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0034-7450/$ – see front matter © 2013 Asociación Colombiana de Psiquiatría. Publicado por Elsevier España S.L. Todos los derechos reservados.
IS N: 0 34-7450
Año 49 / Volumen 42
/ Junio
Original article
“When I Want to Cry I Can’t”: Inability to Cry
Following SSRI Treatment
Jorge Carlos Holguín-Lew
* and Vaughan Bell
Departmento de Psiquiatría, Universidad de Antioquia, Colombia
Visiting Senior Research Fellow, Institute of Psychiatry, King’s College, London, United Kingdom
Article history:
Received September 19, 2012
Accepted January 1st, 2013
Adverse effects
* Corresponding author.
Email: (J.C. Holguín Lew).
We describe seven cases of patients with an inability to cry after treatment with
selective serotonin re-uptake inhibitor (SSRI) medication, even during sad or distressing
situations that would have normally initiated a crying episode, in the light of the role of the
serotonergic system in emotional expression.
Case series drawn from patients attended in a secondary care psychiatry service.
While excessive crying without emotional distress has been previously reported
in the literature, and is associated with reduced serotonin function, these reports suggest
cases of the reverse dissociation, where emotional distress and an urge to cry was present,
but crying was impaired.
Although the case series presented here is new, these cases are consistent
with the neuroscience of crying and their relationship with serotonergic function, and
provide preliminary evidence for a double dissociation between subjective emotional
experience and the behavioural expression of crying. This helps to further illuminate the
neuroscience of emotional expression and suggests the possibility that the phenomenon is
an under-recognised adverse effect of SSRI treatment.
© 2012 Asociación Colombiana de Psiquiatría. Published by Elsevier España, S.L.
All rights reserved.
«Cuando quiero llorar, no lloro»: incapacidad para llorar tras el
tratamiento con inhibidores selectivos de la recaptación de serotonina
Se describen los casos de 7 pacientes con incapacidad para llorar tras trata-
miento con un inhibidor de la recaptación de serotonina (ISRS), situación que se presenta
aun en situaciones estresantes o tristes, que normalmente les habrían iniciado una res-
puesta de llanto. Los casos se examinan a la luz de lo que se conoce acerca del papel del
sistema serotoninérgico en la expresión emocional.
Serie de casos de pacientes que acuden a un servicio de atención secundaria en
Palabras clave:
Efectos adversos
“Cuando quiero llorar, no lloro,
y a veces lloro sin querer…”
Canción de Otoño en Primavera,
Rubén Darío)
Dysfunctions in emotional modulation, experience, and
ex pres sion are frequent in patients with both primary
and secon dary psychiatric disorders. Uncontrollable or
involuntary crying has been widely reported after many
types of neurological damage or disease, where it may be
labelled as ‘pathological laughing or crying’, ‘pseudobulbar
affect’, ‘emotionalism’ or ‘involuntary emotional expression
disorder’ (IEED) to name but a few of the many terms in use.
Conversely, while crying is most typically associated with
mood disorders, evidence that depression leads to more
frequent crying, or, conversely, that severely depressed
individuals lose their capacity to cry, is mixed, and little
reliable empirical evidence for the connection between mood
pathology and crying can be found in the literature.
it is clear from the clinical literature that crying behaviour and
emotional distress can dissociate, so people who experience
involuntary crying may not necessarily experience the
subjec tive emotional feeling that usually accompanies these
This paper reports on 7 cases that demonstrate
the reverse dissociation, an inability to cry after intervention
with selective serotonin reuptake inhibitor (SSRI) medication,
despite the subjective emotional feeling of sadness and the
urge to cry, indicating a perhaps under-recognised adverse
effect and providing further evidence for the neural basis of
crying regulation.
Previous studies on the possible neurological basis of
pathological crying have not come to any clear conclusions as
to which neural circuits are implicated in the condition and, to
complicate matters for those specifically interested in crying, it
is often the case that excessive crying and excessive laughing
are studied as the same phenomenon. The first and still
influential theory of pathological laughing and crying suggests
that it results from ‘disinhibition’ or ‘release phenomenon’ after
damage to the voluntary inhibitory mechanisms in the upper
brain stem.
 However, it has become increasingly clear that
excessive crying is not obviously linked to damage to any one
specific brain area.
 Indeed, prior reports based on lesion data
have implicated a wide range of specific cortical and subcortical
areas, with recent theories focusing on two major pathways:
the cerebro-ponto-cerebellar pathway
 and the cortico-limbic-
subcortico-thalamic-ponto-cerebellar network.
In a recent
review of the literature, however, Nieuwenhuis-Mark et
 noted that the most commonly implicated areas from the
lesion data include the limbic system, brain stem and frontal
lobes, as well as evidence for excessive crying being linked to
a greater level of overall damage and a lower ratio of serotonin
transporter (SERT) binding ratios in the brain stem.
The link with serotonin transporter has emerged from two
neuroimaging studies that have used radioligand binding
to understand serotonin function in stroke patients with
pathological crying. A single-photon emission computed
tomography (SPECT) study by Murai
 found lower SERT binding
ratios in the midbrain and pons in pathological crying patients
compared to non-affected controls, while a positron emission
tomography (PET) study by Møller, Andersen et al
found a
globally lower level of 5HT
receptor binding associated
with pathological crying. This is in line with evidence that
serotonergic medication is an effective treatment for excessive
 and that it typically resolves crying episodes at lower
doses than are needed to treat depression. Furthermore,
resolution of excessive crying typically occurs within days,
in contrast to the several weeks typically needed for the mood
elevating effects.
 In line with this, excessive crying is
recognized as a symptom of SSRI discontinuation syndrome.
From this evidence, a clear prediction emerges that the
over-modulation of serotonergic pathways would induce
the inability to cry in some patients. However, this is a topic
that has rarely been addressed in the clinical literature.
In fact, to our knowledge, only two minor reports exist. In a
letter to the editor, Oleshansky et al
 discussed 3 patients who
seemingly ‘lost’ their ability to cry after starting treatment
with SSRI medication with examples of specific episodes that
typically caused crying in the past but no longer triggered a
tearful response. In addition, a short report by Opbroek et
described 15 patients with sexual dysfunction after SSRI
treatment, of which 60% (n
9), reported that they experienced
Mientras el llanto excesivo sin estrés emocional ya se había descrito en la
literatura asociado con una función serotoninérgica reducida, los presentes reportes
apuntan casos de la disociación inversa, en los que el estrés emocional y la urgencia de
llorar se encontraban presentes, pero con incapacidad para el llanto.
Aunque la serie de casos aquí presentada es nueva, concuerdan con la neurociencia
del llanto y su relación con la función serotoninérgica, y proveen evidencia preliminar para
una disociación doble entre la experiencia emocional subjetiva y la expresión conductual
del llanto. Esto ayuda a elucidar la neurociencia de la expresión emocional y apunta la
posibilidad de que el fenómeno sea un efecto adverso poco detectado del tratamiento con
© 2012 Asociación Colombiana de Psiquiatría. Publicado por Elsevier España, S.L.
Todos los derechos reservados.
the ability to cry ‘a lot less than usual’. However, no con textual
details were given, so it is difficult to say to what extent this
effect may have been due to changes in exposure to emotional
stimuli, changes in appraisal of emotional events, or a loss of
ability to control tears, all three of which are cited as possible
processes having an effect on crying frequency.
In the present study we report a series of 7 psychiatric
patients without neurological damage who presented with
an inability to cry during treatment with SSRIs, even during
extremely sad or moving situations that were cited as likely
to have previously initiated a crying episode. We discuss
implications for serotonergic models of emotional control and
the understanding of how subjective emotional feeling and
emotional expression may dissociate.
Case Reports
Case 1
A female patient aged 43, presented to psychiatric consultation
due to a depressive episode, with profound sadness and
anhedonia, sleep disturbance, low energy, negative cognitions,
and difficulties in concentration. On the first consultation, she
scored 27 on the Beck Depression Inventory version 1A (BDI).
A neurological examination and recent CT scan reported no
abnormalities and she had no history of neurological disease
or acquired brain injury. A general physical examination
found no abnormalities and blood, glucose, thyroid, hepatic
function and creatinine tests were all in the normal range.
The patient was started on escitalopram 10 mg/day. After
five weeks of treatment she reported feeling quite well and
her score on the BDI reduced to 8, within the ‘no depression’
range. After 2 months of treatment, she felt she was no longer
depressed and considered that her day-to-day functioning,
relationships and quality of life had returned to normal.
However, she mentioned she had noticed something that
seemed very curious to her — her pet dog had died one week
ago and although she felt very sad and wanted to cry, she was
unable. She reported the experience as puzzling: “I felt a bit
strange, you know… I really wanted to cry, and I was feeling
like if I was on the brink of doing it, but it is like if my face
and my eyes could not do it”. She was emphatic in saying that
she was not apathetic, that her capacity for enjoying life was
preserved, that it was something only affecting her capacity
for crying. She did not want to stop the medication, fearing
a relapse. The patient has continued taking the medication,
and the inability to cry has persisted. She considered this as
a curious but tolerable side-effect, although she wondered if
being unable to cry would have later consequences because of
“repressed sad feelings”, considering crying as cathartic and
that being unable to cry might “not be good for your mental
Case 2
A 23 year-old male patient presented to psychiatric
consultation with a history of obsessive compulsive
disorder commencing around the age of 15. His obsessions
included intrusive thoughts concerning obscenities and
contamination. His compulsions were restricted to washing
rituals. He did not tolerate sertraline, because of nausea and
sleepiness, and he was subsequently started on fluvoxamine
which was increased to 300 mg/day and was tolerated well.
After 8 weeks of taking fluvoxamine, severity, frequency
and interference of both obsessions and compulsions were
greatly diminished. He reported no comorbid depression, but
fulfilled criteria for generalised anxiety disorder, although
he reported that he felt his tendency for excessive worry had
improved with treatment. After four months of treatment
he noticed that he was unable to cry. Two weeks before the
consultation he ended his romantic relationship and felt sad,
wanting to cry, but could not, as if his “capacity for crying
was frozen”. He was neither apathetic, nor depressed (BDI
score 7). After discussing the matter with him, he preferred
not to change fluvoxamine treatment, because, apart from
the inability to cry, he was very satisfied with the results
of the treatment and considered this side effect a minor
Case 3
A 30 year-old male patient presented to consultation because of
a depressive episode that started at least 5 months previously,
with a score of 25 on the BDI. This was his third major
depressive episode. A CT scan, neurological examination,
thyroid levels, and other general laboratory exams were
normal. The patient had a history of good response and
remission with sertraline 100 mg/day in all previous episodes
and was subsequently restarted on this treatment regime.
After 8 weeks of treatment, his depression was in remission,
scoring 5 (‘no depression’) on the BDI. However, he noticed
that he was unable to cry, even when feeling sad. He described
the situation where his mother was diagnosed with a severe
coronary disease, and, although he felt very sad and wanted
to cry, he couldn’t because “it was as if I had no tears, as
if my face didn’t remember how to cry”. He remembered
having the same experience during previous treatments, but
he did not feel the need to mention it. Subsequent to this
point, the patient has been on the treatment for 12 months,
and the inabi lity to cry has diminished, although he says that
it is still present to a certain degree. He considers that crying
could be healthy on some occasions, but that usually he was
not a “very tearful person” and that he only tended to cry and
being excessively moved by events when depressed or with
severe stressors.
Case 4
A 45 year-old female patient presented to consultation with
her fourth depressive episode. She had previously been
prescribed buproprion and venlafaxine but these treatments
were abandoned because of side-effects (mainly headache,
constipation, irritability and dizziness). She also had previous
treatment with fluoxetine 20 mg/day that she tolerated
better, although with diminished libido. After discussing
alternatives, the patient was prescribed citalopram 20 mg/day.
A CT scan, neurological examination, thyrioid test and other
medical examinations were normal. The initial BDI score was
23. After 4 weeks, she reported feeling much better and quite
comfortable with the citalopram (BDI score 13). However,
after week 12 she complained of diminished sexual desire
and a delay in reaching orgasm. Although in her opinion, the
side-effect was less than with fluoxetine, she was motivated
to request a consultation to discuss alternatives. During the
meeting she remarked “a quite surprising inability to cry”.
She noticed that when watching very moving films (an event
that almost always led her to cry) she “simply couldn’t cry”.
She reported no apathy, depression, anhedonia or other mood
manifestations (BDI score 9). She found that the experience of
not being able to cry was surprising, but not really distressing.
Buspirone, up to 40 mg/day for 6 weeks, was added to her
treatment regime in an attempt to address the sexual
side-effects. Sexual function improved although not to levels
previous to treatment. She also noticed that her ability to cry
had improved (e.g., she would shed tears in a very moving
movie, she cried during a memorial service and found that in
both occasions “it felt right and relieving to cry”). She remains
on both treatments and feels satisfied with them.
Case 5
A 60 year-old woman presented to consultation with a
seventh major depressive episode and a history of previous
treatments with sertraline and escitalopram. CT scan was
reported as normal for her age, with no evidence of vascular
disease or atrophy or other findings that would make think
about a neurological disease. Although she had a history of
hypothyroidism, she was on treatment and a recent thyroid
work-up was within normal range. She was subsequently
prescribed escitalopram 10 mg/day and, after 7 weeks of
treatment, she reported significant improvement. However,
she noted that she was unable to cry when going to the
cemetery to visit her husband’s grave or when one of her
grand children had an accident. She felt that “I was very
sad but I was like dry inside. I wanted to cry, but couldn’t
shed a single tear”. After 10 weeks, her depression was
markedly improved although her inability to cry continued.
She is still on the same treatment and the inability to cry
continues without change although the patient does not feel
this side-effect warrants a change of treatment. She was not
concerned by the inability to cry in itself, but she considered
that the fact she was not able to shed tears when visiting her
late husband’s tomb “was not right”.
Case 6
A 35 year-old male patient reported to consultation with a
third depressive episode. A neurological examination found
no abnormalities, and other medical tests (blood, thyroid, HIV,
blood sugar, etc.) were normal. The patient had no prior history
of previous pharmacological treatment. He was started on
escitalopram 10 mg/day and reported that his depression had
significantly improved after 4 weeks. However, he complained
about a significant decrease in sexual desire and delayed
ejaculation. He also noticed that, paradoxically, when feeling
sad, he was unable to cry. For example, he remembered that
he saw reports of hostages being released he felt very moved,
saying “emotionally I was crying, but in my face no change
happened”. Similarly during a very difficult argument with
his boyfriend he remembered that “I wanted to cry, I feel
like crying, but my body doesn’t respond, like if my crying
apparatus is broken”. He wanted to wait longer before thinking
about changing his medication hoping that the sexual side
effects would subside. He experienced the inability to cry as
something curious, but not especially distressing. However,
he wanted to be able to cry in appropriate situations, for
example, during a memorial service, because it seemed to
him that not being able to cry in some circumstances might
not be polite or healthy. Several weeks later, he went on a
three day trip, and forgot to take his medication. Besides
the usual discomfort due to sudden SSRI discontinuation,
he had several “crying spells”. He described these spells as
“crying without reason, like veritable storm of tears”. He
was emphatic in denying any sad mood accompanying the
crying spells. After a further consultation, the patients started
mirtazapine, that was not well tolerated due to excessive
sleepiness. Subsequently, he was prescribed brupropion, and
had a noticeable increase in anxiety and irritability. Finally,
he was started on reboxetine, that effectively treated his
depression without sexual dysfunction. He has reported no
further episodes of an inability to cry.
Case 7
A 34 year-old female patient reported to consultation owing
to an onset of a major depressive episode. The patient had
a prior diagnosis of dysthymia and double depression (a
concept used more widely in the Americas, that describes
an acute episode of major depressive disorder superimposed
on dysthymia
), and had a history of good symptomatic
response to paroxetine. She was therefore restarted on
paroxetine 20 mg, but after 5 weeks the response was still
partial and therefore the dosage was increased. Three weeks
later she reported having continued improvement and after
12 weeks she was reported feeling significantly improved and
did no longer qualified for a diagnosis of major depression.
However she complained of low sexual desire and delay in
orgasm. She also noticed that “When I want to cry, I can’t. It’s
like my body had forgotten how to cry. I try, but I can’t.” For
example, one of her neighbours died, an event that usually
would have led her to cry, but he was not able to do so. She
noticed a similar inability after arguments with her partner
or mother. She was concerned whether being unable to cry
was normal or whether it would have negative consequences.
However, she preferred to continue paroxetine treatment,
because of the improvement of her mood symptoms. In
order to improve sexual response, burproprion 150 mg/day
was added. After several weeks, sexual desire and response
improved. However, her inability to cry has continued.
We have reported 7 cases in which patients treated with
a diverse range of SSRIs presented with an inability to cry
after several weeks of treatment, even when distressed and
in situation which would normally lead to crying. This was
recounted by patients as if the bodily systems involved in
crying were “frozen”, had “broken” or that the “body had
forgotten how to cry”, in which the patients demonstrated
a dissociation between the presence of subjective feelings
of distress and an urge to cry; and the expressive, motor
components of affect. It is important to emphasise that the
patients were neither apathetic nor blunted in their feelings
— i.e. their subjective experience of emotion was preserved.
Significantly, several of the patients reports that this
inability manifested itself in situations where they would
normally have cried on previous, pre-treatment, occasions;
that they appraised the situation as emotionally distressing;
and that they experienced an urge to cry. Nieuwenhuis-Mark
et al
have criticised some earlier studies of crying, noting
that they often do not specifically address differences in
exposure to emotional stimuli, changes in appraisal of
emotional events, or the control of the urge and expression of
tears, and it is notable that, unlike the present study, neither
of the previous two reports of reduced crying after SSRI
allow these factors to be fully accounted for.
These case studies provide further evidence of the
importance of serotonergic systems in the control of crying.
While all SSRI medication is thought to derive its clinical
effect from the high affinity for the serotonin transporter
and the in creases in the efficiency of post-synaptic
5HT transmission,
the secondary effects of individual
compounds are remarkably variable. Indeed, compounds
associated with inability to cry in the present study have a
range of secondary effects: fluvoxamine on sigma-1 receptors,
paroxetine on muscarinic receptors, sertraline on dopamine
receptors, and citalopram and escitalopram on histamine
receptors (review in Carrasco et al
). The fact that in the
present study an inability to cry was associated with a range
of SSRIs with differing secondary effects suggests that it
is the primary action on increasing synaptic availability
of serotonin which mediates the effect. This is in line
with clinical evidence that SSRIs can treat pathological
 that SSRI discontinuation can lead to crying spells
and the radioligand neuroimaging evidence of lower serotonin
turnover in subcortical areas associated with pathological
crying after stroke.
It is notable that all patients reported here described
a dissociation between crying and subjective feelings
of sadness. Indeed, this dissociation has been reported
previously, although typically in its opposite form, where
pathological crying is present without the subjective
emotional component. This has been reported in cases of
acquired brain injury, stroke, multiple sclerosis, amyotrophic
lateral sclerosis, Parkinson’s disease and Alzheimer’s disease
(see review in Wortzel et al
), as well as a side-effect of
deep brain stimulation to the caudal internal capsule
and the subthalamic nucleus.
 While this dissociation
is most commonly reported after neurological disorder, as
the phenomena of experienced emotion without the normal
behavioural expression is known in schizophrenia, where
diminished facial expression of emotion can be accompanied
by a full subjective emotional experience.
From a psychopathological point of view, an understanding
of how expression and subjective emotion may dissociate
is still in a very preliminary state with a more refined
conceptualisation still lacking. With this in mind, we
offer a tentative classification of how syndromes could be
categorised by the distinction of emotional expression and
emotional experience (table 1).
At present, the justification for our classification is largely
based on clinical observation: patients complain of excesses
or deficits in the experience of some emotions and/or their
expression. On the basis of the value of dissociation in
cognitive neuropsychiatry research
, this plausible although
tentative descriptive classification suggests that there may be
distinct mechanisms underlying subjective experience and
emotional expression (importantly, beyond the simple control
of the musculature), although exactly how distinct and how
separable in terms of cognitive and neural subsystems
remains to be seen. For example, we would expect at the least
a significant two-way feedback between the experience and
expression components considering evidence that voluntarily
forming expressions can have a reciprocal effect on mood
(e.g. Kleinke et al
It is also notable that the patients reported here did not
report apathy or emotional blunting, suggesting that inability
to cry was dissociated from both. This is important as each
can evidently present as symptoms of major depression,
and moreover, each has been reported as a result of SSRI
 In this case series, however, an inability to cry
was associated with other ‘inhibitory’ side-effects: in cases 4,
6 and 7, sexual dysfunction was apparent and, interestingly,
intervention to counteract or compensate for this well-known
serotoninergic side-effect also reversed the inability to cry.
In patient 6, the reversal of inability to cry can be considered
extreme, because of the subsequent presentation of crying
spells on unplanned withdrawal of citalopram. Although
there is no research that addresses this directly, we wonder
whether these ‘inhibitory’ effects may be on a continuum,
Absent or diminished
Present or excessive
Absent or
Apathy, negativism
Pathological crying
and/or laughing
Gelastic seizures
Crying spells (e.g. SSRI
Present or
Affective blunting
or flat affect
Facial akinesia
Inability to cry
Mood lability
Excessive tendency
to cry
Table 1 – Examples of affective symptoms classified
as disorders of emotional experience and expression
where greater serotonergic modulation has an increasingly
inhibitory effect on some function or patients to the point of
apathy at the most extreme end of the spectrum.
With regards to the possible clinical effects of an
inability to cry, it is notable that the experience was
reported as noteworthy enough to mention to a doctor but
not particularly distressing in itself. The reporting of this
experience in a clinical context remind us of the social
and cultural components of emotional expression that
form part of the attribution that something seems out of
the ordinary or emotionally ‘wrong’ and it is notable that
several of the patients mentioned that they were concerned
about the consequences for their mental health, reflecting
the widespread view that crying is cathartic.
empirical support for the catharsis hypothesis is mixed and
the cathartic effect of crying has been found to be modulated
by the response of others, as much as any intrinsic value
to crying itself.
 Perhaps most relevantly, a recent study,
albeit solely on women,
 found that while the majority
(89%) reported relief from crying, those with symptoms of
depression, anxiety, anhedonia and/or alexithymia reported
that crying left them feeling worse or just the same. However,
in this case series, the majority of patients had recovered from
their index diagnosis while being unable to cry, and it is not
clear from this evidence whether this inability prevents them
from accessing a useful form of emotional release, protects
them from unhelpful crying spells (particularly considering
the psychological and neurobiological vulnerability factors
still present in recovered depressed patients
), or has no
effect either way.
We report a dissociation between intact subjective emotional
distress and impaired ability to cry related to the use of SSRI
medication. Although the study has limitations inherent
to case series (mainly selection bias and retrospective
analysis) we hope that it stimulates further research in
this area particularly in light of its theoretical support
from the previous literature on the serotonin system and
crying. From a clinical perspective an inability to cry may
diminish the tolerability and acceptability of treatment
for the patient, particularly in light of the popularly
accepted ‘cathartis model’ of crying despite the fact that
the current literature does support the popular idea
that being unable to cry is emotionally harmful. From a
scientific perspective, the clinical dissociation of emotional
experience and expression suggests a distinction between
underlying cognitive and neurobiological mechanisms and
provides a basis for further prospective studies in this area.
Conflicto de intereses
Jorge Holguin Lew ha sido conferencista remunerado en activi-
dades académicas financiadas por Astra Zeneca, Lundbeck,
Jannssen, Novartis, Eli-Lilly y Servier. Ha asistido a congresos
y actividades académicas en donde su desplazamiento, inscrip-
ción y estadía ha sido financiada por estas casas farmacéuticas.
No posee acciones de ninguna de estas compañías ni recibe
honorarios por afiliación laboral directa.
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