Post stroke depression


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A Teaching Project geared toward RN's role in assessing for Post- stroke Depression and

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  • Under Reported- Many stroke patients may not receive effective treatment because their mood disorder goes un-diagnosed. Many do not recognize the signs of PSD and instead attribute it to the grief process experienced from loss of function. It is difficult to determine the significance of abnormal mood in patients with stroke-related disability, and some studies have postulated that doctors may be reluctant to diagnose PSD due to thecontinued uncertainty about the balance of benefits and risks of antidepressants for stroke sufferers.However, depression is an important complication of stroke that may impede rehabilitation, recovery, quality of life, and caregiver health. Furthermore, stroke associated depression may reduce survival and increase the risks of recurrent vascular events. Caregiver Health- Depression worsens the stroke patient's quality of life and that of his or her family. Caregivers may experience negative impact in their own physical and emotional health when assuming the caregiver role. PSD also imposes a burden on healthcare services. Two studies have shown that, 1 and 3 years after the first hospitalization for stroke, PSD patients had more and lengthier inpatient stays and outpatient visits than non-depressed stroke patients.
  • Stroke recovery can be negatively affected by depression, especially major depression, because it can cause the stroke survivor to lose their motivation to recover and to become less compliant with their rehabilitation program.PSD may alsoincrease functional dependence; depressed stroke patients show a higher failure to return to previous work activities PSD has been linked to higher mortality at 1 year after stroke and afterwards
  • These are just some of the risk factors that contribute to the occurrence of PSD.A complex interaction between genetic and non-genetic factors likely plays an important role in PSD development, with individual genetic susceptibility being influenced by either environmental or biological factors (stress or stroke lesions), or both .Development and intensity of depressive symptoms seem to increase with the severity of functional impairment. Thus, depressive symptoms, particularly minor forms of PSD, may be the expression of the patient's strategy for coping with handicap.
  • DSM IV defines post-stroke major depression as "a mood disorder due to stroke with major depressive-like episodes". The DSM-IV criteria define minor depression for research purposes as the presence of one of the cardinal symptoms of depression for at least 2 weeks, in association with more than one but fewer than 3 additional symptoms of major depression. Cluster symptoms:Decreased energy, or a constant fatigue.Insomnia, decreased amounts of sleep, or sleeping too much.Loss of appetite, or a sudden increase, or decrease in weight.Problems concentrating, decision making, or memory loss.Worthless, helpless, or guilt feelings.Thoughts of death, or suicide, in extreme cases attempted suicide.Chronic aches, or pains that cannot be treated successfully.
  • Incidence- 10-50% of stroke survivors experience this form of PSD. Generally there is a recovery 2 years following the stroke event but the patient may suffer from reoccurrences.Etiologyand affect on Brain-It is hypothesized that the monamine pathways linking the brainstem to the cortex have been interrupted. This can affect the frontal lobe which contains most of the dopamine-sensitive neurons in the cerebral cortex. The dopamine system is associated with attention, long-term memory, planning, reward, and drive. It can also affect the executive functions of the frontal lobe which control the ability to recognize future consequences resulting from current actions and to choose between good and bad actions.The biological or psychological mechanisms we discussed may by themselves cause PSD, but more likely the two interact over the entire PSD risk period. Perhaps in the earliest stage after stroke the biological changes are more influential, tending to disappear as the brain heals, while the psychological factor may become more important later on, when the reality of life after the stroke sets in.Suicidal ideation has been mainly associated with this severeform of depression and the risk may remain high within the first 5 years after stroke. So when the RN is screening for depression, they should also be on the lookout for suicide risk expressed by indirect verbal cues and nonverbal behavior patterns.
  • A diagnosis of dysthymia rather than a depressive illness is made becauseeither there are not enough symptoms present to fulfill the diagnostic criteria for a depressive illness or the symptoms are not present for the majority of time but may come and go for a few days at a time.Dysthymia appears to respond differently to treatment compared to depressive illnesses.There is less evidence that psychotherapies work. Etiology- Not fully understood, DRD depression is thought to have no connection to the brain lesion’s location but more connected to the severity of the damage.Prevalence- Develops in 15-40 percent of post-stroke Response to treatment: Some studies indicate that antidepressants may be of some help, but it appears they can take months (rather than two to four weeks) to start working. As a result, a great deal of patience is called for on both the part of the patient and the doctor.People with dysthymia are at increased risk of also developing a full-blown depressive illness on top of their ongoing depressive symptoms. This is sometimes called 'double depression', meaning dysthymia plus a depressive illness.However, if dysthymia lasts past 2 years, this minor form has a greater chance of becoming a major depressive disorder.
  • To truly be signs of PSD, symptoms must be affecting their daily life and not just be passing in nature.
  • Complete adherence to criteria for major depression is not always possible in stroke patientsDiagnosis of PSD in stroke survivors may be hindered by a number of circumstances, including commonly occurring cognitive impairments such as aphasia, agnosia, apraxia and memory disturbances. The stroke itself may be the cause of poor concentration, psychomotor retardation, or lack of energy, sleep disturbances and loss of appetite, all of which also fit into the profile of depressive symptoms . Emotionalism, anosognosia (denial of the neurological deficient) or fatigue can also limit the patient's capacity to express or communicate depressive symptoms, making it hard to clearly understand what the patient is experiencing.
  • In light of understanding PSD’s diagnostic challenges, I thought it might be good to review the effect a stroke can have on the patient, depending on the site of damage. It is important to note that researchers have found no correlation between stroke site and prevalence of PSD.In our next slide we are going to talk about possible assessment tools that can aid nurses in identifying PSD. By taking a look at this diagram we see that both patients that suffer from left or right sided strokes can be difficult to assess.For example, a patient with right sided stroke may be experiencing memory deficits, so they may not be able to recall recent symptoms or even a previous struggle with depression.On the other hand a patient suffering from left sided stroke, may have the clarity of mind to describe the symptoms, but have trouble expressing it is words due to speech or language deficits.
  • So what are some tools we might use to screen a patient for PSD? I’ve listed a couple that have statistically been proven to be useful in the assessment process, though each has it’s limitations. Let’s take a look at them. The Hamilton Rating scale-The HDRS was mainly designed to monitor changes in depression severity over time in patients with a previous diagnosis of depression. Nevertheless,it has been shown to be sensitive enough to be used with thestroke population . There are two versions of this scale (14 and 21 items) and they emphasize somatic and behavioral symptoms of depression, while symptoms such as anhedonia, poor concentration and non- reactivity of mood are excluded. One advantage of the HDRS scale lies in its ability to identify depression in patients with pre-existing cognitive impairment. The Beck Depression Inventory-The advantages of the BDI test include a low reliance on somatic symptoms and the fact that it is simple, not very time consuming and requires no training to administer. On the other hand, one of its main limitations is a tendency to overestimate depressive symptoms in female stroke patients.Another limitation to point out is it can determine the existence of depression and is sensitive to variations in depressive disorder over time, but it is not useful for distinguishing between major and minor depression. IMPORTANT: PSD diagnosis depends primarily on clinical examination, which should be supplemented by objective data (selected scales) and subjective data (interview with the patient and/or family).Objective Data scalesObservation scales that offer reliable and valid assessment of post-stroke depression include the Clinical Global Impression Severity Scale (CGI-S) and the Signs of Depression Scale (SDSS). When assessing aphasic patients, RN’s can point to "yes" or "no" choices and record nonverbal responses. Involving family members and staff caregivers is an adaptive strategy for assessing depression even when aphasia is present.The CGI-S - requires clinicians to have psychiatric experience as they compare the individual being assessed with typical cases.The SDSS-initially developed as a tool for screening depression in elderly medical patients. SDSS is an easytocomplete tool specifically for nurses and caregivers to use in the assessment of post-stroke depression
  • It is currently recommended that patients be evaluated for depression in the first month after stroke and monitored at regular intervals afterwards, particularly those with risk factors associated with PSD development. ( Ask group what some of those risk factors were)Ideally, patient’s would be screened on each visit for changes in symptoms, giving health care staff a clear picture of what is going on with the patient and making it easier to identify PSD onset.Despite the challenge of aphasia and other cognitive impairments, early interviews with family members can help distinguish expected grief reactions from clinical depression. Completing self-report and observational scales at different times will offer data that can be used to measure the depression, as well as the stroke patient's response to treatment.
  • PSD symptoms can be long-lasting and may even continue for several years after stroke. In a study conducted byRobinson and coworkers, during their baseline assessment major depression was identified in almost a third of patients; of these, 60% were still depressed 1 year later. Minor depression was found on initial evaluation in a fifth of patients and persisted in 60% for 2 years afterwards *124 In order to accurately assess, the RN must be able to correctly interpret the patient’s responses and objective data he/she gathers. There are some symptoms that can be misinterpreted. On the next couple sides, we will take a look at a few RN’s commonly come across.
  • Apathy and depression are often confused. Sometimes apathy signals a depressed mood or is a sign ofpartially treated depression, whereas in other cases, it occurs in the absence of depression. Apathy is a motivational disorder characterized by emotional unconcern or indifference and loss of ability to initiate routine activities. In a study done in Sydney, Australia, apathy and depression were not correlated in 167 patients at 3 months after stroke. The study also found that apathy was associated with attention and processing speed deficits, whereas depression was associated with deficits in memory and executive function. (the ability to recognize future consequences resulting from current actions or the ability to choose between good and bad actions and degrees of better and best) The RN must carefully assess what the patient is subjectively reporting and differentiate apathy from depression. If you find this difficult to do , there are specific scales designed to distinguish depression from apathy.If apathy is the root cause, psychosocial therapy or counseling may be a treatment modality. If depression is the root, the patient may need to start an antidepressant.
  • Identifying distinctions among crying behaviors is an important aspect of assessing post-stroke depression. Although crying is an expected coping response, frequent and sustained bouts of crying can also be an indication of depression. Observing crying responses in relation to whether a motivating stimulus or trigger is present is a critical distinction. For example, when crying occurs while discussing loss experienced from the stoke, the behavior is a reflection of mood; there is an identifiable trigger. But when crying occurs frequently and continues for long periods of time, depression is likely present. Facial expressions and the presence of tears may be apparent in both mood and depressive crying, so it isn’t a definitive measure. But by assessing the congruence between crying and mood or affect of sadness, the RN will be able to better distinguish whether this is a symptom point towards a post-stroke depression diagnosis.Other crying behaviors, such as pathologic crying, emotionalism, and catastrophic reactions, are disorders of emotional expression rather than symptoms of a depressive mood disorder. Pathologic crying or laughing occurs without any triggering event and may be related to damage in the motor areas of the cerebral cortex and brainstem.Emotionalism occurs when the patient has difficulty controlling his emotional behavior and may suddenly start crying (or, less commonly, laughing) for no apparent reason; this may be related to damage in the right cerebral hemisphere.Catastrophic reactions are expressed when crying is accompanied by anxiety, aggressive behavior, swearing, or withdrawing and may be triggered by a task made difficult or impossible by a neurologic deficit, such as trying to move a hemiplegic hand. Pathologic crying, emotionalism, and catastrophic reactions often coexist with post-stroke depression, but they're separate conditions that require separate treatment approaches.
  • TreatmentAs we discussed earlier, a large numberof stroke survivors affected by depression remain without treatment because their condition goes unnoticed or treatment is considered unnecessary since depression is seen as a normal emotional reaction to the physical impairment induced by stroke.Antidepressant therapy- When treating elderly stroke patients, the health care team has to factor in the patient’s medical comorbidities and often, polypharmacy. The elderly population is particularly at risk for adverse side effects of antidepressant. Behavioral and Alternative methods are the preferredmethod of treatment for mild mood disorders, but can be used in conjunction with antidepressant therapy. Psychosocial therapy combined with antidepressant hasbeen shown to be moresuccessful in preventing recurrentdepression in older adults than medication alone or psychosocialtherapy.
  •  After post-stroke depression is determined to be present, other SSRI antidepressant medications, such as Prozac, Zoloft and Paxilhave been effective. An RN should consider with any drug therapy, dosages required to achieve therapeutic blood levels may be lower or even half the usual dose and may take time to titrate in patients who are medically ill. SSRI antidepressants may take longer to absorb, distribute, metabolize, and be eliminated. RN should watch for sign and symptoms of Serotonin Syndrome before administering.Selective serotonin reuptake inhibitors (SSRIs)First line medication choiceProzac:Dosage: For adults the treatment of depression and obsessive compulsive disorder, a dose of 20 mg/day, taken in the morning, is recommended as the initial dose. The maximum Prozac dose should not exceed 80 mg/day. Side Effects and Precautions: The most common side effects seen in people taking Prozac include anxiety, insomnia, drowsiness, headache, diarrhea and rash. Alcohol beverages should be avoided. Unless directed by a physician, Prozac should be avoided if patient is recovering form a heart attack or if they have liver disease or diabetes. Drug Interactions: Do no take Prozac while using an MAO inhibitors, it can cause serious life-threatening reactions. Must wait at least 14 days after stopping an MAOI before taking Prozac. Also, wait at least 5 weeks after stopping Prozac before taking an MAOI. Zoloft:Dosage: For adults the initial dose is 50 mg/day. Maximum dose is 200 mg/day. Side Effects and Precautions: Abdominal pain, agitation, anxiety, constipation, decreased sex drive, diarrhea, dizziness, headache, decreased appetite, insomnia and nausea. Alcoholic beverages should be avoided while taking Zoloft and over-the counter remedies should be used with caution. Drug Interactions: Do not use this drug while taking an MAO inhibitor. Paxil:Dosage: The usual starting does is 20 mg/day, taken as a single dose, usually in the morning. At intervals of at least 1 week, the physician may increase the dosage by 10 mg/day, up to a maximum of 50 mg/day. Side Effects and Precautions: Abnormal ejaculation, constipation, decreased appetite, decreased sex drive, diarrhea, dizziness, sleeplessness, nausea, weakness, and vertigo. Paxil should be used cautiously by people with a history of manic disorders and those with high pressure in the eyes (glaucoma). Paxil should be used cautiously with people that have a history of seizures. Alcohol beverages should be avoided. Drug Interactions: Paxil should never be taken with a MAOI or combined with thioridazine, or taken within 2 weeks of starting or stopping a MAOI. 
  •  Elavil:Dosage: The usual starting dosage is 75 mg/day divided into 2 or more smaller doses. The doses may be gradually increased to 150 mg/day. The total daily dose is generally never higher than 200 mg. Side Effects and Precautions: Rapid heartbeat, constipation, dry mouth, blurred vision, sedation, and confusion. Elavil should not be taken if recovering from a heart attack, unless directed by the physician. Alcohol beverages should be avoided. Elavil may be needed to be taken regularly for several weeks before it becomes full effective. A dosage should not be skipped. Drug Interactions:Elavil should not be taken with MAOIs Pamelor:Dosage: The usual starting dosage is 25 mg/day, 3 or 4 times per day. Doses above 150 mg/day are not recommended. Side Effects and Precautions: Anxiety blurred vision, confusion, dry mouth, heart attack, hallucinations, heart beat irregularities and high blood pressure. Pamelor must be taken regularly to be effective. Skipping doses is not recommended. Alcohol beverages should be avoided. Drug Interactions:Pamelor should not be taken with MAOIs. Ludiomil:Dosage: The recommended initial dose is 75mg daily 2 or 3 divided doses. The maximum recommended dose is 150 mg/day. Side Effects and Precautions: Stomach upset, loss of appetite, nausea, dizziness, blurred vision, low blood pressure. Alcohol beverages should be avoided. Ludiomil is usually not given to people with irregular heart beats or low blood pressure. Contraindicated in known or suspected seizure disorder. Drug Interactions:Ludiomil should not be taken with MAOIs 
  • Novel AntidepressantsWellbutrin:Dosage: No single dose of Wellbutrin should exceed 150 mg. The maximum recommended dosage is 450 mg/day. Side Effects and Precautions: Agitation, constipation, dizziness, dry mouth, and headache. Wellbutrin is associated with an increased risk of seizure. Alcohol beverages should be avoided. Drug Interactions: Do not take Wellbutrin with MAOIs or with any drug that lowers the seizure threshold. Effexor:Dosage: The usual starting dose of Effexor is 75 mg/day divided into 2 or 3 smaller doses. Maximum dose is 375 mg/day. Side Effects and Precautions: Abnormal ejaculation, anxiety, blurred vision, constipation, weight loss, and impotence. Alcohol beverages should be avoided. Drug Interactions: Do not take Effexor with a MAOI. Remeron:Dosage: The usual starting dose of Remeron is 15 mg taken before going to sleep. Maximum dosage is 45 mg/day. Side Effects and Precautions: Abnormal dreams and thinking, constipation, dizziness, dry mouth, flu-like symptoms, increased appetite, sleepiness, and weakness. Rameron makes some people drowsy or less alert, and may affect judgment and thinking. Alcohol beverages should be avoided. Drug Interactions: Never combine Remeron with a MAO Inhibitor.
  • Monoamine oxidase inhibitors (MAOIs) You can see that I’ve added a photo some wine and cheese. These are just a few of the foods that contain high levels of tyramine. Whenever a Doctor prescribes an MAOI, I encourage you to refer a patient for a dietary consult. The list of foods that can affect patients branches into cheese (except for cottage cheese or cream cheese), chocolate (excessive amounts), dry sausage, fava bean pods, liver, meat extract, pickeled herring, sauerkraut, yeast extract, and yogurt.Nardil:Dosage: The usual starting dose is 15 mg 3 times a day. Maximum does is 90 mg/day. Side Effects and Precautions: Constipation, dizziness, dry mouth, headache, liver problems, sexual problems, sleep disturbances, weight gain, and water retention. Taking Nardil with the following food or beverages can cause serious, potentially fatal, high blood pressure. Avoid: Alcohol beverages, caffeine (excessive amounts) , foods high in tyramine. Drug Interactions: All other antidepressants, other MAOIs, amphetamines, nasal decongestants, asthma inhalants, appetite suppressants. Marplan:Dosage: Recommended initial dosage is 10 mg twice daily. Caution is indicated in patients or whom dose of 40 mg/day is exceeded. Side Effects and Precautions: Dizziness, tiredness, problems sleeping, constipation, and dry mouth. Marplan could cause an attack of extremely high blood pressure, which may be fatal. Avoid foods high in tyramine. Drug Interactions: All other antidepressants, other MAOIs, appetite suppressants, and antihistamines. Parnate:Dosage: The usual dosage for Parnate is 30 mg/day. Maximum dose is 60 mg/day. Side Effects and Precautions: Blood disorders, diarrhea, drowsiness, dry mouth, insomnia, muscle spasm, rapid or irregular heartbeat, water retention, and weakness. The most dangerous reaction to parnate is a surge in blood pressure, which sometimes has been fatal. Avoid foods high in tyramine. Drug Interactions: Avoid other MAOIs, other antidepressants, amphetamines, and antihistamines.
  • Cognitive therapy- is a structured approach requiring trained health professionals that focuseson the environment, behavior and cognition and is based on the principle that certain trains of thought lead to certain mood states. In therapy, patients learn how to challenge dysfunctional thoughts or beliefs that are associatedwith low mood and to collaboratively establish more functionalthoughts or beliefs. Patients suffering from either aphasia or cognitive impairments are not well suited for this therapy. ProblemSolving Therapy- focuses on systematically teaching individuals skills that will improve their ability to deal with their own specific everyday problems.Psychosocial behavioral intervention-One program implemented by a nurse involved giving participants written stroke recovery materials from the American Stroke Association, including information about depression, and meeting with a study interventionist once a week for 8 weeks. Participants completed a medication diary and were encouraged to include family members and caregivers in the meetings. The intervention, in combination with antidepressants, reduced post-stroke depression significantly and the effect was sustained for up to 2 years.
  • RN’s should askpatients, if they are able to speak , to describe situations in which they've tackled overwhelming challenges in the past. This can give the RN insight into what kinds of coping mechanisms the patient values and has experience using. The RN should also ask family members to describe how the stroke patient coped with previous difficulties.Assessment of previous coping strategies should also include askingabout previous responses to loss and typical expressions of anger and anxiety, as well as patterns of crying. This can help the RN determine if the response post-stroke is abnormal for this patient. Also the RN should take a detailed history that includes previous episodes of depression. By assessing previous psychiatric history, including treatments that worked and those that didn't, a nurse can gather the necessary information the health care team needs develop an individualized plan. Other methods worth mentioning include:Repetitive transcranial magnetic stimulation-a noninvasive method of triggering brain activity by exciting neurons with electromagnetic induction-may be an effective and safe alternative for stroke survivors who don't respond to antidepressants. Music Therapy-Listening to music during the early post-stroke stage can enhance cognitive recovery and prevent negative mood. Music therapy 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. Acupuncture - shows promise in treating post-stroke depression with fewer adverse reactions than antidepressants.
  • This integrated clinical approach should be routinely available for stroke patients to reduce the considerable negative personal and social consequences of PSD.
  • The desired outcome of PSD treatment is an empowered patient participating in their recovery process!
  • Slide 12Body diagram of stroke Slide 28 Stroke survivor t-shirt
  • Post stroke depression

    1. 1. Post-Stroke Depression:<br />A Nurses Guide<br />Presented by Rachel Lambert <br />
    2. 2. Objectives<br />RN will understand the prevalence, roadblocks and importance of identifying PSD<br />RN will be able to identify the risk factors and signs and symptoms of PSD<br />RN will be familiar with the assessment tools used in identifying PSD<br />RN will be familiar with treatments to combat PSD<br />
    3. 3. Who does PSD affect?<br />1 out of every 3 post-stroke patients<br />Largely under-reported<br />If not treated PSD can affect<br />Rehabilitation<br />Recovery<br />Quality of Life<br />Caregiver health<br />Survival <br />Health Care System <br />
    4. 4. Effect of PSD on Recovery<br />Depression may jeopardize a patient’s ability to meet functional goals and to reintegrate into society<br />The incidence of complications (e.g., skin breakdown, urinary tract infections), hospital length of stay, and medical costs expenses may all increase because of depression.<br />PSD has been linked with higher mortality rate<br />
    5. 5. Risk Factors for Post Stroke Depression<br />Female gender <br />Age 60 or younger <br />Divorced <br />Alcoholism <br />Non-fluent aphasia <br />Having a major motor or cognitive deficit<br />Nursing- home/Rehab placement<br />Lack of Social Support <br />
    6. 6. Types of Post-Stroke Depression<br />Major Depressive Disorder<br />Dysthymic Reactive Depression<br />
    7. 7. Diagnostic Criteria for Major Depressive Disorder<br />At least one cardinal symptom :<br />low mood or diminished interest in almost all activities plus<br />three or four cluster symptoms for a minimum total of five symptoms. <br />Both the cluster and cardinal symptoms should be present for at least 2 weeks and denote a change from a previous functioning condition.<br />
    8. 8. Major Depression<br />Incidence and Recovery<br />Etiology<br />Effect on Brain Function<br />Suicidal Ideation<br />
    9. 9. Dysthymic Depression<br />Prevalence<br />Duration of two years<br />Response to treatment<br />Antidepressants<br />Risk of double depression<br />
    10. 10. Sign and Symptoms of PSD<br />Significant lack of energy<br />Lack of motivation<br />Problems concentrating<br />Difficulty finding enjoyment in anything<br />Sleep disturbances<br />
    11. 11. Why does PSD often go undiagnosed?<br />Diagnosis of PSD is challenging in the acute and chronic aftermath of stroke<br />Stroke symptoms can mask depression symptoms making it hard to distinguish the root of the impairments a patient is experiencing<br />
    12. 12. Stroke Impairments<br />
    13. 13. What are some tools to Identify PSD?<br />Self –report scales<br /><ul><li>Hamilton Rating Scale for Depression</li></ul><br />Beck Depression Inventory<br /><br />Objective Data Scales:<br /><ul><li>Clinical Global Impression Severity Scale (CGI-S)
    14. 14. Signs of Depression Scale (SDSS)</li></li></ul><li> Timing of Evaluation<br /> Evaluation should occur the first month following a stroke<br /> Patients should be monitored at regular intervals, depending on risk factors and presenting symptoms<br /> Families should be included in the evaluation process<br />
    15. 15. Onset of PSD<br />Occurs in all phases of stroke recovery<br />Peak incidence and severity of depression occur between 6 months and 2 years after stroke <br />
    16. 16. Apathy vs. Depression<br />Apathy is a motivational disorder that can occur in the presence or absence of depression<br />Apathy associated with attention and processing Speed deficits<br />Depression associated with memory and executive function issues<br />By understanding the differences, the proper intervention can be determined<br />
    17. 17. Crying Behaviors<br />Identifying distinctions among crying behaviors is an important aspect of assessing post-stroke <br /> RN must be able to distinguish crying that's congruent with a mood of sadness from other crying behaviors<br />Pathologic crying , Emotionalism, Catastrophic Reactions<br />
    18. 18. Treatment<br />Treatments that have been proven to be effective include: <br />Antidepressant medications<br />Behavioral therapy <br />Alternative therapy<br />
    19. 19. Selective Serotonin reuptake Inhibitors (SSRIs)<br />First line medication choice<br />Dosage/Side Effects/ Drug Interactions<br /><ul><li>Prozac
    20. 20. Zoloft
    21. 21. Paxil</li></li></ul><li>Tricyclic and Teracyclic Antidepressants<br /> Dosage/Side Effects/Drug Interactions<br />TCA’s<br />Elavil<br />Pamelor<br />Ludiomil<br />
    22. 22. Novel Antidepressants<br />Dosage/Side Effects/Drug Interactions<br />Wellbutrin<br />Effexor<br />Remeron<br />
    23. 23. MAOI Inhibitors<br />Monoamine oxidase inhibitors (MAOIs)<br />Dosage/Side Effects/Drug Interactions<br />Nardil<br />Marplan<br />Parnate<br />
    24. 24. Behavioral Therapy<br />Cognitive therapy<br /> thoughts lead to moods<br />Problem-solving therapy<br />mental health professionals meet with stroke survivors to facilitate awareness of problems and help develop solutions<br />Psychosocial behavioral intervention<br />stroke survivors are provided with opportunities to interact with educational materials and interventionists<br />
    25. 25. Alternative Therapy<br />Utilizing pre-existing coping techniques<br />Repetitive Transcranial Magnetic Stimulation<br />Music Therapy<br />Acupuncture<br />
    26. 26. RN’s Role<br />A multidisciplinary health team is essential in PSD screening, diagnosis, treatment, monitoring and prevention of potential complications. <br />RN plays an important role in <br />Identifying risk factors<br /> Effectively Screening Patients <br />Educating patients and their families on treatment options to combat PSD<br />
    27. 27. Nursing Considerations<br />A post-stroke patient may need spiritual support, counseling with a provider who has experience with the diagnoses, and support groups<br />Providing resources including printed materials, websites, and organizations is helpful for the patient and family members<br />Assess the patient’s and family’s perception of the diagnoses, and coping mechanisms<br />
    28. 28. Nursing Considerations<br />If the patient is intubated and unable to speak, identify alternative methods of communication<br />Review prescribed medications (antidepressants) with patient and /or family members e.g. side effects and dosages<br />Encourage patient and family to prioritize needs and learn to accept help<br />
    29. 29. Desired outcome<br /> An empowered patient able to participate in their recovery process!<br />
    30. 30. References<br />Brodaty, H Sachdev, P Withall A, Altendorf, A Valenzuela , MJ Lorentz, L. “Frequency and clinical, neuropsychological and neuroimaging correlates of apathy following stroke - the Sydney Stroke Study.” Psychol. Med. 35(12), 1707-1716 (2005).<br />“Depression Trumps Recovery “-Excerpted and adapted from "Depression Trumps Recovery," appearing in Stroke Connection Magazine September/October 2003. (Science update May2008)<br />Fralick-Ball, Susan. “Post-stroke depression: early assessment and interventions can promote optimal recovery.” ADVANCE Newsmagazines<br />Gaete, J and Bogousslavsky, J. "Post-stroke depression." Expert Review of Neurotherapeutics 8.1 2008 Jan: 75-92. Academic OneFile. Web. 15 Jan. 2011. <br />Hackett, M. L., et. al. “Management of Depression after Stroke; A Systematic Review of Pharmacologic Therapies.“ Stroke; 2005 May;36:1092-1097.<br />Lökk, Johan Delbari, A . “Management of depression in elderly stroke patients .“ Neuropsychiatric Disease and Treatment 2010:6 539–549<br />Melrose, Sheley PhD, RN. ”How to uncover post-stroke depression.” Nursing Made Incredibly Easy! 2010 July/Aug; 8 (4):31 - 37.<br />Mitchell ,PH Veith, RC Becker, KJ Buzaitis, A Cain, KC Fruin,M et al. “Brief psychosocial-behavioral intervention with antidepressant reduces poststroke depression significantly more than usual care with antidepressant: living well with stroke: randomized, controlled trial.” Stroke 2009;40:3073-8.<br />Paolucci, Stefano. “Epidemiology and treatment of post-stroke depression.” Neuropsychiatric Disease Treatment. 2008 February; 4(1): 145–154. Published online 2008 February. PMCID: PMC2515899<br />Stradling, Dana RN, BSN, CNRN. September 25, 2009 .“Stroke and depression: continuing education course for the RN.”Published online 2009 September .<br />