Caffeine Induced Psychotic Exacerbation

Tibrewal, Prashant; Dhillon, Rohan

doi:10.3109/00048674.2010.529605

Cited by 6 publications

(11 citation statements)

References 9 publications

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“…In particular, the adenosine reuptake inhibitor dipyramidole used as an adjuvant with the antipsychotic haloperidol significantly decreased psychotic symptoms in schizophrenia patients (Akhondzadeh et al, 2005; Akhondzadeh et al, 2000). In addition, the acute use of the competitive adenosine receptor antagonist caffeine affects dopaminergic neurotransmission and is known to worsen psychosis in persons with schizophrenia; further, an acute dose of caffeine may cause psychosis in susceptible persons (Cerimele et al, 2010; Hedges et al, 2009; Tibrewal and Dhillon, 2011; Williams and Gandhi, 2008). Together these data suggest that adenosine dysfunction might be implicated in human psychosis and that therapeutic adenosine augmentation might be a rational approach for intervention.…”

Section: Adenosine-dependent Mechanisms and Therapeutic Applicationsmentioning

confidence: 99%

Comorbidities in Neurology: Is adenosine the common link?

Boison

Aronica

2015

Neuropharmacology

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Comorbidities in Neurology represent a major conceptual and therapeutic challenge. For example, temporal lobe epilepsy (TLE) is a syndrome comprised of epileptic seizures and comorbid symptoms including memory and psychiatric impairment, depression, and sleep dysfunction. Similarly, Alzheimer’s disease (AD), Parkinson’s disease (PD), and Amyotrophic Lateral Sclerosis (ALS) are accompanied by various degrees of memory dysfunction. Patients with AD have an increased likelihood for seizures, whereas all four conditions share certain aspects of psychosis, depression, and sleep dysfunction. This remarkable overlap suggests common pathophysiological mechanisms, which include synaptic dysfunction and synaptotoxicity, as well as glial activation and astrogliosis. Astrogliosis is linked to synapse function via the tripartite synapse, but astrocytes also control the availability of gliotransmitters and adenosine. Here we will specifically focus on the ‘adenosine hypothesis of comorbidities’ implying that astrocyte activation, via overexpression of adenosine kinase (ADK), induces a deficiency in the homeostatic tone of adenosine. We present evidence from patient-derived samples showing astrogliosis and overexpression of ADK as common pathological hallmark of epilepsy, AD, PD, and ALS. We discuss a transgenic ‘comorbidity model’, in which brain-wide overexpression of ADK and resulting adenosine deficiency produces a comorbid spectrum of seizures, altered dopaminergic function, attentional impairment, and deficits in cognitive domains and sleep regulation. We conclude that dysfunction of adenosine signaling is common in neurological conditions, that adenosine dysfunction can explain comorbid phenotypes, and that therapeutic adenosine augmentation might be effective for the treatment of comorbid symptoms in multiple neurological conditions.

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Section: Adenosine-dependent Mechanisms and Therapeutic Applicationsmentioning

confidence: 99%

Comorbidities in Neurology: Is adenosine the common link?

Boison

Aronica

2015

Neuropharmacology

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“…Moreover, many authors declared that caffeinated energy drinks had adverse effects on the brain such as anxiety, stress, hyper movement, headache, and fatigue [14,15]. Others declared more adverse effects including depression, sleep disturbance and irritability [16,17].…”

Section: Introductionmentioning

confidence: 99%

Effect of caffeinated energy drinks on the structure of hippocampal cornu ammonis 1 and dentate gyrus of adult male albino rats

2020

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Energy drinks are available worldwide and frequently consumed to increase energy level and compensate lack of sleep. Energy drinks consumers aim to improve their cognitive functions. Red Bull is the most popular energy drink consumed in Egypt. However, the link between the impact of energy drinks on the structure of hippocampal cornu ammonis 1 (CA1) and dentate gyrus (DG), a highly vulnerable brain regions to various insults, has not yet documented. To study the effect of energy drinks on structure of hippocampal CA1 and DG of adult male albino rats. Twenty one adult male albino rats were divided into three groups; group I control group, groups II and III received Red Bull, with a dose of 3.75 ml/kg/day orally using gastric tube for four and eight consecutive weeks respectively. At the end of the experiment, brains were dissected and hippocampal specimens were processed for histopathological and immunohistochemical studies. Histopathological examination of hippocampal sections in group II revealed vacuoles, decrease thickness of pyramidal cell layer with irregular dark or ghost nuclei. However, changes were more severe in group III with cracks in pyramidal cell layer, massive vacuolation and signet ring cells. Moreover, star shaped astrocytes and glial fibrillary acidic protein immuno-reactivity were more abundant in group III than in group II. Caffeinated energy drinks produced neurodegenerative changes and reactive astrocytosis in hippocampal CA1 and DG of adult male albino rats. These changes were duration-dependent being more severe in longer duration of intake.

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“…Tibrewal and Dhillon (2011) reported the case of a 52-year-old man with schizophrenia who showed aggravated psychotic symptoms after a few weeks of increased coffee consumption (up to 20-25 cups of coffee/ day). The addition of olanzapine for the control of acute psychotic symptoms was ineffective, but after restricting caffeine consumption without further adjustment of psychotropic medications, his psychotic symptoms disappeared over 10 days (Tibrewal and Dhillon, 2011). Cerimele et al (2010) reported a similar case in which a 43-year-old man with schizophrenia showed aggravated psychotic symptoms after daily consumption of up to 8-10 cans of energy drinks (3629-4536 mg of caffeine/day) for 8 weeks.…”

Section: Influence Of Caffeine On Psychotic Symptomsmentioning

confidence: 98%

“…Without any modification of his psychotropic medication, and by simply halving his caffeine intake, his paranoid symptoms disappeared over 3 weeks (Hedges et al, 2009). Tibrewal and Dhillon (2011) reported the case of a 52-year-old man with schizophrenia who showed aggravated psychotic symptoms after a few weeks of increased coffee consumption (up to 20-25 cups of coffee/ day). The addition of olanzapine for the control of acute psychotic symptoms was ineffective, but after restricting caffeine consumption without further adjustment of psychotropic medications, his psychotic symptoms disappeared over 10 days (Tibrewal and Dhillon, 2011).…”

Section: Influence Of Caffeine On Psychotic Symptomsmentioning

confidence: 98%

“…The association between caffeine consumption and the development or aggravation of psychotic or mood symptoms has long been observed (Hedges et al, 2009;Cerimele et al, 2010;Tibrewal and Dhillon, 2011). Despite this observed association and despite the frequent use of caffeine by many psychiatric patients, very few studies have evaluated the effects of caffeine use on the development and aggravation of psychiatric symptoms, and clinical psychiatrists often underestimate or do not consider these effects.…”

Section: Introductionmentioning

confidence: 96%

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Caffeine-induced psychiatric manifestations

Wang

Woo

Bahk

2015

International Clinical Psychopharmacology

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The association between caffeine consumption and various psychiatric manifestations has long been observed. We present two cases that show the ability of caffeine to induce psychotic and manic symptoms, and we also review the extant literature on caffeine-induced psychiatric manifestations. On the basis of our own and others' findings, we suggest that caffeine may be related to not only de-novo psychotic or mood symptoms but also to aggravation of pre-existing psychotic or mood disorders. We therefore suggest that caffeine consumption among patients with mood or psychotic symptoms should be assessed carefully in clinical practice as part of routine psychiatric evaluations.

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Caffeine Induced Psychotic Exacerbation

Cited by 6 publications

References 9 publications

Comorbidities in Neurology: Is adenosine the common link?

Comorbidities in Neurology: Is adenosine the common link?

Effect of caffeinated energy drinks on the structure of hippocampal cornu ammonis 1 and dentate gyrus of adult male albino rats

Caffeine-induced psychiatric manifestations

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