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Mood instability is common to many diseases that affect the brain. This is certainly true of all forms of dementia. A range of moods can be found from continuous depression or mania to episodes of laughing or crying. Often times such episodes are involuntary and inappropriate to the situation in that they don’t reflect what is going on around the patient. These episodes might be a disorder known as Pseudobulbar Affect or PBA. PBA has been described by a variety of other names such as Affective Instability or Post Stroke Emotionality. It can be very distressing because it is often not under the patient’s control and may occur in any public or social situation. Thus, PBA may lead to embarrassment, secondary anxiety, and depression from constantly anticipating when an episode might happen.
Treatments for PBA have traditionally had modest results at best. Typically a medical investigation is begun to find a source of the unstable mood but it usually ends up being attributed to an underlying neurological condition whether it be a form of dementia, a stroke, multiple sclerosis, traumatic brain injury or whatever. Often times efforts are made to adjust the environment – seeking a diminution of the symptoms. This effort rests upon the idea that something in the environment is there (or missing) and contributing to the distress. While it may be true that a stable and stress free environment may be helpful, this strategy generally does not reach to the root of PBA. It is likely too that many environmental changes for such patients are made to seclude them as the outbursts can be annoying to other patients, staff or even family. Many higher functioning patients will actually seclude themselves fearing more embarrassing episodes in public.
It is generally thought that PBA is caused by a disconnection between the supervising frontal lobe structures and the deeper emotional centers in the brain. Consider what happens when the spine is disconnected from the superior cerebral structures such as is the case in a head injury or stroke. After a period of flaccid paralysis there is often (depending upon the nature of the injury) a spastic paralysis with distinctive reflexive posturing of the arms and legs. This seems to me similar to what happens in PBA.
In the end, the disconnection between the frontal lobe and emotional centers usually remains permanant due to the irreversibility of the neurological disorder which caused it. Medication treatments of PBA therefore have been focused on calming down the emotional spasticity. I have used everything available in the psychopharmacologic arsenal to achieve this – antidepressants, mood stabilizers, antipsychotics and antianxiety medications, all with very limited results.
Fortunately, there is now a medication available specifically for PBA. Nuedexta (Avanir Pharmaceuicals) is approved by the FDA for inappropriate laughing or crying due to any underlying neurological condition. This medication is safe in terms of side effects and in my experience often leads to a dramatic improvement in PBA symptoms. There are specific patients who should not be on Nuedexta. These include those with un-paced complete heart block, users of quinidine, and those on MAOI inhibitors. A baseline EKG is often recommended as a precaution. This is an important new medication but like all medications should only be used under the supervision a licensed practitioner with adequate knowledge of the drug.