A woman, identified only as “Maddie”, in her late 70s, found that she could not stop crying — a week after she woke up with a stroke that rendered half her body useless. The only time she did not cry was when she was asleep, greatly disrupting her rehabilitation sessions.

Yet, when asked whether she felt depressed, Maddie replied, “I'm confused about why this is happening. I don't think so.”

A condition often mistaken for depression


Maddie had had a history of depression, but it was well under control with the use of an antidepressant. Moreover, her psychologist observed that she exhibited no other criteria that were necessary to diagnose depression — such as ‘loss of interest in usual activities, poor sleep and appetite, low energy and weak concentration’.

‘Maddie was experiencing extreme, uncontrollable expressions of sadness without the accompanying emotion’, noted her psychologist, Daniel Shalev.

In fact, Maddie was suffering from the pseudobulbar affect (PBA) — a condition usually secondary to many neurological diseases, including amyotrophic lateral sclerosis (ALS, or Lou Gehrig's disease), multiple sclerosis, Parkinson's disease and stroke — which is characterised by involuntary emotional expression such as laughing or crying.

According to a 2011 study published in Advances in Therapy, the estimated US population with PBA was in the range 1.8 to 7.1 million. Less than half (41%) were diagnosed, and only half were given medication for their symptoms. Many were treated based on mistaken diagnoses.

The symptoms of PBA are easily attributed wrongly to conditions like depression and anxiety, due to the fact that sufferers experience decreased quality of life and social isolation — factors common to other psychiatric disorders. The likelihood of such confusion increases when the sufferer has past diagnoses of such disorders, as in Maddie’s case.

Disruptions in the brain’s emotional circuit


Certain regions of the brain are known to be responsible for the contextual expression of emotion. These include the frontal lobe, which provides the context for emotional expression, the cerebellum and brain stem, which regulates emotional reflexes, and the pons, which translates the impulses of the brain to action and emotional expression.

In Maddie’s case, her stroke had involved a blockage in the blood vessels supplying her brain stem, injuring her pons and disrupting this emotional circuit.

PBA results in an extreme disjunction between the sufferer’s feelings and their expression, causing them to question the integrity of their own thoughts and feelings. Maddie was no exception, and for her, ‘the diagnosis was liberating’ — enabling her to ‘trust her thoughts and feelings again’.

Treatment using antidepressants


PBA is often treated with dextromethorphan and quinidine, the first FDA-approved drugs to combat the condition. Its exact mechanism of action is not clear, but it is known to block glutamate — one of the major excitatory neurotransmitters in the brain. This reduces the frequency of abnormal neural signaling in the brain; and thus, resulting in a reduced degree of inappropriate emotional outburst.

However, dextromethorphan-quinidine is not recommended for patients with certain arrhythmias, such as complete heart block, or a history of heart failure. Maddie did not have any such condition; however, dextromethorphan-quinidine was ‘a risky choice’ for her as the drug could potentially interact with the antidepressant she was already consuming.

Instead, according to Dr. Shalev, ‘there was another class of medications that might help her brain regulate itself: another antidepressant’. Specifically, he recommended a low dose of a selective serotonin reuptake inhibitor (SSRI). These are antidepressants which increase serotonin in the synapses between neurons.

Interactions with Maddie’s antidepressant would be unlikely, as the latter involved another neurotransmitter, norepinephrine.

After just five days on medication, Maddie found that the frequency of her crying outbursts had dwindled to less than once daily. Such quick response to an increase in serotonin in the synapses differentiates PBA from depression, which typically takes weeks before the effect is seen.

Several weeks of rehabilitation and treatment later, Maddie’s crying outbursts were reduced to a frequency which matched the context. Though still troubled with the aftereffects of her stroke, Maddie remained optimistic.

“At least I'll get to be with my grandchildren again,” she lamented with a smile. MIMS

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Sources:
https://www.scientificamerican.com/article/a-vastly-underdiagnosed-brain-disorder-that-brings-frequent-tears/
https://link.springer.com/article/10.1007/s12325-011-0031-3
http://www.strokeassociation.org/STROKEORG/LifeAfterStroke/RegainingIndependence/EmotionalBehavioralChallenges/Pseudobulbar-Affect-PBA_UCM_467457_Article.jsp#.WRRcMILbvIU
http://www.mayoclinic.org/diseases-conditions/pseudobulbar-affect/symptoms-causes/dxc-20198593