Novel Therapies for Cognitive Dysfunction Secondary to Substance Abuse - Psychiatric Times
SUBSTANCE ABUSE: ADDICTION & RECOVERY
Novel Therapies for Cognitive Dysfunction Secondary to Substance Abuse
Brief Screening, Referral, and Cognitive Rehabilitation
By Antonio Verdejo-García, PhD | June 8, 2011
Dr
Verdejo-García is Researcher and Lecturer at the Department of
Clinical Psychology and Institute of Neuroscience, Universidad de
Granada, Spain. He reports no conflicts of interest concerning the
subject matter of this article.
Advances in the fields of neuropsychological assessment and neuroimaging have enormously expanded our knowledge about the profile and severity of cognitive deficits in patients with substance use disorders.
Neuroscience studies have complemented this knowledge by revealing the neural adaptations induced by different substances (dopamine, glutamate, or serotonin) on specific cellular systems and by showing the structure and dynamics of brain systems, including frontostriatal systems and paralimbic networks involved in motivation and cognitive control.1,2
Typical cognitive deficits
Patients with substance use disorders have common cognitive impairments in frontal-executive control skill centers related to planning, working memory, inhibition, and decision making, as well as alterations in episodic memory, selective attention, and emotional processing.3 Moreover, certain drugs have more robust effects on particular cognitive functions3:
• Psychostimulants, on inhibition and flexibility
• Opiates, on planning and fluency
• Cannabis, on episodic memory
• Alcohol(Drug information on alcohol), on a wide range of executive functions as well as on visual-spatial and psychomotor skills
These
deficits are not ubiquitous among patients with substance use
disorders, and there is considerable variability in the degree of
cognitive dysfunction depending on a number of drug use parameters, such
as quantity, frequency, and duration of use. Heavier users typically
display greater impairments. Greater quantity and longer duration of
cocaine use are associated with poorer response inhibition and
flexibility; longer duration of heroin use is associated with poorer
flexibility; heavier cannabis use is linked to poorer episodic memory,
working memory, and reasoning; and heavier alcohol use relates to
poorer updating of information and less adaptive decision making.4The causality of these deficits is still disputed, since a certain degree of cognitive dysfunction (linked to disinhibition) may preexist and be further exacerbated by drug exposure.5 Current neurobiological models assume that impulsivity (as a trait) may confer vulnerability for the onset and progression of substance use disorders, whereas prolonged exposure may induce relatively persistent deficits in memory, attention, and different executive functions (as a state).2,5 This evolution is mediated by neuroadaptations in the frontostriatal systems that provoke a transition from goal-directed (impulsive) toward outcome-detached (compulsive) behavior.6,7
Individual differences in genetic makeup (including genes involved in cognitive functioning or those involved in drug pharmacodynamics) and in rates of cognitive maturation and ageing are also thought to contribute to the differential impact of vulnerability as well as drug exposure in the cognitive status of patients with substance use disorders.8,9
Relevant to both causal pathways (vulnerability and neuroadaptations) is the neuropsychological concept of executive functions, which refers to a group of abilities involved in the production, monitoring, and readjustment of goal-directed behavior. Executive functions are directly involved in planning, updating of relevant information (working memory), control of prepotent inappropriate responses (inhibition), detection and correction of errors (flexibility), and adaptive decision making.10 They are also indirectly involved in successful encoding and retrieval of information (episodic memory), attentional control (sustained, selective, and dual attention), affective responsiveness, and self-awareness.11 Anatomically, they are tightly associated with the functioning of the frontostriatal systems.12
It is not surprising that study results have shown that patients with disorders related to different substances have common cognitive impairments in planning, working memory, inhibition, and decision making (core executive functions), as well as in episodic memory, selective attention, and emotional processing (executive function–related processes). Partial spontaneous recovery of cognitive function is manifest during abstinence, although different profiles of drug use and different cognitive skills are associated with different rates of recovery.3 However, certain skills, such as response inhibition, self-regulation, and decision making, are persistently impaired even after several months of abstinence.3,13
Psychiatric Times. Vol. 28 No. 6
Pages: 1 2 3 4
SUBSTANCE ABUSE: ADDICTION and RECOVERY
Novel Therapies for Cognitive Dysfunction Secondary to Substance Abuse
Brief Screening, Referral, and Cognitive Rehabilitation
By Antonio Verdejo-García, PhD | June 8, 2011
Dr Verdejo-García is Researcher and Lecturer at the Department of Clinical Psychology and Institute of Neuroscience, Universidad de Granada, Spain. He reports no conflicts of interest concerning the subject matter of this article.
The prevalence and durability of cognitive deficits in patients with substance use disorders raises the need to develop specific assessment and rehabilitation strategies. This is pertinent because general deficits in cognitive function and specific deficits in executive functions are robustly associated with worse drug treatment outcomes, including poorer adherence, shorter retention, and greater risk of relapse.14-16
In this article, I propose the use of a brief screening instrument for frontal-executive deficits in patients with substance use disorders and provide examples of novel treatment interventions aimed at addressing these deficits.
Instruments to assess substance use–related cognitive deficits
Key manifestations of cognitive/executive dysfunction among patients with substance use disorders are:
• Difficulties in understanding complex instructions
• Distractibility
• Premature or disinhibited responses
• Thought and behavioral inflexibility
Some other symptoms may be neglected by the patient but stressed by significant collaterals, including problems with initiating and planning novel activities, disorganized behavior, lack of insight into his or her mistakes, and lack of concern about the consequences.
Insight is often lacking in the patient, which underscores the need for the clinician to effectively screen for cognitive dysfunction. If cognitive impairment is suspected in light of clinical observations and interviews, I recommend the use of a brief screening instrument to detect frontostriatal systems–derived cognitive, behavioral, and emotional deficits. For example, the Frontal Systems Behavior Scale (FrSBe) is a sensitive instrument used to detect frontostriatal-related deficits in patients with substance use disorders.17-19
The FrSBe is composed of 46 items (rated on a 1 to 5 Likert scale) that yield 3 scores for symptoms of apathy, disinhibition, and executive dysfunction (working memory, planning, or awareness deficits), as well as an overall score of frontostriatal-systems dysfunction. The scale includes a self-report and a collateral report. Both reports have shown adequate reliability indices, but the use of the latter is especially recommended when the patient’s insight deficits are overtly manifest.17 The scale also possesses norms extracted from the healthy population of the United States, which provides easy classification of patients as impaired or nonimpaired in comparison with demographically adjusted norms.
If the information from the clinical interviews and the scale’s scores converges to suggest at least mild cognitive impairment (below 1.5 standard deviations [SDs] in some of the FrSBe scales), the clinician can complement the assessment by administering a brief battery of neuropsychological tests focused on those cognitive abilities with well-known implications for addiction treatment prognosis (Table). Response inhibition is measured with the Stroop test, the Wisconsin Card Sorting Test (WCST) is used to measure flexibility/perseveration, decision-making capacity is measured using the Iowa Gambling Task (IGT).14-16
The Stroop test measures response inhibition, and it is based on the interference effect driven by the demand of naming the color of a word that is printed in a color incongruent with the name (eg, the word blue printed in red).20 The test consists of 3 conditions. The first condition (W) presents the words red, blue, and green printed in black ink, and patients are requested to read aloud these words. The second condition (C) presents strings of XXX printed in the same 3 colors, and patients have to name the colors as quickly and accurately as possible. The third condition (WC) introduces the interference effect: the words red, blue, and green are printed in incongruent colors and patients have to name the color and ignore the word. The interference score (IS) is calculated by subtracting a weighted mean of the first 2 conditions from the third condition [IS = WC 2 (C 3 W)/(C + W)]; then results are compared with normative values to evaluate the degree of impairment.
The WCST21 is a measure of flexibility to change. It measures response patterns in the face of changing schedules of reinforcement. The clinician presents 4 stimulus cards; the shapes on the cards differ in color, quantity, and design. The patient is given a stack of 64 cards that he has to sort according to initially unknown criteria. However, the examiner knows the criteria (the first sorting criterion is the color of the shapes, the second is the design of the shapes, and the third is the number of shapes) and provides trial-by-trial feedback of the correctness or incorrectness of each card sorted.
Patients try to sort the cards correctly by adjusting their performance to the ongoing feedback. Critically, the sorting criteria change across the test (without any overt warning from the examiner): after 10 consecutive hits in sorting by color, the criterion changes to shape, and then to number.
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by Richard Ash | June 16, 2011 8:24 PM EDT
I am a pancreatic cancer survivor ( 7 years ) but will have lifetime pain as the tumor was lying against the celiac sheath on the perineural nerve and had to be scraped. I take 1200 MG daily of MS-Contin ER in addition to 100MCH Fentanyl patches every three days and, 10/325 Hydrocodone for breakthough pain. I am managed by the Pain Clinic at Vanderbilt in Nashville.
I hold down a full time job of excruciating attention to detail. Creating Excel, Word and Powerpoint quotations, proposals and Statements of Work for Account Executives. ( I was an Outside Sales Rep for 25 years in Hi-Tech selling to Fortune 100 companies )
Your article on the effect of opiods on attention and other executive deficits is of interest to me as I now have to be a bit more careful in reviewing my work before submission. There is a small increment of ADD as I will spontaneously stop working to check personal emails, browse the internet on articles related to our core expertise or take a break and turn upthe volume on the wall TV in the office. I work alone, in an office outsie the home but on my property.
But, these are conscious decisions. I don't suddenly find myself away from the task at hand, rather it is a break from the tedium and, I do ( as stated ) have to be cautious about grammar and diarrhea of the keyboard.
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