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Idiopathic Thrombocytopenia Purpura

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Gym today

I went to the gym and I was trying to ask this lady to fix my machine and I started crying and I kept apologizing to her and she stated that she understood and I said it was because I had a stroke in my brain and she said she never know anyone who had what I have but she worked with people that had different problems.

I apologized anyway and she said anytime I needed her help with anything she would be honored to help me.


What Happened

I met a lady at Bible Study. Her name was Toby. She came to a Mary Kay party we were having for one of the girls. She was nice and she prayed with me or over me because I told her that I cry.

I usually get home about 9:00 at niht and the outide light is on, but not tonight everything was dark and off, I guess my husbamd was a little upset.


I went to Virginia to visit my Mother & Family

I went to Virginia to visit my mother who is 87 years old. She is going through Alheimer Disease. She is staying with my sister and half the time she doesn’t know her. When I was crying my mother would say what are you crying for, stop that crying and she would be hollering at me. When I say Mommy I can’t just stop until I’m finish. But I know she doesn’t understand so I just don’t let her she me crying any more.

My sister, my neices and everyone was there. It was a very nice time. I am glad I went. I had an awesome time there.


I cry. Recovery

how do you feel as
hurdles you have had to get over
thing you find really hard
all types of things like this.

1. The things I find that is really hard for me was setting up a website that
was almost impossible for me to do. I could not remember this or that.
My son set up my website for me and he didn’t really know how but he did
it anyway. On Saturday and Sundays I have to go with my husband to play bingo
and I couldn’t talk to any one because I would cry and I did not want all
those people seeing me cry so I just didn’t talk. If I had a bingo my
husband would yell bingo for me because I could not yell it for myself.
Sometimes I still have a tendency to cry but mostly I don’t.

2.The hurdles I had to get over with my crying was my husband and my son. I
didn’t care about anyone else but them. Whenever I had to speak to my son I cried.
How can I cry to speak to my own child. That was very hard for me. Extremely hard.
He would always say I understand you cry when you say something to anybody not only
me but he didn’t understand that I didn’t want to cry when I spoke to him he was my
child from birth.

Where my other hurdle came in was with my husband, how can I cry with my husband.
I was married to him for 14 years and I couldn’t explain to him good enough what
I was actually crying about. I would take him to work and pick him up. Sometimes
I would cry and sometimes not. If he only said hello when he got into the car,
I would cry. He really didn’t understand it. He would tell me to stop crying all
the time, but of course I could not until I was actually finished crying. It is
and was a nightmare.

3. All types of things like this would make me cry like when I go to the supermarket.
The girl at the checkerout counter would ask me for my phone number and I would
start crying. I go the health food supermarket and they ask me for something and I cry.
I go to the pharmacy and they ask me something, I cry. I go pay a loan for my husband,
and ask me something, I cry. I go to pizza hut for something and they ask me something,
I cry. Every where I go, I cry. Isn’t that crazy. I’m sorry but if you have what
I have its just plain crazy


Doctor’s note

Ms. Brathwaite:
I am sorry that you have had a hard time to find me. Yes I have
studied pathological laughing and crying syndrome and your case sounds
close to what I have seen in many of my patients.
Before I can help you further, please provide me with the following
– report of your most recent MRI (if you have the actual scans on a
CD, that would help me greatly)
– triggers for your crying/ actual examples from daily life
– any change in your mood when you cry/ or before you cry.
– how many times a day before you started on citalopram.
You can visit my lab’s website at http://lbcn.stanford.edu and check
the Etc section where there is an audio report from NPR about this
There are also some news pieces from Boston Globe and other media that
you can find in our website.


Josef Parvizi MD PhD
Assistant Professor
Department of Neurology and Neurological Sciences
Stanford University


Recovering from a strokw

FYI, you can read and distribute this paper in case you want someone
to know more about your condition


Patients with various neurologic disorders exhibit exaggerated or
inappropriate episodes of laughter, crying, or both without an
apparent motivating stimulus or in response to stimuli that would
not have elicited such an emotional response before the onset of
the underlying disease. During these episodes, patients have
difficulty controlling their emotional expression according to the
contextual information. In contrast, patients with mood disorders
have a pervasive and sustained change in their emotional experience
and thus exhibit spells of laughter or crying because of an
underlying mania or depression. This article focuses on the clinical
presentation, diagnosis, prevalence, and proposed pathophysiological
mechanisms of and available treatment options for this
clinical phenomenon.
Mayo Clin Proc. 2006;81(11):1482-1486
MSA = multiple system atrophy; PLC = pathological laughter and crying
Many patients with neurologic disorders exhibit uncontrollable
episodes of laughing, crying, or both
that are either exaggerated or contradictory to the context in
which they occur. Patients report that their episodes are at
best only partially amenable to voluntary control, and unless
they experience a severe change of mental status, they
often have insight into their problem and judge their emotional
display as inappropriate and out of character.
The cardinal feature of the disorder is a pathologically
lowered threshold for exhibiting the behavioral response of
laughter, crying, or both. An affected individual exhibits
episodes of laughter and/or crying without an apparent
motivating stimulus or in response to stimuli that would not
have elicited such an emotional response before the onset
of their underlying neurologic disorder. In some patients,
the emotional response is exaggerated in intensity but is
provoked by a stimulus with an emotional valence congruent
with the character of the emotional display. For example,
a sad stimulus provokes a pathologically exaggerated
weeping response instead of a sigh, which the patient
normally would have exhibited in that particular situation.
However, in some other patients, the character of the emotional
display can be incongruent with, and even contradictory
to, the emotional valence of the provoking stimulus or
may be incited by a stimulus with no clear valence. For
example, a patient may laugh in response to sad news or cry
in response to stimuli with no emotional undertone, or,
once provoked, the episodes may switch from laughing to
crying or vice versa.
Various terms have been used interchangeably to describe
the problem of laughing and crying in these patients. The
most widely used terms are pseudobulbar affect, pathological
laughter and crying, emotional lability, emotionalism,
and emotional dysregulation. Terms such as forced crying,
involuntary crying, pathological emotionality, and emotional
incontinence have also been used, although less
frequently. In some instances, authors have used the same
term for clinically different conditions, and in other instances,
different terms have been used synonymously to
describe the same clinical presentation. Because the disorder
is primarily a problem with laughing and crying
rather than exhibiting all kinds of emotional displays, the
displays are out of character and disproportionate to the
context in which they occur, and the condition can lead to
social and personal distress and functional impairment,
we use the term pathological laughter and crying (PLC)
in this article, which we believe is a clear and concise
descriptor of the condition and has historical roots in classical
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
Mayo Clin Proc. • November 2006;81(11):1482-1486 • www.mayoclinicproceedings.com 1483
Accurate estimates of the incidence and prevalence of PLC
in the setting of each specific neurologic disorder are lacking.
This may be in part due to confusion in the literature
about the nosology and terminology of this clinical condition,
as described previously. This confusion notwithstanding,
there appears to be considerable potential for errors in
estimating the incidence and prevalence of impaired emotional
regulation. Patients and their family members may
be unaware that such episodes develop in the context of
neurologic disorders.1 If clinical researchers do not ask
specifically about symptoms of impaired emotional regulation
and if the nosological distinctions described previously
are not considered, these symptoms may be either
unrecognized or misinterpreted as a symptom of a mood
disorder. Conversely, some studies have attempted to estimate
the prevalence of the problem generally in clinical
referral samples, which may lead to overestimates of the
incidence and prevalence of this disorder.
With these caveats in mind, it is informative to review
the reported scope of the problem in some neurologic disorders.
Among patients with traumatic brain injury,2,3 the
prevalence of this condition during the first year after injury
is estimated at 5% to 11%. The disorder occurs in 10%
of patients with multiple sclerosis,4-6 49% of patients with
amyotrophic lateral sclerosis,7 11% to 34% of patients with
stroke,8-10 5% of patients with Parkinson disease and the
noncerebellar type of multiple system atrophy (MSA),11
and 37% of patients with the cerebellar type of MSA.12
The scope of the problem in patients with dementia is
controversial. In one report,13 the authors defined the problem
as simply “observable sudden changes in emotional
expressions,” which they observed in about 74% of mildly
to moderately impaired patients with Alzheimer disease.
Starkstein et al14 used the Pathological Laughter and Crying
Scale15 in their study of 103 patients with Alzheimer
disease. Of these 103 patients, 40 had PLC. Of note, however,
21 of these 40 patients also had an underlying congruent
mood disorder. The authors labeled these patients
as having “emotional lability,” which they defined as
“pathological laughing and crying with an underlying
mood disorder.”
Despite the problems associated with accurately estimating
the incidence and prevalence of PLC, the limited
data available suggest that this problem occurs with a frequency
considerably higher than is generally recognized by
physicians. In light of the frequency of the neurologic
conditions in which impaired regulation of emotional expression
develops, numerous patients may be expected to
have PLC and might benefit from its identification and
Several scales are available to identify and characterize
PLC.15-17 Among these, the 2 most commonly used in clinical
research studies are the Pathological Laughter and Crying
Scale15 and the Center for Neurologic Study-Lability
Scale.15-17 The items included in these scales cover the
triggering factors, frequency, duration, and involuntariness
of PLC events, issues that overlap minimally with items
included in scales for the assessment of mood disorders
(for example, the Hamilton Depression Rating Scale and
the Beck Depression Inventory), supporting the differences
in these diagnostic constructs.
Assessment scales developed specifically for characterizing
the problem of laughing and crying may be useful in
clinical trials. Using such scales to screen patients at risk
for PLC and to follow their progress may also be practical.
However, we strongly believe that the diagnosis of the
condition remains a bedside issue. As suggested by the
content of assessment scales for this disorder, a single
screening question regarding the presence of frequent
laughing or crying spells may be sufficient to identify
patients with impaired regulation of emotional expression.
Once the patient’s answer is confirmatory, other routine
questions are warranted to discern whether the patient’s
uncontrollable episodes of laughing or crying are related to
an underlying mood disorder.
In the clinical setting, PLC is often unrecognized. In cases
in which the physician notices spells of uncontrollable
laughing or crying, the condition can often be misdiagnosed
as a mood disorder. However, a thorough evaluation
can lead to proper differentiation of these 2 conditions.
Mood is an emotional state sustained over relatively long
periods, days to weeks or more. Patients with depression
feel depressed most of the time, and thus their emotional
display of crying is primarily a reflection of their underlying
depressed mood. By contrast, patients with pathological
crying exhibit the emotional display in the absence of a
pervasive and sustained depressed mood. The crying occurs
only paroxysmally and is uncontrollable and involuntary.
Such episodes may even occur in the absence of any
congruent changes in the mood of the patient. Crying due to
depression is associated with signs such as anhedonia,
decreased energy, psychomotor slowing, feelings of hopelessness
and helplessness, and suicidal ideation as well as
poor concentration and anxiety. Likewise, patients with
bipolar disease may exhibit laughter or crying during their
cycles of cheerfulness, irritability, and depression. In addition,
these patients have associated problems of grandios-
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
1484 Mayo Clin Proc. • November 2006;81(11):1482-1486 • www.mayoclinicproceedings.com
ity, poor judgment, hyperactivity, pressured speech, poor
sleep, and increased energy. Patients with PLC report none
of these symptoms and, in fact, are often embarrassed by
their episodes of laughing or crying.
Importantly, although PLC and mood disorders appear
to be different clinical entities, they may coexist in the
same patient.12,15,18 Robinson et al15 reported that almost
half of their patients with PLC had coexisting depression.
However, resolution of pathological laughing or pathological
crying seems to be independent of the resolution of
depression in these patients and has no relationship with
the changes in anxiety or aggression scores.15 A recent
study found that all patients with the cerebellar type of
MSA who exhibited pathological laughter and/or crying
also had depression.12
The coexistence of pathological emotional expression
(eg, PLC) and pathological emotional experience (eg,
mood disorders) is an important observation because it
poses limitations in diagnosis and research and will certainly
influence the physician’s choice of treatment.
Pathological laughter and crying often responds to the
same treatments used for mood disorders. However, in
patients with PLC, the beneficial effects of these medications
are evident within days of treatment initiation and
occur in response to much lower dosages than those usually
prescribed for the treatment of mood disorders.12,15,18,19
Schiffer et al18 studied the effect of amitriptyline, a
tricyclic antidepressant, in 12 multiple sclerosis patients
with PLC using a mean dosage of 58 mg/d and compared
its effect to that of placebo in a 30-day, double-blind,
crossover study. They reported a significant improvement
in PLC symptoms in 8 patients taking amitriptyline with no
effect on their coexisting depression. Robinson et al15 administered
nortriptyline in dosages as high as 100 mg/d in
14 stroke patients with PLC and compared its effectiveness
to placebo in 14 other patients with stroke. They
reported significantly greater improvement of PLC in patients
given nortriptyline than in those receiving placebo
and no significant change in the depression status of these
Selective serotonin reuptake inhibitors have also been
used for treatment of PLC. In an open-label study by
Seliger et al,20 all 13 patients (8 with stroke and 5 with
multiple sclerosis) who received 20 mg/d of fluoxetine
reported a decrease in the number of laughing or crying
episodes within 3 to 14 days. Andersen et al21 compared
citalopram, 10 to 20 mg/d, to placebo in 16 consecutive
patients with stroke in a crossover study. They found that
daily crying episodes decreased by 50% in all 13 patients
receiving citalopram compared to only 2 patients who received
placebo. In a double-blind, placebo-controlled
study, Burns et al22 determined that sertraline in dosages up
to 50 mg/d was effective in 13 of 14 patients with PLC and
stroke, whereas placebo produced a beneficial response in
9 of 14 patients (P=.041). Muller et al23 conducted an openlabel
study of 26 patients with PLC after traumatic brain
injury. Thirteen patients were treated with citalopram, and
13 others received paroxetine in a single daily dose of 10 to
40 mg. Significant improvement was seen in 92% of patients,
with rapid onset of effect within 1 to 3 days.
AVP-923 is a new compound that consists of 30 mg of
dextromethorphan and 30 mg of quinidine, which inhibits
the metabolism of dextromethorphan by cytochrome P-450
2D6 enzyme. In a recent randomized, double-blind study
by Brooks et al,24 140 patients with amyotrophic lateral
sclerosis and PLC were randomized to receive dextromethorphan
plus quinidine (n=70) vs dextromethorphan
(n=33) or quinidine (n=37) alone in twice-daily doses. The
authors reported approximately 2-fold lower scores on the
Center for Neurologic Study-Lability Scale in the group
that received dextromethorphan plus quinidine compared
to the groups receiving only dextromethorphan or quinidine.
Moreover, 52% of the patients receiving dextromethorphan
plus quinidine were symptom free during the
last 2 weeks of the study compared to 23% of patients
taking dextromethorphan alone and 12% of patients taking
quinidine alone. Statistically significant improvement in
quality-of-life and quality-of-relationship scores were seen
in the patients receiving the combination treatment compared
to those receiving either drug alone. Adverse effects
reported in the group receiving dextromethorphan plus quinidine
included nausea (33%), dizziness (20%), and somnolence
(13%), resulting in a 24% discontinuation rate in the
group receiving the combination regimen compared to 6%
and 5% in the dextromethorphan and quinidine groups,
respectively. In a study by Panitch et al,25 150 patients with
multiple sclerosis and PLC were randomized to receive
dextromethorphan plus quinidine (n=76) or placebo (n=74).
Patients receiving the active compound experienced significant
improvement of their PLC symptoms as well as
their quality-of-life and relationship scores. Laughing and
crying episodes occurred 4.7 times per week in the group
receiving dextromethorphan plus quinidine compared to
11.5 episodes per week in the placebo group. Headaches
were the most commonly reported adverse effect in both
groups, but the only statistically significant adverse event
was dizziness (26.3% in the dextromethorphan plus quinidine
group vs 9.5% in the placebo group). Discontinuation
of the study medication because of adverse events occurred
in 16% of the dextromethorphan plus quinidine group compared
to 11% in the placebo group.
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
Mayo Clin Proc. • November 2006;81(11):1482-1486 • www.mayoclinicproceedings.com 1485
In summary, although several agents have been shown
to be effective in the treatment of PLC, head-to-head
comparative clinical trials are needed to determine whether
any of the aforementioned treatment options are superior in
efficacy or adverse-effect profile.
Given the therapeutic effect of serotonergic agents in patients
with PLC, it has been suggested that a serotonergic
dysfunction is responsible for the impaired emotional regulation
in these patients.21 The fact that a chemical agent,
such as serotonin, is helpful in treating a condition does not
necessarily imply a causal relationship between the agent
and the condition. However, understanding how serotonergic
substitution can improve emotional experience in patients
with mood disorders while also being effective in
patients who have pathological regulation of emotional
expression is important.
The hypothesis proposed by Oppenheim and
Siemerling26 in 1886 and subsequently by Kinnier Wilson27
in 1924 was that impaired emotional regulation results
from disinhibition of a presumed brainstem center for
laughter and crying due to lesions of the voluntary motor
pathways in the descending corticobulbar tracts. As previously
published,28 this explanation has several limitations.
For example, if the inhibitory pathways are damaged in
these patients, why do they not laugh or cry constantly, or
why do they sometimes exhibit a response contradictory to
the emotional valence of the triggering stimulus? Moreover,
why do many patients with this condition lack the
typical features of pseudobulbar palsy? The hypothesis of
disinhibition assumes that a proper operation of emotional
expression is based on a balance between inhibitory and
excitatory inputs to a presumed brainstem center for laughing
and crying. On the basis of the current knowledge of
brain anatomy and function, there is no single brainstem
center for laughter and crying. Rather, a network of
brainstem nuclei is involved in the generation of movements
associated with the acts of laughter or crying, and it
remains to be determined how this network is regulated by
the cerebral cortex. Which cortical structures are involved,
and how do they exert their control over the brainstem
network? Feinstein et al6,29 have shown that the involuntary
and uncontrollable emotional behavior in patients with
multiple sclerosis correlates directly with poor performance
in tests of prefrontal function. This suggests that the
prefrontal cortices, rather than the primary motor cortices
as Oppenheim and Siemerling26 and Kinnier Wilson27 had
suggested, are important for the control of emotional behavior.
30 However, questions remain. For instance, to what
extent and through which pathways do the prefrontal cortices
regulate the operation of the brainstem network? Is this
regulation made possible through direct corticobulbar pathways
or indirectly through additional structures such as the
cerebellum, as suggested recently?12,28,31
A thorough understanding of the etiology and pathophysiology
of PLC awaits further elucidation of the neural
basis of human emotion and of the neurotransmitters and
networks involved in its regulation and coordination.
Meanwhile, the recognition, diagnosis, and treatment of
this clinical entity is important to help patients and their
caretakers enhance their quality of life and relationships.
1. Arciniegas DB, Topkoff J. The neuropsychiatry of pathologic affect: an
approach to evaluation and treatment. Semin Clin Neuropsychiatry. 2000;5:
2. Zeilig G, Drubach DA, Katz-Zeilig M, Karatinos J. Pathological laughter
and crying in patients with closed traumatic brain injury. Brain Inj. 1996;10:
3. Tateno A, Jorge RE, Robinson RG. Pathological laughing and crying
following traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2004;16:
4. Minden SL, Schiffer RB. Affective disorders in multiple sclerosis: review
and recommendations for clinical research. Arch Neurol. 1990;47:98-
5. Feinstein A, Feinstein K, Gray T, O’Connor P. Prevalence and
neurobehavioral correlates of pathological laughing and crying in multiple
sclerosis. Arch Neurol. 1997;54:1116-1121.
6. Feinstein A, O’Connor P, Gray T, Feinstein K. Pathological laughing
and crying in multiple sclerosis: a preliminary report suggesting a role for the
prefrontal cortex. Mult Scler. 1999;5:69-73.
7. Gallagher JP. Pathologic laughter and crying in ALS: a search for their
origin. Acta Neurol Scand. 1989;80:114-117.
8. House A, Dennis M, Molyneux A, Warlow C, Hawton K. Emotionalism
after stroke. BMJ. 1989;298:991-994.
9. Morris PL, Robinson RG, Raphael B. Emotional lability after stroke.
Aust N Z J Psychiatry. 1993;27:601-605.
10. Kim JS, Choi-Kwon S. Poststroke depression and emotional incontinence:
correlation with lesion location. Neurology. 2000;54:1805-1810.
11. Siddiqui MS, Kirsch-Darrow L, Fernandez HH, Jacobson CE IV, Okun
MS. Prevalence of pseudobulbar affect in movement disorders and its mood
correlates: a prospective study of 754 consecutive patients [abstract]. Neurology.
2006;66(suppl 2):A369. Abstract P06.156.
12. Parvizi J, Joseph J, Press D, Schmahmann JD. Pathological laughter and
crying in multiple system atrophy—cerebellar type. Mov Disord. In press.
13. Haupt M. Emotional lability, intrusiveness, and catastrophic reactions.
Int Psychogeriatr. 1996;8(suppl 3):409-414.
14. Starkstein SE, Migliorelli R, Teson A, et al. Prevalence and clinical
correlates of pathological affective display in Alzheimer’s disease. J Neurol
Neurosurg Psychiatry. 1995;59:55-60.
15. Robinson RG, Parikh RM, Lipsey JR, Starkstein SE, Price TR. Pathological
laughing and crying following stroke: validation of a measurement
scale and a double-blind treatment study. Am J Psychiatry. 1993;150:286-
16. Newsom-Davis IC, Abrahams S, Goldstein LH, Leigh PN. The emotional
lability questionnaire: a new measure of emotional lability in amyotrophic
lateral sclerosis. J Neurol Sci. 1999;169:22-25.
17. Smith RA, Berg JE, Pope LE, Callahan JD, Wynn D, Thisted RA.
Validation of the CNS emotional lability scale for pseudobulbar affect (pathological
laughing and crying) in multiple sclerosis patients. Mult Scler. 2004;
18. Schiffer RB, Herndon RM, Rudick RA. Treatment of pathologic laughing
and weeping with amitriptyline. N Engl J Med. 1985;312:1480-1482.
19. Schiffer R, Pope LE. Review of pseudobulbar affect including a novel
and potential therapy. J Neuropsychiatry Clin Neurosci. 2005;17:447-454.
20. Seliger GM, Hornstein A, Flax J, Herbert J, Schroeder K. Fluoxetine
improves emotional incontinence. Brain Inj. 1992;6:267-270.
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
1486 Mayo Clin Proc. • November 2006;81(11):1482-1486 • www.mayoclinicproceedings.com

Questions About PLC
1. Which one of the following statements describes the
condition of PLC, as defined in this article?
a. Patients have congruent mood but exaggerated
episodes of laughter and/or crying
b. Patients have incongruent mood and inappropriate
episodes of laughter and/or crying
c. Patients have exaggerated and inappropriate
episodes of laughter and/or crying due to an
underlying mood disorder
d. Patients have exaggerated and inappropriate
episodes of laughter and/or crying but no comorbid
mood disorder
e. Patients have exaggerated and inappropriate
episodes of laughter and/or crying independent of
any comorbid mood disorder
2. Which one of the following is currently prescribed for
the treatment of PLC?
a. Neuroleptics
b. Antiepileptics
c. Selective serotonin reuptake inhibitors and tricyclic
d. Dextromethorphan
e. Quinidine
3. Which one of the following statements defines the
relationship between PLC and mood disorders?
a. It is not possible to differentiate PLC from any mood
b. By definition, patients with PLC cannot have
comorbid depression or mania
c. Higher dosages and longer durations of
antidepressant therapy are needed for the treatment
of PLC
d. Laughing and crying in patients with PLC are
caused by a pathological mood
e. Mood disorders are a sustained problem of
emotional experience, whereas PLC is a
paroxysmal problem of exaggerated and/or
inappropriate emotional expression
4. Which one of the following neurologic conditions is
most frequently associated with PLC?
a. Amyotrophic lateral sclerosis
b. Multiple sclerosis
c. Stroke
d. Epilepsy
e. Alzheimer disease
5. According to recent clinical trials, which one of the
following treatment options is effective for the
treatment of PLC?
a. 30 mg of dextromethorphan once a day
b. 30 mg of quinidine once a day
c. 30 mg of dextromethorphan plus 30 mg of quinidine
once a day
d. 30 mg of dextromethorphan plus 30 mg of quinidine
twice a day
e. 30 mg of dextromethorphan plus 300 mg of
quinidine twice a day
Correct answers:
1. e, 2. c, 3. e, 4. a, 5. d
21. Andersen G, Vestergaard K, Riis JO. Citalopram for post-stroke pathological
crying. Lancet. 1993;342:837-839.
22. Burns A, Russell E, Stratton-Powell H, Tyrell P, O’Neill P, Baldwin R.
Sertraline in stroke-associated lability of mood. Int J Geriatr Psychiatry.
23. Muller U, Murai T, Bauer-Wittmund T, von Cramon DY. Paroxetine
versus citalopram treatment of pathological crying after brain injury. Brain Inj.
24. Brooks BR, Thisted RA, Appel SH, et al, AVP-923 ALS Study Group.
Treatment of pseudobulbar affect in ALS with dextromethorphan/quinidine: a
randomized trial. Neurology. 2004;63:1364-1370.
25. Panitch HS, Thisted RA, Smith RA, et al, Pseudobulbar Affect in Multiple
Sclerosis Study Group. Randomized, controlled trial of dextromethorphan/
quinidine for pseudobulbar affect in multiple sclerosis. Ann Neurol.
26. Oppenheim H, Siemerling E. Mitteilungen uber Pseudobulbarparalyse
und akute Bulbarparalyse. Berl Klin Wochenschr. 1886;46.
27. Wilson SAK. Some problems in neurology, II: pathological laughing and
crying. J Neurol Psychopathol. 1924;4:299-333.
28. Parvizi J, Anderson SW, Martin CO, Damasio H, Damasio AR. Pathological
laughter and crying: a link to the cerebellum. Brain. 2001;124:1708-
29. McCullagh S, Moore M, Gawel M, Feinstein A. Pathological laughing
and crying in amyotrophic lateral sclerosis: an association with prefrontal
cognitive dysfunction. J Neurol Sci. 1999;169:43-48.
30. Wild B, Rodden FA, Grodd W, Ruch W. Neural correlates of laughter
and humour. Brain. 2003;126(pt 10):2121-2138.
31. Parvizi J, Schiffer R. Pathological crying in a patient with a cerebellar
cyst. J Neuropsychiatry Clin Neurosci. In press.
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.


More Conversation with Dr. Smith

Hello, my name is Karen, thank you for bringing your concerns to Just Answer, before, I continue on with my reply to you..please know that I am very sorry to hear of your suffering a stroke..and the effects of this with regards continuous tearfulness..


What is known and researched is that of strokes leading to personality changes and emotional imbalances( to name but a few of the devastating effects)…and that stroke survivors often find that crying, anger, and laughter occur more easily than they did before the stroke. In some stroke patients, “emotional lability” occurs, when crying and laughter become uncontrollable…though documentation of this is somewhat limited..

A way of letting other Drs becoming much more informed of this would be by getting in touch with ‘AMA American Medical Association’..who publish the American Medical Journal’ and this gets circulated throughout America .. I have posted their website for you to highlight paste and view..for contact details..Failing this perhaps a news article in your city newspaper would be another option..with an appropriate eye catching heading for Dr’s to see and note.It has been documented over the years that indeed Citalopram is used in treatment of traumatic brain damage..

I have also posted a very informative ( though short) blog from a G Anderson of Neurology University Hospital..below..who actually wrote an article about continueous weaping with regards to a stroke..though, this article was posted in Feb 1995..yet it might be worth while writing to him never the less.

Andersen G.

Department of Neurology, Aarhus University Hospital, Denmark.
1995 Feb;6(2):105-11.


Sadly, there is not a lot of information available concerning the connection..and I wish you well if you proceed in making contact with those mentioned above..and hope that it has been helpful to you…if it has please ‘accept’ my response as it does help us greatly to keep this valuable service going for you and others in the future..
blessings in your recovery

Karen Smith, DipCoun, BMin
Professional Counsellor
Accept Answer

You replied

Monday, October 25, 2010 10:36 PM EST
Dear Dr. Smith

I am familiar with Dr. Andersen who wrote that article and I have sent him a email but he has not responded to me. Neithertheless, I will keep trying.



You have accepted an Answer!
From Karen Smith

Monday, October 25, 2010 11:29 PM EST
Hello, thank you for your reply..Oh, that is good you are familiar with Dr Andersen and his work…if he has indeed moved on perhaps it would be another option to address it to the head of the Department of Neurology, he/she might well take it a step further for you or it could be well be sent on to Dr Anderson..The next very useful option to perhaps consider would be the American Medical Journal as mentioned..if at all possible..as this permeates right across the USA throughout all hospital boards…Doctors..
Best wishes
Karen Smith Clinical Dip

Karen Smith, DipCoun, BMin
Professional Counsellor
Add Bonus

You replied

Tuesday, October 26, 2010 8:06 AM EST
I will do that as it needs to be dealt with. Thank you for all your help Karen.



You have received an Answer!
From Karen Smith

Tuesday, October 26, 2010 3:28 PM EST
Hello, thank you again for your reply …its a privilege to have been here for you…
blessings in your work..take good care.

Karen Smith, DipCoun, BMin
Professional Counsellor


My correspondence with Dr. Karen Smith

I am a patholical cryer, that is a person who cry all the time but its not because of depression. I had a stroke and it left me crying. I want to know if you ever heard of it. There doesn’t seem to be anybody who knows about it and I want to know is there anyone I can write to to get doctors to know about this, I am from Rock Hill, South Carolina.


Optional Information:
Gender: Female
Age: 54

Already Tried:
In November 2006 which was Thanksgiving weekend, my mother and my sister came down to visit me. My mother was from New Jersey and my sister was from Virginia. So my sister kept telling me that there was something wrong with my face it was twisted and my husband said that my words was slurring and I said no it wasn’t and I didn’t pay tham any mind. So it was time for my mother and sister to leave so I took them to Charlotte, North Carolina to the bus station. When me and my husband was coming back home, he told me go by the hospital to get a check up so I did. When I got to the hospital and they checked me they told me that I had 7 mini strokes and they kept me there. I was floored and thought they didn’t know what they were talking about. I stayed in the hospital for about two weeks. Then I went home and everything was alright, but then one day I was home by myself and I noticed that I was crying. I was looking at some picture on television and I was crying for nothing because it was nothing for me to cry about because there was no violence in the whole picture or anything like that. Then I just cried for any reason no reason then when someone spoke to me and I had to answer them I cried. So I went to the doctor and I cried. My doctor sent me to see a psychiatrist and he gave me some medicine and he said that he never had a patient that just cried. So after going there for a while I stopped going because he wasn’t helping me and my doctor he gave me the same medicine I was taking from the psychiatrist. So then I went to the Medical client and they did not help me either. So I could not get any help from no doctor in Rock Hill. So it was just me and my crying for two years. I told my nephew Larry and he couldn’t take it and he did some research and he found some doctor who had heard of it (what I had) he had worked on patients and done some research on different patients of his and found out that Citalopram.


I was in the hospital!

Wednesday morning 9/29/10, I took my husband to work and when I

came back home, I was still feeling tired. I tested my sugar that morning

and it was 120. So I figured it would be alright for me to go sleep for a

couple of hours so I went to sleep and woke up about 10:00 or 10:30

that morning and I went to the kitchen to make me some juice and as I

was trying to open it to start making the juice I felt lightheaded and I fell

out. I knew I could not stay on the floor because I didn’t want no

grasshoppers or roaches or anything else crawling on me so I got up. I

don’t know how I did it but I got up off that floor. I went and got into

the bed and I must have passed out. My husband found me on the bed

and called the ambulance. I did not know anything until 11:00 or 12:00

that night that’s when I came too. Thats when it began, the medicine,

blood pressure, blood work, food, sugar shot, it just goes on and on.

Well, I was on my way back from recovery. At first the doctors thought

that I was having another stroke but after the test and all that they saw

that it wasn’t a stroke. I had peumonia. I knew I a had a cold, coughing

sometime, but I thought it was going away. I didn’t know that it turned

into peumonia. They checked out my heart, it was fine. Then my foot

was still hurting from the fall but they didn’t know that because I was

unconscious at the time when I came in. Then when I had to get ready

to go donstairs I told them that my foot was hurting and I could not

stand on it. So they eventually gave me a boot to put on my foot and so

it would not move around all the time. On Thursday, we had a bible

study in the hospital and everybody came to read their bible with me. It

was the most exciting thing that happen to me. What seemed like a life

time to me, they finally let me go home. My recovery was not from a

stroke, but from peumonia and a fractured foot. But it was a recovery.


In other words all the improvement they will make will probably be in the six months following the stroke with little to no improvement after that.

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