====== Bipolar disorder ======

{{rss>https://pubmed.ncbi.nlm.nih.gov/rss/search/1JAk5IMbg5blNNG7IdSR_AG-KWCi1ic1GG8kIlNyvNKWyULwxQ/?limit=15&utm_campaign=pubmed-2&fc=20240902060835}}
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[[Bipolar]] disorder (BD) is a complex [[psychiatric disorder]] that is often underrecognized, misdiagnosed, and challenging to detect. 
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Brain [[oscillation]]s have gained great attention in [[neuroscience]] as functional building blocks of [[cognitive]]-sensory processes. Research has shown that oscillations in "alpha," "beta," "gamma," "delta," and "theta" [[frequency]] windows are highly modified in the brain [[pathology]], including in patients with a [[cognitive impairment]] like [[bipolar disorder]] (BD). The study of changes in brain oscillations can provide fundamental knowledge for exploring [[neurophysiological biomarkers]] in cognitive impairment. Lu et al. review findings from the role and molecular basis of abnormal neural oscillation and [[synchronization]] in the symptoms of patients with BD. An overview of the results clearly demonstrates that, in cognitive-sensory processes, [[resting]] and evoked/event-related [[electroencephalogram]] (EEG) spectra in the delta, theta, alpha, beta, and gamma bands are abnormally changed in patients with BD showing psychotic features. Abnormal oscillations have been found to be associated with several neural dysfunctions and abnormalities contributing to BD, including abnormal [[GABA]]ergic [[neurotransmission]] signaling, hippocampal cell discharge, abnormal hippocampal [[neurogenesis]], impaired [[cadherin]], and synaptic contact-based cell adhesion processes, extended [[lateral ventricle]]s, decreased [[prefrontal]] cortical [[gray matter]], and decreased hippocampal volume. Mechanistically, impairment in calcium voltage-gated channel subunit alpha1 I, neurotrophic tyrosine receptor kinase proteins, genes involved in the brain [[neurogenesis]] and [[synaptogenesis]] like [[WNT3]] and [[ACTG2]], genes involved in the cell adhesion process like [[CDH12]] and [[DISC1]], and gamma-aminobutyric acid (GABA) signaling have been reported as the main molecular contributors to the abnormalities in resting-state low-frequency oscillations in BD patients. Findings also showed the association of impaired synaptic connections and disrupted membrane potential with abnormal beta/gamma oscillatory activity in patients with BD. Of note, the synaptic [[GABA]] [[neurotransmitter]] has been found to be a fundamental requirement for the occurrence of long-distance synchronous gamma oscillations necessary for coordinating the activity of neural networks between various brain regions
((Lu Z, Wang H, Gu J, Gao F. Association between abnormal brain [[oscillation]]s and [[cognitive]] [[performance]] in patients with [[bipolar disorder]]; Molecular mechanisms and clinical evidence. Synapse. 2022 Jul 18. doi: 10.1002/syn.22247. Epub ahead of print. PMID: 35849784.)).

===== Treatment =====

[[Bipolar disorder treatment]].


===== Quality of Life =====

Patients with depression or bipolar disorder have smaller functional and quality of life improvements after surgery compared to patients without psychiatric comorbidities
((Tetreault L, Nagoshi N, Nakashima H, Singh A, Kopjar B, Arnold P, Fehlings MG.
Impact of Depression and Bipolar Disorders on Functional and Quality of Life
Outcomes in Patients Undergoing Surgery for Degenerative Cervical Myelopathy:
Analysis of a Combined Prospective Dataset. Spine (Phila Pa 1976). 2017 Mar
15;42(6):372-378. doi: 10.1097/BRS.0000000000001777. PubMed PMID: 27398891.
)).

===== Risk factors =====

In bipolar disorder (BD), [[C reactive protein]] (CRP) is associated with increases in several cardiovascular risk factors, suggesting that systemic inflammation could be a shared driving force for both outcomes of BD and cardiovascular risk. Further longitudinal research is needed in this area to verify causality, including an examination of actual cardiovascular disease. Non-pharmacological and pharmacological treatments with anti-inflammatory effects should also be investigated, particularly in patients with increased CRP, for their potential to reduce cardiovascular risk in BD
((Marshe VS, Pira S, Mantere O, Bosche B, Looper KJ, Herrmann N, Müller DJ, Rej 
S. C-reactive protein and cardiovascular risk in bipolar disorder patients: A
systematic review. Prog Neuropsychopharmacol Biol Psychiatry. 2017 Jul 29. pii:
S0278-5846(17)30163-X. doi: 10.1016/j.pnpbp.2017.07.026. [Epub ahead of print]
Review. PubMed PMID: 28764912.
)).

===== Case reports =====
A 50-year-old ambidextrous male with co-morbid attention deficit hyperactivity disorder (ADHD) inattentive type, obsessive-compulsive disorder (OCD), and a family history of BPD suffered a motor vehicle [[collision]] (MVC) resulting in a grade II concussion. New onset BPD was diagnosed one-year after a concussion following an involuntary admission and led to the patient self-terminating his medications and suffering a hypertensive crisis and aortic dissection, and stroke. One year later, the patient was again involuntarily admitted for a [[suicide attempt]]. Bipolar disorder persisted unchanged indefinitely. This case study may serve as a real-world example of the DiSM in the etiology of BPD post-concussion
((Sabatose KW, Cufino N, Hahn W, Ibatullin M. Concussion May Result in New-Onset Bipolar Disorder: A Case Report. Cureus. 2024 Jul 17;16(7):e64731. doi: 10.7759/cureus.64731. PMID: 39156286; PMCID: PMC11329324.))