Sedative, Hypnotic and Anxiolytic Use Disorder DSM-5 304.1 (F13.1)

Sedative, Hypnotic and Anxiolytic Use Disorder DSM-5 304.1 (F13.1)

DSM-5 Category: Substance-Related and Addictive Disorders


Self-medication or pharmaceutical treatment for anxiety and insomnia has taken place throughout history, and the problems these can cause have been recognized since ancient times. Alcohol, opium and the two in combination (laudanum) were among the first widely used and frequently misused sedative and anxiolytic drugs, and bromide salts, paraldehyde and chloral hydrate were in medical use by the end of the 19th century. Barbiturates were synthesized in 1903, meprobamate in 1950 and the benzodiazepine chlordiazepoxide in 1959, setting the stage for the great proliferation of sedative-hypnotic drugs and anxiety medications that has continued to the present day (Lader, 2011).

The problem of compulsive and maladaptive use of these drugs, as with other psychoactive substances, has been divided into 2 categories, substance abuse and substance dependence (American Psychiatric Association, 2000). The syndrome of substance abuse has recently involved the consumption of drugs in a way that is harmful to the user of others, while substance dependence has meant the compulsive need to use drugs in order to function normally, with withdrawal symptoms if the drug(s) cannot be obtained. The distinction between “abuse” and “dependence” was based on the concept of abuse as an early or mild phase of abnormal substance use and dependence as a later and more severe manifestation. This is not always the case, and abuse of a substance can be severe while some individuals dependent upon a drug to function may not misuse it as severely or have withdrawal symptoms. In addition, “dependence” and “addiction” have often been used interchangeably, and dependence upon a drug does not necessarily mean addiction, a situation exemplified by insulin, anticonvulsants and sometimes chronic pain regimens.

Recent revisions of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 2013) have combined substance abuse and substance dependence into Substance Use Disorder, in which substance use results in distress or functional impairment, specified by drug and graded on a continuum from mild to severe. The not-infrequent “polysubstance addiction” is addressed as separate substance use disorders, although the overarching criteria are the same for most substances. More symptoms of problematic substance use have been added to the criteria and a diagnosis of mild use disorder now requires 2 or 3 of these rather than a single manifestation for substance abuse. Drug craving has been added to the list of symptoms because this occurs frequently, but the requirement for drug-related legal problems has been removed because this often does not occur. A single disorder (gambling) has been placed in a new category of behavioral addictions because of similarities between gambling addiction and substance use disorders in clinical features, psychiatric comorbidity, physiology, brain origin and response to treatment. Internet gaming and overconsumption of caffeine have been placed in Section III of the Manual, for further study and possible later inclusion as diagnoses. These changes have elicited both accolades and criticism (Edwards, 2012).

Symptoms of Sedative,Hypnotic and Anxiolytic Use Disorder

Barbiturates have been more stringently controlled in the United States, and benzodiazepines are more frequently abused because of perceived greater safety and more frequent prescribing for sleep or anxiety problems. There are two broad categories of patients who become dependent upon sedative-hypnotic or anxiolytic medications: those who take them for symptomatic treatment of a neurologic or psychiatric disorder and those who use them in non-medical settings, sometimes for self-medication for psychiatric symptoms but also to enhance euphoria or curb withdrawal from other drugs. Patients prescribed high doses of sedative-hypnotic agents or treated for more than 1 month are at risk for dependence, especially with a past history of alcohol or prescription drug abuse, and family history of alcoholism may confer a genetic predisposition to benzodiazepine dependence.In the absence of dose escalation or deliberate use of the prescription to produce euphoria, however, there is not necessarily a link between chronic benzodiazepine use and use disorder (Stern, Fricchione, Cassem, Jellinek & Rosenbaum, 2010).

Relatively small doses may cause drowsiness, motor impairment and impaired judgement. Accident risk is greatest in the first weeks of benzodiazepine use or with increasing dosage or use of long-half-life agents. Anterograde amnesia, the inability to learn new information with preserved retrieval of previously-learned information is a common effect of benzodiazepines, and is in fact a therapeutic goal during procedures.Intoxication, stupor, coma and respiratory depression are more common with barbiturates due to steep dose-response curves; curves for benzodiazepines are flatter, and these complications are more often due to the combination of benzodiazepines with other central nervous system depressants (Smink, Egberts, Lusthof, Uges & deGier, 2010).

Withdrawal involves autonomic overactivity, tremor, insomnia, psychomotor agitation or anxiety, hallucinations and convulsions after hours to days of abstinence. Rebound of insomnia, anxiety or other symptoms for which the sedatives or anxiolytics were prescribed may occur within days of cessation but will subside over time; reappearance of a mood or anxiety disorder may also occur after drug discontinuation but does not subside with time.Withdrawal from low (therapeutic) doses of benzodiazepines generally does not occur if the drug had been prescribed for less than 4 months, but when present involves anxiety, insomnia, restlessness, tremor, incoordination, anorexia, nausea and vomiting, hyperpyrexia and diaphoresis, and may progress to delirium and seizures. Withdrawal from high doses generally causes these symptoms and is more rapid and more severe with short-acting drugs like alprazolam than with long-half-life agents like clonazepam; withdrawal usually begins 1 to 2 days after stopping short-acting sedative-hypnotics, and peaks in 1 to 3 days, while withdrawal from longer-acting drugs begins in about a week. A protracted withdrawal syndrome with depersonalization, sensory illusions and heightened perceptions may develop in those with alcoholism or abuse of other sedative drugs. Prolonged mild withdrawal with anxiety, irritability and insomnia may occur for months in patients who stop benzodiazepines after taking therapeutic doses for long periods (Wiviott-Tishler, Wiviott & Hyman, 1996).

Diagnostic Criteria for Sedative,Hypnotic and Anxiolytic Use Disorder

The new diagnosis requires at least 2 of the following criteria. The disorder is mild if 2-3 criteria are met, moderate if 4-5 are present and severe with 6-7 or more.

  • Continuing to use a substance, in this case a barbiturate, benzodiazepine or other sedative-hypnotic, despite negative personal consequences.
  • Repeated inability to carry out major functions at work, school or home on account of use.
  • Recurrent use in physically hazardous situations
  • Continued use despite recurrent or persistent social or interpersonal problems caused or made worse by use.
  • Tolerance, as manifested by needing a markedly increased dose to achieve intoxication or desired effect, or by markedly diminished effect with continued use of the same amount.
  • Withdrawal with the characteristic syndrome, or use of the drug to avoid withdrawal.
  • Using more of the drug or using for a longer period than intended.
  • Persistent desire to cut down use, or unsuccessful attempts to control use.
  • Spending a lot of time obtaining or using the substance or recovering from use.
  • Stopping or reducing important occupational, social or recreational activities due to use.
  • Craving or strong desire to use.

Treatment for Sedative,Hypnotic and Anxiolytic Use Disorder

Benzodiazepine intoxication or overdose can be reversed with flumazenil, which competitively inhibits the benzodiazepine binding sites on the GABAA receptor and thereby reverses the effects of the drugs; it does not always reverse respiratory depression, and can cause seizures, particularly in patients with epilepsy or who overdose with tricyclic antidepressants also (Veariah, Dyas, Cooper, Routledge & Thompson, 2012). Barbiturate overdose may require dialysis, but the rate of barbiturate excretion can be increased by alkalinizing the urine with intravenous sodium bicarbonate, followed by a tapering dose of phenobarbital (Kawasaki, Jacepraro & Rastegar, 2012).

Withdrawal can be prevented by tapering doses of benzodiazepines or phenobarbital; it is recommended to convert the current dose of a short-acting benzodiazepine to the equivalent dose of longer-acting diazepam and then decrease the dose in 2-week decrements to 75, 50, 25, 12.5 and 0 per cent of that. Melatonin and anticonvulsants, particularly carbamazepine, gabapentin, topiramate and possibly pregabalin, are also helpful for withdrawal by reversing kindling and improving comorbid psychiatric symptoms (Vissers, Knipschild & Crebolder, 2007; Bobes, Rubio, Terián, Cervera, López-Gómez & Vilardaga, 2012). Severe delirium due to withdrawal from high doses of barbiturates can be managed by giving pentobarbital 200 mg orally and then 100 mg per hour to a total of 600 mg, until sedation, nystagmus and reduction of pulse and blood pressure occur; thereafter, 30 mg of Phenobarbital can be given orally for every 100 mg of pentobarbital that has been given, and the dose can be tapered on subsequent days by 10 per cent per day. Adding melatonin 5 mg or zolpidem 10 mg a night to a tapering dose of sedative-hypnotic benzodiazepine will reduce the insomnia and restless sleep common during detoxification (Riemann & Perlis, 2009).

Cognitive behavioral therapy is supported by controlled trialsl in chronic insomnia patients, in whom psychotherapy also improved sleep (Vicens, Socias, Mateu, Leiva, Bejarano & Sempere, 2011). Twelve-step programs, specifically Pills Anonymous although fellowships for alcohol, narcotic and cocaine problems may also be helpful, are also appropriate for recovering patients to consider.


American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, ed. 4. Washington, DC, APA Press.

American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders, ed. 5. Arlington, VA, APA Press.

Bobes, J., Rubio, G., Terián, A., Cervera, G., López-Gómez, V. & Vilardaga, I. (2012). Pregabalin for the discontinuation of long-term benzodiazepine use: an assessment of its effectiveness in daily clinical practice. Eur Psychiat, 27(4): 301-307.

Edwards, G (2012). “The Evil Genius of the Habit”. DSM-5 seen in historical context. J Stud Alcohol Drugs, 73(4): 699-701.

Kawasaki, S.S., Jacaprapro, J.S. & Rastegar,D.A. (2012). Safety and effectiveness of a fixed-dose Phenobarbital protocol for inpatient benzodiazepine intoxication. J Subst Abuse Treatment, 43(3): 331-334.

Lader, M. (2011). Benzodiazepines revisited – will we ever learn? Addiction, 106(12): 2086-2109.

Riemann, D. & Perlis, M.L. (2009). The treatments of chronic insomnia: a review of benzodiazepine receptor antagonists and psychological and behavioral therapies. Sleep Med Rev, 13(3): 205-214.

Smink, B.E., Egberts, A.C., Lusthof, K.J., Uges, D.R. & deGier, J.J. (2010). The relationship between benzodiazepine use and traffic accidents: A systematic literature review. CNS Drugs, 24(8): 639-653.

Stern TA, Fricchione G, Cassem NH, Jellinek MS & Rosenbaum JF (2010). Drug-addicted patients. In, Massachusetts General Hospital Handbook of General Hospital Psychiatry, ed. 6. Philadelphia, W.B. Saunders.

Veariah, A., Dyas, J., Cooper, G., Routledge, P.A. & Thompson, J.P. (2012). Flumazenil use in benzodiazepine overdose in the U.K.: a retrospective survey of NPIS data. Emerg Med J, 29(7): 565-569.

Vissers, F.H., Knipschild, P.G., Crebolder, H.F. (2007). Is melatonin helpful in stopping the long-term use of hypnotics? A discontinuation trial. Pharm World, 29(6): 641-646.

Wiviott-Tishler, L., Wiviott, S.D. & Hyman, S.E. (1996). Sedative hypnotics and anxiolytics. In, Freidman, L., Fleming, N.F., Roberts, D. & Hyman, S.E. (eds). Sourcebook of Substance Abuse and Addiction. Baltimore, Williams and Wilkins, pp. 203-217.

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