Transcranial Magnetic Stimulation

Transcranial magnetic stimulation

Transcranial magnetic stimulation (TMS)  TMS uses electromagnetic induction to induce weak electric currents using a rapidly changing magnetic field; this can cause activity in specific or general parts of the brain with minimal discomfort, allowing the functioning and interconnections of the brain to be studied. A variant of TMS, repetitive transcranial magnetic stimulation (rTMS), has been tested as a treatment tool for variousneurological and psychiatric disorders including migraines, strokes, Parkinson's disease, dystonia, tinnitus, depression and auditory hallucinations.

Background

The principle of inductive brain stimulation with eddy currents has been noted since the 20th century. The first successful TMS study was performed in 1985 by Anthony Barker and his colleagues in Sheffield, England Its earliest application demonstrated conduction of nerve impulses from the motor cortex to the spinal cord, stimulating muscle contractions. The use of magnets rather than a direct electric current to the brain reduced the discomfort of the procedure and research and allowed mapping of the cerebral cortex and its connections.

Effects on the brain

The exact details of how TMS functions are still being explored. The effects of TMS can be divided into two types depending on the mode of stimulation:

§  Single or paired pulse TMS causes neurons in the neocortex under the site of stimulation to depolarize and discharge an action potential. If used in the primary motor cortex, it produces muscle activity referred to as a motor evoked potential (MEP) which can be recorded on electromyography. If used on the occipital cortex, 'phosphenes' (flashes of light) might be perceived by the subject. In most other areas of the cortex, the participant does not consciously experience any effect, but his or her behaviour may be slightly altered (e.g. slower reaction time on a cognitive task), or changes in brain activity may be detected using sensing equipment.

§  Repetitive TMS produces longer-lasting effects which persist past the initial period of stimulation. rTMS can increase or decrease the excitability of the corticospinal tractdepending on the intensity of stimulation, coil orientation and frequency. The mechanism of these effects is not clear although it is widely believed to reflect changes in synaptic efficacy akin to long-term potentiation (LTP) and long-term depression (LTD).

Risks

Although TMS is often regarded as safe, the greatest acute risk of TMS is the rare occurrence of induced seizures and syncope. More than 16 cases of TMS-related seizure have been reported in the literature, with at least seven reported before the publication of safety guidelines in 1998, and more than nine reported afterwards. The seizures have been associated with single-pulse and rTMS. Reports have stated that in at least some cases, predisposing factors (medication, brain lesions or genetic susceptibility) may have contributed to the seizure. A review of nine seizures associated with rTMS that had been reported after 1998 stated that four seizures were within the safety parameters, four were outside of those parameters, and one had occurred in a healthy volunteer with no predisposing factors. A 2009 international consensus statement on TMS that contained this review concluded that based on the number of studies, subjects and patients involved with TMS research, the risk of seizure with rTMS is considered very low.

Besides seizures, other risks include fainting, minor pains such as headache or local discomfort, minor cognitive changes and psychiatric symptoms (particularly a low risk ofmania in depressed patients). Though other side effects are thought to be possibly associated with TMS (alterations to the endocrine system, altered neurotransmitter andimmune system activity) they are considered investigational and lacking substantive proof.

Other adverse effects of TMS are:

§  Discomfort or pain from the stimulation of the scalp and associated nerves and muscles on the overlying skin;this is more common with rTMS than single pulse TMS,

§  Rapid deformation of the TMS coil produces a loud clicking sound which increases with the stimulator intensity that can affect hearing with sufficient exposure, particularly relevant for rTMS (hearing protection may be used to prevent this),

§  rTMS in the presence of incompatible EEG electrodes can result in electrode heating and, in severe cases, skin burns.Non-metallic electrodes are used if concurrent EEG data is required.

Clinical uses

ses of TMS andThe u rTMS can be divided into diagnostic and therapeutic uses.

Diagnostic Use

TMS can be used clinically to measure activity and function of specific brain circuits in humans. The most robust and widely-accepted use is in measuring the connection between the primary motor cortex and a muscle to evaluate damage from stroke, multiple sclerosis, amyotrophic lateral sclerosis, movement disorders, motor neuron disease and injuries and other disorders affecting the facial and other cranial nerves and the spinal cord.TMS has been suggested as a means of assessing short-interval intracortical inhibition (SICI) which measures the internal pathways of the motor cortex but this use has not yet been validated.    Therapeutic Use

A TMS therapy device

Studies of the use of TMS and rTMS to treat many neurological and psychiatric conditions have generally shown only modest effects with little confirmation of results.However, publications reporting the results of reviews and statistical meta-analyses of earlier investigations have stated that rTMS appeared to be effective in the treatment of certain types of major depression under certain specific condition.TMS devices are marketed for the treatment of such disorders in Canada, Australia, New Zealand, the European Union, Israel and the United States

A meta-analysis of 34 studies comparing rTMS to sham treatment for the acute treatment of depression showed an effect size of 0.55 (p<.001)This is comparable to commonly reported effect sizes of pharmacotherapeutic strategies for treatment of depression in the range of 0.17-0.46.However, that same meta-analysis found that rTMS was significantly worse than electroconvulsive therapy (ECT) (effect size = -0.47), although side effects were significantly better with rTMS. An analysis of one of the studies included in the meta-analysis showed that one extra remission from depression occurs for every 3 patients given electroconvulsive therapy rather than rTMS (number needed to treat 2.36).There is evidence that rTMS can temporarily reduce chronic pain and change pain-related brain and nerve activity, and TMS has been used to predict the success of surgically implanted electrical brain stimulation for the treatment of pain.

Other areas of research include the rehabilitation of aphasia and motor disability after strong tinnitus,Parkinson's disease tic disorders and the negative symptoms of schizophrenia.TMS has failed to show effectiveness for the treatment of brain death, coma, and other persistent vegetative states.

It is difficult to establish a convincing form of "sham" TMS to test for placebo effects during controlled trials in conscious individuals, due to the neck pain, headache and twitching in the scalp or upper face associated with the intervention. "Sham" TMS manipulations can affect cerebral glucose metabolism and MEPs, which may confound results.This problem is exacerbated when using subjective measures of improvement. Depending on the research question asked and the experimental design, matching this discomfort to distinguish true effects from placebo can be an important and challenging issue.

One multicenter trial of rTMS in depression used an active "sham" placebo treatment that appeared to mimic the sound and scalp stimulation associated with active TMS treatment. The investigators reported that the patients and clinical raters were unable to guess the treatment better than chance, suggesting that the sham placebo adequatelyblinded these people to treatment.The investigators concluded: "Although the treatment effect was statistically significant on a clinically meaningful variable (remission), the overall number of remitters and responders was less than one would like with a treatment that requires daily intervention for 3 weeks or more, even with a benign adverse effect profile". However, a review of the trial's report has questioned the adequacy of the placebo, noting that treaters were able to guess whether patients were receiving treatment with active or sham TMS, better than chance.In this regard, the trial's report stated that the confidence ratings for the treaters' guesses were low.

FDA actions

In January 2007 an advisory panel of the United States Food and Drug Administration (FDA) did not recommend clearance for marketing of an rTMS device, stating that the device appeared to be reasonably safe but had failed to demonstrate efficacy in a study of people with major depression who had not benefitted from prior adequate treatment with oral antidepressants during their current major depressive episod The panel agreed that "unblinding was greater in the active group, and considering the magnitude of the effect size, it may have influenced the study results."However, the FDA determined in December 2008 that the rTMS device was sufficiently similar to existing devices that did not require a premarket approval application and allowed the device to be marketed in accordance with Section 510(k) of the Federal Food, Drug, and Cosmetic Act for "the treatment of Major Depressive Disorder in adult patients who have failed to achieve satisfactory improvement from one prior antidepressant medication at or above the minimal effective dose and duration in the current episode". The user manual for the device warns that effectiveness has not been established in patients with major depressive disorder who have failed to achieve satisfactory improvement from zero and from two or more antidepressant medications in the current episode and that the device has not been studied in patients who have had no prior antidepressant medication..

In July 2011 the FDA published a final rule in the Federal Register that classified the rTMS system into class II (special controls) (see: Medical device#Classification) "in order to provide a reasonable assurance of safety and effectiveness of these devices". The rule identified the rTMS system as "an external device that delivers transcranial pulsed magnetic fields of sufficient magnitude to induce neural action potentials in the prefrontal cortex to treat the symptoms of major depressive disorder without inducing seizure in patients who have failed at least one antidepressant medication and are currently not on any antidepressant therapy". An FDA guidance document issued in conjunction with the final rule describes the special controls that support the classification of the rTMS system into Class II.

Response to FDA decision

Soon after the FDA cleared the device, several members of Public Citizen stated in a letter to the editor of the medical journal Neuropsychopharmacology that the FDA seemed to have based its decision on a post-hoc analysis that did not establish the effectiveness of rTMS for the treatment of depression. The writers of the letter expressed their concern that patients would be diverted from therapies such as antidepressant medications that have an established history of effectiveness.

Health insurance considerations

Commercial health insurance

In july 2011, the Technology Evaluation Center (TEC) of the Blue Cross Blue Shield Association, in cooperation with the Kaiser Foundation Health Plan and the Southern California Permanente Medical Group, determined that TMS for the treatment of depression did not meet the TEC's criteria, which assess whether a technology improves health outcomes such as length of life, quality of life and functional ability.The TEC's report stated that "the meta-analyses and recent clinical trials of TMS generally show statistically significant effects on depression outcomes at the end of the TMS treatment period. However, there is a lack of rigorous evaluation beyond the treatment period", which was, with a few exceptions, one to four weeks.The Blue Cross Blue Shield Association's medical advisory panel concluded that "the available evidence does not permit conclusions regarding the effect of TMS on health outcomes or compared with alternatives.”

In 2012, several commercial health insurance plans in the United States, including Anthem, Health Net, and Blue Cross Blue Shield of Nebraska and of Rhode Island, covered TMS for the treatment of depression. In contrast, UnitedHealthcare issued a medical policy for TMS in 2012 that stated there is insufficient evidence that the procedure is beneficial for health outcomes in patients with depression. UnitedHealthcare noted that methodological concerns raised about the scientific evidence studying TMS for depression include small sample size, lack of a validated sham comparison in randomized controlled studies, and variable uses of outcome measures^] Other commercial insurance plans whose 2012 medical coverage policies stated that the role of TMS in the treatment of depression and other disorders had not been clearly established or remained investigational includedAetna, Cigna and Regence.

Medicare

In early 2012, the efforts of TMS treatment advocates, including a Rhode Island physician who used TMS in her practice to treat patients with depression, resulted in the approval for the New England region of the first Medicare coverage policy for TMS in the United States. However, in August 2012, the Medicare administrative contractor for the Centers for Medicare and Medicaid Services jurisdiction covering Arkansas, Louisiana, Mississippi, Colorado, Texas, Oklahoma and New Mexico determined that, based on limitations in the published literature,

"... the evidence is insufficient to determine rTMS improves health outcomes in the Medicare or general population. ... The contractor considers repetitive transcranial magnetic stimulation (rTMS) not medically necessary when used for its FDA-appproved indication and for all off-label uses."

American Medical Association category codes

In 2011, the American Medical Association established three Category I CPT® Codes to be used for the reporting and billing of therapeutic repetitive transcranial magnetic stimulation treatment services.The three codes effective January 1, 2012 are:

§  90867 – Therapeutic repetitive transcranial magnetic stimulation (TMS) treatment; initial, including cortical mapping, motor threshold determination, delivery and management

§  90868 – Therapeutic repetitive transcranial magnetic stimulation (TMS) treatment; subsequent delivery and management, per session

§  90869 – Therapeutic repetitive transcranial magnetic stimulation (TMS) treatment; subsequent motor threshold re-determination with delivery and management

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Technical information

TMS - Butterfly Coils

TMS uses electromagnetic induction to generate an electric current across the scalp and skull without physical contact. A plastic-enclosed coil of wire is held next to the skull and when activated, produces a magnetic field oriented orthogonally to the plane of the coil. The magnetic field passes unimpeded through the skin and skull, inducing an oppositely directed current in the brain that activates nearby nerve cells in much the same way as currents applied directly to the cortical surface.

The path of this current is difficult to model because the brain is irregularly shaped and electricity and magnetism are not conducted uniformly throughout its tissues. The magnetic field is about the same strength as an MRI, and the pulse generally reaches no more than 5 centimeters into the brain.

Coil types

The design of transcranial magnetic stimulation coils used in either treatment or diagnostic/experimental studies may differ in a variety of ways. These differences should be considered in the interpretation of any study result, and the type of coil used should be specified in the study methods for any published reports.

The most important considerations include:

§  the type of material used to construct the core of the coil

§  the geometry of the coil configuration

§  the biophysical characteristics of the pulse produced by the coil.

With regard to coil composition, the core material may be either a magnetically inert substrate (i.e., the so-called ‘air-core’coil design), or possess a solid, ferromagnetically active material (ie, the so-called ‘solid-core’ design). Solid core coil design result in a more efficient transfer of electrical energy into a magnetic field, with a substantially reduced amount of energy dissipated as heat, and so can be operated under more aggressive duty cycles often mandated in therapeutic protocols, without treatment interruption due to heat accumulation, or the use of an accessory method of cooling the coil during operation. Varying the geometric shape of the coil itself may also result in variations in the focality, shape, and depth of cortical penetration of the magnetic field. Differences in the coil substance as well as the electronic operation of the power supply to the coil may also result in variations in the biophysical characteristics of the resulting magnetic pulse (e.g., width or duration of the magnetic field pulse). All of these features should be considered when comparing results obtained from different studies, with respect to both safety and efficacy.

A number of different types of coils exist, each of which produce different magnetic field patterns. Some examples:

§  round coil: the original type of TMS coil

§  figure-eight coil (i.e. butterfly coil): results in a more focal pattern of activation

§  double-cone coil: conforms to shape of head, useful for deeper stimulation

§  four-leaf coil: for focal stimulation of peripheral nerves

Design variations in the shape of the TMS coils allow much deeper penetration of the brain than the standard depth of 1.5 cm. Circular, H-shaped, double cone coils and other experimental variations can induce excitation or inhibition of neurons deeper in the brain including activation of motor neurons for the cerebellum, legs and pelvic floor. Though able to penetrate deeper in the brain, they are less able to produced a focused, localized response and are relatively non-focal.

ALCOHOL DEPENDENCE

Defining "alcohol dependence

The view of alcohol dependence as a separately recognized disorder first appeared in the 1960s as the "disease concept of alcoholism" (Jellinek, 1972, 2002). In the 1970s, the "alcohol dependence syndrome" was described, along with the cognitive, behavioral, and physiological changes associated with it (Edwards, 1986; Edwards & Gross, 1976; Edwards & Lader, 1990).

Several views exist on the etiology of alcohol dependence (Peele, 1985). There is evidence that in some individuals, alcohol dependence is a manifestation of underlying traits that include a genetic predisposition (Bierut et al., 2002; Cloninger, 1999; Cloninger, Bohman, & Sigvardsson, 1981; Crabbe, 2002; Walters, 2002). Alcohol dependence is often associated with other conditions, such as depression and anxiety, and there is compelling evidence to support a strong familial component (Davids et al., 2002; Schuckit, Kelsoe, Braff, & Wilhelmsen, 2003). It is also widely recognized that alcohol dependence can occur as a result of the cultural and social influences on an individual (Heath, 1986; Jung, 2000). Similarly, culture plays an important role in how dependence is viewed within a society (Bennett, Janca, Grant, & Sartorius, 1993; Bennett, Miller, & Woodall, 1999; Grant & Ritson, 1990; Gureje, Vazquez-Barquero, & Janca, 1996).

A medical perspective on alcohol dependence has allowed evidence-based diagnostic criteria to be developed to assist in identifying dependent individuals. This model of alcohol dependence has increasingly gained currency around the world and is accepted as the basis for its classification and diagnosis through the International Classification of Disease, ICD (World Health Organization, 1994) and the Diagnostic and Statistical Manual of Mental Disorder, DSM (American Psychiatric Association, 1994).

Alcohol dependence is classified as one of several substance-related disorders involving psychoactive substances, including alcohol. According to the ICD-10, the dependence syndrome is a "cluster of behavioral, cognitive, and physiological phenomena that develop after repeated substance use and that typically include a strong desire to take the drug, difficulties in controlling its use, persisting in its use despite harmful consequences, a higher priority given to drug use than to other activities and obligations, increased tolerance, and sometimes a physical withdrawal state" (World Health Organization, 1994).

A similar definition in DSM-IV requires the presence of at least three of the following six symptoms within a 12-month period for a positive diagnosis of alcohol dependence:

1. Tolerance: increasing amounts of alcohol are needed to produce the desired effect in a given individual. Where the threshold for tolerance lies varies from one individual to another.

2. Withdrawal from the absence of alcohol:  characterized by a number of physiological symptoms, most commonly tremor, anxiety, sweating, agitation and restlessness, nausea, and diarrhea. Depression and sleep disorders are also common. Further drinking generally relieves these symptoms.

3. Salience of drinking: a dependent individual’s drinking occupies higher priority than other interests or obligations. Typically, hobbies and interests, once important, have been put aside to make room for a greater focus on drinking.

4. Craving: an individual’s compulsion to drink, triggered by any number of external cues or "primed" by the first drink or two.

5. Impaired control: an individual's lack of control over drinking and difficulty setting consumption limits. At the same time, a dependent individual tends to be acutely aware of the need to curb his or her drinking.

6. Continued use despite harm: continued harmful drinking despite awareness of the adverse effects.

Certain drinking patterns are characteristic of alcohol dependence, primarily those that have been described as the "narrowing of the drinking repertoire." These patterns are rigid and not easily changed by external influence. The dependent individual’s drinking pattern is driven by considerations such as avoiding the symptoms of withdrawal. However, certain drinking patterns may also lead to the development of alcohol problems culminating in dependence (Cloninger et al., 1981; Cloninger, Sigvardsson, & Bohman, 1996). Heavy steady chronic drinking at sufficiently high levels can lead to the physiological changes that result in alcohol dependence.

Treatment approaches

For individuals who are diagnosed with alcohol dependence, treatment may be appropriate and can take on a variety of forms. Careful consideration should be given to which approach is most fitting, most likely to elicit the desired effect, and most compatible with a particular culture (Room, 1998; Schmidt & Room, 1999). The effectiveness of different approaches to treatment hinges upon the cultural setting in which they are applied and the prevailing societal views on dependence and priorities. In general, treatment is administered with the goal of allowing the affected individual to resume normal functioning.

There are various approaches to treating alcohol problems. They can be divided into two groups, depending on the severity of the problem: (1) treatment approaches directed at alcohol-dependent individuals and severe problem drinkers, and (2) approaches that target those who are not yet dependent, but are at high risk. The choice of which treatment is appropriate depends to a large extent on the severity of the problems being addressed. Some individuals may require only minor behavioral modifications to address emerging problems. For those whose drinking patterns have resulted in more serious and established negative consequences, more intensive secondary and tertiary prevention may be needed.

A variety of treatment approaches exists, each of them appropriate for particular individuals and less so for others (Babor et al., 2003; Babor & Del Boca, 2003; Enoch & Goldman, 2002). They include behavior modifications, support groups, as well as pharmacological treatment. Some treatment has as its goal abstinence from alcohol, while other approaches seek to change the pattern of drinking to one that is moderate and compatible with a healthy and balanced lifestyle. Whatever the final goal, most treatment comprises three stages: detoxification to minimize withdrawal, rehabilitation, and maintenance. Which approach and end result is best for a particular individual should be determined on a case-by-case basis (Kadden, Longabaugh, & Wirtz, 2003; Longabaugh & Wirtz, 2003, 2001).

The following is an overview of some of the commonly used approaches to treatment of alcohol dependence.

Self-help or mutual help groups aspire to abstinence from alcohol. They include Alcoholics Anonymous (AA), developed in the United States, in which an individual submits to a higher power in the process of "recovery" (Humphreys, 2003). AA members make a fresh resolve each day not to drink. Other similar groups exist with modifications that make them appropriate for different cultures. These include the Swedish Links movement, the Croix Bleu, and others (Gossop, 1995). A dominant approach in some countries of Southern and Central Europe—e.g., in Italy and Croatia—relies on Clubs for Alcoholics in Treatment, CATs (Hudolin, 1964; Hudolin, 1984). Unlike AA, these are often integrated into the social health services system and rely heavily on the family as integral to the self-help group. Self- and mutual help groups exist as both residential and non-residential programs.

Early identification and brief intervention emphasizes that it is possible for individuals to modify their problematic drinking patterns (Babor, Higgins-Biddle, Saunders, & Monteiro, 2001; Bien, Miller, & Tonigan, 1993). Inherent in this approach is the notion that it is possible for individuals to learn to drink responsibly, especially if they are diagnosed early and before problems have become severe. Brief interventions have been tested across cultures and have been found to be widely effective at reducing problematic drinking. They have also been successfully applied in the treatment of diverse populations, including young people with problem drinking patterns. Another advantage of this approach is that it is quick and efficient to administer and can therefore be implemented in settings where resources may be scarce.

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Motivational interviewing centers on the idea that individuals with problematic drinking patterns may recognize the negative aspects of their behavior, but need assistance in making the decision to change. This is achieved through motivational techniques to encourage the patient to set realistic and attainable goals, using positive feedback to encourage and sustain progress and change. The approach is oriented toward drinkers with problems, but not severe dependence, and its final goal is a changed drinking pattern rather than abstinence.

The community reinforcement approach includes behavioral techniques designed to support the individual in overcoming dependence. In general, it is most appropriate for those who are alcohol-dependent or have severe problems. The approach identifies high-risk situations that encourage and contribute to the individual’s problematic drinking and endows the patient with skills aimed at problem solving and at avoiding such situations. Skills include vocational training, recreational activities, marriage counseling, and avoiding situations where the risk for drinking and drunkenness is high. The patient is also taught skills to avoid relapse.

Psychological therapy and aversion therapy are also used to reduce problematic drinking (Parks, Marlatt, & Anderson, 2001). Aversion therapy relies on associating alcohol with highly negative contexts (e.g., nausea induced by various medications, such as the drug Antabuse) or other negative cues. Other methods include teaching social skills to deal with stressors and to facilitate problem solving or developing skills aimed at reducing or controlling drinking (e.g., refusing or just sipping drinks). Psychotherapy is employed as an approach for general drinking problems and also for alcohol dependence.

Pharmacotherapy is also commonly used to assist individuals with alcohol dependence by easing the symptoms of withdrawal and easing craving. Disulfiram (Antabuse), naltrexone, and acamprosate are among the most common drugs used for treatment (Drummond, 2001; O'Malley & Froehlich, 2003; Rubio, Ponce, & Manzanares, 2002; Soyka & Chick, 2003).

The effectiveness of various treatment approaches has been assessed in populations of individuals with drinking problems and those with alcohol dependence. According the data, the most successful approaches include brief intervention and motivational enhancement, followed by pharmacotherapy and skills therapy. Various self- and mutual help approaches, despite their popularity, are less effective and, according to some research, no more effective than no treatment. Counseling approaches have been shown to be the least effective means of addressing treatment.

It should be noted, however, that many treatment approaches may be combined with others, enhancing their overall effectiveness. Clearly, the sooner a problem can be identified and addressed, the greater are the chances for success. Patients’ relapse into earlier behaviors remains the main obstacle to the effectiveness of treatment.

Implications for policy and prevention

Many problems related to alcohol abuse (and dependence) are associated with trauma and injury. As a result, for many individuals suffering from these consequences, the emergency room and trauma departments at hospitals are a point of first contact with health care providers. Thus, emergency rooms offer an important point of access to patients and opportunity for treatment (Hungerford & Pollock, 2003).

Assessing admitted patients for alcohol dependence and increased risk for dependence has proven an effective approach to reducing problems. Assessment can be accompanied by psychiatric assistance and followed up through social workers. In addition, the provision of brief interventions has shown reduced injuries requiring emergency treatment, shorter hospital stays, and reduced alcohol consumption.

In addition to emergency rooms, other venues can also be used to provide brief interventions for individuals who abuse alcohol (Fernandez Garcia et al., 2003). Doctor’s offices and general health services are a useful venue, but not accessible in many parts of the world. Use can be made of the resources available within a particular community, including the training of non-medical personnel to provide assessment or counseling where it is not possible to prevent the emergence of problems or to arrest them at a less advanced stage of development, approaches for dealing with dependence, including treatment, are needed. As a starting point, it should be recognized that alcohol dependence is a manifestation of a clinical condition, not criminal behavior. Punitive measures and incarceration may temporarily put the affected individuals out of circulation, but have not been shown to have an impact on changing behavior.

Treatment may be the only viable solution for many of these individuals and, therefore, the provision of treatment services is an essential part of a comprehensive and effective alcohol policy. It has been shown that different groups of individuals require different approaches to treatment. Aside from cultural differences in how alcohol problems in general and dependence in particular are perceived, appropriate treatment for women may be different from that offered to men (Acharyya & Zhang, 2003; Ashley, Marsden, & Brady, 2003), and young people also require separate approaches.

Treatment services are clearly a necessary component of any healthcare system. Ideally, they should cover a range from assessment to therapy and follow-up care. How these services they are integrated into the system varies from country to country, depending on local priorities and resources. Adequate healthcare includes ensuring that treatment opportunities and facilities are available, and also educating health care professionals about alcohol dependence. Those providing health care should be able to recognize symptoms of dependence and direct individuals to appropriate further care.

Cost is clearly a consideration, especially for countries where health care is inadequate or where priorities need to be set clearly, not only with regard to alcohol, but around health issues in general. However, as effectiveness studies have shown, some of the less extensive and thus costly approaches, including early identification and brief intervention are actually among the most effective. They can be administered through a variety of less formal channels and do not hinge upon access to health providers.

It is also important to bear in mind that alcohol dependence, like alcohol abuse, does not affect only the dependent individual but also his or her family and others. Children of alcohol-dependent individuals are more likely to experience behavioral problems and the general stress of dealing with a dependent individual takes a heavy toll on the immediate surroundings in a variety of different ways. It is important, therefore, to make available the necessary support structure

Included in this support structure is a role for the community as a whole, including employers, families , and educators, not only the health sector. Offering a broad support network can assist in both prevention and treatment.

Conclusions

Alcohol dependence is a condition clearly defined by diagnostic criteria. While alcohol dependence includes abusive drinking patterns, it is not interchangeable with alcohol abuse and, indeed, not all those who abuse alcohol are dependent.

NURSING MANAGEMENT WHEN PATIENT WITH DELIRIUM

Introduction

Organic mental disorders are behavioral or psychological disorders associated with transient or permanent brain dysfunction and include only those mental and behavioral disorders that are due to demonstrable cerebral disease or disorder either primary or secondary.

The presence of following features requires special attention in identifying organic mental disorders:

•          First episode

•          Sudden onset

•          Older age of onset

•          History of drug and alcohol use disorders

•          Concurrent medical or neurological disorder

•          Neurological signs or symptoms like seizure ,impairment in consciousness, head injury, sensory or motor disturbances

•          Presence of confusion , disorientation ,memory impairment or soft neurological sign.

•          Prominent visual or other non auditory hallucinations

 The disorder can be subcategorized into the following categories :

•          Delirium

•          Dementia

•          Organic amnestic syndrome

•          Other organic mental disorders

Definition

Delirium is not a clinical entity but a symptom-complex of manifold etiology. Its presence signifies acute cerebral insufficiency and often represents a medical and/or psychiatric emergency.Though some forms of delirium have distinctive features, the fundamental phenomena are common to all, with clouding of consciousness the sine qua non. The condition has two major components: (1) the basic "acute brain syndrome" and (2) associated release phenomena.Clinicians must first make the vital differentiation between delirium and "functional" mental disorder, then proceed with the elucidation of the underlying diagnosis and the concurrent organization of symptomatic and etiologic treatment.Proper treatment combines management of the acute brain syndrome with general and specific procedures for control of the underlying condition. Dealing with the symptom-complex itself involves the principles and practice of sedation, hydration, and nutrition, nursing care and supportive measures. Provided the basic organic condition is treatable, the prognosis today is usually good.

According to DSM IV TR delirium is characterized by a disturbance of consciousness and a change in cognition that develop rapidly over a period of time.

History:

In the English literature delirium was applied to an organic brain syndrome with impaired consciousness. In contrast, in France délire was originally used to describe a primary disturbance of perception. In 1909 Bonhoeffer defined delirium as a clinical pattern of acute brain failure.  In the past it was known in different names such as acute confusional state, acute brain syndrome, acute organic reaction , toxic psychosis, metabolic encephalopathies  .

Epidemiology:

Delirium is a common problem in all health care settings, with a prevalence of 0.4% in general population, 1.1% in general population aged >55 years, 9–30% in general hospital admissions and 5–55% in elderly general hospital admissions.

Predisposing factors :

A.  Metabolic causes:

•          Hypoxia

•          Hypoglycemia

•          Hepatic encephalopathy, uremic encephalopathy

•          Cardiac failure ,cardiac arrhythmias

•          Water and electrolyte imbalance(water ,Na+,K+, Mg ++,Ca++)

•          Metabolic acidosis

•          Fever, anemia, hypovolemic shock

B. Endocrine causes

•          Hypo-hyper pitutairism

•          Hypo-hyper –thyroidism

•          Hypo-hyper –parathyroidism

•          Hypo-hyper –adrenalism

C. Drugs (both ingestion and withdrawal causes delirium) and poisons

•          Digitalis ,quinidine ,anti-hypertensive’s

•          Alcohol, sedatives ,hypnonitics

•          Tri cyclic antidepressants  and antipsychotics

•          Anti convulsants –levo dopa

•          Salicylates ,steroids ,pencillin,insulin

•          Methyl alcohol ,heavy metals

D. Nutritional deficiencies

•          Thiamin, niacin, pyridoxine ,folic acid ,B12

E. Systemic infections:

•          Acute and chronic (e.g. septicemia, pneumonia and endocarditis)

F. Intracranial causes:

•          Epilepsy

•          Head injury, subarachnoid hemorrhage ,sub dural hematoma

•          Intracranial infections e.g. meningitis, encephalitis cerebral malaria

•          Stroke ,hypertensive encephalopathy

•          Focal lesions e.g. right parietal lesions

G. Miscellaneous

•          Post operative states

•          Sleep deprivation

•          Heat ,electricity and radiation

Possible causes of delirium, can be described with  the well-known I WATCH DEATH mnemonic.

The DSM IV TR differentiates between the disorders of delirium by their etiology ,although they share a common symptom presentation . Categories of delirium includes :

•          Delirium due to general medical condition

•          Substance induced delirium

•          Substance intoxication delirium

•          Substance withdrawal delirium

•          Delirium due to multiple etiologies

1. Delirium due to general medical condition : In this type the delirium is due to direct result of the physiological consequences of a general medical condition. Such conditions include systemic infections, metabolic disorders, fluid or electrolyte imbalances, hepatic or renal disease ,thiamine deficiency, post operative states, hypertensive encephalopathy, postictal states and sequelae of  head trauma.

2. Substance induced delirium:   this disorder is characterized by the symptoms of delirium  that are attributed to medication side effects or exposure to a toxin.  The following medications are reported to cause substance induced delirium : anesthetics, analgesics, antiasthamatic drugs ,anticonvulsants ,antihistamines, antihypertensive, antimicrobials, antiparkinsonian drugs immunosuppressive agents ,lithium ,muscle relaxants and psychotropic medications .

3. Substance induced delirium : Delirium may arise within minutes to hours after taking relatively high dose of certain drugs such as cannabis ,cocaine and hallucinogens .

4. Substance withdrawal delirium:  it occurs after reduction or termination of sustained usually high dose use of certain substances such as alcohol, sedatives, hypnotics or anxiolytics.

5. Delirium due to multiple etiologies : It is associated with more than one cause. It may be the result of combined effect of general medication ad substance use.

Clinical features: 

Delirium is characterized by the following features:

•          Impairment of consciousness is the key feature that separates delirium from most other psychiatric disorders. There is a continuum between mild impairment of consciousness and near unconsciousness. There is fluctuation in intensity, and symptoms are often worse at night. The patient may be unmistakably drowsy, but milder states are easy to miss, especially by those who are unfamiliar with the patient's normal intellectual performance. They may be apparent only in reduced or slowed performance on bedside cognitive testing. There is disorientation in time, place, and the identity of other people.

•          Appearance and behaviour: the patient looks unwell and behaviour may be marked by agitation or hypoactivity, by a fluctuation between these states, or by a mixture of them—for example, a drowsy patient plucking aimlessly at the bedclothes.

•          Mood is frequently labile, with perplexity, intermittent periods of anxiety or depression, or occasionally of other mood states such as elation and irritability. Usually, the mood states have an empty and transitory quality.

•          Speech: the patient may mumble and be incoherent.

•          Perception: visual perception is the modality most often affected. Illusions and misinterpretations are frequent. For example, a patient may become agitated and fearful, believing that a shadow in a dark room is actually an attacker. Visual hallucinations also occur. The small living creatures which may be seen in delirium tremens are the best-known example. Auditory and tactile hallucinations also occur. Complex sensory distortions, such as colours being experienced as tastes, would suggest intoxication with hallucinogens.

•          Cognition: there are abnormalities in all areas of cognitive function. Memory registration, retention, and recall are all affected. Mild cases may show their most pronounced abnormalities in slow performance on tasks or in the wandering of attention away from the task at hand.

•          Orientation: in obvious cases, orientation in person, time, and place will all be disturbed. Milder degrees of disorientation will need to be interpreted in the context of the individual patient. For example, it may be considered not abnormal for a person who has been seriously ill in hospital for a long time to be unaware of the day of the month.

•          Concentration is impaired, for example, on tests such as ‘serial sevens' or ‘days of the week backwards'.

•          Memory disturbances are seen, with impaired registration (e.g. digit span), short-term recall (e.g. name and address), and long-term recall (e.g. current news items). After recovery from the illness there is usually (but not always) amnesia for the illness.

•          Insight is usually impaired. The patient will have no understanding of why a psychiatric assessment has been requested

•          The disturbance of sleep wake cycle most commonly insomnia at night with day time drowsiness

•          Diurnal variation is marked usually with worsening of symptoms in the evening and night (called sun downing )

Diagnosis

ICD 10  diagnostic criteria : According ICD 10 , for definite diagnosis of delirium ,symptoms should be present in each one of the following areas .

•          Impairment of the consciousness and attention (on a continuum from clouding to coma, reduced ability to direct ,focus ,sustain and shift attention )

•          Global disturbance of cognition ( perceptual distortions: illusions and hallucinations most often visual ; impairment of abstract thinking and comprehension with or with out transient delusions ,but typically with some degree of incoherence ,impairment of immediate recall  and of recent memory but relatively intact remote memory ;disorientation for time as well as  in more severe cases for place and person.

•          Psychomotor disturbances ( hypo or hyper activity and unpredictable shifts from one to one another ;increased reaction time increased or decreased flow of speech and enhanced startle reactions )

•          Disturbance of sleep walk cycle (insomnia or in severe cases total sleep loss or reversal of the sleep walk cycle ;day time drowsiness ,nocturnal worsening of symptoms ,disturbing dream or nightmares  which may continue as hallucinations after awakening)

•          Emotional disturbances .e.g. depression, anxiety or fear, irritability ,euphoria ,apathy.

•          The onset is usually rapid and the course diurnally fluctuating and total duration of the condition much less than 6 months .

Differential diagnosis of delirium

•          Functional psychotic disorders can mimic the positive features of delirium, such as hallucinations.

•          Stupor due to severe depression or mania can be mistaken for a diminished level of consciousness.

•          Dementia

•          Amnestic disorders, such as Korsakov's syndrome, also occur in clear consciousness, but the cognitive deficits are concentrated in short-term memory. Immediate recall (e.g. digit span) is normal in amnestic disorders, and long-term memory is relatively preserved: both are impaired in delirium.

•          Sleep disorders (e.g. narcolepsy) and various forms of epilepsy (e.g. the rare petit mal status epilepticus in children) may also need to be excluded.

Physical and laboratory examinations :

•          A bedside mental status examination or Mini Mental Status Examination or neurological signs can be used to document the cognitive impairment and to provide a base line from which to measure the patients clinical course .

•          The Confusion Assessment Method is also widely used because it is reliable, brief, and applicable to a variety of settings

Confusion Assessment Method

•          Delirium diagnosed if (a) + (b) + one of either (c) or (d):

•          Acute onset and fluctuating course: Evidence of an acute change in mental status from the patient's baseline that changes in severity during the day

•          Inattention: Patient has difficulty focusing attention, e.g. is easily distractible or has difficulty keeping track of conversation

•          Disorganized thinking: Patient's thinking is disorganized or incoherent, as evidenced by rambling or irrelevant conversation and unclear or illogical flow of ideas

•          Altered consciousness: A rating of a patient's level of consciousness as other than alert (normal) i.e. vigilant or hyper alert, lethargic or drowsy, stuporus  or comatose

•          Physical examination reveals the cause of delirium

•          Laboratory work up include CBP, electrolytes, thyroid function tests, ECG , EEG  ,chest x ray ,blood ,urine , and CSF cultures .

•          EEG:  It shows a generalized slowing of activity

Management :

Four key steps in management of delirium are –

•          Addressing the underlying causes,

•          Maintaining behavioural control,

•          Preventing complications,

•          Supporting functional needs

The  management strategies include both nonpharmacologic and pharmacologic interventions.

Nonpharmacologic Interventions

Physical Interventions:

•          Initial interventions include general measures to support cerebral function, such as intravenous hydration and appropriate nourishment.

•          Supplemental oxygen has been found to be highly effective in patients who develop delirium with pneumonia.

•          Physical restraints, once a mainstay in the treatment of delirium, are now used only when all pharmacologic and nonpharmacologic interventions have failed.

 Environmental Interventions:

•          The hospital environment is a significant factor in the management of delirium. Environmental manipulations are directed toward providing the right amount of stimulation for the patient, encouraging sleep, maximizing the patient's ability to perceive the environment accurately, maintaining safety, and achieving familiarity and consistency for the patient.

•          Over stimulation should be avoided, because it contributes to both confusion and insomnia

•          Under stimulation is probably a more common problem and is perhaps equally injurious. Delirious patients who are left alone without stimulation often withdraw and begin to respond more to internal stimuli than external stimuli. In such situations, regular interaction with hospital staff can be helpful. It is often appropriate to place the delirious patient in a room close to the nursing station or other workstation

•          Sun downing can be lessened by leaving a radio on in the patient's room

•          It has long been recognized that, in certain cases, the hallucinations of delirium can be specifically treated: visual hallucinations by controlled visual stimuli, auditory hallucinations by music and other meaningful external sounds, and olfactory hallucinations by the introduction of odors or scents

•          To help the patient perceive the environment accurately, adequate daytime lighting and a night light should be provided

•          Hearing aids, eyeglasses and other devices that assist sensory perception should be used whenever possible and should not be put away during a delirious episode

•          One of the most helpful interventions is having family members stay with the patient. Family members should also be encouraged to bring personal effects from home, because some patients with delirium are greatly comforted by the presence of familiar photographs or objects.

Cognitive Interventions:

Reorientation is one of the most easily accomplished cognitive interventions. The first step is to place a clock and a calendar where the patient can see them easily. The patient should then be verbally reoriented to time and place several times over the course of the day. Repetition is recommended to compensate for memory impairment in the delirious patient.

Psychologic Interventions:

The delusions expressed by a patient should not be directly disputed. Instead, alternative explanations of events should be offered, and frequent reassurance should be given.

Pharmacologic Interventions

•          100 mg of B1 IV for thiamine deficiency and IV fluids for fluid and electrolyte imbalances

•          Symptomatic management: as many patients are agitated , emergency psychiatric treatments may be needed. Small doses of benzodiazepines (lorazepam or diazepam)  or antipsychotics (haloperidol)  may be given orally or parenterally.

Prognosis:

Resolution of symptoms may take longer in patients with poor pre morbid cognitive function, incorrect or incomplete diagnosis of contributing factors, and structural brain diseases treated with large doses of psychoactive medications prior to the onset of acute medical illness. For some patients, the cognitive effects of delirium may resolve slowly or not at all.

Patient Education

•          Educating families and patients regarding the etiology and course of disease is an important role for physicians.

•          Educate the patient, family, and primary caregivers about future risk factors.

•          Families may worry that the patient has brain damage or a permanent psychiatric illness. Providing reassurance that delirium often is temporary and is the result of a medical condition may be beneficial to both patients and their families.

•          Suggest that family members or friends visit the patient, usually one at a time, and provide a calm and structured environment. Encourage them to furnish some familiar objects, such as photos or a favorite blanket, to help reorient the patient and make the patient feel more secure.

Nursing management :

Assessment

•          Client history : from the clients history ,nurses should assess the following areas of concern.

•          Type ,frequency, and severity of mood swings,

•          Personality  and behavioral changes

•          Catastrophic emotional reactions  

•          Cognitive changes such as problems with attention span ,thinking process ,problem –solving

•          Language difficulties

•          Orientation to person ,place, date and situation

•          Appropriateness of social behavior

Physical assessment :

Assessment should focus on two main areas

•          Signs of damage to the nervous system

•          Evidence of diseases of other organs

Nursing diagnoses :

1. Risk for trauma related to impairment in cognitive and psychomotor function

Outcome criteria : Client will not experience injury

Interventions:

•          Arrange furniture and other items in the room to accommodate clients disabilities

•          Store frequently used items within easy access

•          Do not keep bed in elevated position

•          Assist the client with ambulation

•          Keep a dim light on at night

•          Frequently orient the client to place ,time and situation

•          Soft restraints may be required if client is very disoriented and hyperactive

2. Disturbed thought process related to cerebral degeneration as evidenced by disorientation, confusion, memory deficits  and inaccurate interpretation of the environment

Outcome criteria: client will interpret the environment accurately and maintain reality orientation to the best of his or her cognitive ability

Interventions:

•          Frequently orient the client to reality. Use clock and calendars with large numbers that are easy to read

•          Notes and large bold signs may be used as reminders

•          Keep explanation simple

•          Discourage rumination of delusional thinking

•          Talk about real people and real events

•          Monitor for medication side effect

3. Self care deficit related to disorientation ,confusion and memory deficits as evidenced by inability to fulfill the ADL

Outcome criteria: client will accomplish the ADLs to the best of his or her ability. Unfulfilled activities may be kept by caregivers

Interventions:

•          Identify the self care deficits and provide assistance as required

•          Provide guidance and assistance for independent actions

•          Provide a structured schedule of activities that does not change from day to day

•          Provide for consistency in assignment of daily caregivers

•          Perform ongoing assessment of clients ability to fulfill nutritional needs ,ensure personal safety ,follow medication regimen and communicate need for assistance with activities that she or he cannot accomplish independently

•          Involve the family members in the care of the patient

Conclusion

Delirium or acute confusional state is a transient global disorder of cognition. The condition is a medical emergency associated with increased morbidity and mortality rates. Early diagnosis and resolution of symptoms are correlated with the most favorable outcomes. Therefore, it must be treated as a medical emergency.

References

1.         Henry WD, Mann AM. Diagnosis and treatment of delirium.. Can Med Assoc J. 1965 Nov 27;93(22):1156-66.

2.         Mary TC. Psychiatric Mental Health Nursing –Concept of Care.3rd ed. Philadelphia: F.A. Davis Publishers; 2005

3.         Fortinash K M, Worret P H. Psychiatric Nursing Care Plans.5th ed. Philadelphia: Mosby Publications; 2007.

4.         Kaplan HI, Sadock BJ. Synopsis of Psychiatry, Behavioral Sciences/ Clinical Psychiatry .9th ed. Hong Kong: William and Wilkinson Publishers ;1998

5.         Gelder M G, López-Ibor J J, and Andreasen N. New Oxford Textbook of Psychiatry .London Oxford University Press ;2000

6.         Stuart GW, Laria MT. Principles and Practices of Psychiatric Nursing. Ist ed. Philadelphia: Mosby Publishers; 2001.

7.         The ICD 10