Hwang et al. BMC Neurology (2017) 17:122
DOI 10.1186/s12883-017-0901-7

CASE REPORT

Open Access

Paroxysmal freezing of gait in a patient
with mesial frontal transient ischemic
attacks
Hee Won Hwang, Seung Ha Lee, Chul Hyoung Lyoo and Myung Sik Lee*

Abstract
Background: Rare patients have been reported who developed a mixture of gait disturbances following a focal
lesion in the frontal lobe. Thus, the exact location of frontal lesion responsible for a specific gait disturbance is not
well defined.
Case presentation: We describe a 47-year-old man who experienced two episodes of paroxysmal freezing of gait
of the right leg. During the attacks, he had no motor weakness, sensory change, or disequilibrium. He had past
history of panic attacks. Recently, he had been under severe emotional stress. T2 and diffusion brain magnetic
resonance imaging scans were normal. So far, the most likely clinical diagnosis might be functional freezing of gait.
However, magnetic resonance angiography showed atherosclerosis in the proximal left anterior cerebral artery.
Perfusion scans showed a delayed mean transit time in the left mesial frontal lobe. He developed two more attacks
during the four months of follow up.
Conclusions: The presented case illustrates that the mesial frontal lobe may be important in the pathophysiology
of freezing of gait. We speculate that the supplementary motor area may generate a neuronal command for the
initiation of locomotion that in our case may have been inhibited by a transient ischemia.
Keywords: Mesial frontal lobe, Transient ischemic attack, Freezingof gait, Locomotor block

Background
Freezing of gait (FOG) is defined as episodic brief
absence or marked reduction of forward progression of
the feet despite the intention to walk [1]. Patients with
frontal gait disorder may have FOG. However, they
frequently have widespread cerebrovascular lesions and
present various combinations of additional gait disturbances including start and turn hesitation, short steps,
shuffling, and postural instability. Thus, in patients with
frontal gait disorder, exact location of brain lesion
responsible for FOG is difficult to decipher [2].
Rare patients have been reported who developed FOG
following a focal lesion involving the dorsal midbrain
tegmentum, suggestive of important role of mesencephalic
locomotor region in the locomotor initiation [3–5].
However, frontal lobe, especially the supplementary motor
* Correspondence: mslee@yuhs.ac
Department of Neurology, Gangnam Severance Hospital, Yonsei University
College of Medicine, Eonjuro 211, Gangnam-gu, Seoul, South Korea

area, plays also a prominent role in the initiation and control of human locomotion [1]. Here, we describe a patient
who developed paroxysmal FOG of the right leg associated with left mesial frontal transient ischemic attacks
(TIAs).

Case presentation
A 47-year-old man visited the emergency room due to
two incidents of transient locomotor blocks. He had a
past history of panic attacks. Recently, he had been
under severe emotional stress. When he attempted to
walk at the pedestrian crossing on the green light, his
right foot was glued to the ground. He sat down and
massaged his right leg with both hands. Several seconds
later, he could walk normally again. Two hours later,
when he attempted to run while walking, his right foot
was again stuck to the ground for several seconds.
During the attacks, there were no knee trembling of the
frozen leg. He denied any motor weakness, sensory
change, or dyskinesia of the arms or legs. On

© The Author(s). 2017 Open Access 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.

Hwang et al. BMC Neurology (2017) 17:122

Page 2 of 4

Fig. 1 a Diffusion axial brain MRI scan shows no abnormalities. b Cerebral MR angiography shows atherosclerotic narrowing in the left anterior
cerebral artery (arrow). c Perfusion axial brain MRI scan shows delayed mean transit time in the left mesial frontal lobe

neurological examination, he had no motor, sensory, or
cerebellar dysfunctions. T2 and diffusion brain magnetic
resonance imaging (MRI) scans were normal (Fig. 1a).
However, magnetic resonance (MR) angiography
showed atherosclerosis in the proximal left anterior
cerebral artery (Fig. 1b). Perfusion scans showed a delayed mean transit time in the left mesial frontal lobe,
including the supplementary motor area and cingulate
cortex (Fig. 1c). Routine laboratory tests were all
normal, including CBC, liver function tests, renal
function tests, urine analysis, electrocardiography, and
chest x-ray studies. There was no hyperlipidemia.
Screening tests for autoimmune disease (e.g. ANA,
Ani-dsDNA antibodies, P-ANCA, C-ANCA, AntiCardiolipin antibodies Ig M andIg G) were all negative. Transthoracic echocardiography study showed no
abnormalities. Interictal electroencephalography (EEG)
studies revealed no abnormalities. During four

months of follow up period, he had been treated with
low dose aspirin, but he developed two more attacks
when he attempted walking.

Conclusion and discussion
The presented case developed paroxysmal locomotor
blocks. There were no motor weakness, sensory changes,
or cerebellar ataxia. The attacks were induced by sudden
movements of the leg as in paroxysmal kinesigenic dyskinesia, but there was no dyskinesia. Unlike the typical
FOG observed in patients with degenerative parkinsonism,
the present patient developed FOG in open spaces and
there was no hastening or alternating knee trembling-like
leg movements. Besides, he did not have any parkinsonian
features [1]. T2 and diffusion weighted brain MRI studies
showed no lesions (Fig. 1a). He had past history of panic
attacks and recently had been under severe emotional

Table 1 Reported patients with gait disturbances or postural instabilities following a lesion confined to the frontal lobe
Reference

Lesion sites

Gait disturbances
& postural instabilities

Other neurologic deficits

Characters of lesion

Sakakibara et al. [14]

bilateral medial frontal

shuffling gait

tinnitus, deafness, hallucination,
versive seizure, disorientation,
inattention

MRI: neurosarcoidosis

Chung et al. [19]

Lt. medial frontal

gait initiation disturbance

severe bilateral lower extremity
bradykinesia

MRI: ischemic stroke

Nadeau et al. [20]

Bilateral parasaggital
white matter

gait ignition difficulty

bilateral paratonia, retropulsion in
sitting position

MRI: Primary CNS
lymphoma

Ducruet et al. [15]

Rt. medial frontal

ataxic gait

Lt. hemiparesis

CT: hemorrhage

Wada et al. [16]

Rt. SMA

astasia

Robbins et al. [18]

Rt. Parasagittal frontal

freezing of gait

speech impairment, axial
bradykinesia, balance disturbance

MRI: cortical vein
thrombosis

Frassanito et al. [17]

Rt. basal frontal

gait instability

Della et al. [21]

Bilateral frontal

gait apraxia

Present case

Lt. mesial frontal

freezing of gait of the right leg

MRI: infarction

MRI: tumor excision
spastic paraplegia, disequilibrium,
loss of postural reflexes

CT computerized tomography, MRI magnetic resonance imaging, SMA supplementary motor area

MRI: infarction
MRI: ischemia

Hwang et al. BMC Neurology (2017) 17:122

stress. So far, the most likely clinical diagnosis might be a
functional FOG [6].
However, cerebral MR angiography showed atherosclerosis in the left anterior cerebral artery (Fig. 1b) and
perfusion MR scans showed ischemia in the left mesial
frontal lobe (Fig. 1c). The presented case did not develop
sensory dysfunctions or motor weakness during the attacks, probably because the lesion was remote from the
sensory pathways and unilateral proximal limb receives
motor inputs from the bilateral supplementary motor
areas [7]. Indeed, about 20% of patients with anterior
cerebral infarctions develop neither leg weakness nor
sensory changes [8].
FOG occurs rarely as a form of bilateral akinetic
seizure. Such FOG is precipitated by standing up, gait
initiation, turning, stumbling, or startle induced by
unexpected auditory or tactile stimuli [9]. Because mesial frontal epileptic discharge can hardly be detected by
conventional EEG studies, epileptic origin of FOG can
not be excluded in the presented case [10]. However, increased neuronal excitability in TIA causes dyskinesia
(so call ‘shaking TIA’) rather than epileptic motor arrest
[11]. FOG has been reported in patents who had
widespread cerebral and bilateral basal ganglia lesions
associated with hypoxia, carbon monoxide poisoning,
wasp sting allergy, orpantothenate kinase associated neurodegeneration, as well as primary degenerative parkinsonism [12]. A recent neuronal network mapping study
attributed FOG to the dorsal medial cerebellum [13].
FOG may also occur in patients with a focal brain lesion.
The most often reported focal lesion is in the unilateral
or bilateral dorsal midbrain tegmentum [3–5]. However,
some patients had progressive worsening of gait disturbances and extensive subcortical white matter changes
that obscured the causal relationship between the midbrain lesion and FOG [3].
We reviewed the literature and identified eight
patients who developed gait disturbances or postural
instabilities following a focal lesion in the frontal lobe.
As the present case, seven of the eight patients had
lesions in the mesial frontal lobe (Table 1) [14–21]. They
developed various gait disturbances, inducing ataxic gait,
shuffling gait, astasia, or FOG. At least four patients
have been reported who developed FOG following a
mesial frontal lesion associated with cortical vein thrombosis, lymphoma, or infarction [18–21]. However, they
had additional neurological deficits that may disturb
locomotor initiation (e.g. short steps, severe leg bradykinesia, spastic paraplegia, paratonia, retropulsion, loss of
postural reflexes, and balance disturbance).
The presented patient developed isolated paroxysmal
FOG associated with mesial frontal TIAs. This finding
indicates that the mesialfrontal lobe, probably the supplementary motor area, generates a neuronal command

Page 3 of 4

for the initiation of locomotion. The mesial frontal lobe
lesion seemed to disrupt transmission of a locomotor
initiation command from the mesial frontal cortex to
the locomotor pattern generators in the subcortical (e.g.
nucleus accumbens and ventral pallidum), brainstem
(e.g. pedunculopontine nucleus, cuneiform nucleus, and
subcuneiform nucleus),and spinal cord [1, 22].
Abbreviations
ANA: Anti-nuclear antibodies; Anti-dsDNA: Anti-double stranded DNA
antibodies; C-ANCA: Cytoplasmic anti-neutrophil cytoplasmic antibodies;
CBC: Complete blood counts; FOG: Freezing of gait; MR: Magnetic resonance;
MRI: Magnetic resonance imaging; P-ANCA: Perinuclear anti-neutrophil cytoplasmic antibodies
Acknowledgements
Not applicable.
Funding
We received no funding support.
Availability of data and materials
All data are presented in the manuscript. There are no additional data.
Authors’ contributions
HWH collected data, analyzed and wrote the manuscript. SHL analyzed the
data and revised the manuscript. CHL analyzed the data and revised the
manuscript. MSL designed the study, analyzed the data and revised the
manuscript. All authors read and approved the final manuscript.
Ethics approval and consent to participate
Not applicable.
Consent for publication
Written informed consent for participation and publication was obtained.
Competing interests
The authors declare that they have no competing interests.
Received: 21 May 2017 Accepted: 21 June 2017

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