In his article “New-Onset Psychosis: Check Caffeine Use,” Whiting describes a patient his team treated at the Naval Medical Center in Portsmouth, Virginia for psychotic symptoms who ingested a high amount of caffeine regularly. The patient, Ms. P, was 19 years old and reported visual hallucinations, paranoia, and the inability to organize thoughts. Ms. P drank four cups of coffee on an average day, plus three or four more and two or three Monster energy drinks if she was on duty.¹ According to Whiting, Ms. P was ingesting about 22 mg/kg of caffeine per day. Ms. P was asked to reduce her caffeine intake and return in two weeks for a follow-up.¹

Two weeks later, Ms. P reported that her caffeine intake consisted of a cup of coffee or a Monster every now and then. She felt less paranoid, slept better, and had less thought disruption.¹ However, as her progress deteriorated over the next four weeks, she was prescribed ziprasidone 20 mg/day.¹ The medicine was tolerated well, and Ms. P retired from the military for medical reasons.¹

Statistics show that alcohol use disorders, also referred to as AUDs, frequently go untreated. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) conducted the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) in both 2001 and 2002, which calculated alcohol abuse and dependence at 4.65 percent and 3.81 percent, respectively.[2] Using those results, Cohen and colleagues found that just 14.6 percent had ever received treatment.[3] A second study conducted by Dawson and colleagues focused on those whose onset of alcoholism occurred a year before the NESARC study.[4] Concerning treatment, Dawson and colleagues found that just 25.5 percent had ever received such, with 5.4 percent reporting the use of formal treatment, 3.1 percent reporting the use of a 12-step program, and 17 percent reporting the use of both.[5]

In 1989, the NIAAA conducted Project MATCH, where patients were first categorized by certain factors—such as alcohol involvement, cognitive impairment, psychiatric disorders, gender, and motivation to change—and then randomly referred to a 12-week treatment: a 12-step program, cognitive-behavioral therapy, or motivational enhancement therapy.[6] After the treatment was complete, patients were followed for one year at three-month intervals, to track drinking patterns, quality of life, and their utilization of other treatments. As a result, those with low psychiatric severity were found to be best suited with 12-step treatments.⁶

Peer-run mutual help groups (MHGs) remain effective in aiding those dependent recover, as they are available at peak times of weakness: nights and weekends.¹ Also, since members are able to contact each other for support, chance of relapse decreases. However, many do not continue to attend MHG’s, leading researchers to both focus on extended treatments which provide continuous care and reach beyond the traditional methods.¹

With the growing use of technology, alcoholism treatments are expanding their availability to cell phones and the Internet. Online social support groups, Internet-based interventions, email, and text messaging all are able to provide supports.¹ Gustafson and colleagues report on a cell phone-based support for patients who finish inpatient treatment, called Addiction Comprehensive Health Enhancement Support System (A-CHESS).[7] The technology offers social support, motivation, and coping strategies, which researchers believe will show a reduced number of patients’ drinking days.⁷

Myers, Roozen, and Smith report the Community Reinforcement Approach (CRA) helps patients convert their lifestyles to healthy and drug-free, through becoming involved in alternate activities.[8] The activities focus the patients on their family and other social relationships as well as their employment. The approach also enlists the help of the patients social relationships to maintain an alcohol-free environment.⁸

Researchers have also found that cost-effective treatments are the most successful, and the Federal parity legislation and health care reform has allowed more treatments to be so. Stewart and Horgan explain that the Federal parity law has required group health plans that offer mental health and addiction services to cover the services comparably to medical and surgical services, lifting some financial burden from the patient.[9] They believe this will cause changes to private and public insurance plans, as well, and may also expand Medicaid eligibility.⁹

With treatment for alcohol use disorders improving, multiple approaches are available to fit the needs of many different patients, and they are becoming more affordable and technological as well. This only allows for further improvements in the future.

More than one in 10 U.S. children live with an alcoholic parent and are at increased risk of developing a host of health problems of their own, according to a new government study released on Thursday.

Researchers at the Substance Abuse and Mental Health Services Administration (SAMHSA) analyzed national survey data from 2005 through 2010 and found that, on average, 7.5 million children — about 10.5 percent of the country’s under-18 population — lived with a parent abusing alcohol during any given year.

Most of those kids — an average of 6.1 million each year — lived in two-parent households where one or both of the adults had a drinking disorder, the researchers found.

Of the 1.4 million children who lived in a single-parent home where the adult had a drinking issue, the overwhelming majority — 1.1 million — were in female-headed households, SAMHSA said.

The researchers said children living with alcoholics were at greater risk of suffering from a number of mental health problems, including depression and anxiety.

The children were also more likely to be abused or neglected by their parents, more likely to have cognitive or language deficiencies, and four times more likely to develop alcohol problems of their own, the researchers said.

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Corr states that EBM has consistently been behind the mark in child and adolescent psychiatry as pharmacological treatment trials of the population are limited.¹ According to Walkup and colleagues, using children in scientific studies was usually avoided, as was the scientific causes of child psychopathology.[3] Also, historically using medicine to treat children was hindered; therefore, reason for pharmacotherapy studies was lacking.¹ However, as things are now changing, advancements have been made through several trials. With more trials, Corr states that applying EBM will bring credibility to the field of psychiatry, as well as awareness of the science behind it. Mental illnesses will be viewed as having a biological basis.¹

Even still, Corr states there continue to be gaps. First, insufficient research has delayed Food and Drug Administration (FDA) approval of medicine for the psychiatric treatment of children and adolescents.¹ Therefore, clinicians are forced into off-label uses of medicines, leading credibility of such to be challenged as the FDA has yet to support such treatments. Second, children and adolescents can be difficult to clearly diagnose, as more often several visits to a clinician are required before there is a full understanding of the child.¹ Also, as children continue to grow and develop, their diagnoses may develop and change; therefore, reevaluating and modifying treatment is crucial.¹

Clinician preparation in EBM is crucial to its future in the field of child and adolescent psychiatry. Medical schools begin to form the basis of good clinical practice in order to prepare future clinicians for using EBM.¹ Frequently, during fellowships and residencies clinicians are offered the opportunity to practice applying the principles of EBM, as such is a core requirement of the Accreditation Council for Graduate Medical Education (ACGME).¹ According to Corr, it is not enough—more should be done in preparation, such as incorporating EBM into fellowship training with case conferences.¹ Green and colleagues found that such training was associated with better examination scores.[4] However, Corr explains her struggle with EBM during her fellowship as the differences in instructors’ approaches. Some rely on objective data while others insist upon using clear-cut pathways for pharmacologic treatment.¹ However, again, Corr states that it is about treating the patient and not the diagnosis.

Overall, Corr believes that increasing the number of clinical trials conducted regarding child and adolescent psychopharmacology will ultimately acknowledge EBM as standard practice within the field of psychiatry.¹

The drug disulfiram (Antabuse) was introduced in the 1940s, with the intent to help alcohol dependent persons abstain from heavy drinking. Now, newer medicines, such as naltrexone and it’s intramuscular injection Vivitrol and acamprosate (Campral), have proven effective for drinking abstinence, especially when paired with behavioral therapies. Currently, four medicines are FDA-approved for the treatment of alcohol dependence: Antabuse, Naltrexone, Campral, and Topiramate.[2]

Antabuse works by interfering with the body’s ability to metabolize alcohol by way of blocking the break down of acetaldehyde by the enzyme aldehyde dehydrogenease. Therefore, the body accumulates a large amount of acetaldehyde, causing the adverse effects of nausea, vomiting, palpitations, and headache.[3] With the effects being immediate, the medication supports a person’s motivation to avoid alcohol; however, the effects may also make medication compliance difficult, and the medicine is proven to be most successful when administered by someone other than the dependent, such as a healthcare provider or family member.[4]

Naltrexone, an opiate antagonist, works by blocking the μ-receptors of the brain,[5] successfully decreasing both the overall number of drinks consumed by the dependent[6] and the number of days the dependent consumed large amounts of alcohol.[7] Taking the oral dose of 50 to 100 mg per day over a period of three months has shown to prevent relapse, especially when combined with medical management.⁶ During a six-month trial, the monthly injection of 380 mg of Extended-Release Vivitrol kept the dependent adhered to medication and showed results of 32 percent remaining abstinent for a period of six months, compared to 11 percent who received a placebo.[8] The adverse effects experienced were minor, including nausea, headache, and dizziness; however, persons with liver disease and opiate pain management can not use naltrexone or Extended-Release Vivitrol.3

Campral became approved for treating alcohol dependency in 2004, and although how exactly it works is unknown, it has been studied and used largely in various other countries around the world.3 According to Littleton and Zieglgansberger, it is believed to balance the excitatory and inhibitory pathways of the brain, those that are altered by alcohol use.[9] The medicine has shown to improve abstinence rates and prolong the time before the dependent’s first drink.[10] Generally, Campral’s side effects were gastrointestinal; therefore, use in persons with liver disease is admitted. However, persons with kidney impairments are not recommended to use the drug.3

Topiramate, the fourth approved medicine, is an anticonvulsant; however, it has shown to reduce alcohol and cigarette use.[11] At a dosage of 300 mg per day, the drug works by assisting GABA neurotransmitter functioning and opposing glutamate activity, with adverse effects including cognitive dysfunction, abnormal sensations, anorexia, and taste abnormalities. The medication has exhibited the infrequent effects of metabolic acidosis, acute myopia, and secondary narrow-angle glaucoma.3

With current approved medicines having only a moderate effect at treating alcohol dependency, studies identifying new, more effective medicines are underway.3 The selective serotonin reuptake inhibitors line of depression-treating medicines have not shown effectiveness among persons with early-onset dependence; however, some studies concluded it may be with later-onset alcoholism when used in conjunction with naltrexone.[12] According to Addolorate, Leggio, Ferrulli, et al’s study, the “Effectiveness and safety of baclofen for maintenance of alcohol abstinence in alcohol-dependent patients with liver cirrhosis,” medicines that target the GABA and glutamate neurotransmitters may be promising methods of treatment.[13] With early intervention, gabapentin, another anticonvulsant, has also shown promise of effectiveness.⁶

As most medicines focus mainly on those who are alcohol dependent, those who abuse the substance yet do not meet the criteria for dependence may also benefit from such treatment.3 Young adults fall into the category, as they are mostly interested in only decreasing their drinking instead of abstaining.3 Therefore, motivational interventions like the Brief Alcohol Screening and Intervention for College Students (BASICS) offer personalized feedback and strategies for refraining from alcohol-induced harm. While the interventions alone proved effective, coupled with medicine, it would help reduce drinking even further.⁸

Unfortunately, studies of the effects of prenatal alcohol exposure encounter certain obstacles. As data pertaining to alcohol consumption during pregnancy is collected through self-reporting, many women either deny or underreport considerably the amount of alcohol they have consumed while pregnant.[2] With no reliable biomarkers available for credible testing, self-reporting is the main collection route. Bailey and Sokol state that the reported amount of prenatal drinking in the United States is likely significantly lower than the actual amount, which skews research regarding consumption thresholds. Therefore, no amount of alcohol consumed during pregnancy should be considered “safe.” Additionally, false self-reporting causes some prenatal drinkers to become classified as “nondrinkers,” leading risk outcomes for nondrinkers to increase falsely. This further blurs the research regarding the effects alcohol has on a fetus.

As research is uncovering certain factors that increase a woman’s risk of adverse effects from prenatal drinking, the level of “safe” alcohol use becomes more unclear.¹ Sokol reports that women older than 30 have an increased risk of poor pregnancy outcomes if prenatal drinking is involved, as well as women who are of certain racial and ethnic backgrounds.¹ Therefore, an amount that will not have an adverse effect on one woman may cause serious effects for another.

Another obstacle for researchers of prenatal alcohol effects is how alcohol consumption is measured.¹ While many studies measure alcohol in drinks, exactly what a drink is may vary significantly. Different beverages contain different amounts of alcohol, and some may consider a drink to be x amount of ounces while others consider a drink to be y. Therefore, questionnaires which inquire the specific details regarding consumption should be utilized during screenings.¹

Women who engage in prenatal drinking are more likely to be older, unmarried, to have experienced a larger amount of stress, to suffer from a mental health condition, and to be of a lower socioeconomic status.[3] As these factors also increase poor pregnancy outcomes, it becomes difficult to pinpoint alcohol as the sole factor of such. However, studies of animal subjects, with the ability to control other causing factors, have shown alcohol to cause outcomes such as spontaneous abortion, stillbirth, preterm delivery, and SIDS.¹

Typically, spontaneous abortion refers to fetal demise before 20 weeks gestation, and, according to Kline, occurs in 20 percent of pregnancies.[4] While the reason for spontaneous abortion is often unknown, prenatal alcohol use has been defined as one risk factor. In fact, women who consume more than three alcoholic drinks per day have three times the risk of having a spontaneous abortion than those who do not engage in prenatal alcohol use.[5] Henderson and colleagues conducted a study in 2007 examining the risks of light prenatal alcohol use on a fetus and reported no consistent evidence linking the two.[6] However, moderate to heavy levels remains linked through research.

Stillbirth, the fetal demise after 20 weeks gestation, is shown to be another poor pregnancy outcome when prenatal alcohol use occurs.¹ Kesmodel and colleagues report that the consumption of more than five drinks per week increases the risk of stillbirth by three times, and animal studies stand to support the risk.[7] Aliyu and colleagues conducted a study in 2008 of more than 600,000 human births and found that the risk of stillbirth was 40 percent more likely if prenatal alcohol use was involved.[8] Aliyu and colleagues separated women by early stillbirth, earlier than 28 weeks gestation, and later stillbirth, after 28 weeks gestation, and found that alcohol use was associated more with early stillbirth than late.⁸ The study also screened for other stillbirth-causing factors within their results. Burd and colleagues reports prenatal alcohol use to be linked with placental dysfunction, smaller placental size, and impaired blood and nutrient flow to the fetus.[9]

Preterm birth usually refers to fetuses delivered prior to 37 weeks gestation; however, they are further categorized as mildly preterm, between 32 and 36 weeks gestation, and extremely preterm at less than 32 weeks gestation.¹ Studies focusing on the association between prenatal alcohol use and preterm birth have been controversial. In 2000, Kesmodel and colleagues reported that consuming more than 10 drinks per week puts the fetus three times more likely to be born premature;[10] however, in 2009, O’Leary and colleagues found there to be no association between prenatal alcohol use and preterm birth.[11] Due to the smaller group sizes of the studies, the significance of the evidence either pose is minor. In 2007, Sokol and colleagues conducted a larger study of 3,000 women, which found that there was in fact an association between prenatal alcohol use and extreme preterm delivery.[12] The study was found to be scientifically significant due to group size and control of outer-lying factors. Sokol and colleagues reported that if all women abstained from drinking, two out of every five preterm births would have been avoided.¹²

Bailey and Sokol state that prenatal alcohol use within the early stages of pregnancy increases a child’s risk of SIDS. Iyasu and colleagues conducted a study in which first trimester binge drinking was shown to be directly linked to SIDS, by three times the likeliness.[13] However, consuming alcohol during the later stages of pregnancy has not yet shown significant statistics. Therefore, more evidence is needed in order to link alcohol to SIDS, which the Prenatal Alcohol and SIDS and Stillbirth Network are currently researching.¹

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Finer and Henshaw report that fifty percent of pregnancies in the United States are not planned, and with manic episodes bringing about impulsive behavior, women with bipolar disorder who are of reproductive age should be advised of the risks of an unplanned pregnancy and prescribed effective birth control.[2] However, several mood stabilizers are known to decrease the effectiveness of oral contraceptives, and several oral contraceptives are known to decrease the effectiveness of mood stabilizers.[3] Therefore, women with bipolar disorder should be educated about supplementary forms of birth control.

According to Vemuri and Williams, prenatal counseling should begin at least three months before pregnancy, and the risks associated with pregnancy and mood stabilizers should be mentioned when the patient is first started on medication, even if the woman is not planning to become pregnant.¹ If possible, medication during the first trimester of pregnancy should be avoided due to risk of malformation of the fetus, and should be supplemented with increased psychosocial and clinical supports to monitor for relapse. Also, prenatal vitamins are strongly recommended, especially for those who have previously been pregnant or are on antiepileptic medications.[4]

Not always is medication able to be avoided during pregnancy, and if not, a minimum effective dose should be used of just one stabilizer.¹ The treatment decisions should be made with both the mother and significant other, as the significant other should monitor the mother for symptoms of relapse throughout the pregnancy and also to make sure both understand the risks associated with taking mood stabilizing medication while pregnant. Women diagnosed with bipolar disorder may relapse when medication is suddenly discontinued, showing signs of insomnia, impulsivity, suicidal ideations and attempts, and reduced self-care.¹ Therefore, in some cases, based upon the severity of the disorder, continuing certain medication is preferred to complete discontinuation.

Mood stabilizers valproate, carbamazepine, and lithium pose the greatest risks for fetus malformation, and are therefore recommended by Viguera, Whitfield, and Baldessarini to be avoided before and during a women’s pregnancy.[5] Valproate, especially with doses over 800 mg/day, poses a six to 13 percent risk of fetus malformation when taken during pregnancy, specifically targeting the neural tubes, cardiac, and facial features.² Yonkers, Wisner, and Stowe have reported heart rate deceleration, abnormal vocal tone, and growth retardation to be adverse fetal effects,[6] and Meador, Baker, and Browning have found it to cause lower IQ scores, and in some cases, autism.[7] Carbamazepine is also known to cause malformations of the neural tube, cardiac, and facial features,[8] as well as vitamin K deficiencies.[9] Lithium has shown a fetal malformation rate of 2.8 percent, and therefore it is recommended that women who are taking lithium during pregnancy undergo an ultrasound and echocardiogram between 16 and 18 weeks to scan for effects such as prematurity, hypothyroidism, liver abnormalities, respiratory effects, and diabetes.[10] Levels of the medication should be monitored, and due to fluid shifts during delivery, the risk of lithium toxicity becomes present.

Women with bipolar disorder are at risk for postpartum mania and psychosis, which will usually occur soon after delivery.¹ Counseling and medication during the postpartum period are imperative to the well being of both the mother and the baby. Because four percent of women diagnosed with postpartum psychosis commit infanticide, monitoring of mother-child interactions is critical.¹ Lithium therapy has shown to decrease the risk of postpartum psychosis when given within 48 hours of delivery.¹ Also, allowing the mother to receive adequate sleep with minimal disruption has shown to stabilize mood.

However, all mood-stabilizing medications have been discovered to pass into breast milk; therefore, a mother breastfeeding while on such medications needs to be trained to recognize the signs of neonatal toxicity.¹ Many processes that breakdown the medications are premature in infants, which can lead to their bodies obtaining high levels of the drugs. It is recommended the mother not breastfeed but instead pump or use formula, which would also allow her to obtain an adequate amount of sleep for mood stabilization as well.¹

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When ecstasy first emerged as a faddish street drug, it was sought after by Caucasian adolescents and young adults who indulged in the nightclub and rave scenes; however, over time it has become popular among a wider range of ethnic groups.[3] Ecstasy is also used as a component in a multiple-drug venture that includes marijuana, cocaine, methamphetamine, ketamine, Viagra, and other substances, both legal and illegal, prominent among urban gay males.[4]

Predominantly, ecstasy effects the neurons in the brain that use serotonin to communicate with other neurons, increasing and extending the serotonin signals. Serotonin regulates a person’s mood, aggression, sexual activity, sleep, and sensitivity to pain. As ecstasy resembles the chemical structure of serotonin, it will cause the excessive release of the neurotransmitter by the neurons. Therefore, using ecstasy  can cause a person to become confused, depressed, have trouble sleeping, and can create severe anxiety. While ecstasy has similar effects on norepinephrine and dopamine, it is minor compared to that of serotonin. The time period in which the user experiences the adverse effects varies. With some, the effects are experienced soon after using the drug, while others experience such effects days or even weeks after.

The National Institute on Drug Abuse suggests ecstasy is not safe for human consumption, as studies of the drug using animal research have proven it to be damaging to the brain.[5] Users of ecstasy are shown to perform poorer than nonusers on cognitive and memory tests, and one study conducted by Ricaurte and McCann determined that just four days of use caused damage to the serotonin nerves that was still present up to seven years later.[6]

As ecstasy is known to bear similar physical effects as stimulants such as cocaine and amphetamines, including increased heart rate and escalated blood pressure, the adverse effects due to such are abundant. According to the National Institute on Drug Abuse, users may experience lesser effects such as muscle tension, teeth clenching, nausea, blurred vision, faintness, and chills/sweating, or even greater effects of circulatory problems and heart disease.[7]

Other adverse effects can even be deadly. Taken in high doses, ecstasy may impede upon the body’s ability to regulate it’s own temperature, which can cause it to increase and consequently produce liver, kidney, and heart failure—all of which can lead to death. Therefore, combining ecstasy with other drugs—such as ephedrine, cough suppressants, ketamine, caffeine, cocaine, marijuana, or alcohol—can increase the chance of adverse effects.[8]

Ecstasy is proven to be an addictive drug.[9] After performing a survey of adolescent and young adult users, Cottler, Womack, Compton, and Ben-Abdallah found that 43 percent of users qualified as dependent in accordance with the Diagnostic and Statistic Manual of Mental Disorders IV diagnostic criteria.[10] According to Stone, Storr, and Anthony, when withdrawing from the drug, users may experience fatigue, loss of appetite, depression, and trouble concentrating.

While specific treatments for ecstasy addiction are non-existent, cognitive-behavioral therapy has shown to be effective in relieving the habit.[11] Such therapy will work to modify the user’s thinking and behaviors that are related to their drug abuse, allowing them to learn and utilize positive stress-coping strategies instead. Coupled with support group therapy, recovery has proven even more promising.[12]

Auditory hallucinations are defined as “perceptions of sounds without identifiable external stimuli.”¹ Commonly, this form of hallucination is connected with the psychiatric disorder schizophrenia. Between 60 and 90 percent of patients who suffer from schizophrenia experience auditory hallucinations in the form of voices.[2] Formed and complex hallucinations, sometimes a patient will even experience multiple voices at once.[3] However, schizophrenia is not the only cause of auditory hallucinations. Mood disorders may also cause milder forms, and diseases of the middle and inner ear may cause a patient to experience a consistent buzzing sound or various other unformed noises.² Patients suffering from partial seizures may also experience auditory hallucinations, frequently a perception of music, but sometimes a command or an unformed sentence.[4] According to Curie and colleagues, who examined 514 patients with temporal lobe epilepsy, 17 percent experienced auditory hallucinations during seizure activity.[5] Another cause of auditory hallucinations is alcoholic hallucinosis, a syndrome caused by alcohol withdrawal. Patients with alcoholic hallucinosis tend to experience vocal hallucinations, which oftentimes are threatening or accusatory.² However, sometimes musical hallucinations are present, as well. Other causes of auditory hallucinations are CNS neoplasms, stroke, mania, delirium, posttraumatic stress disorder, and hallucinogens.¹

According to Ali and colleagues, visual hallucinations are “visual sensory perceptions in the absence of external stimuli”¹ and occur in numerous physical and psychiatric conditions.Between 16 and 72 percent of patients suffering from schizophrenia and schizoaffective disorder experience vivid visual hallucinations that commonly include family members, animals, and religious figures.[6] Sometimes, patients with major depressive disorder or bipolar disorder will experience visual hallucinations as well.¹ Also, visual hallucinations are the most common type of hallucinations associated with delirium, as patients with this condition will often see small animals or insects.¹ Another condition commonly linked to visual hallucinations is migraine. Thirty-one percent of migraine sufferers experience an aura, which is almost always accompanied by visual symptoms.[7] Epilepsy patients who have occipital seizures will most likely experience fragmented visual hallucinations, such as bright spots that flash throughout seizure activity.[8] Also, visual hallucinations are common in patients with Dementia with Lewy Bodies (DLB), and occur in more than 20 percent of cases.[9] Oftentimes, patients with DLB will see people or objects that are not there. Similar to DLB, half of patients with Parkinson’s disease will experience visual hallucinations which will sometimes move.[10]

Ali and colleagues define olfactory hallucinations as “smelling odors that are not derived from any physical stimulus.”¹ Several psychiatric conditions may cause olfactory hallucinations, such as schizophrenia, depression, bipolar disorder, eating disorders, and even substance abuse.[11] Patients with schizophrenia may believe the odor is coming from an external source, while patients with depression may believe the source is internal.[12] Also, Olfactory Reference Syndrome causes olfactory hallucinations, as it is a condition in which patients believe they are the source of a foul odor and will proceed to bathe excessively and overuse deodorants, perfumes, and colognes, as well as withdraw socially.¹² Other causes of olfactory hallucinations include tumors affecting the medial temporal lobe and mesial temporal sclerosis, Alzheimer’s disease, and dementia.¹

Less common than auditory and visual hallucinations are gustatory, tactile, and somatic hallucinations. Patients with gustatory hallucinations experience taste alterations, a sensation of thirst, or excess salivation.¹ Gustatory hallucinations are often caused by temporal lobe disease, parietal operculum lesions,[13] and sinus disease.[14] Tactile hallucinations, affecting the sense of touch, are often described as either crawling insects or pressure on the skin.[15] Frequently, tactile hallucinations are associated with substance abuse, especially cocaine and amphetamine, and obsessive-compulsive disorder (OCD).¹⁵ Somatic hallucinations are abnormal body sensations and physical experiences.¹ Ali and colleagues give the example of a person feeling they do not have a stomach while they are eating. Scientists believe that somatic hallucinations are caused by the activation of the postcentral gyrus, parietal operculum, insula, and inferior parietal lobule of the brain.[16]

Ali and colleagues describe multiple conditions associated with several different types of hallucinations, most commonly auditory and visual. They state that proper diagnosis of hallucinations is important, as there are several physical and psychiatric causes of each, and in order to ensure effective treatment, a correct diagnosis must be made.

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) had defined a recommended limit of alcohol consumption: men younger than 65 should consume no more than four drinks per day or 14 drinks per week and women of any age and men older than 65 should consume no more than three drinks per day or seven drinks per week.[5] The NIAAA also defines a “drink” as 12 ounces of beer, five ounces of wine, or 1.5 ounces of distilled spirit. Drinking above the NIAAA’s recommended limit is defined as “hazardous” or “at-risk” use.[6] Twenty percent of the country’s population are at-risk drinkers who do not meet the criteria of dependence set by the DSM-IV.⁶ Frequently, the psychiatric population falls into this category and yield problematic effects, such as reduced medicine compliance, an increase in suicide attempts, an increase in symptom severity, and an increase in functional impairments.[7]

Usually, intervention strategies for problem drinkers have focused on primary care settings and have been developed as efficient and quick.⁴ The five to 15 minute interventions focus on educating the patient on risks associated with their drinking, as well as developing a goal to cut back on consumption.[8] Abstinence is recommended for persons dependent, but it is not necessary for those who are not.⁶ Results have shown that the mini-interventions are effective in reducing a patient’s drinking at both six and 12-month follow-ups, by approximately four drinks per week.⁸ Also, the interventions have shown to reduce suicide attempts, domestic violence incidents, assaults, and even child abuse.² Implementing such interventions into a psychiatric setting would not be difficult.

Goulding and Fleming recommend physicians and psychiatrists use an approach referred to as the “Five A’s of Intervention,” which are ask, advise, assess, assist, and arrange.4 The first “A”, ask, is useful when sparking a conversation with a patient regarding their alcohol use. Goulding and Fleming state that asking about a wide range of topics, such as nicotine, exercise, and other health-related issues, will help to seem routine and decrease the chances of a patient becoming defensive. If the patient reports using alcohol, the physician should follow up with a second question regarding how often the patient has exceeded the recommended amount of drinks per day in the past year. If the patient has exceeded the recommended amount more than once, Goulding and Fleming state the screening should then move to assess the patient’s weekly alcohol intake, perhaps by using a chart that specifies what specifically constitutes a “drink.” These questions will help a physician determine whether or not the patient is a problem drinker.

Goulding and Fleming recommend that the physician “advise,” or provide feedback to problem drinkers; however, it is important for them to keep an empathetic tone and non-confrontational manner.⁴ When possible, the physician should relate the drinking to different aspects of the patient’s life, such as health, family, financial, and social, and recommend that the patient change their habit.⁴ When doing so, the physician should always recommend the patient change, rather than command it, and also state they are willing to help the patient achieve the goal.⁴ Goulding and Fleming state the physician should then “assess” their patient’s willingness to change. Oftentimes, connecting the risky drinking to personal consequences will encourage the patient to agree to changes and set goals to reduce drinking amounts.⁴

After the goal is initiated, the physician may “assist” with designing an appropriate treatment plan. Discussing strategies such as pacing, switching between alcoholic and nonalcoholic beverages, and keeping a drinking diary, along with offering handouts, will aid patients in preparing themselves to reach their goal.⁴ Goulding and Fleming recommend the physician help the patient identify problem situations and offer tips on how to avoid or manage them, often with the support of a family member or a friend.⁴ For patients not willing to make changes, the physician should review the benefits of cutting back and the risks of continued drinking, as well as discussing any barriers the patient may face when making changes.⁴ Finally, Goulding and Fleming suggest the physician schedule a follow-up appointment with the patient, to check on progress made and obstacles encountered. Specifically, a follow-up phone call two weeks after the initial appointment followed by a one-month check-up is ideal.⁴

Goulding and Fleming state that problem drinking is not always properly addressed in psychiatric settings.⁴ A study conducted by Barnaby and colleagues examined 200 psychiatric patients, in which 49 percent reported problem drinking; however, only 27 percent had medical records reporting alcohol use.[9] Screening tools, such as CAGE or AUDIT, are not routinely used in psychiatric settings, and Goulding and Fleming believe that the tools would be helpful in identifying problem drinkers.⁷ Milner and colleagues report brief interventions used within psychiatric settings led to decreased drinking by an average of seven drinks per week over a period of six months.[10] Therefore, Goulding and Fleming offer the “Five A’s of Intervention” as a helpful tool that may be used by physicians and psychiatrists both to identify and intervene with patients who are problem drinkers.

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