Post-Stroke Depression

Early assessment and interventions can promote optimal recovery.
By Susan Fralick-Ball, PsyD, MSN, CH

As sequelae to a right-sided or left-sided (ischemic) stroke, occurring in both the young and old, post-stroke depression (PSD) is a real and present danger to optimal stroke recovery. In the U.S., there are over 700,000 strokes annually, at a rehabilitation cost of over $58 billion dollars. Making the most of full physical and mental health recovery needs to be at the core of stroke treatment.

PSD remains recognized, yet under-diagnosed and under-treated. Many in our population do not know or recognize the signs of stroke or depression in themselves or others, thus possibly leading to overwhelmingly negative outcomes of brain events.

Various experts agree there are two forms of PSD: major endogenous, psychotic depression and minor, dysthymic reactive depression. With endogenous PSD, the monoamine pathways linking the brain stem to the cortex - and frontal lobe executive functioning - have been interrupted. Ten to 50 percent of stroke survivors experience this form of major PSD. Generally, there is full recovery from the depression in 1-2 years following the traumatic stroke event.

Dysthymic reactive depression has no connection to brain lesion locus and becomes apparent in 15-40 percent of post-stroke clients, with varying degrees of recovery over the subsequent 2 years. If depression reduction does not occur within the first few years, the minor form of PSD can become a major depressive disorder, necessitating longer-term medical and psychological treatment to help alleviate the symptoms of this devastating form of depression.

Symptoms

Typical symptoms of depression include a sense of hopelessness that disrupts one's ability to function, sleep disturbances, radical changes in eating patterns, lethargy, social withdrawal, irritability, fatigue and lowered self-esteem that leads to the sense of uselessness. Suicidal thoughts may ensue. In PSD, these signs can result from vascular changes and psychological reactions to disability and often are provoked by the lesion.

The neurophysiology of stroke indicates a probable disruption of amine-containing pathways by stroke lesion. Noradrenergic and serotonergic cell bodies in the brain stem (locus coeruleus and midline raphe nucleus of lower pons and medulla, respectively) send messages through the medial forebrain to frontal cortex for interpretation and executive orchestration.

Depression may be caused by depletion of total available norepinephrine and/or serotonin, or interference with receptor sites. Agitation, confusion, tremor, myoclonus and hyperthermia may result as a serotonin syndrome emerges post-stroke. Serotonin syndrome is a triad of rapid-onset cognitive, autonomic and somatic toxic effects ranging from mild to life-threatening after administration of therapeutic dosages of serotonin and/or concomitant medications.

Signs and symptoms include mental confusion, hypomania, hallucinations, agitation, headache, coma, shivering, sweating, hyperthermia (>104° F), hypertension, tachycardia, nausea, diarrhea, muscle twitching, hyperreflexia and tremor. Other manifestations include metabolic acidosis, rhabdomyolysis, seizures, renal failure and disseminated intravascular coagulation (DIC) secondary to the hyperthermia.

Serotonin antagonists and stoppage of the serotonin medication must be instituted immediately when this syndrome occurs. Benzodiazepines are indicated to control agitation. Antipyretics are not indicated since the increased body temperature is due to muscular activity, not a temperature set-point abnormality. Direct-acting sympathomimetics (e.g., epinephrine, etc.) may be needed to counter the autonomic symptoms. Serotonin syndrome differs from neuroleptic malignant syndrome in subtle ways, yet classic differential includes hyperkinesias and clonus for serotonin syndrome and bradykinesia with "lead pipe" rigidity for neuroleptic malignant syndrome.

Lasting Effects

Severe PSD may eventually involve physiological changes, e.g., diurnal mood variation, early morning waking and loss of appetite.

Differences in the presentation of PSD appear when considering right-sided versus left-sided lesions. The lasting psychological effects following a brain event in the right hemisphere include significant variance from the person's normal emotional output and relative lack of control. Many of the lesions to the right frontal and parietal lobes leave impairments for recognizing emotions expressed through tone of voice, identification of facial expressions, and difficulty expressing emotion through facial movements, as well as anhedonia (severe lack of interest in people/interests).

Cerebral ischemia leads to decrease in acetylcholine release, which may cause many of the post-stroke behavioral changes. Mania and hypomanic reactive responses are more common with right-sided versus left-sided lesions.

Patients with right-sided stroke lesions become desocialized. This often is the beginning of strain on social contact and communication. A family history of psychiatric disorders or having had a previous left-sided stroke increases the risk of PSD in right-sided stroke patients.

Left-sided lesions in the frontal or basal ganglia areas (putamen and/or caudate nucleus) often result in major depression. An increased catastrophic response is thought to be due to an inability to up-regulate serotonin receptors since serotonin binding is greater on the right. Vascular lesions also may interfere with serotonin transduction throughout the brain.

It also is possible to classify depressive symptoms post-stroke into direct and indirect cause-and-effect responses. Indicators for reactional depression include:
• aphasia;
• amnesia and cognitive impairments;
• anosognosia (denial of disability);
• denial of depressive signs;
• aprosodia (poor speech comprehension);
• catastrophic reaction;
• neurological apathy syndromes (e.g., frontal lobe syndrome);
• dementia.

Often, the signs of PSD are clinically similar to the depression associated with dementia of the Alzheimer's type.
Indirect symptoms are linked to factors common to many severely ill, hospitalized or stroke patients: controlled appetite due to tube feedings or dysphagia, frequent awakenings with a total poor sleep pattern, significant time in bed or being relatively immobile, delirium, or speech disruptions. Many of these post-stroke outcomes severely hamper the effectiveness of physical, occupational, speech/language and psychological therapies.

PSD related to lesion location can be characterized by the following:
• Bilateral lesions in the anterior frontal and temporal lobes and caudate nucleus are associated with increased risk of PSD.
• Left basal ganglia lesions at the head of dorsolateral caudate result in apathy and poor initiation.
• Incidence and severity of PSD increase with close proximity to left frontal pole lesions.
• Emotion-related processing impairments are greater with right hemisphere and frontal lobe lesions, since they serve emotional communication.
• Frontal lobe anterior and middle cerebral artery lesions result in apathy.
• Left anterior subcortical lesions show greater incidence of PSD than on the right side.
• When lesions are within 40 percent of either frontal pole, the PSD rate is 60 percent or greater.

Cerebrovascular disease also is found concomitantly with cardiovascular disease. When adding the co-condition of depression, the mood disorder is found both independently and additively when both heart disease and brain injury occur.

For many years, experts have recognized the incidence of depression following myocardial infarction, cardiac valvular disease, hypertension and dysrhythmias. Depression also remains an enduring predictor of post-cardiac incident morbidity and mortality, often severely affecting rehabilitation, return to sexual function and adherence to therapeutic regimen. With the advent of selective serotonin reuptake inhibitors (SSRIs) for the treatment of depression, there has been increased use of this treatment that features relatively few cardiac side effects.

Women, Stress & PSD

Additionally, women's response to stress and PSD differs from men's. Women carry a higher stroke burden than the men, both because women have a longer life expectancy - and strokes occur at late ages for many women - and because most stroke deaths occur in women. Women ages 45-54, while continuing to be active mothers, employees, spouses, possible grandmothers and/or caretakers for older parents, are twice as likely as men in the same age bracket to have strokes.

Differences between the sexes in relation to stroke are increasingly being recognized. For example, among stroke survivors, women tend to have worse outcomes than men due to more-severe pre- and post-stroke disability, and an increased likelihood of post-stroke institutionalization and loss of independence for women.

Being female raises more questions regarding the occurrence of PSD:
• Is pre-stroke depression already in place (with depression nearly twice as prevalent in women than men)?
• Has there been an extremely erratic or sudden loss of estrogen during menopause?
• During menopause, have sleep issues contributed to depression?
• Have general social issues and stress contributed to depression?

Since female communication and language systems in the brain are more cross-hemispherically connected, they often suffer significant speech/language deficits during stroke, resulting in reactive PSD. Women also have been lax in noting and reporting initial symptoms of stroke when emergency treatment can be initiated to limit the type and amount of stroke sequelae.

Psychotherapy

Treatment of PSD includes psychotherapy, medication and time from insult. As of our current assessment, only one-third to less than one-half of all post-stroke patients are adequately treated for depression.

Assessment of symptoms is problematic since there is no gold standard for diagnosis after recent stroke; however, rating scales are available and help with initial and ongoing evaluation of symptoms (Hamilton Rating Scale for Depression, Beck Depression Inventory, etc.) According to the Diagnostic and Statistical Manual, Version IV (DSM-IV), major depressive disorder often is used to describe PSD if five or more symptoms of depression are present for 2 or more weeks. Treatment of PSD also improves cognitive impairments or limitations imposed by stroke, e.g., orientation, memory, language and hand-eye coordination.

Both individual and group psychotherapy help the post-stroke patient regain emotional control and adjust to the loss of function and compromised self-image/self-esteem. The mode of therapy can be adapted to encompass any present cognitive and language deficits. Cognitive-behavioral, interpersonal, psychodynamic and eclectic forms of psychotherapy have been successful to alleviate or subdue many of the PSD symptoms. Inpatient and outpatient patient stroke groups, spousal support groups and discharge support groups are paramount to a smooth transition from hospital to rehab to aftercare venues, whether in long-term communal care or return to home.

Antidepressants

Antidepressants and psychostimulants often are the key medications used to help the post-stroke individual through recovery from depression. Psychostimulants may be useful for reducing the negative effects of PSD, e.g., anhedonia, and promoting return of executive functioning, such as organization, goal setting and achievement, initiating activities and self-monitoring. A combination of methylphenidate and Prozac during the early stroke recovery period can dramatically improve mood, apathy and initiation by 50-82 percent.
Antidepressants from the classifications of tricyclics, SSRIs and newer atypical groups are used, according to the symptoms demonstrated by individual patients. Antidepressants are frequently prescribed for 1 year post-stroke; stopping medications before 1 year lends to vulnerability of developing another depressive episode.

Of course, individuation is always considered. When medication is indicated, most patients are advised to stay with a particular medication regimen for a minimum of 6 months, with reevaluation throughout the trial period.

Tricyclics improve ADL function, improve appetite, lift general symptoms of depression and can help with insomnia, yet unfortunate anticholinergic side effects, especially in elderly stroke patients (dry mouth, dry eye, lowered GI motility, sedation, syncope, dysrhythmias, delirium) may cause discontinuation of this class of medication. SSRIs and the atypical antidepressants target serotonin and/or norepinephrine reuptake. Elevation of mood and improvement of depressive symptoms as rated on various depression rating scales frequently takes a minimum of 3-6 weeks and can take several months post-stroke. The addition of talk-based therapy during this time is highly encouraged.

Less traditional forms of assistance to lower the effects of PSD include music therapy, which tends to increase the production of dopamine to suppress aversive symptoms and pain; increases cross-hemispheric connectivity to music and lyrics; and enhances alertness, motivation, reward, attentiveness and executive functioning. Following middle cerebral artery stroke, brain plasticity and the laying down of renewed neural networks may be boosted. Music also has been demonstrated to modulate emotional arousal and decrease cortisol levels with respect to negative cardiovascular activity.

In summary, the goals and interventions for the care of a patient with PSD include the following:
• Act quickly to encourage the patient or family members to report stroke and symptoms of depression.
• Educate the patient and family about the symptoms, prevalence and treatment of PSD.
• If depressive symptoms persist and interfere with the patient's ability to function, treatment should be initiated.
• Treat with medication and therapy for optimal relief from PSD.
• Obtain baseline and serial depressive symptom ratings throughout treatment.

Susan Fralick-Ball is the owner of PsychMedEd, Blue Bell, PA.
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