Preventing And Treating Depression After Stroke
A recently published Cochrane review examined trials that looked at interventions to prevent depression after stroke. They found 12 trials that fulfilled the criteria for inclusion . None of the included drug trials indicated a prophylactic effect of antidepressant medication, compared to placebo. However, one trial of psychotherapy had a small but significant effect size.
Since that review was published, a more recent study has compared the effect of early versus late antidepressant treatment on a functional outcome measure in 62 stroke patients. They found that early, prophylactic treatment led to an enhanced functional outcomean effect that persisted over the two years of the study.
Treatment trials have indicated that SSRI treatments and other antidepressants are superior to placebo. There have also been small trials supporting the use of transcranial magnetic stimulation.
The Importance Of Movement
Exercise of all kinds can be vitally important for all PD patients, says Dr. Savica. Those who exercise a minimum of 2.5 hours a week significantly slow the decline in their quality of life compared to those who dont. Exercise has also been shown to play a big role in mood. People with PD who exercise more are less likely to experience anxiety or apathy than those who exercise less. Get moving with regular walking, water aerobics, Tai Chi, dance, Pilates, weight traininganything thats enjoyable enough to stick with it long term.
Bottom line: Yes, depression and anxiety are statistic likelihoods with Parkinsons psychosis, but your loved one is not a statistic, and you have options. Start with a call to their doctor to assess treatment options, then consider which therapies and lifestyle enhancements weve outlinedmaybe search for a gentle water-aerobics class or a weekly low-key lunch with friendsmight be doable. It may take trial and error, but there is a very real chance that better days are ahead.
Depression, Anxiety, and Psychosis:Movement Disorders Clinical Practice. Affective Correlates of Psychosis in Parkinsons Disease.
- Anxiety in PD:Frontiers in Neuroscience. Neuropsychiatric Disorders in Parkinsons Disease: What Do We Know About the Role of Dopaminergic and Non-dopaminergic Systems?
The Case Of Fluvoxamine Maleate
The role of serotonergic drugs in PD associated with depression has been receiving considerable attention amongst the research community . As a link between DA and the development of depression in patients with PD has been suggested, the pathophysiological features of both PD and depression have in common DA pathway dysfunction and depletion and/or 5-HT deficit . It has been suggested that an increase in serotonergic tone may indirectly influence DA function and may contribute to increased motor activity which is partially blocked by DA antagonists . Studies have shown that depression may be associated with an abnormal level of DA . As studies have also shown that brain regions affected by abnormal DA processing may also be affected when 5-HT is abnormally processed, we hypothesize that Fluvoxamine maleate treatment may play a role in improving the chemical imbalance caused by low levels of DA in the brain .
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Diagnosis Of Depression In Parkinsons Disease
Diagnosing depression in PD can be particularly difficult because of the clinical overlap between the two syndromes.
Symptoms that are common to both depression and idiopathic Parkinsons disease include motor slowing, bradyphrenia, sleep and appetite disturbance, weight loss, loss of interest and concentration, and reduced libido. The body language of depression looks similar to that of PD at first glance. The patient often appears hunched with a lack of an obvious affective response and spontaneity .
Symptoms that may help in the diagnosis of depression in people with PD include
pervasive low mood with diurnal variation
early morning wakening
pessimistic thoughts about the world, themselves, and the future
Table 1 lists the Diagnostic and statistical manual, 4th revision criteria for major depressive episode.
DSM-IV criteria for major depressive episode
Depression should be considered in any patient whose function deteriorates notably over a few days or weeks.
Differential diagnosis of depression in Parkinsons disease
A variety of mood disorders have been described in the setting of neurosurgery for PD. These include transient dysphoria during surgery . More chronic changes in mood have also been described following pallidotomy and deep brain stimulation although definitive studies have not been performed in this area.
Dopamine Hypothesis Of Depression
Dopamine is produced in the substantia nigra pars compacta in the midbrain. Dopaminergic projections in both the mesocortical and the mesolimbic systems are known to be disturbed by stress . Dopaminergic pathways are part of the reward system and the effects of chronic stress on reward perception that lead to depression can occur because of the interaction between the dopaminergic system and the HPA axis and between the dopaminergic system and the serotonergic system . Studies have demonstrated that early psychological stress that activates the HPA axis, exacerbates DA depletion and is associated with a decrease in DA synthesis in the brain . Auffret et al. and Leentjens, have shown that symptoms of depression can be improved by administration of DA agonists highlighting the possibility of antidepressant drugs to have an affinity to DA receptors. Since DA depletion may accompany depression, some antidepressant drugs may act on both dopaminergic and serotonergic systems to exert their antidepressant effect . Therefore, DA deficiency resulting from early life stress may in some instances predispose an individual to depression and eventually to neurodegenerative diseases such as PD.
Suicidal Behaviour In Ms
Suicidal ideation is very common in MS. In one study, a quarter of clinic attenders with MS had suicidal ideation sometime in the week before their attendance. Around 3% of people with MS will kill themselves. A study of the cause of death in 3000 people with MS over 16 years indicated that 15% of the deaths were recorded as suicide. Other studies have confirmed this increased risk and indicated that additional risk factors for suicide in MS include being male, young age of onset, previous history of depression, social isolation, and substance abuse. A study comparing MS patients with and without lifetime suicidal ideation could distinguish the groups by severity of depression, social isolation, and alcohol abuse. This study also noted that patients with suicidal ideation often were not in receipt of psychiatric evaluation.
The differential diagnosis of depression in MS includes adjustment disorders, paroxysmal changes in mood , and mood changes in relation to drugs for MS.
A number of drugs used to treat MS or its symptoms have been implicated as risk factors for low mood. There are case reports of steroid induced low mood in MS and other disorders. All the anti-spasticity drugs have been associated with low mood . There are also case reports of psychiatric changes following the abrupt discontinuation of baclofen and other anti-spasticity drugs. This means that history taking in respect to depression should include a detailed drug history.
How Does Alcohol Affect Parkinsons Medication
The interaction between Parkinsons medications and alcohol is a common topic on MyParkinsonsTeam. I miss my red wine and whiskey on occasion, one member wrote. I found that it just makes my meds stop working. Another member said, My husband has been told he shouldn’t drink with his meds.
I have to limit myself to one Scotch on the rocks now, a MyParkinsonsTeam member said. I used to have three or four, but the side effects are too bad. Another wrote, Never really a good idea to mix alcohol with meds.
Whether you decide to continue your current drinking habits, cut down, or eliminate alcohol altogether, its important to listen to your body and have open conversations about these topics with your neurologist.
If you find yourself drinking alcohol to cope with other issues, such as depression and anxiety, you may find that healthy practices such as physical activity can help. In addition, participating in activities such as tai chi, yoga, and meditation may help ease the symptoms and complications of PD.
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What The Research Says
Researchers believe that depression and anxiety in Parkinson’s are due to changes in brain chemistry that are caused by the disease itself. The same pathways that create dopamine in the brain which are impacted in PD also create the brain chemical serotonin, which regulates mood, appetite and sleep. Scientists think that the effect of Parkinson’s on serotonin, as well as other brain chemicals that support mood, is responsible for symptoms of depression and anxiety.
The Michael J. Fox Foundation actively pursues research that can shed light on the connection between mood changes and Parkinson’s and lead to treatment breakthroughs for people living with the disease. The MJFF-funded Study of Antidepressants in Parkinson’s Disease found that certain antidepressants eased depression in people with Parkinson’s without worsening movement symptoms. Still, more work remains to find more and better treatments for depression and anxiety. Researchers are looking at several different therapies: medications such as buspirone for anxiety, as well as cognitive behavioral therapy and non-invasive brain stimulation for both depression and anxiety. Join recruiting studies in your area through MJFF’s online tool Fox Trial Finder.
Depression In Parkinsons Disease
Diagnosis and management of depression in Parkinsons disease is important for two main reasons: firstly, depression is common in PD , and secondly depression causes significant morbidity in terms of quality of life, disability , and carer stress. This effect is independent from the effect of motor disability.
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Finding The Right Treatment
One hallmark of PD is the reduction of dopamine, the neurotransmitter involved in controlling movement, kidney function, sleep, motivation, learning, and pleasure. So a first-line treatment is dopamine agonists , medications that mimic the neurotransmitter’s actions and restore normal movement and mood. Over time, though, the same medicine that saved your loved ones life may cruelly turn on them. After many years, these drugs can cause hallucinations, paranoia, compulsion, and memory loss, says Dr. Savica. If so, he starts fresh with a whole new, non-DA drug regimen. There are a lot of ways we can tailor the treatment to the patient. Psychosis is not always an eventuality.
Depression and/or anxiety might be treated with antidepressants by the neurologist, but most doctors will also recommend talk therapy. Since symptoms of psychosis generally first appear between ages 55 and 65 and become more common in people ages 70+, its worthwhile finding a psychologist or psychiatrist who specializes in geriatrics, says Dr. Savica. In one study, PD patients who received cognitive-behavioral therapy by geriatric therapists experienced significantly less depression than those who didn’t. One caveat: Therapy wont help with psychosis symptoms, says Dr. Quinn, but it can help ease the associated depression and anxiety.
What Is Samhsas National Helpline
SAMHSAs National Helpline, , or TTY: is a confidential, free, 24-hour-a-day, 365-day-a-year, information service, in English and Spanish, for individuals and family members facing mental and/or substance use disorders. This service provides referrals to local treatment facilities, support groups, and community-based organizations. Callers can also order free publications and other information.
Also visit the online treatment locators.
Getting Help For Mood Changes
When a person with PD experiences mood changes, they may withdraw from seeking help. However, talking about symptoms with a healthcare professional helps create more of a sense of control and enables the doctor to better understand how PD is affecting the patient. Many treatment options are available to relieve mood disorders like depression and anxiety.1
Common Symptoms Of Drug
The motor features of PD are often very easy to see via a neurologic exam in a doctors office. Rest tremor for example, is seen in virtually no other illness and can therefore be very important in diagnosing PD. But there is one other common condition that induces the symptoms of PD, including a rest tremor, which must be considered every time PD is being considered as a diagnosis, and that is drug-induced parkinsonism.
Parkinsonism is not technically a diagnosis, but rather a set of symptoms including slowness, stiffness, rest tremor, and problems with walking and balance. This set of symptoms can be caused by PD, but also can occur as a side effect of certain prescription medications .
A number of medications can cause parkinsonism because they block the dopamine receptor and thereby mimic the symptoms of PD that are caused by loss of dopamine neurons in the brain. Reviewing a patients medications is therefore a critical step for a neurologist when seeing someone with parkinsonism. Anti-psychotics and anti-nausea treatments make up the bulk of the problematic medications, although there are other medications that can also cause parkinsonism. The primary treatment for this type of parkinsonism is weaning off of the offending medication, if possible.
How Does Depression Work
Depression is more than simply feeling sad. It’s a common condition that interferes with how you function in your everyday life, whether at home or work.
Why depression occurs in some people and not others remains unclear, although it’s likely that some combination of your DNA and environmental factor play a role.
One interesting theory relating to the development of depression in PD revolves around stress and the neurotransmitter dopamine.
We know that psychological stress activates your hypothalamic-pituitary-adrenal axis and that depression is associated with HPA-axis hyperactivity.
Activation of the HPA axis triggers the release of cortisol, which leads to all sorts of inflammatory and hormone changes in your body, including the possible lowering of dopamine production in your brain.
Since PD is also characterized by the loss of dopamine in the brain, experts believe that low dopamine levels from early life stress may make a person more vulnerable not only to depression but also eventually to PD. Even more, depression may be a risk factor for developing PD later on in life.
Identifying And Treating Depression
Between 17 to 50 percent of patients with Parkinsons have depression. Depression and Parkinsons have so many similar-looking symptoms that it is hard to tell the difference between them.
Its important to note, however, that depression is not a reaction to the disability. Rather, it seems to be related to the degeneration of specific neurons in Parkinsons disease itself.
Typical symptoms include:
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Symptoms Of Depression In Parkinsons Disease
The symptoms of depression in PD can be difficult to tease apart from the symptoms of PD itself.
For example, apathy, which is a lack of energy or interest in everyday activities, is a symptom of various mental health disorders, including depression. Apathy is also common in patients with PD, whether or not they have depression.
Fatigue is another common and disabling symptom of PD that may also occur with depression. The fatigue of PD can worsen underlying depression or vice versa, creating a vicious cycle that can be challenging to untangle and treat.
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Serotonin Hypothesis Of Depression
Serotonin is mainly produced in the dorsal raphe nucleus . Serotonin transporters take up released serotonin from the synaptic cleft into serotonergic neurons in a manner that helps to modulate various functions in the brain including mood and emotion . The striatum, the amygdala, and the prefrontal cortex are regions of the brain that are innervated by serotonergic neurons . These brain regions including the dorsal raphe nucleus which is part of the brains serotonergic system, are activated during early maternal stress . Abnormal 5-HT levels in these brain areas have been associated with depression . Pre-clinical and clinical studies have demonstrated that early life stress affects 5-HT levels in the brain and this may lead to depression . Selective serotonin re-uptake inhibitors are a class of antidepressant drugs commonly used to treat depression . SSRIs work by blocking 5-HT re-uptake thus increasing the availability of 5-HT in the synaptic cleft as well as its chance to bind to receptors in the post-synaptic membrane . Therefore, by restoring the levels of monoamines and their transporters in the brain, SSRIs drugs are appropriate treatments to address early life stress dysfunction that predisposes to depression later in life.
Read More About Parkinsons And Depression In Our Brochure
Parkinsons disease is generally considered a neurological disorder. However, because of the frequency of mood and other psychiatric complications, PD could also be considered as a neuropsychiatric disease. In fact, James Parkinson himself observed in 1817 that depression is commonly associated with PD.
Read more about depression and its connection to Parkinsons Disease here:
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Q: Is There Greater Awareness Now Of The Link Between Depression And Parkinsons Disease
A: Absolutely and thats a good-news story. Its stimulated an increased awareness about screening people with Parkinsons for depression. There has even been talk in the Parkinsons community about adding depression along with other nonmotor symptoms, like REM sleep behavior disorder to the diagnostic criteria. That would be huge.
Targeting Parkinsons-Linked Protein Could Neutralize 2 of the Diseases Causes
Researchers report they have discovered how two problem proteins known to cause Parkinsons disease are chemically linked, suggesting that someday, both could be neutralized by a single drug designed to target the link.
Environmental Toxins And Parkinsons Disease
Neuronal cell death in PD may also be triggered by exposure to toxic substances or environmental factors which precipitate the symptoms of the disease as they render the brain vulnerable to subsequent physiological chronic stress . The environmental cause of PD mainly refers to exposure to dopaminergic toxins 6-hydroxydopamine , 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine , paraquat and rotenone as these toxins are known to induce formation of reactive oxygen species and oxidative stress which may result in neuronal cell death .
DA is one of the common neurotransmitters present in most parts of the central nervous system . The mesocortical, mesolimbic, nigrostriatal and tubero-infundibular pathways are the four main pathways that play a key role in dopaminergic signaling . DA cannot cross the blood brain barrier, therefore, it is synthesized from tyrosine which is carried into the brain via amino acid transporters . At the dopaminergic neuron level, tyrosine is then converted into dihydroxyphenylalanine by tyrosine hydroxylase then finally into DA by aromatic L-amino acid decarboxylase . DA is then stored in the vesicle until an action potential allows the vesicle to be discharged into the synapse . Monoamine oxidase is the enzyme that is responsible for breaking down excess DA and is known to similarly act on 6-OHDA inducing oxidative stress resulting in apoptosis .
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