Psychiatric Annals

MEDICAL ILLNESS AND DEPRESSION 

Depression and Its Treatment in Neurological Disease

Jorge Luis Maldonado, MD; Francisco Fernandez, MD; Enrique Sergio Garza-Trevino, MD; Joel K Levy, PhD

Abstract

Mood disorders are commonly found in patients with neurological diseases, and their frequency in this population is greater than in the general population1"10 (Table 1). Patients may report mood disturbances that range from normal sadness to major depressive and organic mood disorders. Because the suicide risk is also increased in many of the neurological disorders,11,12 patients need to be carefully assessed. The reported deaths by suicide in patients with epilepsy (5%), spinal cord injury (9%), head injury (9%), Huntington's disease (HD; 7.8%), multiple sclerosis (MS; 17%), and acquired immunodeficiency syndrome (36%) are significantly higher than in the general population (1.4%), and suicidal ideation is almost always a symptom of depression in neurological patients.

Depression may actually precede any clinical manifestation of a primary neurologic disorder, as is often the case in patients with HD.5 Depression may also occur more frequently early in the course of the neurological illness, as in Alzheimer's dementia (AD)13 or post-stroke depression (PSD).14 Progression of the neurological disease or the involvement of specific brain areas, as in MS,15 may be associated with significant depression. Thus, formulating an accurate diagnosis of depression in patients with neurological disease may be difficult because many of the usual diagnostic indicators of depression are also common to neurological impairment. Medications used for the treatment of neurological disease,16"18 such as phénobarbital, zidovudine, bromocriptine, corticosteroids, levodopa, and valproic acid, may induce depressive symptoms.

Depression may affect the prognosis of patients with primary neurological disease by preventing recovery, by accelerating the patient's deterioration, or by increasing the risk of complications. Depressed patients show greater impairment in activities of daily living, cognitive functioning, and ability to participate meaningfully in rehabilitation programs.19'21 Yet, depression is both underdiagnosed and undertréated in neurological patients. A thorough approach to the neurological patient includes a realistic appraisal of the psychosocial situation and a comprehensive neurobehavioral assessment to address all elements associated with depressive illness in neurological disease.

DIAGNOSTIC CONSIDERATIONS

Diagnosing depression in patients with neurological diseases is often difficult. Many clinicians tend to rely on "psychological" rather than "somatic" symptoms of depression to fulfill diagnostic criteria for depression in neurologically ill patients. However, as with aphasie patients, many neurologically impaired patients are unable to report symptoms due to communication problems, memory problems, or lack of awareness, and the diagnosis of depression can easily be missed. An all-inclusive approach to the diagnosis of depression in patients with neurological diseases is the most clinically effective. If all symptoms are counted toward the diagnosis of depression, regardless of the specific etiology, then symptoms of questionable neurological or psychological origin will nonetheless be considered valid diagnostic indicators. To this end, caregivers, as surrogate reporters, may be helpful in diagnosing mood disorders in these patients.22,23 Caregivers often report objective signs that can account for a more accurate diagnosis of depression.

Table

Psychostimulants (methylphenidate and dextroamphetamine) have been tried in patients with PSD, PD, and neurotrauma. A single double-blind, placebo-controlled trial of dextroamphetamine demonstrated statistically significant gains in recovery of motor function without treatment-emergent side effects42 in stroke patients. Patients with PD have shown limited benefits from stimulants in both depression and movement disorders. Stimulants may be particularly useful in HIV-infected patients in whom TCAs are contraindicated or have been ineffective. Stimulants are also beneficial in HTV-infected patients who suffer from both depression and cognitive impairment/dementia. There is little experience with the use of psychostimulants in patients with other neurological diseases, and caution is recommended if used in these patients.

There are no reports of treatment of depression in neurologically ill patients using newer medications such as venlafaxine, nefazodone, and mirtazapine; however, these medications are probably…

Mood disorders are commonly found in patients with neurological diseases, and their frequency in this population is greater than in the general population1"10 (Table 1). Patients may report mood disturbances that range from normal sadness to major depressive and organic mood disorders. Because the suicide risk is also increased in many of the neurological disorders,11,12 patients need to be carefully assessed. The reported deaths by suicide in patients with epilepsy (5%), spinal cord injury (9%), head injury (9%), Huntington's disease (HD; 7.8%), multiple sclerosis (MS; 17%), and acquired immunodeficiency syndrome (36%) are significantly higher than in the general population (1.4%), and suicidal ideation is almost always a symptom of depression in neurological patients.

Depression may actually precede any clinical manifestation of a primary neurologic disorder, as is often the case in patients with HD.5 Depression may also occur more frequently early in the course of the neurological illness, as in Alzheimer's dementia (AD)13 or post-stroke depression (PSD).14 Progression of the neurological disease or the involvement of specific brain areas, as in MS,15 may be associated with significant depression. Thus, formulating an accurate diagnosis of depression in patients with neurological disease may be difficult because many of the usual diagnostic indicators of depression are also common to neurological impairment. Medications used for the treatment of neurological disease,16"18 such as phénobarbital, zidovudine, bromocriptine, corticosteroids, levodopa, and valproic acid, may induce depressive symptoms.

Depression may affect the prognosis of patients with primary neurological disease by preventing recovery, by accelerating the patient's deterioration, or by increasing the risk of complications. Depressed patients show greater impairment in activities of daily living, cognitive functioning, and ability to participate meaningfully in rehabilitation programs.19'21 Yet, depression is both underdiagnosed and undertréated in neurological patients. A thorough approach to the neurological patient includes a realistic appraisal of the psychosocial situation and a comprehensive neurobehavioral assessment to address all elements associated with depressive illness in neurological disease.

DIAGNOSTIC CONSIDERATIONS

Diagnosing depression in patients with neurological diseases is often difficult. Many clinicians tend to rely on "psychological" rather than "somatic" symptoms of depression to fulfill diagnostic criteria for depression in neurologically ill patients. However, as with aphasie patients, many neurologically impaired patients are unable to report symptoms due to communication problems, memory problems, or lack of awareness, and the diagnosis of depression can easily be missed. An all-inclusive approach to the diagnosis of depression in patients with neurological diseases is the most clinically effective. If all symptoms are counted toward the diagnosis of depression, regardless of the specific etiology, then symptoms of questionable neurological or psychological origin will nonetheless be considered valid diagnostic indicators. To this end, caregivers, as surrogate reporters, may be helpful in diagnosing mood disorders in these patients.22,23 Caregivers often report objective signs that can account for a more accurate diagnosis of depression.

Table

TABLE 1Prevalence of Depression in Patients With Neurologic Diseases

TABLE 1

Prevalence of Depression in Patients With Neurologic Diseases

Table 2 lists the mood disorders according to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV).24 Table 3 lists depressive disorders not included in the DSM-IV. Although the most frequent diagnosis in neurological patients is depression secondary to the primary neurological disorder, we also have to- consider psychoactive substances and medication side effects as significant sources of depressive symptoms, and a detailed list of illicit, over-the-counter, and prescribed medications needs to be reviewed with the patients and their families. Other medical conditions can coexist and can contribute to or induce depression. A medical work-up is necessary to diagnose or exclude other medical illnesses.

Depression and Dementia

The two most frequent dementias, AD and multi-infarct dementia (MID), have a clinical presentation that often includes depression. Dementia and depression frequently coexist even in patients who have no prior history of major depression. Pathological crying is also frequent in patients with dementia, and although pathological crying and depression are not necessarily related, they are significantly associated with each other.25

Huntington's disease is a dementia characterized by a variety of neuropsychiatrie symptoms as part of its clinical presentation. Patients frequently present with increased irritability and aggressive behavior, which often precedes the appearance of depressive symptomatology. When patients are depressed, the aggression is often directed toward themselves, with a high incidence of suicide, particularly in 50- to 69year-old patients. The spectrum of anxiety/ depression commonly antedates the presentation of the movement disorder. The characteristic depressive symptoms observed in this group of patients include apathy, anhedonia, a sense of worthlessness, helplessness, hopelessness, and low self-esteem, which reflect dysfunction of the caudate nucleus, striatum, and prefrontal subcortical circuits.6 A higher prevalence of depression is found in white patients with a family history of mood disorders.

Depression is the most common neuropsychiatrie disorder of Parkinson's disease (PD).9 Patients with PD can have significant dementia with marked impairment in language and memory functions.20 Depression may be a prominent symptom in PD, and its presence is often the first clinical manifestation of a dementing process (ie, the "pseudodepression" of dementia). Studies have failed to correlate depression in PD to age of patients, length of illness, degree of disability, or gender.9 There seems to be a correlation between depression and severity of cognitive impairment, gait, and postural changes in PD.

Although the lifetime prevalence for major depressive disorders in patients infected with the human immunodeficiency virus (HTV) is approximately 30%,4 it is estimated that close to 85% of patients will have manifestations of a mood disturbance that will go from normal sadness to a major depressive disorder. They will also have mood changes because of medications, psychoactive substances, or other medical illnesses. Cognitive changes are also frequent, and approximately 70% of HrV-infected individuals will have an HrV- associated minor cognitive/motor disorder (Table 4). Earlier signs and symptoms reflect involvement of the subcortical areas, and 20% to 30% of the patients will fulfill diagnostic criteria of HTV-associated dementia (Table 5). Patients initially have cognitive deficits in memory registration, storage and retrieval, psychomotor speed, information processing, and fine motor function. In late stages, aphasia, agnosia, apraxia, and impairment of other cortical and motor functions become progressively more severe.26 A complete medical evaluation is mandatory in the HIV-infected patient to search for reversible organic causes of both the mood disorder and the cognitive dysfunction.

Table

TABLE 2Depressive Disorders According to the DSM-IV

TABLE 2

Depressive Disorders According to the DSM-IV

Depression and Stroke

Several studies have replicated the relationship between lesion location and PSD.2,14,23 Patients with left frontal cortex and left anterior subcortical (basal ganglia) lesions show higher frequency of depression than patients with lesions in any other locations. In the right hemisphere, the more posterior the lesion, the higher the frequency of depression during the acute phase; however, this correlation seems to change during the months after the stroke. Patients with cerebellar and brainstem lesions who develop PSD have a shorter course of depressive symptoms.

The majority of patients with PSD develop symptoms shortly after the stroke. However, of the non-depressed group after the stroke, one third will develop depression at 2-year follow up.2

Depression and Epilepsy

Depression is also highly prevalent in the population of patients with epilepsy. Risk factors for the development of depressive symptoms aré left hemisphere epileptic focus, which produces dysfunction of the left limbic system, male gender,27 multiple antiepileptic medications, and a decreased frequency of generalized tonic-donic seizures,18 which may be related to the amount of medications used by patients. Depression in these patients is manifested mainly through psychological factors, including pessimism, low self-esteem, sad mood, and low energy level.17

Depression and Demyelinating Disorders

Patients with MS have a high prevalence of depression, which is predominantly characterized by anger, worry about the future, irritability, and discouragement.28 The location of the lesions and the amount of brain damage by MS correlates with the appearance of depressive symptoms. Clark et al15 studied thé relationship between sleep disturbance, depression, and lesion site, finding that right and left frontal white matter and the deep white matter of the right insula were the most related to sleep disturbance, regardless of the cause of the lesion, but only patients with these lesions due to MS showed higher depressive scores in the scales used.

Table

TABLE 3Depressive Disorders Not Included in DSM-IV

TABLE 3

Depressive Disorders Not Included in DSM-IV

TREATMENT CONSIDERATIONS

The selection of the pharmacologic treatments for depression in neurological diseases continues to be based on the clinician's experience. All antidepressants are equally effective, and treatment efforts are oriented mainly to use the drug that will be safest for an individual patient. In the case of patients with neurological illnesses, this becomes more complex because they are more susceptible to the effects of psychoactive medications and display greater sensitivity due to blood brain-barrier alterations, physical changes associated with chronic illness (eg, malnutrition, pharmacokinetic changes associated with advanced age), and a greater risk of suicide. As a general rule, psychotropic medications are used with greater caution and at lower doses in patients with neurological diseases.

Generally, the tricyclic antidepressants (TCAs) are probably the most commonly used antidepressants in patients with neurological diseases. They may be especially useful in patients with significant insomnia or mild to moderate agitation. They are best tolerated by patients who are not significantly compromised by their underlying neurological disease. The TCAs decrease seizure threshold, especially clomipramine, Imipramine, amitriptyline, amoxapine, and maprotiline, and therefore their usé in patients with epilepsy should be avoided.29 If a TCA is required in this population, doxepin is thought to be relatively safé.30 Orthostatic hypotension may limit TCA use in debilitated patients or in patients with cerebrovascular insufficiency who may already have had a stroke. The anticholinergic effect of TCAs can aggravate the cognitive disorder of neurologically impaired individuals and/or precipitate delirium. In HIV/AIDS patients, the excessive drying of mucous membranes from anticholinergic effects may predispose them to develop or worsen oral candidiasis, and the more anticholinergic TCAs should be avoided. The anticholinergic effect may also worsen the movement disorder in patients with HD31 but may be beneficial for patients with PD.32 Doxepin has been reported to cause parkinsonism and should be avoided in PD patients.33 Amoxapine should also be avoided in PD patients due to its dopamine-blocking effect, which may worsen parkinsonian symptoms.

Table

TABLE 4Criteria for Clinical Diagnosis of HI V-1 -Associated Minor Cognitive/Motor Disorder*

TABLE 4

Criteria for Clinical Diagnosis of HI V-1 -Associated Minor Cognitive/Motor Disorder*

Monoamine oxidase inhibitors (MAOIs) are also very effective in treating depression in patients with neurological diseases. However, the dietary restrictions, potentially lifethreatening pharmacologic interactions, and the significant orthostasis associated with them may limit their use. Obviously, patients taking L-dopa or other dopamine agonists should not take MAOIs because of the possibility of precipitating a hypertensive crisis. Selegiline, a selective type B MAOI at low doses (10 mg/day), can be safely administered to patients taking L-dopa or other dopamine agonist, and may have an antidepressant effect even in low doses.34 At higher doses (20 mg/day) however, it is non-selective, and the same restrictions as with other MAOIs are mandatory. Moclobemide, a reversible MAOI type A, can be safely used, because it is free of pharmacologic interactions, even with tyramine-containing foods.35 Its major limitation is that it is not available in the United States, and patients have to get it from other countries. It is best not to use MAOIs in HIV-infected patients, because their nutritional status is often already compromised, and theoretically, MAOIs are incompatible with zidovudine, which has catechol-o-methyltransferase - inhibiting effects.36

The selective serotonin reuptake inhibitors (SSRIs) have become popular alternatives to the TCAs because they have fewer side effects and are easily titrated. However, pharmacodynamic and pharmacokinetic interactions are important. For example, blood levels of anticonvulsants need to be monitored to prevent toxicity. In PD patients who take the MAOI selegiline, the use of SSRIs should probably be avoided because a serotonin syndrome could be precipitated with this combination. Further study is required to determine if the increase in seizure threshold observed in animal studies37 is applicable to humans and to determine the safety of SSRIs in patients with PD, because there are conflicting reports about changes in the movement disorder with the use of fluoxetine.38,39

Other second-generation agents, such as bupropion, have improved PD symptoms, but in many PD patients, bupropion failed to improve the depressive symptoms.40 Patients on this medication are also at risk for developing psychotic symptoms or worsening dyskinesia, and therefore it should be used cautiously. Bupropion should be avoided in patients with epilepsy, although at the recommended doses of 150 mg or less per dose or 450 mg or less per day, it seems to carry no greater risk than other antidepressants. Because it has an activating effect, it may be beneficial for withdrawn or anhedonic patients. HrV-infected patients usually tolerate it well; however, their central nervous system pathology must be considered, because seizures can be precipitated or aggravated in these patients.40 Trazodone may be beneficial in demented patients with agitation,41 but at antidepressant doses, the risks due to orthostasis may outweigh the benefits.

Table

TABLE 5Criteria for Clinical Diagnosis of HI V-1 -Associated Dementia Complex*

TABLE 5

Criteria for Clinical Diagnosis of HI V-1 -Associated Dementia Complex*

Psychostimulants (methylphenidate and dextroamphetamine) have been tried in patients with PSD, PD, and neurotrauma. A single double-blind, placebo-controlled trial of dextroamphetamine demonstrated statistically significant gains in recovery of motor function without treatment-emergent side effects42 in stroke patients. Patients with PD have shown limited benefits from stimulants in both depression and movement disorders. Stimulants may be particularly useful in HIV-infected patients in whom TCAs are contraindicated or have been ineffective. Stimulants are also beneficial in HTV-infected patients who suffer from both depression and cognitive impairment/dementia. There is little experience with the use of psychostimulants in patients with other neurological diseases, and caution is recommended if used in these patients.

There are no reports of treatment of depression in neurologically ill patients using newer medications such as venlafaxine, nefazodone, and mirtazapine; however, these medications are probably safe and efficacious in this population.

Electroconvulsive therapy (ECT) is, in general, a safe and very effective treatment for depression. It is useful in treating seizures43 because it raises the seizure threshold. When ECT is used in the epileptic population, anticonvulsants should be continued through the treatment course, although a higher electrical dose will probably be required. The transitory decline in cognitive functioning with ECT may be even greater in patients who have dementia; however, even in these patients, the net effect on cognition may be one of improvement. In PD patients, both depression and movement disorder can respond to ECT.44 A decrease in dopaminergic drug dosage before the course of ECT may decrease the post-ECT confusion. In PSD, the treatment is also efficacious and has minimal complications. If patients become depressed immediately after the stroke, it is advisable to wait for a complete resolution of the cerebral edema and the return of the intracranial pressure to normal values.

CONCLUSIONS

Patients with neurological illnesses have a higher prevalence of depression and suicide than other patient populations as well as than the general population at large. Signs and symptoms of depression are now detected earlier, allowing prompt and more aggressive management of these potentially devastating complications in patients with neurological disease.

The treatment of the depressive disorders in patients with neurological illnesses should be individualized, and careful attention should be paid to the patient's psychiatric,neurocal,and general medical conditipn.Quantitative and qualitative improvements in function can be achieved with most antidepressant therapies. These pharmacologic interventions may help ameliorate the depression and remediate various neurobehavioral and motor abnormalities associated with the neurological disease.

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TABLE 1

Prevalence of Depression in Patients With Neurologic Diseases

TABLE 2

Depressive Disorders According to the DSM-IV

TABLE 3

Depressive Disorders Not Included in DSM-IV

TABLE 4

Criteria for Clinical Diagnosis of HI V-1 -Associated Minor Cognitive/Motor Disorder*

TABLE 5

Criteria for Clinical Diagnosis of HI V-1 -Associated Dementia Complex*

10.3928/0048-5713-19970501-09

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