The Corpus Callosum

Poststroke Laughing and Crying

The Journal of Psychiatry and Neuroscience (Canadian,
bilingual), an open-access publication, has a regular column entitled
Psychopharmacology for the Clinician (Psychopharmacologie
).   Typically the column contains a case
report and a brief discussion of practical issues in treatment.

The most recent (September 2007) issue describes a case of poststroke
pathological laughing and crying (PLC).  PLC is a mysterious
condition, something that is impossible to explain using behavioral or
psychodynamic theory.  

After a stroke, 7 to 48 percent of patients experience disinhibition of
emotional displays, including crying and/or laughing.  In some
patients, the threshold for activation of these displays is reduced.
 In others, the displays appear to be entirely spontaneous.
 It is not directly harmful, but it is annoying. Moreover, it
can lead to some degree of disability because it can be disruptive.

Note that this is not due to poststroke depression or mania.
 Although affective disorders commonly occur after stroke, PLC
is not associated with a full set of symptoms that would support a
diagnosis of mania or depression.

Now, you might think that an antidepressant would not have any effect,
since the patients do not have depression.

However, such expectations next to useless in psychiatry.  The
only way to learn anything in psychiatry is to try it and see what
happens.  So, what happens when a person with PLC takes an

treatment of poststroke pathological laughing and crying

Peter Giacobbe, MD
Alastair Flint, MBA 60-year-old man with left-sided limb
weakness after a stroke was referred for assessment and treatment of
depression. The patient reported that, after his stroke 2 weeks ago,
he has been crying “for no reason” several times a
day. He
described that the crying spells last several seconds and cannot be
resisted. The patient denies depressed mood or symptoms consistent
with a mood disorder. On examination, stereotyped paroxysms of crying
lasting 5–10 seconds were noted during the interview,
to any emotional themes discussed. The patient was diagnosed with
pathological crying and was started on citalopram 10 mg orally at
night. On follow-up, he reported that his crying spells stopped
within days of initiating the selective serotonin reuptake inhibitor
(SSRI) medication…

The column reviews the (scant) literature on the subject,
indicating that several studies have shown that antidepressants are
effective.  Curiously, they take effect within a few days, a
time scale too short for an antidepressant effect.  So they
work by some other mechanism, but that mechanism is not known.

…In pooled data of 93 people from these
placebo-controlled trials of nortriptyline, fluoxetine, sertraline and
citalopram 96% of patients who received antidepressant medication
demonstrated a greater than 50% reduction in the number of crying
episodes at the end of the treatment trials, compared with 27.5% of
patients who received placebo, yielding a number needed to treat (NNT)
of 1.5…

So not only does the response occur quickly, it occurs in a high
percentage of people.  An NNT as low as 1.5 is unusual in
psychiatry, as it is in most areas of medicine.


  1. #1 stumpy
    October 11, 2007

    I’ve seen several instances of the pathological crying, such as the case report presented here — but I’ve never seen a case of pathological laughing following a CVA. Do antidepressants work in these cases too?

  2. #2 Joseph j7uy5
    October 11, 2007

    I was only able to find a few specific references to that, although I did not look very hard…

    J Neuropsychiatry Clin Neurosci. 1998 Fall;10(4):453-5.
    Rapid response of emotional incontinence to selective serotonin reuptake inhibitors.
    Nahas Z, Arlinghaus KA, Kotrla KJ, Clearman RR, George MS.

    Medical University of South Carolina, Department of Psychiatry, Charleston, SC 29403, USA.

    Emotional incontinence (EI) is a perturbing condition characterized by uncontrollable outbursts of exaggerated, involuntary facial expressions and pathological crying or laughter. There is increasing evidence that serotonergic neurotransmission may be damaged in EI. The authors report 4 pathological crying cases (3 poststroke and 1 with multiple sclerosis) and 1 case of pathological laughter after traumatic brain injury. EI improved dramatically with three different selective serotonin reuptake inhibitors (fluoxetine, sertraline, and paroxetine) in the context of these different CNS diseases.

    PMID: 9813792 [PubMed – indexed for MEDLINE]


    Clin Neuropharmacol. 2005 Sep-Oct;28(5):249-51.
    Mirtazapine treatment for pathological laughing and crying after stroke.
    Kim SW, Shin IS, Kim JM, Lim SY, Yang SJ, Yoon JS.

    Department of Psychiatry, Chonnam National University Medical School, Republic of Korea.

    Selective serotonin reuptake inhibitors (SSRIs) have been recognized as the treatment of choice for pathological laughing and crying (PLC), which is a common, distressing condition that follows stroke. There have been few reports about other treatment options for PLC. Here, the authors report rapid responses to mirtazapine in two patients with poststroke PLC who failed to respond to SSRIs or bupropion. In the first case, a 63-year-old woman with severe long-standing crying spells that had persisted for 3 months responded well to low-dose mirtazapine within a few days; she could not tolerate citalopram or sertraline. In the second case, both the laughing and crying spells of a 64-year-old woman were improved within a few days of mirtazapine administration, after they had not responded to bupropion. This is one of the first reports to suggest that mirtazapine may be an alternative to SSRIs for treating poststroke PLC.

    PMID: 16239769 [PubMed – indexed for MEDLINE]

  3. #3 Greg P
    October 11, 2007

    The literature may be scant, but the practical experience is commonplace.

    There is ample literature on so-called post-stroke depression. Now why do I use this qualifier? The problem is, and I’ve psychiatrists make this mistake, that diagnosing depression after stroke is more difficult than many think.
    It begins with the fact that many of the usual indicators of depression, such as reduced energy, “vegetative signs”, decreased appetite, altered sleep, even a depressed mood, can be related to the physical effects of the stroke, or in the of depression (as a generic symptom) is to some degree expected after a life-changing event — do you think people are happy about having a stroke?
    Experience shows us that strokes in the dominant hemisphere (most often left) produce a lot of apparent signs of depression but not necessarily depression. Strokes in the nondominant hemisphere can oftne produce a problem with sensing the mood of others and perhaps the self as well.
    The bottom line in rehab is, in my view, looking at how the patient is performing in the rehab setting. If they are participating in therapies, making progress, seem to get enough rest in spite of what may be a marked change in sleep patterns, then they are not substantially depressed, and typically these patients do not report depression. On the other hand, if someone in spite of reporting no mood problems, is not performing up to expectations (given their brain lesion) in therapy, hostile, finding ways of getting out of going to therapy, “always” tired, this is someone at high suspicion for depression.
    With these “pathological” emotional states it’s important to treat the patient, not those around them. It may be that the crying is really only upsetting to the family or staff (and this does come in degrees of severity), and it’s not interfering with progress, and overall the patient is optimistic.
    Now, having said this, let me recount something else not so much seen in the literature. We do see patients, seemingly without depression, mood Ok, eating Ok, sleeping Ok, who are just not improving as one would expect based on the size and location of their stroke. In many cases there will be frontal lobe involvement and some kind of premotor problem — the patient either seems unable to perform/begin a task or once begun performs it quite well. These patients, when given an SSRI, will frequently show a sudden improvement in neurologic function, to the point that I may start the drug and the next day the therapists are coming up to me and saying, “What did you do with Mr. X? He’s like a different person today.” These patients, I believe, have some kind of organic frontal lobe problem that is overcome by SSRIs. I have seen this time and time again. One thing to add, important in these days of the pushing of generics, is that I try to avoid the older SSRIs like fluoxetine and paroxetine, since these frequently do two bad things: increase spasticity and cause hallucinations in this patient population.

    One of the problems trying to analyze this and publish it is that the ability to say a particular patient will respond or not respond is something I have not yet figured out. I will say that just generally putting patients on SSRIs is not sensible – this is a subpopulation with a particular collection of issues.

  4. #4 Greg P
    October 11, 2007

    Something else:
    I also see quite a number of patients with ALS, and this is well-known to have an incidence of pathological laughter/crying, something both at the same time or one leading to the other, and here also, probably for the same substrate reasons, SSRIs can be useful, but I emphasize can. One particular SSRI may be better than another, and other atypical antidepressants may also be of use.

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