Discussion
The data presented characterize the
neuropsychological performance of individuals diagnosed
with methamphetamine-induced psychosis.
The results indicate impairment in several abilities
related to executive function and memory.
Given that testing occurred many years after the
initial MAP diagnosis, the fi ndings suggest that
methamphetamine users who experienced at least
one prior psychotic episode have lasting cognitive
impairments that may refl ect brain damage.
Nearly half of the sample was re-hospitalized for
MAP but analyses confi rmed that their cognitive
performance did not differ from those who were
not re-hospitalized. Likewise, there was no effect
of route of administration on cognitive impairment.
Cognitive dysfunction can limit adherence
to treatment and negatively infl uence outcomes
and results of neurocognitive assessments can
shed light on the neurological underpinnings of
methamphetamine-induced psychosis and related
psychoses. As mentioned, methamphetamine is
a moderator, infl uencing the relationship between
dopamine functioning and cognitive performance.
The cognitive dysfunction exhibited by these MAP
patients involves brain regions such as the prefrontal
cortex, which has dopaminergic systems vital
to the formation of attentional sets and switching
behavior16. Results support the assumption that
MAP patients, like methamphetamine users, have
altered dopamine function.
These data are distinctive from an earlier
study of Thai MAP patients who completed
neurocognitive testing. It appears that the two
samples of patients vary in their patterns of cognitive
ability; performance scores of the current
sample on Trail Making A/B appear poorer while
Stroop scores are nearly equivalent17. A notable
distinction between these two groups of Thai
MAP patients is that the prior sample completed
testing at their fi rst hospitalization for MAP while
for the current sample; approximately six years
passed since their fi rst hospitalization for MAP.
This evokes the question of whether what we
are seeing in the current sample is progressive
cognitive impairment from the time of the initial
diagnosis. A comparative analysis of a subset
of patients who participated in both studies is
underway to answer this question.
As one would anticipate, the MAP
patients’ scores were considerably poorer than
those of the normative samples. Executive function,
attention, inhibition, visuoperceptual processing,
and working memory components all appear
impaired in the patients with psychosis compared
to the normative control samples.
Future research comparing neuropsychological
performance of MA-dependent samples with
and without methamphetamine-induced psychosis
is warranted to understand the cognitive impairment,
if any, that psychosis contributes above
and beyond the impairment seen with chronic MA
use. Another line of research that awaits evaluation
is the comparison of cognitive performance
of MAP patients by country, which would provide
information about cultural, educational, and ethnic
differences and their potential infl uences on MAP
etiology, prognoses, and treatment. Assessment
of the relationship and the potential progression
of cognitive decline with duration of methamphetamine
use and emergence of MAP symptoms
warrant future study. Limitations. When interpreting
these data one should take into account that this
study was limited because of its cross-sectional
design. While this prohibited evaluation of cognitive
functioning prior to the onset of MAP symptoms,
future analyses will assess a subset of MAP participants
who completed repeated neurocognitive
testing over several years. A second limitation
is the lack of objective verifi cation of sustained
abstinence over the course of the follow-up
timeframe. This may be a minor factor however,
as all participants provided urine negative for
methamphetamine at the time of testing, implying
no use in at least a few days. The lack of Thai
norms made it impossible to calculate statistical
signifi cance of the cognitive impairment.
Conclusion
This descriptive study characterizes the
neuropsychological performance of individuals with
methamphetamine-induced psychosis. Continuing to
investigate cognitive performance in MAP patients
in Thailand and in other countries will provide a
better understanding of the etiology and consequences
of MAP. Additionally, neuropsychological
testing may be a valid diagnostic tool to distinguish
methamphetamine abuse from methamphetamineinduced
psychosis, or to inform clinicians trying
to treat individuals with MAP.
Acknowledgments
Support for this research provided by
the National Institute on Drug Abuse grant # U01
DA017394.
DiscussionThe data presented characterize theneuropsychological performance of individuals diagnosedwith methamphetamine-induced psychosis.The results indicate impairment in several abilitiesrelated to executive function and memory.Given that testing occurred many years after theinitial MAP diagnosis, the fi ndings suggest thatmethamphetamine users who experienced at leastone prior psychotic episode have lasting cognitiveimpairments that may refl ect brain damage.Nearly half of the sample was re-hospitalized forMAP but analyses confi rmed that their cognitiveperformance did not differ from those who werenot re-hospitalized. Likewise, there was no effectof route of administration on cognitive impairment.Cognitive dysfunction can limit adherenceto treatment and negatively infl uence outcomesand results of neurocognitive assessments canshed light on the neurological underpinnings ofmethamphetamine-induced psychosis and relatedpsychoses. As mentioned, methamphetamine isa moderator, infl uencing the relationship betweendopamine functioning and cognitive performance.The cognitive dysfunction exhibited by these MAPpatients involves brain regions such as the prefrontalcortex, which has dopaminergic systems vitalto the formation of attentional sets and switchingbehavior16. Results support the assumption thatMAP patients, like methamphetamine users, havealtered dopamine function.These data are distinctive from an earlierstudy of Thai MAP patients who completedneurocognitive testing. It appears that the twosamples of patients vary in their patterns of cognitiveability; performance scores of the currentsample on Trail Making A/B appear poorer whileStroop scores are nearly equivalent17. A notabledistinction between these two groups of ThaiMAP patients is that the prior sample completedtesting at their fi rst hospitalization for MAP whilefor the current sample; approximately six yearspassed since their fi rst hospitalization for MAP.This evokes the question of whether what weare seeing in the current sample is progressivecognitive impairment from the time of the initialdiagnosis. A comparative analysis of a subsetof patients who participated in both studies isunderway to answer this question.As one would anticipate, the MAPpatients’ scores were considerably poorer thanthose of the normative samples. Executive function,attention, inhibition, visuoperceptual processing,and working memory components all appearimpaired in the patients with psychosis comparedto the normative control samples.Future research comparing neuropsychologicalperformance of MA-dependent samples withand without methamphetamine-induced psychosisis warranted to understand the cognitive impairment,if any, that psychosis contributes aboveand beyond the impairment seen with chronic MAuse. Another line of research that awaits evaluationis the comparison of cognitive performanceof MAP patients by country, which would provideinformation about cultural, educational, and ethnicdifferences and their potential infl uences on MAPetiology, prognoses, and treatment. Assessmentof the relationship and the potential progressionof cognitive decline with duration of methamphetamineuse and emergence of MAP symptomswarrant future study. Limitations. When interpretingthese data one should take into account that thisstudy was limited because of its cross-sectionaldesign. While this prohibited evaluation of cognitivefunctioning prior to the onset of MAP symptoms,future analyses will assess a subset of MAP participantswho completed repeated neurocognitivetesting over several years. A second limitationis the lack of objective verifi cation of sustainedabstinence over the course of the follow-uptimeframe. This may be a minor factor however,as all participants provided urine negative formethamphetamine at the time of testing, implyingno use in at least a few days. The lack of Thainorms made it impossible to calculate statisticalsignifi cance of the cognitive impairment.ConclusionThis descriptive study characterizes theneuropsychological performance of individuals withmethamphetamine-induced psychosis. Continuing toinvestigate cognitive performance in MAP patientsin Thailand and in other countries will provide abetter understanding of the etiology and consequencesof MAP. Additionally, neuropsychologicaltesting may be a valid diagnostic tool to distinguishmethamphetamine abuse from methamphetamineinducedpsychosis, or to inform clinicians tryingto treat individuals with MAP.AcknowledgmentsSupport for this research provided bythe National Institute on Drug Abuse grant # U01DA017394.
การแปล กรุณารอสักครู่..
