Bassani et al. BMC Res Notes (2017) 10:109
DOI 10.1186/s13104-017-2425-z

BMC Research Notes
Open Access

CASE REPORT

Crying spells triggered by thumb‑index
rubbing after thalamic stroke: a case report
R. Bassani1,2, C. Rosazza3, L. Ghirardin1, V. Caldiera3, E. Banco2, C. Casati2 and L. Tesio2,4*

Abstract
Background: Pathologic crying, devoid of any emotional counterpart, is known to occur as a consequence of various brain stem, cortical hemispheric and cerebellar lesions or, quite exceptionally, of “dacrystic” epilepsy. The case
reported here suggests that thalamic lesions may also cause crying spells, under the special circumstances described
below.
Case presentation: After a mild left thalamic stroke a caucasian 77 years old man presented with crying spells with
no emotional counterpart, triggered by thumb-index rubbing of his right hand. Only a modest sensation loss on
right infra-orbital and nose-labial areas and the first three right fingers could be detected at clinical examination. The
circumstances and processes leading to the crying spells were investigated, together with their neural substrate. Brain
computerized tomography (CT), magnetic resonance imaging (MRI) and functional magnetic resonance imaging
(fMRI) were conducted. Neurophysiologic studies included Video-Electroencephalography, Electromyography, motor
and sensory Evoked potentials. Active thumb-index rubbing, passive fingertips stimulation and interaction of sensorymotor stimulation with cognitive/speech activities were tested under different paradigms. A treatment with pregabalin (75 mg twice a day) was attempted. CT and MRI showed a small ischemic infarct in the left ventral postero-lateral
thalamus, while fMRI led to the expected findings, i.e. a bilateral activation of the hand motor representation during
the crying-triggering right-hand finger rubbing activity. Sensory potentials evoked from stimulation of the right
upper limb were the only abnormal neurophysiologic test. Crying spells could be invariably evoked by both real and
imagined active finger rubbing, in either the left of right hemi-space. Rubbing by an examiner was ineffective. Immersion in water (18 °C) but not oiling of the fingertips prevented the symptom. Administration and discontinuation of
pregabalin 75 mg daily could be associated with suppression and reappearance of the symptom, respectively.
Conclusions: In this patient loss of sensation seemed to generate crying spells rather than the more common
allodynia. As a matter of speculation, both symptoms might represent responses to a sensory loss, but in this case the
pathway might have been selectively affected providing inhibition from the lateral to the medial segment of the VPLT,
which is linked to the anterior cingulate (limbic) cortex engaged in emotional behaviour.
Keywords: Crying, Cerebrovascular disease, Thalamus, Stroke, Case report
Background
Despite being rare, pathologic crying, devoid of any emotional counterpart, is known to occur as a consequence
of various brain stem and hemispheric cortical lesions
[1] or, quite exceptionally, of “dacrystic” epilepsy [2]. To
the Authors’ knowledge, lesions of the thalamus has been

never suggested as a source of this symptom. The case
is presented here of a man suffering from disabling crying spells after a mild thalamic stroke. The symptom was
only triggered by thumb-index rubbing of the contralesional hand. This case can stimulate hypotheses concerning the role of the thalamus in crying control.

*Correspondence: luigi.tesio@unimi.it
2
Department of Neurorehabilitation Sciences, Istituto Auxologico
Italiano, IRCCS, Milan, Italy
Full list of author information is available at the end of the article

Case presentation
A caucasian man aged 77 was admitted to the emergency
room with symptoms indicative of a right brachial monoparesis and facio-brachial tingling paresthesiae. Brain

© The Author(s) 2017. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License
(http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium,
provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/
publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Bassani et al. BMC Res Notes (2017) 10:109

computerized tomography (CT) was negative for acute
lesions. Approximately 3 h following the onset of symptoms the patient was transferred to a stroke unit where
he underwent intravenous thrombolysis with alteplase
0.9 mg kg−1.
The procedure was well tolerated with no side effects.
The patient was then discharged, despite still suffering of
right facio-brachial paresthesiae. A brain CT performed
4 days after the event showed an ischemic lesion to the
left ventral-posterior lateral thalamus (VPLT).
Two weeks after the event a new symptom was
observed by the patient and reported to the first Author.
A crying spell, inclusive of tears but devoid of any emotional substrate, was triggered whenever the patient
rubbed the tips of his right hand thumb and index fingers. The examiner established through a stopwatch that
the frequency of the movement had to be at least 1 Hz.
The crying spell started in 5–10 s and faded 3–5 s after
the movement stopped. The symptoms were also triggered by various daily activities such as using cutlery and
playing cards, thus impairing the patient’s social interaction. No pain was reported. The patient adapted to his
condition by wearing a thick glove on his right hand. A
series of tests was started 8 weeks after the acute event.
Written informed consent was obtained from the patient.
Representative motor tests are shown in the video provided with the Additional file 1. Clinical examination
showed a moderate sensory loss on light touch on the
palmar side of the first three right hand fingers, as well as
on the right infra-orbital and nose-labial areas. A videoEEG excluded epileptic seizures during crying spells
(Fig. 1). Motor evoked potentials were normal. Sensory
evoked potentials from stimulation of the left limbs

Page 2 of 7

evidenced increased latency, low voltage and temporal
dispersion (not shown).
The patient was administered a neuropsychological
evaluation in order to describe his cognitive functioning
and to exclude cognitive deficits. Thalamic lesions may in
fact lead to many cognitive impairments, spanning from
decreased consciousness to dementia and including deficits in spatial representation and memory [3], the latter
being of potential relevance for the motor tests described
below. However, the cognitive tests ruled out language,
praxic, executive, attention, spatial attention, memory
and abstract reasoning deficits, as in all tests the patient’s
performance was within the tolerance limits of a reference sample of subjects similar for age and educational
level (details are provided in the Additional file 1). This
was also consistent with the site and the size of the lesion
(see below). Active thumb-index rubbing, passive fingertips stimulation and interaction of sensory-motor stimulation with cognitive/speech activities were tested under
different paradigms, in blocks as shown in Table 1.
One examiner (CC) stimulated the patient for about
20 s in each task. Another examiner (LT) determined
the onset of a crying spell when an evident change in
size and/or frequency of ventilation and a typical grimace developed (usually, within 5–6 s). In this case, the
stimulation was suddenly stopped. Blocks of tasks were
balanced (ABBA sequence). The patient was videotaped.
Representative tasks (marked with asterisk in Table 1) are
shown in the Additional file 2.
During the experimental session, three independent
observers (TL, BR, BE) checked for presence/absence
of the crying spell. In Table 1 the fourth column from
the right gives the observed outcome (onset/absence of

Fig. 1 Video-encehalography before (a) and during (b) thumb-index rubbing of the right hand, causing a crying spell. As soon as the patient starts
crying (left arrow pointing to the electroencephalographic tracing) the ventilation pattern shows a gradual increment both in frequency and amplitude (right arrow pointing to the respiratory tracing)

Bassani et al. BMC Res Notes (2017) 10:109

Page 3 of 7

Table 1 Motor-sensory tasks aimed at investigating the modality of triggering crying spells under finger scrubbing
Main tasks

Blocks

Task alternative modes

Crying-triggering tasks/
modes

On-line video

Light thumb-index rubbing

Eyes open

Left hand; right hand; both

Right hand; both

*

Eyes closed

Left hand; right hand; both

Right hand; both

Eyes closed, imagined movement

Left hand; right hand

Right hand

Eyes open. The “rubbing” hand
is covered and replaced by
another one’s hand rubbing

Left hand; right hand

Right hand

Index and thumb flex but do
not touch each other (finger
tapping)

Left hand; right hand; both

None

Arms straight and crossed, eyes
open

Left hand; right hand; both

Right hand

Passive stimulation

Hand immersion in water, 24 °C

No motion; right hand

None

Hand fingertips stained with
grease

Right hand

Right hand

Passive rubbing of index fingertip (toothbrush)

Right hand; right hallux

No

Warming of hand fingertips
(hair dryer)

Right hand

No

Cognition/speech (narration; reading aloud; month
sequencing; counting
backwards)

*

*

Hands still; right hand “counting Right hand
money”

* Indicate the tests presented in the Additional file 2

crying spells). This was fully reproducible with no exceptions across repetitions of identical tasks and across
observers. It must be highlighted that crying (a) was only
triggered by active rubbing of the fingers (not toes), with
eyes either open or closed, during either a real or imagined task; (b) it persisted when the fingertips were oiled
(olive oil at room temperature 24 °C), but ceased if the
hand was immersed in tap water at 18 °C; (c) it appeared
irrespective of the fact that the hand was placed in the
left or the right hemi-space.
The MRI exam showed an old lacunar infarct in the
left thalamus, likely involving its ventral, posterolateral
portion (VPLT, Fig. 2). This small lesion (6 mm largest
diameter, 83 mm3 volume) appeared characteristically
hypointense in the T1-weighted image (lower left image)
and hyperintense in the T2-weighted image (lower right
image). MRI also showed signs of chronic microvascular
ischemic disease, a common finding in elderly people.
An fMRI exam was also performed (Fig. 2). A blockeddesign sensory-motor task was adopted, with 12 active
blocks (6 for each side) alternating with 8 rest blocks.
The task consisted of active thumb-index rubbing on visual instruction, for 20 s per block. Two examiners (CR,
LT) checked the patient’s performance. The patient was
instructed to stop rubbing when crying started (usually

within 5–6 s) in order to avoid head movements hindering the results of the fMRI task. The sensory-motor task
elicited a typical pattern of activations in the motor and
sensory hand area, which were weaker for the affected
(right) hand (P < 0.001, uncorrected) as the movement
was only briefly performed. Presumably, this asymmetry
also reflected the longer stimulation allowed to the unimpaired hand. During movement of the impaired hand,
the pattern of activation observed with fMRI involved
expected areas, i.e. both the controlateral motor and sensory hand area and the ipsilateral hand area. Pregabalin
was prescribed (75 mg the first day, then 75 mg twice
daily). The crying spells receded within a week. The drug,
however, caused some sedation. After the first week it
was gradually suspended through the subsequent week.
Crying spells reappeared the day after the treatment was
discontinued. The drug was re-administered and crying
spells disappeared again in one week. Under continuous treatment no crying spells were reported during a
6 months period.

Conclusions
An ischemic lesion of the VPLT was the only one visible
brain alteration that could be related to patient’s symptoms. Presumably, this resulted from occlusion of one

Bassani et al. BMC Res Notes (2017) 10:109

Page 4 of 7

Fig. 2 T1 (upper row of panels) AND T2-weighted (lower left panel) magnetic resonance images evidencing a lacunar infarct in the ventral posterolateral portion of the left thalamus. The lesion is millimetric (6 mm longest diameter, 83 mm3 volume) and it appears characteristically hypointense
in the T1-weighted sequence, and hyperintense in the T2-weighted sequence and in Flair (not shown). Diffusion-weighted MR image and apparent
diffusion coefficient map (not shown) do not evidence any associated restriction of water molecules diffusivity, thus confirming that the lesion is
a chronic lacunar stroke. In addition, the magnetic resonance imaging shows the presence of multiple gliotic subcortical and periventricular areas
suggestive of a chronic microvascular ischemic disease, a common finding in elderly people. In the lower right corner the figure shows functional
magnetic resonance images of a sensory-motor task consisting of rubbing the fingers of the affected (right) hand. The movement elicited a typical
pattern of activation of both the controlateral motor and sensory hand area and the ipsilateral hand area (P < 0.001, uncorrected). Images are all
shown in radiological convention (right is left)

or more of the thalamogeniculate arteries [4]. The fMRI
findings were all expected.
The sensory deficit closely matched the one seen in
cases of hand-mouth (“cheiro-oral”) sensory syndromes
caused by a lesion in the VPLT, where representations
of the face and of the hand are very close to each other
[5]. How to classify this case, within the framework of

known neurologic syndromes? The choice depends
on whether the sensory or the behavioural side of the
phenomenon are highlighted. On the sensory side, two
hypotheses can be put forward: the case is an example
of (a) thalamic (Roussy-Dejérine) syndrome [6], or (b) of
allodynia within a poststroke thalamic pain (PSTP) syndrome [7].

Bassani et al. BMC Res Notes (2017) 10:109

a. Classifying the case within the “analgetic” subtype
of thalamic syndromes fits with the lesion site, the
absence of pain, and the moderate alterations in sensation and sensory evoked potentials.
b. A subclinical mechanical allodynia [8] was seemingly
at work. The fingertips stimulation seemed to elicite much more than a pure feeling of touch. While
allodynia is a component of the PSTP syndrome,
yet it belongs to the large family of neuropathic pain
symptoms and is not necessarily associated with thalamic lesions. It may follow pure sensory loss and it
is considered to reflect central “sensitization” stemming from a slow maladaptive plasticity [7, 9]. As it
is the case for most of the allodynic symptoms, also
in this case crying appeared weeks after the lesion.
Consistently with this sensory-allodynic interpretation, suppression of the symptom could be obtained
by immersing the hand in water at 18 °C for a few
seconds. This possibly followed a cooling-related
mild increase of the threshold for touch detection
[10], and indeed lubrication with oil was unsurprisingly ineffective. Presumably, the mere lubrication
(at 24 °C) did not cool the skin and left the tactile
threshold unaffected, although in itself it can influence grip forces and the sense of touch pleasantness
[11]. In addition, the symptom was highly responsive
to pregabalin, known to be effective in neuropathic
pain [12].
Neither hypothesis fits perfectly the clinical picture,
however, due to the absence of pain.
If the crying behaviour per se is highlighted, three more
candidate classifications for this case can be put forward. The case could represent a variant of (a) “disorder
of laughing and crying”—DLC [13], (b) of release of the
palmo-mental reflex and (c) of tickle behaviour.
a.

The case might be reasonably classified as a “negative sensory” variant of DLC. In fact the underlying
pathology is of destructive, not irritative (e.g. epileptic), nature (hence the “negative” connotation) and the
symptom is triggered by stimuli usually unrelated to
crying. The mechanism leading to this type of DLC is
described by its proponents as follows: “Destructive
lesions or diaschisis alter central appraisal and sensory
processing of feelings or emotional or nonemotional
stimuli, leading to inappropriate emotional output
after a stimulus, so that stimuli such as pain and touch
lead to inappropriate emotional output” [13]. The new
classification is consistent with the observation that a
variety of diseases and lesion sites, possibly affecting
shared neural circuits, may lead to similar clinical pictures. In fact, the proponents state that “the concept

Page 5 of 7

of laughter and crying centers should be replaced by
circuits modulating emotional and sensory stimuli”
(italics in the original text) [13].
Neither this classification can encase the whole clinical
picture, however. The fact that crying was only triggered
by active (self ) thumb-index rubbing, both physical and
imagined, remains in fact unexplained.
b. Rubbing of the thenar eminence may be sufficient to
trigger the palmomental reflex [14], both in healthy
infants and in adults after various brain lesions.
Again, the above classification does not fit the clinical
picture. In fact, the palmo-mental reflex can be elicited
by passive (e.g. by another person) rubbing.
c.

In tickle, mild cutaneous stimuli (including rubbing
of the palms) may evoke contradictory feelings (both
pleasant and unpleasant) and complex avoidance
behaviours. It is known that self-tickling is impossible [15]. By contrast, crying spells in the case reported
here could be only evoked by active self-rubbing.

Two main questions thus remain open: (a) why finger
rubbing elicited crying and neither laughing nor pain and
(b) why only self-rubbing, either real or imagined, and
not passive rubbing could trigger the crying spells.
With respect to the former question, one should recall
that laughing and crying both belong to the DLC syndromes. A sudden shift from crying to laughing can be
oserved in the same patient, in response to the same
stimulus (for historical recalls on pathologic laughter and
crying see ref. 1). The site of the crying/laughing switch
(or switches) is presently unknown. For sure, crying and
pain are related. For unknown reasons crying is perhaps
the most primitive and explicit behaviour communicating pain and other danger-related feelings such as hunger
and fear [16]. Yet, in many circumstances healthy adults
can suppress crying. Actually, the behavioural and neurobiological basis of inappropriate, “pathologic” crying still
remains poorly understood [17].
This curious case encourages some speculation on the
site of the damage to the neural circuitries linking (or,
possibly, decoupling) cutaneous sensation and crying.
The lateral thalamus projects to the primary and secondary somatosensory cortices and is considered to be
involved in the discriminative and thermal-nociceptive
dimensions of pain. The medial thalamus (so called “limbic” thalamus) [18] projects to the anterior cingulate cortex and is considered to control, through this projection,
the affective-emotional and behavioural aspects of pain.
In fact, various models of deafferentation pain, typically

Bassani et al. BMC Res Notes (2017) 10:109

presenting with severe emotional characteristics, converge in ascribing symptoms to hypoactivity of the lateral
thalamus, becoming less effective in inhibiting the medial
thalamus and therefore, indirectly, the anterior cingulate cortex [7]. In fact in mammals the cingulate gyrus,
also said the limbic cortex, is part of the crying circuitry
which, in its purely motor component, in all vertebrates
is essentially a brain stem circuitry. The anterior cingulate cortex is hyperactive in mechanic hyperalgesia in
complex regional pain syndromes [19], which are exacerbated by incongruent sensory motor actions as previously highlighted. The thalamo-cingulate pathway is one
of the three major divisions of the limbic system (the
other being the amigdalar and the septal branches). In
the patient described in this work, the thalamic lesion
evidenced through MRI is located in the VPLT, presumably in the small area where both the face and the hand
are represented. As a matter of speculation, the lesion
might have selectively affected the inhibitory lateral-tomedial thalamus projection, thus ultimately dishinibiting
the cingulate cortex and, indirectly, the crying behaviour.
By contrast, the projection from the lateral thalamus to
the primary and secondary cortices might have been relatively spared. This would explain why pregabalin, a drug
which decreases both neuronal hyperexcitability and
neuropathic pain, was effective also in preventing crying.
In 1923 it was proposed that “dishinibtion” of the brain
stem circuits subtending crying could arise from lesion
of areas of the motor cortex specifically dedicated to the
involuntary (emotional) control of brain stem circuits
[20]. This hypothesis has been recently challenged in
favour of a cerebellar origin of the symptom [1] following
a direct lesion or a lesion of afferents originating from the
prefrontal/anterior cingulate cortex. This should imply,
however, a deficit in spatio-motor problem solving tasks,
such as the Stroop and the Tower of Hanoi tests [1]. The
Stroop and the simplified version of the TOH (the London Tower test), however, were normal in this case (see
table in Additional file 1). Also, both the MRI and the
fMRI exams did not provide evidence of alterations in
thalamo-frontal nor thalamo-cerebellar pathways.
With respect to the second question (asking why active,
not passive, rubbing was effective) one can again speculate that the sensory deficits created a mismatch between
the expected and the actual sensory feedback arising
from movement. The so-called action-effect binding [21]
is the basis for the “sense of agency”, the perception that
sensation was caused by one’s own action. A frustrated
sense of agency, both in real and imagined movements, is
a potential source of pain in complex regional pain syndromes [22, 23]. Sensory-motor incongruence can also
exacerbate chronic pain after whiplash injury [24]. On
the other hand, re-matching delusive movements and

Page 6 of 7

providing the expected visual feedback from an amputated limb can decrease phantom limb pain [25, 26].
In a study with Positron Emission Tomography, other
cortical regions have been proven to be involved in perceiving a sensory mismatch (e.g. between vision and
proprioception) and in controlling a movement under
sensory-motor mismatch. These are the right ventral lateral prefrontal cortex and the right dorsal lateral prefrontal cortex, respectively [27]. Again, in the present case no
alterations were detected in these areas at MRI examination, and at fMRI examination during the thumb-index
rubbing task. Only the Supplementary Motor Area of
Area 6 was activated, as a typical pattern elicited during a simple hand movement. Presumably, premotor or
parietal activation would have been be observed if visual
information was presented [27]. Of course, anatomical
lesions and circuital impairments undetectable through
MRI and/or fMRI could not be ruled out.
To sum up, a disinhibition of the thalamo-limbic pathways remains a plausible-although, unproven-explanation for the phenomenon. In this case the lesion might
have been moderate enough to make the limbic activation undetectable at fMRI and the crying spell to require
the simultaneous double triggering of the limbic areas,
i.e. from peripheral stimuli causing hyperexcitation of
the (already dishinibited) medial thalamic circuits, like in
allodynia, and from direct central hyperexcitation of the
limbic cortex caused by a frustrated sense of agency, like
in other pain syndromes.

Additional files
Additional file 1. Neuropsychological assessment. Table S1 contains the
list of tests of neuropsychological assessment, including: (a) Test names.
(b) Scores. (c) References to each of the listed tests.
Additional file 2. Crying spells triggered by thumb-index rubbing after
thalamic stroke. It contains the video of the patient during “index-thumb
rubbing” manoeuvres, showing his crying spells.

Abbreviations
CT: computerized tomography; EEG: electroencephalografy; EMG: electromyography; fMRI: (functional) magnetic resonance imaging; MRI: magnetic
resonance imaging; VPLT: ventral postero-lateral thalamus.
Authors’ contributions
BR clinical data collection, neurological assessment, motor testing, manuscript
drafting. RC, CV standard and functional neuroimaging. GL neurophysiological
assessment. BE and CC cognitive assessment, motor testing. TL design, clinical
assessment, motor testing, manuscript drafting. All authors read and approved
the final manuscript.
Author details
1
Department of Neurological Sciences, Ospedale “G. Salvini”, Garbagnate
Milanese, Italy. 2 Department of Neurorehabilitation Sciences, Istituto Auxologico Italiano, IRCCS, Milan, Italy. 3 Department of Neuroradiology, Istituto
Neurologico “C. Besta”, IRCCS, Milan, Italy. 4 Department of Biomedical Sciences
for Health, Chair of Physical and Rehabilitation Medicine, Università degli Studi
di Milano, Milan, Italy.

Bassani et al. BMC Res Notes (2017) 10:109

Acknowledgements
The authors would like to thank Ing Viviana Rota and Prof. Giuseppe Vallar for
their valuable help.

Page 7 of 7

8.
9.

Competing interests
The authors declare that they have no competing interests.

10.

Availability of data and materials
All data supporting findings are contained in the manuscript and in the
Additional files 1, 2.

11.

Consent for publication
Written informed consent was obtained from the patient for publication of
this Case Report and any accompanying images.

12.
13.

Ethical approval and consent to participate
Not applicable for a case report on this patient that was treated without a
research intention. This case report does not meet the definition of human
research by the United States Department of Health and Human Services or
the Food and Drug Administration guidelines. This is also in accordance with
the ethical manual and guidelines of the World Medical Association (see 59th
WMA General Assembly, Seoul, Republic of Korea, October 2008).

17.

Funding
No funding was provided by any parties.

18.

Received: 11 September 2016 Accepted: 10 February 2017

19.

14.
15.
16.

20.
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