Thinking about cognitive impairment in bipolar disorder: A clinical perspective

Gitlin, Michael

doi:10.1111/bdi.12694

Cited by 2 publications

(3 citation statements)

References 5 publications

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“…Patients with BD I seem to have similar levels of cognitive impairment when compared with BD II patients, although the latter is much less studied [11]. Patients with BD may show selective deficits in approximately a third of cases or broad-based deficits in another third of cases [1].…”

Section: Cognition In Bipolar Disordermentioning

confidence: 99%

“…A recent study from 2017 highlighted the effects of lithium in those with BD across the cognitive domains of attention, psychomotor speed, processing speed, working memory, intellectual functioning, verbal memory, visual memory, and executive functioning [11]. The authors found that lithium does not cause attentional difficulties in BD participants, processing speed was not affected by lithium, however lithium can cause psychomotor slowing that appears to partially ameliorate after lithium withdrawal [34,38].…”

Section: The Effect Of Lithium Across Cognitive Domainsmentioning

confidence: 99%

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Lithium and Cognition in Bipolar Disorder – A Review

Donisan

2020

Ro J Psychiatry Psychother.

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The level of cognitive impairment in patients with bipolar affective disorder (BD) represents a topic of general interest because it is essential when talking about treatment adherence, quality of life, and global burden of disease. Of the treatments currently available for BD, the most studied mood stabilizer is lithium. The mechanisms and effects that lithium has on cognition are not well known. This study aims to review the current knowledge regarding the levels of impairment or improvement of cognition induced by lithium in patients with BD.

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Section: Cognition In Bipolar Disordermentioning

confidence: 99%

Section: The Effect Of Lithium Across Cognitive Domainsmentioning

confidence: 99%

Lithium and Cognition in Bipolar Disorder – A Review

Donisan

2020

Ro J Psychiatry Psychother.

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“…According to the observation that RTG might promote neuroprotection in neurons through its concerted action on Kv2 and Kv7 channels, it results mandatory for future research to deepen plausible favourable effects of this unique molecule on cognitive impairment and functional impairment, a very important target in patients with BD …”

mentioning

confidence: 99%

Retigabine‐ezogabine: A new treatment option for bipolar disorder?

2019

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To the Editors, The M-channels (ie, voltage-gated potassium channels formed by KCNQ2, KCNQ3, and KCNQ 5) has emerged as a promising target for treating bipolar disorder. M-Kv7 channel activators have shown to decrease neuronal excitability and might potentially treat neuronal hyperexcitability disorders like epilepsy and mania. Recent data demonstrate that voltage-gated neuronal Kv7/KCNQ/M-current modulates the excitability and synaptic transmission of prefrontal cortex neurons, suggesting that pharmacological modulation of M-current in the prefrontal cortex may exert beneficial effects on cognitive deficits implicated in the pathophysiology of many neuropsychiatric disorders. Retigabine-Ezogabine (RTG) [D-23129; N-(2amino-4-(4-fluorobenzylamino)phenyl) carbamic acid ethyl ester] is a third-generation antiepileptic drug (AED) with a novel mechanism of action. It produces an augmentation of g-aminobutyric acid-induced currents, a weak blocking effect on sodium and calcium currents and opens neuronal Kv 7.2 to 7.5 (formerly KCNQ2-5), voltage-activated potassium channels, which stabilize via M-current the membrane potential and control neuronal excitability. It has been approved in 2011 by the Food and Drug Administration as an add-on medication to treat seizures associated with epilepsy in adults. RTG was found to have an antimanic-like effect in the amphetamine (AMPH) + chlordiazepoxide (CDP)-induced hyperactivity model in mice, suggesting a potential role in the treatment of mania and possibly in the management of bipolar disorder. Amann et al 1 conducted the first open trial on RTG during a 3-week period in the treatment of hospitalized patients with acute mania. The drug appeared to be ineffective for most of severely manic patients but authors suggest that it may have an acute antimanic effect in some bipolar disorder patients with a lack of a depressogenic effect. RTG was in general well-tolerated at dose of 600-1200 mg/ day. Recently 18 medication-free individuals with major depressive disorder were enrolled in a 10-week open-label study receiving RTG up to 900 mg/day and exhibited a significant reduction of depressive and anhedonic symptoms. In addition, a subgroup of patients showed increased reward learning following treatment. RTG seems to have a low interaction profile; side effects are mainly related to the central nervous system (dizziness, drowsiness, tremor, ataxia), but also affect peripheral organs, such as the bladder, due its relaxing effect on smooth muscle. A growing body of studies supports the theory that bipolar disorder (BD) is strictly linked to structural and functional impairments in various brain regions. Kv/channel openers have been demonstrated to reduce baseline cerebral glucose metabolic activity and increase prefrontal cortical and hippocampal [pSer9]GSK3β levels, similar to standard mood stabilizing agents. Such results highlight the potential of RTG as an adjunctive treatment option in bipolar disorder. The findings that KCNQ expression correlates with drinking and that RTG redu...

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Thinking about cognitive impairment in bipolar disorder: A clinical perspective

Cited by 2 publications

References 5 publications

Lithium and Cognition in Bipolar Disorder – A Review

Lithium and Cognition in Bipolar Disorder – A Review

Retigabine‐ezogabine: A new treatment option for bipolar disorder?

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