Pseudobulbar affect

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Several criteria exist to differentiate between PBA and depression.

Pseudobulbar Affect (PBA), also known as emotional incontinence, is an emotional disturbance characterized by uncontrollable episodes of crying and/or laughing, or other emotional displays. PBA typically occurs as a secondary condition to a neurologic disorder or brain injury.

Signs and Symptoms[edit | edit source]

The main feature of PBA is a pathologically lowered threshold for exhibiting laughter, crying, or both. Affected individuals exhibit episodes of these emotional displays without an apparent motivating stimulus or in response to stimuli that would not have elicited such a response prior to the onset of their underlying neurologic disorder. Some patients may have emotional responses that are exaggerated in intensity but congruent with the character of the emotional display.

However, in other patients, the emotional display can be incongruent with, or even contradictory to, the emotional valence of the provoking stimulus. PBA symptoms can be severe, with persistent and unremitting episodes. Characteristics of PBA episodes include:

  • Sudden and unpredictable onset
  • Typical duration of a few seconds to several minutes
  • Occurrence of multiple episodes per day

Social Impact[edit | edit source]

PBA can significantly affect individuals' social functioning and relationships with others. Sudden, frequent, extreme, and uncontrollable emotional outbursts may lead to social withdrawal and interfere with daily living, social and professional pursuits, and overall healthcare.

Differentiating PBA from Depression[edit | edit source]

PBA is often misdiagnosed as clinical depression, but there are clear distinctions between the two. In depression and grief syndromes, crying is typically a sign of sadness, while the pathological displays of crying in PBA are often in contrast to the underlying mood or greatly excessive. Additionally, PBA episodes are sudden and brief, whereas crying in depression is more sustained and closely related to the underlying mood state. The level of control one has over the crying episodes in PBA is minimal or nonexistent, while in depression, emotional expression can be modulated by the situation.

In some cases, depressed mood and PBA may co-exist. Depression is a common emotional change in patients with neurodegenerative diseases or post-stroke sequelae, often comorbid with PBA. However, comorbidity implies that depression is distinct from PBA and is not necessary for, nor does it exclude, a diagnosis of PBA.

Causes[edit | edit source]

The specific pathophysiology involved in PBA is still under investigation, and the primary pathogenic mechanisms remain controversial. PBA is a secondary condition that occurs due to neurological diseases or brain injuries, resulting from disruptions of neural networks controlling the generation and regulation of emotions. PBA is commonly observed in individuals with neurologic injuries, such as traumatic brain injury (TBI) and stroke, and neurologic diseases like Alzheimer's disease, attention deficit/hyperactivity disorder (ADHD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and PANDAS in children and adults. PBA may also be reported as a symptom of hyperthyroidism, Graves' Disease, or hypothyroidism in combination with depression.

PBA has been associated with various other brain disorders, including brain tumors, Wilson's disease, syphilitic pseudobulbar palsy, and different types of encephalitis. Rarer conditions linked to PBA are gelastic epilepsy, dacrystic epilepsy, central pontine myelinolysis, olivopontinocerebellar atrophy, lipid storage diseases, chemical exposure (e.g., nitrous oxide and insecticides), fou rire prodromique, and Angelman syndrome.

These primary neurologic injuries and diseases are hypothesized to affect chemical signaling in the brain, which in turn disrupts the neurologic pathways controlling emotional expression.

Diagnosis[edit | edit source]

A psychiatrist may diagnose PBA when a subject is crying or laughing uncontrollably for approximately 3–5 minutes without an apparent reason.

Treatment[edit | edit source]

Educating patients, families, and caregivers is crucial for the appropriate treatment of PBA. Crying associated with PBA might be misinterpreted as depression, and laughter may cause embarrassment. It is essential for families and caregivers to recognize the pathological nature of PBA and reassure patients that it is an involuntary syndrome that can be managed. Traditionally, antidepressants such as sertraline, fluoxetine, citalopram, nortriptyline, and amitriptyline have been prescribed with some efficacy.

Medication[edit | edit source]

Dextromethorphan hydrobromide affects the signals in the brain that trigger the cough reflex. It is used as a cough suppressant, although it can sometimes be used medicinally as a pain reliever and recreationally as a drug. Quinidine sulfate affects the way the heart beats and is generally used in people with certain heart rhythm disorders. It is also used to treat malaria. Quinidine sulfate, as a metabolic inhibitor, "increases plasma levels of dextromethorphan by competitively inhibiting cytochrome P450 2D6, which catalyzes a major biotransformation pathway for dextromethorphan," enabling therapeutic dextromethorphan concentrations.

  • Dextromethorphan/quinidine is a combination of these two generic drugs and is the first FDA-approved drug for the treatment of PBA, approved on October 29, 2010.
  • Quinidine sulfate affects the way the heart beats, and is generally used in people with certain heart rhythm disorders. It is also used to treat malaria. Quinidine sulfate, as a metabolic inhibitor, "increases plasma levels of dextromethorphan by competitively inhibiting cytochrome P450 2D6, which catalyzes a major biotransformation pathway for dextromethorphan," enabling therapeutic dextromethorphan concentrations.
  • Dextromethorphan/quinidine is a combination of these two generic drugs, and is the first FDA-approved drug for the treatment of PBA, approved on October 29, 2010.
Pseudobulbar affect Resources
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Contributors: Prab R. Tumpati, MD