Pseudobulbar affect in Parkinson’s disease
Reviewed by Pseudobulbar affect (PBA) in Parkinson’s disease is a condition that causes sudden, involuntary, and exaggerated laughing and crying outbursts that may not match how the affected person typically feels in that moment. Examples are crying intensely when feeling only slightly sad or laughing uncontrollably without feeling happy.
The condition occurs when a nervous system disorder disrupts the brain networks that normally keep emotional responses in check. There may also be alterations in chemicals in the brain that contribute to the condition’s development. Such alterations, which may disrupt brain signaling, may make it harder to regulate emotional expressions such as laughing or crying, triggering uncontrollable PBA episodes.
PBA outbursts are sudden, brief — typically lasting seconds to minutes — and can occur multiple times daily. There is evidence that crying is a more common sign of PBA than laughing. These outbursts can occur at any time, with the affected person’s mood appearing normal between episodes. The condition is easily misdiagnosed as depression or bipolar disorder because outward emotional displays are mistaken for a mood disorder rather than a loss of emotional motor control.
PBA is one of several nonmotor symptoms of Parkinson’s, affecting emotional expression rather than movement.
Distinguishing PBA from depression
PBA in Parkinson’s can be mistaken for depression, because both can involve frequent crying or emotional outbursts. One key difference lies in the pattern of outbursts. PBA outbursts are brief and sudden, while depressive episodes involve a sustained low mood lasting for at least two weeks, with other associated symptoms that can significantly affect a person’s daily life.
Importantly, PBA in Parkinson’s is a disorder of emotional expression rather than emotional feeling. This means that the outward display of laughing or crying does not match what the person is actually feeling inside, or is far more intense than what the individual actually feels. Depression, by contrast, is a mood disorder in which people’s inner feelings align with their outward mood, persistently affecting their overall emotional state and daily functioning over a longer period, of at least two weeks or more.
Another important marker is that PBA itself does not cause somatic — meaning physical or neurovegetative — symptoms. People with depression may experience changes in sleep, appetite, energy levels, and concentration. However, a person with PBA alone does not experience these physical symptoms. Importantly, however, PBA, Parkinson’s, or co-occurring depression can still cause changes in sleep and energy for some people.
Despite these differences, the two conditions frequently co-occur. Studies show that people with a history of depression or those taking antidepressants often score higher on PBA screening tests, partly because both conditions share similar brain pathways and because PBA is often initially misdiagnosed as depression. Similarly, a screening study in an outpatient mental health clinic found that a large proportion of people with depression, bipolar disorder, and schizophrenia scored positive on PBA screening tests, highlighting how easily emotional issues due to psychiatric conditions can overlap with PBA symptoms.
This overlap is why screening tools matter. The Center for Neurologic Study-Lability Scale (CNS-LS) is a popular seven-item questionnaire that helps identify and measure the severity of PBA symptoms, giving doctors a clearer starting point to tell PBA apart from depression. Another screening tool is the Pathological Laughter and Crying Scale, which consists of an 18-question interviewer-administered assessment used by clinicians to measure emotional outbursts.
The following table details some of the main distinctions that differentiate PBA versus depression in Parkinson’s.
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| Feature | PBA | Depression |
|---|---|---|
| Underlying nature | A disorder of emotional expression, not emotional experience | A mood disorder affecting overall emotional state |
| Episode duration | Brief, sudden outbursts, lasting seconds to minutes | Sustained low mood lasting at least two weeks or longer |
| Link to inner feeling | Outward laughing or crying doesn’t match what the person actually feels inside | Outward mood generally reflects inner emotional state |
| Somatic/vegetative symptoms | Usually absent when PBA occurs alone | Changes in sleep, appetite, energy, and concentration are common |
| Voluntary control | Only partially controllable | Not applicable (Represents an overall mood state rather than a sudden physical action or outburst) |
| Underlying cause | Neurological damage or disease, such as Parkinson’s, stroke, traumatic brain injury, multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer’s | Changes in brain chemicals caused by Parkinson’s, along with psychological factors |
What causes PBA in Parkinson’s?
PBA is thought to develop when Parkinson’s affects brain networks involved in controlling emotional expression. This can occur because, in Parkinson’s, certain nerve cells in the brain break down and die. However, scientists do not yet know the exact way in which Parkinson’s causes PBA.
Some researchers believe that PBA stems from damage to the cortico-ponto-cerebellar circuit. This pathway links several important parts of the brain, including the frontal cortex, brainstem, and cerebellum, which help regulate emotional expression.
Normally, this circuit allows the cerebellum to regulate laughing and crying behaviors (emotional expressions), ensuring that they fit the situation. When Parkinson’s or another neurological condition disrupts these connections, the brain may have more difficulty regulating emotional expressions.
Changes in the transmission of brain signals, including signaling involving brain chemicals such as serotonin and glutamate, may also contribute to PBA, although researchers do not yet fully understand their role.
Research suggests a correlation between PBA and altered levels of certain brain chemicals. These include lower levels of serotonin, dopamine, and norepinephrine, along with higher levels of glutamate, in the brain. Because these chemicals carry signals across the brain, an imbalance may make it harder for the brain to keep emotional responses in check.
In Parkinson’s, PBA outbursts can also align with medication timing. Some people notice sudden crying or laughing when the effect of levodopa medication wears off. However, this same wearing off can also cause genuine mood changes, leading to outbursts that actually reflect a person’s underlying emotional state.
How common is PBA in people with Parkinson’s?
Estimates of PBA in Parkinson’s vary widely depending on the screening tool and diagnostic threshold used.
A recent study of 100 people with Parkinson’s employed the CNS-LS questionnaire, which measures the frequency and severity of crying or laughing episodes. Using a standard cutoff score of 13 or higher as indicating PBA symptoms, 41% of patients screened positive. Given a stricter threshold of 17 or higher, which better filters out general mood disorders, about 21% screened positive for PBA symptoms.
Still, an earlier study found that 26% of people with Parkinson’s screened positive for PBA symptoms using a CNS-LS cutoff of 13.
These wide ranges support some concerns that PBA may be underreported and underdiagnosed. Researchers speculate that some clinicians downplay emotional or emotion-like symptoms of Parkinson’s, perhaps due to stigma around mental illness and/or the perception that the disease’s motor symptoms require more urgent and intensive care.
Diagnosis and medical treatments for PBA
Diagnosing PBA starts with a multidisciplinary evaluation. A neurologist, movement disorder specialist, or psychiatrist typically leads this process. Because PBA is linked to several underlying conditions, clinicians focus on identifying its distinct pattern of emotional outbursts.
Clinicians often use the CNS-LS screening questionnaire to determine cases warranting further clinical review. When combined with a detailed clinical interview, this test can help distinguish PBA from depression, anxiety, or other mood disorders, even though symptoms can overlap.
After a diagnosis of PBA, individuals with Parkinson’s may opt to take medications that specifically target PBA symptoms. To date, Nuedexta (dextromethorphan hydrobromide and quinidine sulfate) is the only drug approved in the U.S. specifically to treat PBA.
Medical evidence supports this approach. Patients taking Nuedexta experienced a dramatic reduction in symptoms, cutting the average number of their daily PBA outbursts to 3.9, down from 6.8 before treatment.
However, not everyone can safely take Nuedexta.
The drug should strictly not be used with monoamine oxidase inhibitors (MAOIs), quinidine, quinine, or mefloquine, due to the risk of a dangerous reaction called serotonin syndrome. It also should not be taken within 14 days of using an MAOI because the combination can cause serious health problems.
Other groups potentially vulnerable to Nuedexta side effects include:
- people with certain heart conditions, such as some heart rhythm or electrical problems
- people with myasthenia gravis, a rare long-term condition that causes muscle weakness
- people who have previously had an allergic reaction to dextromethorphan, quinidine, or quinidine-like drugs
Some clinicians may prescribe off-label medications, such as selective serotonin reuptake inhibitors or tricyclic antidepressants. However, these medications are not approved specifically for PBA, and evidence supporting their use is more limited. Also, their potential benefits and risks vary, so it is key to have a physician determine whether the drug is appropriate for specific patients.
Managing PBA episodes
There are some practical strategies that may help in managing PBA episodes. These techniques may ease some of the symptoms:
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| Strategy | How it works |
|---|---|
| Refocusing attention | Redirects a patient’s attention, for example, by counting objects in a room or thinking about something unrelated |
| Posture change | Changes posture abruptly, for instance, by the person straightening up |
| Muscle relaxation and breathing | Relaxes tense muscle groups, particularly the forehead and shoulders, along with slow, deep breathing |
| Switching activity | Doing the opposite of a current action, such as standing instead of sitting |
Recognizing an episode as it starts can be the first line of defense. Cognitive refocusing, which redirects a person’s attention, can interrupt the outburst process before it builds.
Posture and physical relaxation also play a role in immediate symptom management. Straightening posture or changing body position can help disrupt an episode before it escalates, while relaxing muscles and altering body position can further help restore control.
Tracking triggers is a valuable long-term strategy. Keeping a symptom diary can help identify patterns, such as fatigue, stress, or specific times of day that precede outbursts. For individuals with Parkinson’s, noting when episodes occur relative to medication doses can also be useful during medical appointments, helping clinicians tailor treatment plans more effectively.
Social adjustments and open communication are equally vital. Explaining a PBA diagnosis to friends, family, and coworkers helps them understand that outbursts are a neurological pathway disruption, not a reflection of true inner feelings. This openness can reduce the confusion or awkwardness that unexpected outbursts might cause in some people.
Caregiver education matters, too. Family members who know the condition is neurological and not psychological tend to offer more effective reassurance during episodes. Support groups can also provide a space for people with PBA to exchange coping strategies with others facing similar challenges.
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