Changes in Cerebral Blood Flow and Mental State after Amphetamine Challenge in Schizophrenic Patients

Mathew, Roy J.; Wilson, William H.

doi:10.1159/000118564

Cited by 23 publications

(7 citation statements)

References 38 publications

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“…1A). A similar transient increase in CBF immediately following acute MA exposure has been reported in humans exposed to MA (Mathew and Wilson, 1989) and baboons exposed to amphetamine (McCulloch et al, 1978). …”

Section: Discussionsupporting

confidence: 74%

Methamphetamine causes sustained depression in cerebral blood flow

et al. 2011

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The use prevalence of the highly addictive psychostimulant methamphetamine (MA) has been steadily increasing over the past decade. MA abuse has been associated with both transient and permanent alterations in cerebral blood flow (CBF), hemorrhage, cerebrovascular accidents and death. To understand MA-induced changes in CBF, we exposed C56BL/6 mice to an acute bolus of MA (5 mg/kg MA, delivered IP). This elicited a biphasic CBF response, characterized by an initial transient increase (~5 min) followed by a prolonged decrease (~30 min) of approximately 25% relative to baseline CBF -as measured by laser Doppler flowmetry over the somatosensory cortex. To assess if this was due to catecholamine derived vasoconstriction, phentolamine, an α-adrenergic antagonist was administered prior to MA treatment. This reduced the initial increase in CBF but failed to prevent the subsequent, sustained decrease in CBF. Consistent with prior reports, MA caused a transient increase in mean arterial blood pressure, body temperature and respiratory rate. Elevated respiratory rate resulted in hypocapnia. When respiratory rate was Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access

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Section: Discussionsupporting

confidence: 74%

Methamphetamine causes sustained depression in cerebral blood flow

et al. 2011

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“…There have been several studies investigating the effects of amphetamine on CBF. Although different research groups, depending on various measurement techniques, have demonstrated increased (Devous et al 2001;Price et al 2002;Rose et al 2006), as well as decreased (Alhassoon et al 2001;Mathew and Wilson 1989;Polesskaya et al 2011;Wang et al 2001), or unchanged flow (Kimmerly et al 2003) in response to amphetamine, it is mostly assumed in the interpretation of benzamide PET studies that amphetamine induces transient increases in CBF with rapid return to baseline values (Price et al 2002). An amphetamine-induced increase in CBF could increase the delivery of the tracer and we may observe a larger V T , thus possibly underestimating the amphetamineinduced decrease in α2 adrenoceptor binding.…”

Section: Discussionmentioning

confidence: 99%

Amphetamine challenge decreases yohimbine binding to α2 adrenoceptors in Landrace pig brain

2012

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“…In rats, the acute administration of amphetamines is known to increase dopamine release in the (medial) prefrontal cortex. Accordingly, experimental studies show that the administration of amphetamines in laboratory partially relieves the negative symptoms of schizophrenia [29]. In addition, recent results from brain imaging studies schizophrenia would be vulnerable to the rewarding effects of drugs of abuse.…”

Section: Bmentioning

confidence: 99%

Toxic Psychoses as Pharmacological Models of Schizophrenia

Potvin¹,

Stip²,

Roy³

2005

CPSR

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To simplify the understanding of schizophrenia, psychiatry has invested important efforts into the modelling of the disease. For obvious ethical reasons, sleep deprivation and sensory deprivation models have been rejected in the last decades. Thus, the psychotic disorders induced by psychoactive substances remain the main heuristic models of schizophrenia. Most of the work in the pharmacological modelling of schizophrenia has occurred in the sixties and seventies. Still, some observations retain their interest: 1) lasting up to six months, the amphetamine psychosis remains the best model of the positive symptoms of paranoid schizophrenia; 2) hallucinogens such as LSD or psilocybine reproduce, at best, the psychotic phenomenology observed during the first episodes of schizophrenia; 3) anesthetic dissociatives (PCP & ketamine) faithfully reproduce thought disorder, as well as the frontal cognitive deficits and certain negative symptoms of schizophrenia; 4) cannabis reproduces with fidelity the depersonalization states observed among schizophrenics; 5) alcohol hallucinosis could be the best model of the patients' hallucinations; 6) the psychotic disorder induced by muscarinic antagonists is not usually considered as a schizophrenia model, but its occurrence signals that cholinergic dysfunctions could be associated with the cognitive symptoms of the disease. As such, these observations go hand in hand with the common view of schizophrenia as a pathology of general cerebral disconnectivity that would affect a plurality of neurotransmitter systems.

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Changes in Cerebral Blood Flow and Mental State after Amphetamine Challenge in Schizophrenic Patients

Cited by 23 publications

References 38 publications

Methamphetamine causes sustained depression in cerebral blood flow

Methamphetamine causes sustained depression in cerebral blood flow

Amphetamine challenge decreases yohimbine binding to α2 adrenoceptors in Landrace pig brain

Toxic Psychoses as Pharmacological Models of Schizophrenia

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