CASE REPORT

Writing Tremor Secondary to Ischemic Stroke:
A Report on a Case With a Remarkable
Response to Topiramate
Juan P. Paviolo, MD, Gabriela B. Raina, MD, Eugenia Conti, MD, and Federico Micheli, MD, PhD
Abstract: Writing tremor (WT) is a task-specific tremor that occurs only
or mostly while writing with the dominant hand. Secondary cases are extremely uncommon. We report on a patient who, after developing a WT after an ischemic stroke, had a remarkable response to topiramate (TPM).
Case: A 65-year-old right-handed man with a history of arterial hypertension, dyslipidemia, and coronary heart disease presented dizziness and
headache followed by a loss of consciousness and then a right hemiparesis.
He regained his strength on the fifth day. Fourteen days after stroke, he
developed a WT as well as other complications with activities such as
welding (he is a welder) and using a spoon. He was treated with 50 mg/d
of TPM with marked improvement in WT. A few weeks after TPM
was discontinued, the WT symptoms reappeared and he was retreated,
showing the same beneficial reaction.
Electromyographic record showed a 5- to 6-Hz tremor in his right hand,
and a magnetic resonance imaging showed bilateral small frontoparietal
subcortical infarcts.
Conclusions: Primary WT pathophysiology is not well known, and secondary WT as a result of stroke is even less considered. Although patients
with essential tremor benefit with TPM and WT could be a variant of essential tremor, we used TPM with our patient and there was a marked benefit.
Key Words: writing tremor, task-specific tremor, secondary writing
tremor, stroke, topiramate
(Clin Neuropharm 2015;38: 57–59)

A

task-specific tremor is a form of tremor that appears while
performing or attempting to perform a particular task. The
most common form is writing tremor (WT) that manifests only
or mostly during writing with the dominant hand. It is classified
into type A when the tremor appears while writing and type B
when the hand adopts the writing position.1,2 It is controversial
whether primary WT is a variant of essential tremor, which is a
type of focal dystonia or a separate nosological entity because
its pathogenesis remains poorly understood.3
We could find only 1 case of WT secondary to a discrete cortical infarction in the literature.4 Here, we report on a patient who
developed WT after an ischemic stroke and showed a remarkable
improvement with topiramate (TPM).

FIGURE 1. Magnetic resonance image performed 2 years after
stroke: multiple bilateral small images in frontoparietal subcortical
and periventricular region, hyperintense on T2 and Flair sequences.

center. He had experienced dizziness and headache for several
hours followed by a sudden loss of consciousness. When he recovered consciousness, he had a right hemiparesis. Five days later, he
had completely recovered his strength. Two weeks after this, he
developed a mild WT that was initially present only on certain occasions, but after several days, it became present every time he
attempted to write. In addition, a few days later, other specific activities such as welding (the patient is a welder by profession) or
using a spoon to consume soup also triggered the tremor. This
tremor remained stable for almost 2 years. He had no personal
or family history of tremor before the stroke. A therapeutic

CASE REPORT
A 65-year-old right-handed man with a history of arterial hypertension, dyslipidemia, and coronary heart disease had an ischemic stroke 2 years before coming to our movement disorder
Parkinson's Disease and Movement Disorders Program, Hospital de Clínicas
José de San Martín, University of Buenos Aires, Buenos Aires, Argentina.
Address correspondence and reprint requests to Federico Micheli, MD, PhD,
Parkinson's Disease and Movement Disorders Program, Hospital de
Clínicas José de San Martín, Juncal 1695 Piso 5 J, 1062 Buenos Aires,
Argentina; E-mail: fmicheli@fibertel.com.ar.
Conflicts of Interest and Source of Funding: The authors have no conflicts of
interest to declare.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
DOI: 10.1097/WNF.0000000000000069

FIGURE 2. A, Patient writing before treatment. B, Patient writing
7 days after taking 50 mg/d of TPM.

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Clinical Neuropharmacology • Volume 38, Number 2, March/April 2015

Paviolo et al

FIGURE 3. Electromyographic recording: 5- to 6-Hz tremor on his right hand when writing.

attempt with levodopa-carbidopa was made without any improvement. When we first saw him, he had no paresis, ataxia, or sensory
disturbances. He had no resting tremor, and he only exhibited
tremor when writing or adopting a writinglike posture.
The magnetic resonance imaging performed 2 years after
the stroke showed multiple small bilateral images, which were hyperintense on T2 and Flair sequences in the frontoparietal subcortical regions (Fig. 1). He was treated with 50 mg/d of TPM in
which he reported a remarkable improvement on tremor (Fig. 2)
of up to 80%. After a few months, TPM was discontinued, but
the tremor reappeared and only improve again when the drug
was reintroduced (Fig. 3).

DISCUSSION
Only 1% to 4% of the manifestations of stroke are movement
disorders, and of these poststroke involuntary movements, tremor
represents only a small percentage.5–7 The time at onset of movement disorders after a stroke is quite variable, ranging from the
same day to several years after stroke. It is assumed that the delay
between the stroke and the onset of the involuntary movement is
caused by the time required for the partial recovery of motor function and the development of a pathological circuitry.5,8,9 Although
we cannot be absolutely sure that the development of tremor in our
patient was not a coincidence, it is highly suggestive to be a
poststroke tremor because it began 14 days after a stroke and the
patient had no personal or family history of tremor. Another feature of poststroke involuntary movements is that they usually start
gradually and get progressively worse for weeks or months and
then stabilize, as has happened with our patient.9 Primary WT
physiopathology is unknown and even less is known about
poststroke WT. Poststroke movement disorders have been associated with lesions in different locations, although the most common locations are the basal ganglia and thalamus.8 Small vessel
disease, with small deep infarcts, is the most common subtype
leading to involuntary movements.6–8 To our knowledge, this is
the second case of WT secondary to an ischemic stroke. Our case

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is different from the previously reported case because we could
not identify the causal lesion, whereas the previous case had a discrete cortical infarct in the left frontal lobe between the central and
precentral sulci4 that was responsible for the tremor. In our patient,
we observed multiple bilateral small images in the frontoparietal
subcortical region, which were hyperintense on T2 and Flair sequence on magnetic resonance imaging.
Essential tremor and other hyperkinetic movements such
as vascular chorea may respond to treatment with TPM. This drug
has complex action mechanisms, which include blocking voltagegated sodium channels, augmenting γ-aminobutyric acid (GABA)
activity at the GABA-A receptors, antagonizing the a-amino-3hydroxy-5-methyl-4-isoxazolepropionic acid/kainate glutamate receptors, and inhibiting the carbonic anhydrase enzyme.10
It is postulated that the mechanism by which TPM improves vascular chorea could be through GABAergic potentiation
of the indirect pathway of the basal ganglia in vascular chorea.11
For the essential tremor, TPM is believed to act by facilitating GABAergic transmission on olive and cerebellar-thalamiccortical pathways. Furthermore, it has been postulated that, for
symptomatic dystonic tremor resembling essential tremor, therapeutic strategies are the same for essential tremor.12 It is for this
latter mechanism of action that we assume our patient improved
so greatly.
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Clinical Neuropharmacology • Volume 38, Number 2, March/April 2015

Writing Tremor Secondary to Ischemic Stroke

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