Neuroinflammation and psychiatric illness

Neuroinflammation and psychiatric illness

Stress is a constant factor in today’s fastpaced life that can jeopardize our health if left unchecked. These systems, which were previously considered pristinely independent, in fact, interact at myriad levels. The result is a comprehensive yet accessible interdisciplinary introduction to psychoneuroimmunology which also takes you further than the foundations of those fascinating topics by covering the most recent research in HIV/AIDS, autoimmune diseases, and the reactivation of latent herpes viruses. Third, at least in the case of the less serious infectious diseases (colds, influenza, herpes), it considers consistent and convincing evidence of links between stress and negative affect and disease onset and progression. Frankly I’m frustrated that the medical community hasn’t established a cause or a cure in the past 150 years. Since then, an expanding collection of reproducible biological causes, from neurosyphilis, head trauma, stroke, tumor, demyelination and many others caused symptom complexes that overlapped with classic psychiatric disorders [9-11]. All it took was for someone who was thinking about CFS to be exposed to these different literatures and to start fitting them together.

Peripheral immune modulators can induce psychiatric symptoms in animal models and humans [12-19]. Healthy animals injected with pro-inflammatory IL-1β and tumor necrosis factor alpha (TNF-α) cytokines demonstrate ‘sickness behavior’ associated with social withdrawal [12]. Overall, steroid hormones influence the immune response, with estrogens providing a boost to the humoral immune response while androgens, progesterone and glucocorticoids act as immunosuppressors. The healing practice of shamanism is thought to have had its origins in Siberia dating as far back as 20,000 years ago. Medical conditions associated with chronic inflammatory and immunological abnormalities, including obesity, diabetes, malignancies, rheumatoid arthritis, and multiple sclerosis, are risk factors for depression and bipolar disorder [10,12,13,15,17,18]. The immune system is a network of glands, nodes, and organs that work to protect the body from bacteria, viruses, fungi, and other harmful organisms. Only recently have major breakthroughs occurred that have revolutionized our understanding of PNI.

Further, herpes simplex virus, Toxoplasma gondii, cytomegalovirus, and influenza during pregnancy increase the risk of developing schizophrenia [16]. Peripheral cellular [21,22] (Table ), and humoral immunological abnormalities [13,21-23] are more prevalent in psychiatric patients relative to healthy controls. In both pilot (n = 34 patients with major depressive disorder (MDD), n = 43 healthy controls) and replication studies (n = 36 MDD, n = 43 healthy controls), a serum assay comprising nine serum biomarkers distinguished MDD subjects from healthy controls with 91.7% sensitivity and 81.3% specificity; significantly elevated biomarkers for neuropsychiatric symptoms were the immunological molecules alpha 1 antitrypsin, myeloperoxidase, and soluble TNF-α receptor II [23]. We first review the association between autoimmunity and neuropsychiatric disorders, including: 1) systemic lupus erythematosus (SLE) as a prototype of systemic autoimmune disease; 2) autoimmune encephalitides associated with serum anti-synaptic and glutamic acid decarboxylase (GAD) autoantibodies; and 3) pediatric neuropsychiatric autoimmune disorders associated with streptococcal infections (PANDAS) and pure obsessive-compulsive disorder (OCD) associated with anti-basal ganglia/thalamic autoantibodies. As far as the effectiveness of PET scans finding local vagus infection: We don’t know. Between 25% to 75% of SLE patients have central nervous system (CNS) involvement, with psychiatric symptoms typically occurring within the first two years of disease onset. Psychiatric symptoms may include anxiety, mood and psychotic disturbances [97].
Neuroinflammation and psychiatric illness

Hence the throat chakra is disrupted resulting in thyroid disease and autoimmune conditions. Imbued as deity, physicians of today infrequently recognize a need for pastoral or psychiatry consults for our patients. These antibodies include anti-ribosomal P (positive in 90% of psychotic SLE patients) [1], anti-endothelial cell, anti-ganglioside, anti-dsDNA, anti-2A/2B subunits of N-methyl-D-aspartate receptors (NMDAR) and anti-phospholipid antibodies [97]. It is only with major stressors of longer duration, or with major exposure to glucocorticoids, that the immune system does not just return to baseline, but plummets into immunosuppression. On recognition of the cytokine by the CNS, the information is converted to neuroendocrine signals, resulting in chemical messages being sent back to the immune system, with ensuing physiological changes. Autoimmune encephalitides are characterized by an acute onset of temporal lobe seizures, psychiatric features, and cognitive deficits [2,3,99-108]. The pathophysiology is typically mediated by autoantibodies targeting synaptic or intracellular autoantigens in association with a paraneoplastic or nonparaneoplastic origin [3].

Anti-synaptic autoantibodies target NR1 subunits of the NMDAR [100,108,109], voltage-gated potassium channel (VGKC) complexes (Kv1 subunit, leucine-rich glioma inactivated (LGI1) and contactin associated protein 2 (CASPR2)) [101,102,106], GluR1 and GluR2 subunits of the amino-3-hydroxy-5-methyl-l-4-isoxazolepropionic acid receptor (AMPAR) [6,110,111] and B1 subunits of the γ-aminobutyric acid B receptors (GABABR) [3,99,103]. Anti-intracellular autoantibodies target onconeuronal and GAD-65 autoantigens [2,3]. This is done to find tumors. Up to two-thirds of patients with anti-NMDAR autoimmune encephalitis, initially present to psychiatric services [5]. Anti-synaptic antibodies-mediated autoimmune encephalitides must be considered in the differential of acute psychosis [2-6]. Hashimoto’s (chronic thyroiditis) may follow Graves’ disease, and is characterized by a TSH stimulation-blocking antibody (TSBAb) that disrupts the activity of TSH, resulting in damage and atrophy of the gland. Negative psychological states, such as stress, anxiety, and depression, may alter immune system regulation and modulation of peripheral cytokines.

Further, seronegative autoimmune encephalitides can also present with prominent neuropsychiatric disturbances, making diagnosis more elusive [107,112,113]. Activation of STAT3 was inhibited by a blockade of the ß1- and ß2-adrenergic receptors with propranolol, and by blocking of protein kinase A with KT5720, but not with the α-receptor blockers—prazosin (α1) and/or yohimbine (α2). Studies show that these brain-born cytokines can influence peripheral neuroendocrine functions and influence behavioral effects, particularly those associated with the hypothalamus and hippocampus. In a prospective cohort of 29 subjects who met the DSM-IV criteria for schizophrenia, serum anti-NMDAR autoantibodies were found in three subjects, and anti-VGKC-complex autoantibodies were found in one subject [5]. Using more sensitive techniques to detect immunoglobulin G (IgG) NR1 autoantibodies in 100 patients with definite schizophrenia, no autoantibodies were identified [122]. However, this study did not assess autoantibodies targeting the NR2 subunit of NMDAR. Other studies reported significantly increased odds of elevated (≥90th percentile non-psychiatric control levels) NR2 antibody levels (odds ratio (OR) 2.78, 95% confidence interval (CI) 1.26 to 6.14, P = 0.012) among individuals with acute mania (n = 43), but not in chronic mania or schizophrenia [116].

According to the hypothesis, the frequent failure of drug therapy and also one’s own immune system to eliminate infections within vagal ganglia and paraganglia is just like how some drug doses and antibodies do not penetrate the BBB. Anti-basal ganglia antibodies are implicated in Sydenham’s chorea [123]. PANDAS is characterized by acute exacerbations of OCD symptoms and/or motor/phonic tics following a prodromal group A β-hemolytic streptococcal infection. Suggest a well-rounded detox supplement to help patients eliminate toxins from their bodies. For example, Carver [19] published that “finding benefit” among women with breast cancer during the year after diagnosis predicts better adjustment 5 to 8 years after diagnosis.

You may also like