream, with the immuno-inflammatory cascade and induction of IgG-dependent food sensitivity. Alterations in bidirectional signaling between the gastrointestinal tract and the brain, so called “microbiota–gut–brain axis”, may be normalized by dietary immunomodulating factors, including prebiotics and probiotics. In the case of increased IgG concentrations, the implementation of an elimination–rotation diet may prove to be an effective method of reducing inflammation and, in this way, alleviating depressive symptoms.Given complexity and variety of mood disorders, it is necessary to develop improved integration models. Preliminary study results raise hope that the new methods mentioned above, i.e. psychobiotics, prebiotics, an elimination-rotation diet, may be an important addition to the psychiatrist's armamentarium as therapeutic agents improving the efficacy of the treatment for affective disorders [1–3].Disclosure of interestThe authors have not supplied their declaration of competing interest.

scholarly journals Probiotics, Prebiotics and Postbiotics on Mitigation of Depression Symptoms: Modulation of the Brain–Gut–Microbiome Axis

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1000
Author(s):  
Agata Chudzik ◽  
Anna Orzyłowska ◽  
Radosław Rola ◽  
Greg J. Stanisz
Keyword(s):  
Gut Microbiota ◽  
Gut Microbiome ◽  
Depressive Disorders ◽  
Corticosterone Level ◽  
Depression Symptoms ◽  
Symptoms Of Depression ◽  
Bidirectional Communication ◽  
The Central Nervous System ◽  
Communication Pathway ◽  
The Brain

The brain–gut–microbiome axis is a bidirectional communication pathway between the gut microbiota and the central nervous system. The growing interest in the gut microbiota and mechanisms of its interaction with the brain has contributed to the considerable attention given to the potential use of probiotics, prebiotics and postbiotics in the prevention and treatment of depressive disorders. This review discusses the up-to-date findings in preclinical and clinical trials regarding the use of pro-, pre- and postbiotics in depressive disorders. Studies in rodent models of depression show that some of them inhibit inflammation, decrease corticosterone level and change the level of neurometabolites, which consequently lead to mitigation of the symptoms of depression. Moreover, certain clinical studies have indicated improvement in mood as well as changes in biochemical parameters in patients suffering from depressive disorders.

scholarly journals AN UPDATED REVIEW ON THE APPLICATION OF DENDRIMERS AS SUCCESSFUL NANOCARRIERS FOR BRAIN DELIVERY OF THERAPEUTIC MOIETIES

2021 ◽  
pp. 1-9
Author(s):  
SARANYA SASI ◽  
SHARON KUNNATH JOSEPH ◽  
ARYA MANGALATH ARIAN ◽  
SACHIN THOMAS ◽  
AMRUTHA V. U. ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Genetic Material ◽  
Review Article ◽  
Wide Range ◽  
The Central Nervous System ◽  
Systemic Side Effects ◽  
High Degree ◽  
Novel Drug ◽  
Physical And Chemical ◽  
The Brain

It’s been nearly 100 y of effort to study the organization and role of the blood brain-barrier and still, we strive to find better techniques to overcome this barrier to deliver the drugs to the brain effectively with reduced systemic side effects. The advances in nanotechnology have given newer horizons in achieving this goal since the nano-scaled systems can modify an existing drug to have a high degree of sensitivity to the physiological conditions and specificity to reach the target organ. Among the various nanocarriers, dendrimers owing to their unique physical and chemical characteristics, represent a potential therapeutic tool in biomedical and pharmaceutical science. Dendrimers, an established polymeric nanocarrier system of the time, can deliver both drugs and genetic material and are being extensively studied to target the brain. The surface modification of dendrimers can reduce their innate toxicity problems and increase the therapeutic efficacy of brain disorders. This review article is an attempt to update on the potential of dendrimers explored in the past five years as a drug delivery avenue that can be considered as a promising solution in the management of a wide range of disorders affecting the central nervous system, including neoplastic, degenerative, and ischemic conditions. The following search criteria were used to expand the review article with the keywords dendrimers, novel drug delivery, nanoparticles, site-specific drug delivery etc.

scholarly journals Five Decades of Cuprizone, an Updated Model to Replicate Demyelinating Diseases

2019 ◽  
Vol 17 (2) ◽  
pp. 129-141 ◽  
Author(s):  
Jose M. Vega-Riquer ◽  
Gerardo Mendez-Victoriano ◽  
Raul A. Morales-Luckie ◽  
Oscar Gonzalez-Perez
Keyword(s):  
Multiple Sclerosis ◽  
Clinical Signs ◽  
Behavioral Changes ◽  
Demyelinating Diseases ◽  
Histological Changes ◽  
Cerebellar Peduncles ◽  
The Central Nervous System ◽  
Myelin Disorders ◽  
The Brain ◽  
Pharmacological Model

Introduction: Demyelinating diseases of the central nervous system (CNS) comprise a group of neurological disorders characterized by progressive (and eventually irreversible) loss of oligodendrocytes and myelin sheaths in the white matter tracts. Some of myelin disorders include: Multiple sclerosis, Guillain-Barré syndrome, peripheral nerve polyneuropathy and others. To date, the etiology of these disorders is not well known and no effective treatments are currently available against them. Therefore, further research is needed to gain a better understand and treat these patients. To accomplish this goal, it is necessary to have appropriate animal models that closely resemble the pathophysiology and clinical signs of these diseases. Herein, we describe the model of toxic demyelination induced by cuprizone (CPZ), a copper chelator that reduces the cytochrome and monoamine oxidase activity into the brain, produces mitochondrial stress and triggers the local immune response. These biochemical and cellular responses ultimately result in selective loss of oligodendrocytes and microglia accumulation, which conveys to extensive areas of demyelination and gliosis in corpus callosum, superior cerebellar peduncles and cerebral cortex. Remarkably, some aspects of the histological pattern induced by CPZ are similar to those found in multiple sclerosis. CPZ exposure provokes behavioral changes, impairs motor skills and affects mood as that observed in several demyelinating diseases. Upon CPZ removal, the pathological and histological changes gradually revert. Therefore, some authors have postulated that the CPZ model allows to partially mimic the disease relapses observed in some demyelinating diseases. Conclusion: for five decades, the model of CPZ-induced demyelination is a good experimental approach to study demyelinating diseases that has maintained its validity, and is a suitable pharmacological model for reproducing some key features of demyelinating diseases, including multiple sclerosis.

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