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Case Report

Can a stroke present with flexor spasms? A highly rare
experience
Kann sich ein Schlaganfall über Flexorspasmen darstellen? Eine sehr
seltene Erfahrung
Abstract
Involuntary movement disorders are not a common presentation of
basal ganglia ischemia which may be induced by cerebral hemodynamic
insufficiency. In secondary causes of movements disorders cerebrovascular diseases represent up to 22% and involuntary movements develop
after 1–4% of strokes. We describe a case of a middle-aged woman
who presented with intermittent involuntary tonic spasms or seizurelike episodes followed by weakness due to contralateral putaminal infarction. Initially thought to have Todd’s paralysis she was not thrombolysed, but later she developed dense hemiplegia. Flexor spasms are
generally thought to occur in lesions of the spinal cord but they can also
occur in cerebral lesion, may be because of disinhibition of the spinal
cord. Certain other theories also have been narrated, but this field still
needs to be worked upon.

Yasir Mehmood Malik1
Abubaker
Abdulrahman
Almadani1
Jaeed Ahmed Dar1
1 Rashid Hospital, Dubai,
United Arab Emirates

Keywords: stroke, putaminal infarction, flexor spasm, movement
disorder, basal ganglia infarction

Zusammenfassung
Unwillkürliche Bewegungsstörungen sind kein übliches Anzeichen einer
Ischämie der Basalganglien, die infolge cerebraler Minderdurchblutungen auftritt. Unter den zweitrangigen Gründen für Bewegungsstörungen
machen cerebrovaskuläre Erkrankungen bis zu 22% aus und unwillkürliche Bewegungen entstehen in 1–4 % der Schlaganfälle. Wir beschreiben einen Fall einer Frau im mittleren Alter mit intermittierenden unwillkürlichen tonischen Spasmen oder anfallartigen Episoden, gefolgt von
einer Schwäche als Folge eines Infarktes im Putamen auf der kontralateralen Seite. Der Anfangsverdacht war ein epileptischer Anfall (TODD’s
paralysis), so dass eine Thrombolyse nicht durchgeführt wurde. Aber
später entwickelte sich eine ausgeprägte Halbseitenlähmung (Hemiplegie). Flexorspasmen entstehen gewöhnlich bei Läsionen des Rückenmarkes, sie können aber auch bei cerebralen Läsionen entstehen,
möglicherweise aufgrund einer Enthemmung des Rückenmarks. Einige
andere Theorien sind auch erwogen worden, aber dieser Bereich benötigt weitere Bearbeitung und Klärung.
Schlüsselwörter: Schlaganfall, Infarkt des Putamens, Flexorspasmen,
Bewegungsstörungen, Infarkt in den Basalganglien

Introduction
Cerebral ischemia has a wide variety of presentations
which is mainly dependant on the area of involvement.
Ischemia of basal ganglia and surrounding structures can
present with weakness, dystonia or involuntary movements. Post-stroke movement disorders can manifest in
a wide range including Parkinsonism or hyperkinetic

movement disorders such as chorea, ballismus, athetosis,
dystonia, tremor, myoclonus, complexe motor stereotypies
or akathisia. Sudden-onset repetitive tonic spasms of
short duration may be classified under the heading of
involuntary movements and are a very rare manifestation
of basal ganglia infarction.
Tatemichi et al. presumed in a case study the mechanism
of the sudden-onset movement disorder to be cerebral

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Figure 1: Brain CT of the patient taken at presentation which shows only basal ganglia calcification. No early ischemic changes,
no hyperdense artery sign.

ischemia. By using cerebral blood flow studies they supported this concept and demonstrated perfusion insufficiency in a patient at rest with limb-shaking transient
ischemic attacks. The focal perfusion deficit improved
and the patient's symptoms relieved after carotid
endarterectomy [1].
We are going to describe a case who presented in a very
different way. The fact that the diagnosis initially was not
clear, delayed the therapeutic decision. In literature only
2–3 similar cases have been reported so far. Repeated
short lasting flexor spasm-like activity is not a known
presenting feature of cerebral ischemia. It is usually seen
in spinal cord disorders but it can occur in cerebral
ischemia because of an undetermined mechanism.
Various theories have been described which we will discuss here.

Case summary
This is the case of a 57-year-old Indian right-handed woman who was known to have hypertension and ischemic
heart disease and was on regular medication for these
comorbids. On the day of presentation she woke up well
and after 2 waking hours she started having involuntary
movements on the right side of the body. This occurred
5–7 times and was described by the patient like some
tightening spell which would persist for 5–10 sec and
then it relieved by itself. This was followed by a weakness
on the right side of the body which was so severe that
she could not move out of bed. After half an hour the
weakness started improving. When she reached hospital,
her condition had much improved. On examination she
was mildly slow in mental processing, but GCS (Glasgow
Coma Scale) score was 15/15. She had mild dysarthria
but speech assessment and cranial nerves were normal.
In the motor system she had mild weakness with power
of grade 4+/5 in the right sided limbs, both proximally
and distally, and mild hypotonia on the right side. Power
on the left side was normal. Reflexes were normal and
symmetrical on both sides. The other examination results
was unremarkable. We did CT brain which was normal

(Figure 1). Preliminarily we thought of tonic seizure disorder followed by Todd’s paralysis because we did not
witness that episode and were dependant on history. We
thought of stroke/transient ischemic attacks and discussed it with the family. At that time deficit was minimal
and history was also suggesting Todd’s paralysis, so the
unanimous decision was made not to treat as stroke and
just to observe for seizure. Therefore she was not given
thrombolytic therapy, however we loaded her with 300 mg
Aspirin.
After 5 hours we observed involuntary movements on the
right side of the body, which consisted of painful slow
contractions of flexor muscles of hand and forearm along
with dorsiflexion of the ipsilateral foot with a rapid release
after 5–6 seconds (see video (Attachment 1)). Mild
weakness was still persistent since the first spell. We
gave her calcium considering it to be hypocalcemic
spasms (as serum calcium was borderline low), but there
was no response. However it responded to diazepam for
some time and then recurred. As we thought of the possibility of flexor spasms or seizure, she was given a loading dose of phenytoin after what severity and frequency
were reduced.
After 9 hours of onset she developed dense hemiplegia
on the right side. Now on examination she had right upper
motor neuron type facial weakness, dysarthria, power of
0/5 in all muscle groups on the right side with hyporeflexia and hypotonia. The right Babinski sign was positive.
Sensory examination was normal. There was no limb
ataxia. The whole examination of the left side was unremarkable. She was still having the same spasms on the
right side while hemiplegia persisted.
CT brain was repeated and was normal. EEG was normal.
Laboratory investigations were normal except of the high
cholesterol level. MRI brain showed infarction in the area
of the left internal capsule, the putamen and some part
of the thalamus (Figure 2). Echocardiography and carotid
Doppler were normal.
Flexor spasms were improved with phenytoin and weakness also improved with rehabilitation.

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Figure 2: MRI Brain: (1) FLAIR, (2) diffusion weighted and (3) T2w MRI images of the patient showing infarction in the left
putamin and internal capsule area with slight involvement of the left thalamus.

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Discussion
Involuntary movement disorders are not commonly considered as an early sign of basal ganglia ischemia which
may be induced by cerebral hemodynamic insufficiency.
In secondary causes of movement disorders cerebrovascular diseases represent up to 22% and involuntary
movements develop after 1–4% of strokes [2]. Various
post-stroke involuntary movement disorders have been
described with a spectrum of hyperkinetic disorders including chorea, ballismus, athetosis, dystonia, tremor,
myoclonus, parkinsonism, motor stereotypies, and
akathisia [2]. Some of these occur immediately after
acute stroke, whereas others can develop later and a
third category can also present as delayed-onset progressive movement disorders [2]. Such movement disorders
have been observed in ischemic and hemorrhagic stroke
affecting the basal ganglia or their connections. Flexor
spasms are rarely caused by cerebral ischemia [3], and
acute onset flexor spasms are a very rare presentation
of putaminal infarction [4].
Yanagihara T et al. presented a case series in which patients were analyzed for their acute-onset involuntary
movements. EEG was normal and cerebral angiography
revealed either occlusion or high-grade stenosis of the
internal or common carotid artery on the side opposite
of the involuntary movement in all patients. They concluded that the repetitive involuntary movements result
from transient hemodynamic ischemic episodes [5].
Im SH et al. presented a small case series of involuntary
movement disorder induced by cerebral hemodynamic
insufficiency. A common MRI finding in all cases was a
small infarct in the frontal corona radiata, which did not
extend to the cortex or basal ganglia. A perfusion defect
in the frontoparietal subcortical regions was demonstrated by single-photon emission computerized tomography (SPECT) in all patients. Following bypass vascular
surgery improved hemodynamic circulation in the frontoparietal subcortical regions occurred on SPECT scan in
all patients. Their involuntary movements also improved
[6].
Flexor spasms are generally seen in patients with spinal
cord pathologies [3], brain tumor [7], multiple sclerosis
[4], vasculitis and cerebral ischemia.
Glaser GH worked a lot on spasms and spasticity. He
describes that for the spasticity after brain lesion there
are three main physiological mechanisms:
1. exaggerated spinal stretch reflexes, due to release
from and facilitation by supraspinal controls, especially reticular and cerebellar influences,
2. increased susceptibility to proprioceptive stimuli, and
3. possible overactivity in the gamma control system of
the muscle spindles [8]
This last mechanism, which is also the most classically
described, has been studied long ago. Amongst all hypotheses which can explain spasm or spasticity, reduction
of presynaptic inhibition (usually in basal ganglia
ischemia) is the one having been clearly demonstrated

[9]. The spinal reflex is normally inhibited by various
supra-spinal fibers, dorsal reticulospinal pathway is the
most important inhibitory pathway. The motor areas of
the cortex, through corticobulbar pathways, facilitate the
dorsal reticulospinal pathway, augmenting the net inhibitory role down the spinal cord. Lesion of these corticobulbar pathways, either in the cortex or internal capsule,
reduces the inhibitory drive and results in net excitation
of spinal cord activity [10].
It is undetermined whether electrophysiologically it is
possible for an area of infarction or surrounding ischemic
penumbra to generate an ephaptic (aberrant) transmission of otherwise normal axonal impulses which may lead
to some involuntary movements. The therapeutic effectiveness of the Gamma aminobutyric acid-facilitating drug
diazepam would support the theory that the lesion is interfering with inhibitory control [11].
In cerebral lesions the possible mechanism of painful
flexor spasms may be one of the above mentioned
pathological sequence of events, but the exact mechanism is yet to be determined.

Conclusion
Spontaneous flexor spasms as presented here often occur
in patients suffering from spinal lesions or as a poststroke motor sign after cortical ischemic lesions combined
with spasticity, hemiplegia and other symptoms of pyramidal features. As demonstrated in our case spontaneous
flexor spasms can be an early sign of an ongoing stroke
in basal ganglia. Pathomechanisms are not clarified and
need more attention for diagnostics and treatment.

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

Attachments
Available from
http://www.egms.de/en/journals/gms/2014-12/000191.shtml
1. Attachment 1_gms000191.MOV (5224 KB)
Video: Flexor spasm. This video shows intermittent
flexor spasms in the right leg of the patient which
consist of a flexion phase of 4–5 seconds followed
by spontaneous release occurring at frequency of
8–10 per minute. There is no jerky movement, no
extensor muscles contraction. Similar intermittent
flexor spasms occurred in the right arm and hand
simultaneously.

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Corresponding author:
Dr. Yasir Mehmood Malik
Rashid Hospital, Dubai, United Arab Emirates, Phone:
00971502584776
yasirmmalik@gmail.com
Please cite as
Malik YM, Almadani AA, Dar JA. Can a stroke present with flexor
spasms? A highly rare experience. GMS Ger Med Sci. 2014;12:Doc06.
DOI: 10.3205/000191, URN: urn:nbn:de:0183-0001912
This article is freely available from
http://www.egms.de/en/journals/gms/2014-12/000191.shtml
Received: 2013-10-07
Revised: 2014-02-06
Published: 2014-02-27
Copyright
©2014 Malik et al. This is an Open Access article distributed under the
terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You
are free: to Share — to copy, distribute and transmit the work, provided
the original author and source are credited.

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