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Current Psychiatry Reviews
ISSN: 1573-4005 - Expanded Frequency Print & Online
- Now 4 Issues in 2006
Current Psychiatry Reviews
Volume 1, Number 2, June 2005
Contents
Metamphetamine Psychosis: How is it Related to Schizophrenia?
A Review of the Literature Pp. 115-122
Melinda Sweeting and Michael Farrell
[Abstract]
The Role of Cytokine Network in the Pathophysiology
of Schizophrenia Pp. 123-131
Yong-Ku Kim
[Abstract]
Schizophrenia and Idiopathic Unconjugated Hyperbilirubinemia
(Gilbert’s Syndrome) Pp. 133-138
Tsuyoshi Miyaoka and Jun Horiguchi
[Abstract]
Genetics, Perinatal Insult and Schizophrenia: The
Mechanism Underlying an Increased Prevalence of Perinatal
Complications Among Individuals with a Diagnosis of Schizophrenia?
Pp. 139-150
Antonio Preti and Paola Miotto
[Abstract]
Dysfunction of Glia-Neuron Communication in Pathophysiology
of Schizophrenia Pp.151-163
Kenji Hashimoto, Eiji Shimizu and Masaomi Iyo
[Abstract]
Augmentation of Clozapine with Atypical Antipsychotic
Substances Pp. 165-172
Mathias Zink and Harald Dressing
[Abstract]
Neurotrophic Actions of Mood-Stabilizers: A Recent
Research Discovery and its Potential Clinical Applications
Pp. 173-185
Guang Chen, Thomas Creson, Sharon Engel, Yanlei Hao and
Gang Wang
[Abstract]
Interpersonal-Psychological Precursors to Suicidal
Behavior: A Theory of Attempted and Completed Suicide Pp.
187-196
Kimberly A. Van Orden, Katherine A. Merrill and Thomas
E. Joiner Jr.
[Abstract]
mGlu5 Receptors: Neuroanatomy, Pharmacology, and Role
in Drug Addiction Pp. 197-214
M. Foster Olive
[Abstract]
Is it Safe to Drive a Car when Treated with Anxiolytics?
Evidence from onthe-Road Driving Studies During Normal Traffic
Pp. 215-225
Joris C. Verster, Dieuwke S. Veldhuijzen and Edmund R.
Volkerts
[Abstract]
Abstracts
[Back to top]
Metamphetamine Psychosis: How is it Related to
Schizophrenia? A Review of the Literature
Melinda Sweeting and Michael Farrell
There is a body of literature on metamphetamine psychosis
dating back to the 1950’s with a recent resurgence of
interest following increase in use worldwide. Distinct similarities
appear to exist between metamphetamine psychosis and schizophrenia.
The aim of this paper is to critically review the literature
on metamphetamine psychosis.
Searches on Medline, Psycinfo and Cochrane were undertaken,
references were followed and recent editions of major journals
reviewed. There is a vast array of literature on stimulants
and psychosis. I have deliberately limited my data to that
on metamphetamines, only citing other data if particularly
well known and relevant to distinguish. Data in Japanese has
been quoted with reference to where cited.
Metamphetamine psychosis has been observed as a paranoid
hallucinatory state developing gradually with repeated metamphetamine
abuse and possibly continueing after metamphetamine withdrawal.
Also noted is a lasting susceptibility to recurrence of the
paranoid hallucinatory state with neuroleptics preventing
this recurrence. Patients with persistent metamphetamine psychosis
can develop long lasting residual symptoms resembling negative
symptoms of schizophrenia.
In animals intermittent administration of smaller doses of
metamphetamine appears to lead to augmentation of behaviour,
and increases in dopamine and seretonin levels. Also it appears
that a challenge injection or stress can cause the same responses,
which are inhibited by dopamine antagonists. Larger repeated
doses of metamphetamine appear to lead to long lasting depletion
of dopamine and seretonin.
There are clear clinical similarities between metamphetamine
psychosis and schizophrenia altered in both conditions with
the use of antipsychotics. A major as yet unanswered question
is whether metamphetamine can cause schizophrenia.
The literature describes a number of changes in dopamine
and seretonin systems. More research in this field could increase
our understanding of transmitters and receptors, thereby helping
our quest in improved drug development for both illnesses.
[Back to top]
The Role of Cytokine Network in the Pathophysiology
of Schizophrenia
Yong-Ku Kim
A growing body of evidence suggests that cytokines have
a role in schizophrenia. Cytokines are involved in neurodevelopment,
schizophrenic psychopathology, and neurodegeneration, and
these processes are all part of the pathophysiology of schizophrenia.
Cytokines modulate neuronal action, differentiation, and survival
during neurodevelopment and are important factors in the processes
of neurotoxicity and neurodegeneration. Cytokines also play
a role in the activity and survival of neurons that utilize
certain neurotransmitters, particularly dopamine, serotonin,
and glutamate. This paper addresses the potential role of
the cytokine network in the pathophysiology of schizophrenia.
[Back to top]
Schizophrenia and Idiopathic Unconjugated Hyperbilirubinemia
(Gilbert’s Syndrome)
Tsuyoshi Miyaoka and Jun Horiguchi
Idiopathic unconjugated hyperbilirubinemia (Gilbert's syndrome,
GS) is a relatively common congenital hyperbilirubinemia occurring
in 3-7% of the world population. It has been recognized as
a benign familial condition in which hyperbilirubinemia occurs
in the absence of structural liver disease or hemolysis, and
the plasma concentration of conjugated bilirubin is normal.
Recently, it was reported that unconjugated bilirubin had
neurotoxicity in the developing nervous system. The ‘neurodevelopmental
hypothesis’ of schizophrenia was proposes that a yet-unidentified
event occurring in utero or early postnatal life. We have
observed that patients suffering from schizophrenia frequently
present an increased bilirubin plasma concentration when admitted
to the hospital. Therefore, we had notice the relation between
unconjugated bilirubin and the etiology and vulnerability
of schizophrenia.
[Back to top]
Genetics, Perinatal Insult and Schizophrenia: The
Mechanism Underlying an Increased Prevalence of Perinatal
Complications Among Individuals with a Diagnosis of Schizophrenia?
Antonio Preti and Paola Miotto
Recent studies on animals and humans point to the possibility
that environmental events might impact on genetic predisposition
to abnormal reactions after CNS lesion, causing deviations
in the natural course of brain maturation that may result
in neuropsychiatric disorders.
The literature on the genetic basis of obstetric complications
risk is here summarized and linked to the large body of studies
indicating perinatal and prenatal adverse events as significant
antecedents of schizophrenia.
The hypothesis of an important link between obstetric complications
on a genetic basis and the risk of schizophrenia is put forward,
with an illustration of the studies that will allow accepting
or rejecting the proposed hypothesis.
[Back to top]
Dysfunction of Glia-Neuron Communication in Pathophysiology
of Schizophrenia
Kenji Hashimoto, Eiji Shimizu and Masaomi Iyo
Multiple lines of evidence suggest that genetic factors
and environmental factors as well as a dysfunction in the
glutamatergic neurotransmission contribute to the pathophysiology
of schizophrenia. Communication between neurons and glia is
essential for axonal conduction, synaptic neurotransmission,
and information processing, and thus is required for normal
functioning of the nervous system during development and throughout
adult life. A number of studies have demonstrated that the
substances which ommunicate between neurons and glia are altered
in the blood, cerebrospinal fluid (CSF), and postmortem brain
samples of schizophrenic patients. These findings suggest
that neuron-glia communication might be impaired in the brains
of schizophrenic patients. In this article, we review the
imbalance of neuron-glia communication presented in the neurodevelopmental
hypothesis as well as the glutamate hypothesis of schizophrenia.
First, we discuss the role of growth factors (e.g., basic
fibroblast growth factor (bFGF), epidermal growth factor (EGF),
midkine), brain-derived neurotrophic factor (BDNF) and cytokines
in the pathophysiology of schizophrenia. Second, we focus
on the role of endogenous substances (glutamate, glutamine,
D-serine, kynurenic acid, and glutathione), which modulate
the NMDA receptor function, in the pathophysiology of schizophrenia.
[Back to top]
Augmentation of Clozapine with Atypical Antipsychotic
Substances
Mathias Zink and Harald Dressing
The clinical outcome of patients suffering from schizophrenic
psychoses has been considerably improved with typical antipsychotic
drugs, however, up to 40 % of the cases show treatment resistant
symptoms. Even therapy with atypical substances such as risperidone,
olanzapine, quetiapine, sulpiride, amisulpride, and ziprasidone
often fails in reaching complete remission due to resistant
schizophrenic symptoms or dose-limiting side effects. As this
also holds true for monotherapy with clozapine, a substance
with proved efficacy in formerly resistant cases, increasing
numbers of patients receive atypical antipsychotic drugs in
addition to clozapine.
This review systematically evaluates case reports and clinical
investigations on the combined application of clozapine with
other atypical antipsychotic drugs. Details about indication,
methodology and effects of the investigations are summarized.
Only one double blind, placebo-controlled trial on the combination
with sulpiride was found in a total number of 34 publications,
encompassing a total of 1250 patients. Favorable effects on
psychotic symptoms or improvements of clozapine-induced side
effects were described for every combination approach. In
some cases, pharmacokinetic interactions or serious unfavorable
effects were reported.
In conclusion, most of the combination therapies follow a
neurobiological rationale. There are major differences in
the level of evidence regarding their safety, tolerability
and effectiveness. We discuss criteria for the indication
of a clozapine augmentation and differential indication for
existing alternatives. Additional randomized prospective trials
are needed in order to systematically evaluate these strategies.
[Back to top]
Neurotrophic Actions of Mood-Stabilizers: A Recent
Research Discovery and its Potential Clinical Applications
Guang Chen, Thomas Creson, Sharon Engel, Yanlei Hao and
Gang Wang
Recent in vitro and in vivo studies reveal
that mood stabilizers lithium and valproate activate the extracellular
signal-regulated kinase (ERK) pathway and the phosphoinositide
3-kinase (PI3K) pathways. The activations of the ERK and PI3K
pathways are major signaling mechanisms by which neurotrophic
factors modulate neurogenesis, neuronal growth and regeneration,
neuronal survival, and synaptic plasticity. Like neurotrophic
factors, lithium and valproate promote neurite outgrowth and
axonal regeneration in cultured neuronal cells and in injury
models utilizing retinal cells, sciatic nerve, and spinal
cord. These mood stabilizers also enhance neurogenesis in
cultured cortical and hippocampal cells and in the hippocampal
dentate gyrus of adult animals. Treatments with these mood
stabilizers protect cultured cells against a variety of insults
and reduce neuronal loss and associated functional deficits
in animal models of Alzheimer's disease, HIV-associated encephalitis
and dementia, Huntington's disease, ischemia, and Parkinson's
disease. Crosssectional and longitudinal brain imaging studies
show that lithium treatment increases brain N-acetyl aspartate
levels and cerebral gray matter volumes in patients with mood
disorders. These data suggest that mood stabilizers and neurotrophins
share common mechanisms of action that may contribute to their
therapeutic effects.
[Back to top]
Interpersonal-Psychological Precursors to Suicidal
Behavior: A Theory of Attempted and Completed Suicide
Kimberly A. Van Orden, Katherine A. Merrill and Thomas
E. Joiner Jr.
Suicidal ideation is not uncommon in the general population
and is even more prevalent in psychiatric samples; however,
most individuals who experience ideation will not attempt
suicide and even fewer will complete suicide. Despite these
discrepancies, the number of studies investigating risk factors
for serious suicidal behavior (i.e., attempts and completions)
is relatively small. We first review studies in the literature
which focus on the distinction between attempted and completed
suicide and/or which predict completion status. We then highlight
a program of research in our own laboratory which is grounded
in Joiner’s interpersonal-psychological theory of attempted
and completed suicide. The theory posits that serious suicidal
behavior will not occur unless an individual has both the
desire to commit suicide and the ability to do so. Two factors
contribute to an individual’s desire for suicide, a
thwarted sense of belongingness and a sense of perceived burdensomeness
on others, while the ability to commit suicide can be acquired
over time through habituation to the physical and mental pain
involved in self-injury. Finally, we discuss implications
of the theory for assessment and treatment of suicidal behavior.
[Back to top]
mGlu5 Receptors: Neuroanatomy, Pharmacology, and Role
in Drug Addiction
M. Foster Olive
Over the past half century, most studies investigating the
neural substrates of drug addiction have focused on the mesolimbic
dopamine reward circuitry. Yet recent evidence suggests a
critical role for glutamate neurotransmission in addiction-related
behaviors. Glutamate receptors, both ionotropic and metabotropic,
are widely expressed throughout the central nervous system.
Dissection of the role of individual glutamate receptor subtypes
in addictive processes has been aided by the development of
pharmacological ligands selective for glutamate receptor subtypes,
and by the generation of genetically altered rodents in which
the gene encoding an individual glutamate receptor protein
or receptor subunit has been deleted or altered. A pivotal
study identifying a specific role for the type 5 metabotropic
glutamate receptor (mGlu5) in drug addiction was published
in 2001 by Chiamulera and colleagues. These investigators
demonstrated that mice lacking functional mGlu5 receptors
failed to self-administer cocaine and did not exhibit cocaine-induced
hyperlocomotion, while food seeking behavior remained unaltered.
These findings, and a subsequent flurry of other animal studies
utilizing selective mGlu5 antagonists, have confirmed that
inhibition of mGlu5 receptor function reduces drug self-administration
and/or other behaviors induced by abused drugs including cocaine,
amphetamine, nicotine, and alcohol. In this paper these preclinical
studies demonstrating a clear role for mGlu5 receptors in
drug addiction are reviewed. Summaries of the neuroanatomical
distribution, pharmacology and neurotransmitter release-altering
properties of mGlu5 receptors are also given. From this review,
it is clear that additional studies are needed to determine
(1) the efficacy of mGlu5 antagonists in reducing selfadministration
of all drugs of abuse, (2) neuroanatomical loci and neurochemical
mechanisms by which mGlu5 regulate addictive behaviors, (3)
the efficacy of mGlu5 antagonists in various models of craving
and relapse, and (4) the ability of mGlu5 antagonists to alter
various forms of neuronal plasticity associated with acute
or chronic drug exposure. Such studies will hopefully prove
a basis for developing novel mGlu5-based pharmacotherapies
to aid in the treatment of drug addiction in humans.
[Back to top]
Is it Safe to Drive a Car when Treated with Anxiolytics?
Evidence from onthe-Road Driving Studies During Normal Traffic
Joris C. Verster, Dieuwke S. Veldhuijzen and Edmund R.
Volkerts
Background. The majority of those suffering
from anxiety or related disorders are outpatients, and presumably
involved in daily activities such as driving a car. However,
anxiolytic drugs may possess sedative properties that reduce
alertness and produce sleepiness. Therefore, it must be questioned
whether it is safe to drive a car when treated with these
drugs.
Methods. A MEDLINE literature search (keywords
driving and anxiety) and cross-references identified 14 placebo-controlled,
double-blind studies that examined the effects of anxiolytic
drugs on driving ability by conducting the on-the-road driving
test during normal traffic. Primary parameter of the driving
test is the Standard Deviation of Lateral Position (SDLP),
the weaving of the car. Data from epidemiological studies
was summarized as supportive evidence.
Results. After single dose administration
of benzodiazepines and related GABAergic compounds (diazepam,
lorazepam, alprazolam, oxazepam, alpidem, suriclone, zolpidem)
driving performance was significantly impaired. Further, although
tolerance develops, driving studies show that the impairing
effects of benzodiazepines and related GABAergic compounds
may still be present after on week of daily treatment (demonstrated
for diazepam, lorazepam, alpidem, suriclone). Driving performance
was also significantly impaired after single dose administration
of TCAs (imipramine, amitriptyline), but after repeated use
of TCAs tolerance developed to the impairing effects on driving
ability. In contrast, SSRIs (paroxetine, fluoxetine), venlafaxine,
5HT-antagonists (ritanserin, ondansetron) and buspirone produced
no significant impairment on the driving test after both acute
and repeated administration. These findings were in line with
epidemiological evidence.
Conclusions. Patients treated with benzodiazepines,
GABAergic compounds, or TCAs should be cautioned when driving
a car. Driving a car when treated with buspirone, venlafaxine,
5HT-antagonists, and SSRIs seems relatively safe.
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