Mood Symptoms and Syndromes

Mood symptoms are ubiquitous. The language of emotion is found in the most common of ritualized greetings (e.g., “How are you feeling?”) and the most sublime of poetic expressions. At times, however, mood interferes with usual functioning and becomes associated with particular thoughts, feelings, beliefs, and behaviors. This cluster of signs and symptoms is then recognizable as a specific mood syndrome with a characteristic course.

Mood syndromes, in contrast, have no pathognomonic features. When present, they may reflect an underlying delirium or dementia. However, an altered mood that persists for days or weeks in spite of environmental change and in the absence of cognitive impairment or a fluctuating level of consciousness is strong presumptive evidence that a mood syndrome is present. Often, the direction of mood change is clear; however, the patient with an irritable mood or “mixed” mood state (in which elements of euphoria and depression coexist or rapidly alternate) can present a confusrng picture.

T he distinction between mood symptoms and mood syndromes may have particular relevance to the elderly population, as the Epidemiologic Catchment Area (ECA) study found higher rates of depressive symptoms, but lower rates of major depression, in respondents older than 65 compared with those younger than 65 (Romanoski et aL 292, issmanctili.991).

In addition to a prolonged period of altered mood, other signs and symptoms are required to make a diagnosis of a syndrornic mood disorder. These include changes in a person’s ability to experience pleasure, degree of self-confidence, interest in surroundings, and sense of mental and physical vitality. Typically, the direction of these changes is down in depressive disorders and up in mania. Changes in self-attitude are common in mood disorders; despair, guilt, worthlessness, and hopelessness are seen in depression, whereas a feeling of invincibility occurs in mania. Motor activity is frequently affected; in mania it is increased, whereas in depression both restlessness and a slowing or scarcity of movement can be seen. Biologically driven behaviors such as eating and sleeping may be adversely affected and difficulties with memoiy and concentration are often present. Hallucinations can occur and are usually auditory; their content tends to be self-deprecating or hopeless in depression and laudatory in mania. Delusions may be present and are usually “mood-congruent” (i.e., consonant with the direction of mood change). In depression, the predominant themes of delusions are self-deprecating, hopeless, or nihilistic, and in mania, self-aggrandizing. Suicidal ideation or urges, which frequently accompany depression, are of particular concern in the elderly population which has the highest rate of completed suicide of any age group. In DSM-IV (Aincrican Psychiatric Association 1994) each mood syndrome is defined (in part) by a checklist of symptoms, a minimum number of which must be present to make a diagnosis.

Table 23—I. placebo-controlled outcome studies of psychoactive mhications in nursing home residents

Study Medication (mg/day)

Sample Outcome mearures

Results/comments

Beber 1965

Oxazepani (11)-If)) vs.

N = 100 Anxiety and tension

Improvement in a11 parameters was

placebo

mean age = 79 years;

nonpsychotic with chronic

brain syndrome (ii = 20),

mixed atixietyidepression

is = 26), anxiety (is = 43),

or depression (n = 3)

Depression, lethargy, and

autonomic reactions

Irritability, insomnia, agila-

lion, phobic reactions

significantly greater in oxazepam-treated

group than in placebo-treated group

4-I subjects received concomitant treat-

ment with other drugs, including neuro

leptics, antidepressants, hypnotics, anti-

parkinsonian agents. and analgesics

Barrnes et al 1982

Thiorida,ine (mean = 625) vs luxapinc (mean — 10,5) vs placebo .

N = 53 mean age — 143 years; dementia and 3 behavioral symptoms -

BPRS SCAC NOSIE CGI

total scores and global ratings showed modest efficacy with thioridazine and loxapine, not statistically better than placebo Prominent placebo effect

Significant improvement in anxiety, excitement, emotional lability, and uncooperativeness in active treatment groups. but no significant differences in overall efficacy between thioridazine and loxapine Significant improvement on BPRS and SCAG only in subjects with high severity baseline scores

Stotsky 19114

Thioridazine (10-200) vs diazepam (20—10) vs. placebo

N = 237 nursing home patients mean age — 80 years; all nonpsychotic with cognitive impairment, emotional lability, and ADL dysfunction; and agitation. anxiety, depressed mood or sleep disturbance (also studied 273 patients on geriatric wards of state hospitals)

Modified HAM-A Modified NOSIE Global evaluations

Thioridazine was well tolerated with few side effects Thiondazine-treated group improved significantly more than placebo grtasp on all HAM-A items and global evaluations Thioridazine-treated group improved significantly more than

diazepam group on NOSIE and global ratings Insomnia responded better to diazepam. but there was more overall improvement on HAM-A rating wIth thioridazine

Deldin et al 1985

Alaproclate (400) (serotonin uptake inhibitor) vs. placebo

N =40 mean age = 82 years; primary degenerative. multi-infarct, or mixed dementia; not selected on the basis of affective or behavioral symptoms

Intellectual function Motor (unction (A01) Emotional function (includ- ing depressive symptoms) Clinical global evaluation

No difference in efficacy between alaproclate and placebo Severity of dementia ranged f rum mild to severe Behavioral problems not described

Katz et at 1990

Nortnpsylsne (mean = 65.25) vs. placebo

N 30 residents of nursing home or congregate housing mean age = 84 years; major depression (l-IAII-D scores 18)

HAM-D 00$ CGI ,

Significant improvement in patients treated with nortriptyline compared with placebo on HAM-D and CGI. but not on GDS Location (in nursing home yr. congregate housing) not significantly related to response Trend toward decreased nortripsyline response in the nursing home related to higher levels of disability and lower ser um albumin in nursing home patients

Note. ADL = activities of daily living; BPRS: Brief Psychiatric Rating Scale (Overall and Corharn 1962); CGI: Clinical Global Impressions (Guy 1976); GDS = Global Deterioration Scale (Reiskrerg ci al t9M): HAM-A = Hamilton Anxiety Scale (Hanrilton 1959); HAM-D: Hamilton Rating Scale for Depression (Hamilton 1960); NOSIE — Noises’ Observation Scale for Inpatient Evaluation (Honigfeld ci al. 1966); SCAG — Sandoz Clinical Assessment—Geriairic (Shader et at 1974).

Table 12—1. Symptoms of major depressive episode 1. Depressed mood: most of the day, nearly every day, as indicated either by subjective account or observation by others 2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated either by subjective account or Observation by others of apathy most of the time) 3. Significant weight loss when not dieting or weight gain (e.g., more than 5% of body weight in a month) or decrease or increase in appetite nearly every day 4. Insomnia or hypersomnia nearly every day 5. Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down) 6. Fatigue or loss of energy nearly every day 7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick) 8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others) 9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide

Note. Adapted from criterion A in DSM-W (American Psychiatric Association 1994).

The mood syndromes of DSM-III-R (AmcricanfsvchiatricAssociationl98i) included bipolar disorder, major depression, dysthymia, cyclothymia, and adjustment disorder with depressed mood. Bipolar disorder, major depression, and, to a lesser extent, all the other mood disorders are distinguished by their phenomenology, epidemiology, course, and responses to treatment. In turn, each of these disorders is a heterogeneous category made up of various subtypes. Bipolar disorder, for example, is made up of bipolar I (at least one manic episode and usually one or more depressed episodes), bipolar II (at least one hypomanic and one depressed episode), and rapid cycling subtypes. Major depression occurs in many varieties including “melancholia,” in which social withdrawal, sleep or appetite disturbance, and diurnal mood variation are prominent features. Any of these subtypes can in turn be characterized by the presence or absence of psychotic features (i.e., hallucinations, delusions, or catatonia) and may occur in a seasonal pattern. Cyclothymia (alternating bouts of hypomania and mild to moderate depression) and dysthymia (persistent mild to moderate depression) are controversial mood syndromes that resemble personality disorders in their chronicity. These disorders further differ from bipolar disorder and major depression in that no studies have linked them to neuropsychiatric conditions affecting the elderly population.

Minor depression is a mood syndrome that may be of special importance in the elderly population. For example, Rlazer..eLaL(19S9) identified six clusters of depressive symptoms, one of which—characterized by multiple depressive complaints, cognitive impairment, and a lack of association with any of the currently defined depressive syndromes—was unique to the population over age 60. The concurrence of cognitive impairment and depression suggests an association with neuropsychiatric disease.

Emotional incontinence and emotional lability are two important mood syndromes typically seen in elderly patients with neurological conditions. They are not listed in DSM-IV because they are rarely seen in patients without some degree of brain injury.

Emotional incontinence describes a syndrome in which there is a sudden expression of emotion, either laughter or crying, that is not experienced by the patient as accompanied by the emotion usually associated with that affect (Poeck 1969). Other characteristics of emotional incontinence are its rapid onset and precipitation by a minor or inconsequential stimulus. It is almost always associated with signs of pseudobulbar palsy (increased jaw jerk, spastic cranial nerve VII function, and heightened gag reflex), that is, bilateral involvement of corticobulbar fibers. The dissociation between mood and affect seen in emotional incontinence suggests that the control of emotional expression is predominantly in the brain stem, whereas the experience of mood is grounded elsewhere, most likely in the limbic system (Poeck 1969). Tricyclic antidepressants are effective in treating emotional incontinence (RohinsoiteLaLl99.3; Schiffer..et al 1985). In the elderly, emotional incontinence is most commonly seen in individuals with bilateral stroke. Progressive supranuclear palsy and multiple sclerosis are other common causes.

Emotional lability refers to frequent wide swings in mood. These mood swings are said to come on less quickly than do the changes of emotional incontinence, but the validity of this distinction is unclear. Emotional lability is usually precipitated by an upsetting environmental event and appears as an emotional overreaction. This lability is usually precipitated by an upsetting environmental event and appears as an emotional overreaction. This contrasts with the precipitation by a minor or inconsequential stimulus seen in emotional incontinence. Emotional lability can follow lesions in any area of the brain. It is unclear whether a greater amount of tissue destruction or a specific location (e.g., frontal lesions) increases its occurrence.

Summary

Several major points can be made about the neuropsychiatric foundations of mood disorders in the elderly: 1. The prevalence of organic syndromes affecting mood increases over the life span. Thus an underlying neuropsychiatric condition should be suspected in all mood disturbances of new onset in elderly patients. 2. The phenomenology (i.e., signs and symptoms) of “idiopathic” and “secondary” mood disorders affecting elderly patients are essentially identical. Thus the history, physical examination, and ancillary testing are essential tools in the search for potential neuropsychiatric causes of a mood disturbance in an elderly person. 3. Converging lines of evidence suggest that the left frontal lobe plays an essential role in the genesis of “idiopathic” and secondary depression. Modest evidence from similar studies also suggests a role for the basal ganglia. 4. Evidence from neuropathological and functional imaging studies suggests that disruption of cortical and subcortical tracts (from stroke, demyelination, or neuronal degeneration) impairs norepinephrine and serotonin neurotransmission and may increase the likelihood of a mood disturbance (usually depression). Because there are age-related decrements in these neurotransmitter systems (as well as an increase in monoamine oxidase), the concordance of disease-induced and age-related changes in these systems puts the elderly at special risk for developing mood disorders. 5. The treatments that are effective for “idiopathic” mood syndromes are also useful in treating secondary mood syndromes. Removal of the causative agent (e.g., medications or endocrine dysfunction) is sometimes an effective treatment for secondary mood symptoms, but is not always possible. Lower doses of medication are often appropriate in elderly patients. Side effects from medication are more likely to limit therapy in elderly patients than in younger ones. Finally, ECT is an effective treatment for severe depression or mania in elderly patients, and its side effects are often better tolerated than pharmacological therapy.

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Late-Life-Onset Psychoses

Introduction

Late-life-onset psychosis is a fascinating but heterogeneous and insufficiently explored syndrome. To examine it objectively, one should put aside commonly held notions, such as that most cases of late-life-onset psychosis represent coarse brain disease (e.g., Alzheimer’s disease or microvascular pathology) or that early- and late-life-onset schizophrenia merely represent opposite tails of age distribution of the same syndrome. Late-life-onset psychosis is a common condition, accounting for up to 10% of admissions to psychiatric hospitals for patients over age 60 (Bridge and Wyatt 1980a, 1980b; Kay and Roth 1961; Roth1955; Siegel and Goodman 1981). It is feasible that all psychoses, including late-life-onset forms, represent a final common expression of diverse etiopathologies. This diversity is likely to be especially marked in late-life-onset conditions, a viewpoint argued by Holden (I987) and Post (1966). In part, this may be related to a general increase in age-related biological heterogeneity (Jeste and Caliguiri 1991) as well as to the emergence in late life of several neurodegenerative disorders in which psychotic symptoms are common. Late-life-onset psychosis is a disorder classically defined on the basis of clinical phenomenologv but clinicians also define cases, somewhat inconsistently, on the basis of pathological entities (e.g., Alzheimer’s disease) and etiologic descriptions (e.g., amphetamine psychosis). Two useful, but competing, approaches to defining the syndrome are (1) to cast the net broadly (i.e., include all patients with onset of delusions and hallucinations for the first time in late life) and (2) to examine a more narrowly defined group of patients who have late-life-onset delusions and hallucinations, but in the clear absence of an affective syndrome, progressive cognitive impairment, or obvious organic cause. This more restricted syndrome is closer to what has been assumed late-life-onset schizophrenia, or late paraphrenia. Depending on which of these approaches is chosen and which age at onset is used, mixtures of patients will emerge with differing etiopathologies, genetics, brain changes,and responses to treatment (JesIcetaLI9S, l9BBh,1991). The emergence of such heterogeneous patient mixtures is precisely what has occurred with studies of such patients, resulting in a lack of clarity. As late-life-onset psychosis likely comprises a heterogeneous group of etiopathologies, even the narrowly defined group referred to above, which has been assumed by many to be most similar to early-onset schizophrenia, may well exhibit significantly more heterogeneity than would be found among a comparable group of early onset schizophrenic patients, a point made recently (Rabins and Pearison, in press). (The full range of conditions commonly included under the broad umbrella of “late-life-onset psychosis” is discussed in the section “Diagnostic Diversity and Classification of Late-Life-Onset Psychosis” below.)

Treatment and Treatment Response

Differential diagnosis needs first to be confirmed. The mainstay of treatment of late-life-onset psychosis has been neuroleptic drugs, but lack of insight into illness and suspiciousness can result in variable medication compliance. Late-life-onset psychosis patients tend not to seek treatment. The psychiatrist is often involved late in the illness, offering treatment to an uncooperative patient (e.g., see, Almeida et aI.,Jn.press PostI84). As might be expected, medication compliance, depot medication, and use of a community psychiatric nurse for outpatients all favorably affect treatment response (Howard and Jeyy 1992) Despite the paucity of well-organized, double-blind crossover treatment trials, several open trials of neuroleptics have shown substantial improvement in a subgroup of well-characterized late-life-onset psychosis patients. Four studies over a 25-year period are summarized in Table 13-2.

Table 13— Results of neuroleptic treatment in late-life—onset psychosis

6.

Study Complete

Remission

Partial

remission

No

improvement

N

patient

Post 1966 60.5% 31% 8.5% 71

Rabins

etal.1984 . 57% 28.5% 14.5%

34

Pearison

etal. 1989 48% 28% 24% 54

Howard and

Levy 1992 27% 31% 42% 64

Table 13—2. Groups included ma broad classification of “late-life—onset psychosis” patients Elderly early-onset schizophrenia patients Patients with late-life—onset schizophrenia (“late paraphrenia”) Patients with paranoid psychoses without hallucinations Psychotic affective patients Cerebrovascular disease patients: Classic multi-infarct dementia with psychotic symptoms “Multi-infarct disease” Alzheimer’s disease patients with psychotic symptoms Patients with psychoses of miscellaneous causes with and without defined neuropathology Patients in delirious and toxic states Patients with extremes of paranoid or schizoid personality types

Conclusions Late-life-onset psychosis is clearly a heterogeneous and understudied syndrome. Much that is vital to comprehend is still unknown, for example, how best to subdivide the condition meaningfully and, for each resulting separate syndrome, how to determine its precise prevalence and find its important pathophysiological underpinnings. Also remaining obscure are the syndrome’s precise relationship to early-onset schizophrenia, response to treatment, and long-term outcome.

Although neuroimaging has the potential to provide important insights into the underlying pathophysiology, the numbers of subjects studied in most recent studies have been small, and there is a great need for large-scale longitudinal studies with suitable comparison patients (e.g. patients with Late-life-onset affective disorders or elderly patients with early-onset schizophrenia). Finally, neuropathological examination is ultimately needed to clarify the nature of the underlying brain processes. More narrowly defined cases of late-life-onset schizophrenia (or late paraphrenia) appear both more clinically homogeneous and most phenomenologically similar to early-onset schizophrenia. Even when more narrowly defined, late-life-onset psychosis appears to be a more diverse syndrome than early-onset schizophrenia and neurodegenerative changes play a larger etiologic role than formerly envisioned. Evidence suggests that neurodegenerative and neurodevelopmental changes likely contribute to late-life-onset psychosis, but because the relative importance of each is unknown in most cases it is too soon to settle the question of whether early- and late-life-onset schizophrenia are essentially the same condition (a theme discussed by both AImeida.et..al. Perhaps the clearest parallel is with late-life-onset depressive illness (see Chapter 12). There, too, one finds a genetic risk for the appropriate illness (albeit a diminished one compared with early-onset forms of the disease), evidence in some subjects of nonspecific brain changes (identified by neuroimaging techniques), and a likely heterogeneous mixture of delayed “true” cases and “organic phenocopies.” Neuroimaging clearly has the potential to help “biotype” the syndrome and to clarify the question of diversity. However, documenting the choice of index and comparison patients, as well as of control subjects, is critical in this endeavor, as some neuroimaging studies have cast their recruitment net broadly, whereas others have excluded cases with likely “organic” associations. Returning to the theme of affective illness, we believe that Castle and Murray’s view point 1991) that late-life-onset cases of schizophrenia in fact represent affective disorder is unlikely. Our opinion is based on recent observations that late-life-onset schizophrenia and affective disorder comparison patients have different patterns of atrophy on the CERAD (Consortium to Establish a Registiy for Alzheimer’s Disease; Morri&etaLJ9B9) MRI rating scale (AylwardetaLi993; Rahins..eLaLJnpi:ess) and differ phenomenologically (Rahins.et..aL.19.84). Also the types of abnormal premorbid personality reported in late-life-onset schizophrenia and affective disorder differ, the risks of family members being affected with affective disorder versus schizophrenia appear to be different in the two groups, and the syndromes respond to different types of treatment. So far, interactions between the various risk factors reported for late-life-onset schizophrenia, as well as the ability to separate necessaiy from sufficient associations, lack the development of an encompassing theory. As we have stated (Pearlsoat...aLJ..993), the etiology and timing of the structural changes in late-life-onset schizophrenia are unknown. They could be primarily initiated in late life, or alternatively, depend on age-related brain changes unmasking a preexisting (perhaps genetic) vulnerability. If a developmental origin, similar to that proposed for early-onset cases (W ergerl9&7) is also applicable to some cases of late-life-onset schizophrenia (e.g., as we have suggested [Pearison and Rabins 1988]), a vital point to address is why symptomatic onset has been delayed to the seniuni. In this chapter, we have reviewed evidence that such possible precipitants for late-life-onset psychosis could include neuronal loss due to usual aging and vascular or age-related functional changes, especially those affecting females, such as postmenopausal estrogen loss and thus alterations in the relative balance of dopamine D receptors in basal ganglia. The role of late-life brain abnormalities and the relative contributions of 2 neurodegenerative processes versus brain damage secopdary to stroke or microvascular disease remain to be elucidated. Cerebrovascular pathology is likely to prove an important etiologic factor for a significant proportion of late-life-onset major psychiatric illnesses, including psychosis.

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Anxiety Disorders Introduction Anxiety is a normal human emotion in the elderly, as in the young, with adaptive value in that it helps one anticipate and prepare for noxious events. This normal emotion, however, can be considered pathological when it becomes unjustifiably excessive and maladaptive, as in morbid anxiety in clinical situations. This morbid anxiety usually manifests itself in the form of a multitude of cognitive, behavioral, and physiological symptoms, whereas the mental content of such anxiety may range from excessive worrying about everyday concerns regarding job and relationships to episodes of intense anxiety and fear (panic attacks). I use the term anxiety in this chapter to refer to such clinically significant or morbid anxiety, unless specified otherwise.

Table 14—1. Multidimensional symptoms of anxiety

Cognitive

Nervousness

Apprehension

Racing thoughts

Worry

Fearfulness

Irritability

Distractibility

Behavioral

Hyperkinesis

Repetitive motor acts

Stiffness

Phobias

Pressured sp&ch

Startle response

Physiological

Tachycardia

Palpitations

Chest tightness

Dry mouth

Hyperventilation

Paresthesias

Lightheadedness Sweating Urinary frequency

.

Source. Reprinted from SheikhJI: “Clinical Features of Anxiety Disorders,” in The Rsythiatry of Old Age. Edited by CopelandJM, Abou-Saleh MT, Blazer DG. Chichester, England, Wiley, 1993a, p. 107.1. Used with permission.

Table 14-1 lists some examples of multidimensional symptoms that might be experienced by patients with various anxiety disorders. Anxiety disorders are some of the most frequent but least studied of psychiatric illnesses in elderly patients. For example, an analysis of the Epidemiologic Catchment Area (ECA) data by Blazer (1921) indicated a 6-month prevalence of 19.7% for all anxiety disorders in the 65 or older age group, with phobias the most common psychiatric syndrome in elderly women and the second most common in elderly men. Systematic studies of anxiety disorders in elderly subjects, however, remain scant. In this chapter, I begin with a description of the classification of anxiety disorders based on DSM-LV, summarize findings of phenomenology of anxiety disorders in elderly patients from the literature, discuss manifestations of anxiety in certain medical illnesses, present a systematic way of assessing anxiety in the elderly and differentiating it from depression, and summarize treatment methods particularly suited to geriatric anxiety.

Table 14-2. DSM-IV anxiety disorders Panic attack Agoraphobia Panic disorder With agoraphobia Without agoraphobia Agoraphobia without history of panic disorder Specific phobia (simple phobia) Social phobia (social anxiety disorder) Obsessive-compulsive disorder Posttraumatic stress disorder Acute stress disorder Generalized anxiety disorder Anxiety disorder due to a general medical condition Substance-induced anxiety disorder Anxiety disorder not otherwise specified

Source. From American Psychiatric Association 1994. Table 14-2 Clinical Differentiation Between Anxiety and Depression Debate about the unresolved and somewhat controversial issue of whether anxiety and depression lie on the same continuum, or whether they are separate conditions, is a recurring theme in the psychiatric literature. Despite recent advances in our knowledge about the phenomenology and biology of these

Management of Geriatric Anxiety

Effective management of geriatric anxiety can be accomplished by using pharmacological and/or psychological treatments. In the following sections, I provide a summary of the advantages and disadvantages of various treatments, as well as recommendations of their usage in specific anxiety disorders.

Half-life Active Daily dome (aig)

Drug (hour) metabolites Aduk Fidedy

Alprazolain 12—15 Yes 0.25—2.0 0.125—I

Chlordiazepoxide 7-28 Yes 25-100

Clonazepam 18-56 Yes 1-8 0.5-4

Clorazepate 30-200 Yes 15-60 7.5-30

Diazepam 20-60 Yes 5-30 2-15

Loi-azepam 10-20 None 1-6 0.5—3

Halazcpam 15-50 Yes 20-160 20—SO

Oxazepam 5-15 None 15—90 10-45

Pa-azepam 25-200 Yes 20-60 10-20

Table 14-6. Commonly used anxiolytic benzodiazepines a summary of pharmacokinetics

Half-life Active 11Y dome (mg)

Drug (boise) metabolite. Aduk

Aiprazolani 12—15 Yes 0.25—2.0 0.125—1

Chlordiazepoxide 7-28 Yes 25-100 5—SO

Clonazepam 18-56 Yes 1-8 0.5-4

Clorazepate 30-200 Yes 15-60 7.5-50

Diazepani 20-60 Yes 5-30 .2-15

Lorazepam 10-20 None 1-6 0.5—S

Halazepam 15-50 Yes 20-160 20-80

Oxazepam 5-15 None 15-90 10-45

Prazepaxn 25-200 Yes 20-60 10-20

Table 14—7. Potential complications of long-term benzodiazepine use in elderly patients Excessive daytime drowsiness Cognitive impairment and confusion Psychomotor impairment and a risk of falls Depression Intoxication (even on therapeutic dosages) Paradoxical reactions Amnestic syndromes Respiratory problems Abuse and dependence potential Breakthrough withdrawal reactions

Source. Adapted from Sheikh 1992a. Used with permission. Table 14-7 lists potential complications of long-term use of benzodiazepines in the elderly. Buspirone. In double-blind studies (Rickels.andSchweizcr-I98.7; RickekeLaL1982), this anxiolytic medication with partial serotonin-agonist properties has demonstrated efficacy comparable to that of diazepam in patients with geiieralized anxiety disorder. its nonaddictive profile, absence of withdrawal symptoms when discontinued icke1s eLaL19l8), and lack of psychomotor impairment even with long-term usage (Smi1eyandMoskoxvitzI96) seem to be advantages over benzodiazepines in chronic anxiety conditions. Studies in geriatric populations indicate that it is well tolerated, does not cause adverse interactions when coprescribed with other medications (including antihypertensives, cardiac glycosides, and bronchodilators), and is effective for remediation of chronic anxiety symptoms in this population (NapolinlloJ986). It also appears that in both acute and chronic dosing, the pharmacokinetics of buspirone in elderly patients are very similar to those in younger patients (Gammansci at 19&2). Such a profile seems to suggest that buspirone may be a particularly desirable anxiolytic for chronic anxiety.