Cerebrovasc Dis 2003;16:97–98
DOI: 10.1159/000070124

Transient Rotational Vertigo as the Initial
Symptom of a Middle Cerebral Artery Territory
Infarct Involving the Insula
S. Debette a, E. Michelin b, H. Hénon a, D. Leys a
a Research Group on Vascular and Degenerative Cognitive

Decline (EA 2691), Department of Neurology, Stroke Unit,
b Department of Neuroradiology, Lille University Hospital,

Lille, France

Case Report
A 51-year-old man suddenly developed pain in the right cervical
region associated with a right ptosis and lacrimation. During the preceding weeks he had carried heavy burdens. Two weeks later he suddenly experienced a severe rotational vertigo with nausea. A few minutes later occurred a sudden left hemiplegia.
On admission, the drowsy patient had a left-sided hemiplegia, a
partial loss of tactile and vibratory sensations on the left side, a Horner’s syndrome on the right side and a horizontal nystagmus in the
right lateral gaze of very short duration. The acute rotational vertigo
had disappeared after less than 30 min, and there was no nystagmus,
head tilt, or skew deviation on physical examination at bedside. The
patient did not report hearing symptoms such as tinnitus.
The computed tomographic scan was normal on admission.
Duplex ultrasonography of the cervical arteries showed an occlusion
of the right internal carotid artery beginning 1 cm above the carotid
bifurcation. The left carotid and both vertebral arteries were normal.
An MR angiography confirmed that the right internal carotid artery
was occluded with a mural hematoma. A diagnosis of right internal
carotid artery dissection was made.
A cerebral magnetic resonance imaging (MRI) scan revealed multiple supratentorial abnormalities in the territories of the middle
cerebral and anterior choroidal arteries (fig. 1): decreased signal
intensity on T1-weighted images and increased signal intensity on
T2-weighted images in the right hemisphere, involving the superior
part of the caudate nucleus, the lenticular nucleus, the postero-superior part of the posterior limb of the internal capsule, the anterior
infero-medial temporal cortex, the insular cortex involving the short
and long insular gyrus and the transverse and superior temporal
gyrus, as well as retroinsular areas, and the inferior part of the posterior limb of the internal capsule. There was a slightly increased signal
intensity (T2-weighted images) on the lateral part of the thalamus,
adjacent to the internal capsule. There was no lesion on MRI in the
brainstem and in the cerebellum.
An EEG showed normal findings, without paroxysmal discharges. Auditory evoked potentials were normal. Functional vestib-

Case Reports

Fig. 1. Magnetic resonance imaging scan

(FLAIR sequences), revealing an area of high
signal intensity, suggesting an infarct involving the superior part of the caudate nucleus,
the lenticular nucleus, the postero-superior
part of the posterior limb of the internal capsule, the anterior infero-medial temporal
cortex (central territory of the middle cerebral artery), the frontal cortex and the insular
cortex (peripheral territory of the middle cerebral artery), and the inferior part of the
posterior limb of the internal capsule (anterior choroidal artery).

ular explorations were not performed because the vertigo was transient and bed rest was recommended during the acute stage to prevent hemodynamic failure in the territory of the occluded artery.
Anticoagulation was initiated. At 2 months the hemiplegia had
disappeared. However, when the patient stood upright, he exhibited
a slight head and body tilt to the left, which was not measured. He has
now returned home, and is fully independent.
Discussion
This is to our knowledge the first case report of a transient rotational vertigo as the initial manifestation of a middle cerebral artery
(MCA) territory infarct due to an extra-cranial internal carotid artery
dissection.
Rotational vertigo is characteristic for an acute vestibular syndrome [2]. The latter can be the consequence of a lesion located anywhere along the vestibular pathways between the inner ear and the
vestibular cortex via the eighth nerve, brainstem structures such as
vestibular nuclei, medial longitudinal fasciculus, interstitial nucleus
of Cajal, and the thalamic vestibular subnuclei [3, 4]. The vestibular
cortex is not well defined. In the monkey [5, 6] several areas of the
parietal and temporal cortex have been identified to receive vestibular afferents. In humans, there is increasing evidence that the multisensory parieto-insular cortex receives input from the inner ear.

97
Downloaded by:
Stockholms Universitet
198.143.54.1 - 8/14/2015 12:06:33 PM

Rotational vertigo of central origin is usually due either to a
brainstem lesion or temporal lobe epilepsy. It is less well known that
acute rotational vertigo can be secondary to an ischemic lesion in the
vestibular cortex. The only case reported so far occurred in a cardioembolic infarct involving the vestibular and auditory cortices [1].
To our knowledge this is the second reported case of rotational vertigo secondary to a middle cerebral artery territory infarct, but the
first to be transient and to occur in a patient with isolated carotid
artery dissection.

Indeed Penfield and Jasper [7] induced vestibular symptoms by electrical stimulation within the sylvian fissure. Friberg et al. [8] found a
focal increase in cortical blood flow in the same area during caloric
vestibular stimulations and in positron emission tomography and
functional MRI studies the parietoinsular cortex also appears to be
activated by caloric irrigation of the external ear and by galvanic
stimulation of the mastoid. Interestingly, the activation of vestibular
cortex areas exhibits a significant right hemispheric dominance [9].
Descriptions of vestibular syndromes (and particularly of rotational vertigo) of supratentorial origin remain scarce. Dieterich and
Brandt [10] reported a series of 35 patients, 14 of whom developed a
vestibular syndrome due to a dorsolateral thalamic infarct. In a study
of 52 patients with MCA infarcts, the same authors identified a significant, mostly contraversive, tilt of the subjective visual vertical in
23 patients, with an overlapping ischemic area centered on the long
insular gyrus, the adjacent superior temporal gyrus and the transverse temporal gyrus [11]. There is only one report in the literature of
rotational vertigo in a patient with an infarct located in the right posterior insula, involving the long insular and the transverse temporal
gyrus [1]. Vestibular epilepsy [12, 13] was unlikely in our patient
because of the absence of other epileptic symptoms and specific EEG
features.
Thus, this case confirms that the occurrence of an acute rotational
vertigo in a patient with an MCA infarct is not necessarily due to an
associated brainstem infarct or a vestibular epilepsy. As in our case, it
may be transient.
Only a systematic evaluation of all patients with parieto-insular
infarcts could determine the frequency of this symptom. We cannot
exclude the possibility that transient vertigo occurs more frequently,
but is not recognized because other neurological deficits are more
prominent and it is of only short duration.

11 Brandt T, Dieterich M, Danek A: Vestibular cortex lesions affect the perception of verticality. Ann Neurol 1994;35:403–412.
12 Blanke O, Perrig S, Thut G, Landis T, Seeck M: Simple and complex vestibular responses induced by electrical cortical stimulation of the parietal
cortex in humans. J Neurol Neurosurg Psychiatry 2000;69:553–556.
13 Vercueil L, Kahane P, François-Joubert A, Hirsch E, Hoffmann D, Depaulis A, Marescaux C: Basal ganglia involvement in rotational seizures. Epileptic Disord 1999;1:107–112.
Prof. D. Leys
Service de neurologie et pathologie neurovasculaire
Hôpital Roger-Salengro, centre hospitalier et universitaire de Lille
F–59037 Lille (France)
Tel. +33 320 44 68 13, Fax +33 320 44 60 28
E-Mail dleys@chru-lille.fr

a

Acknowledgments
The authors would like to thank Prof. T. Brandt (Munich, Germany) for his helpful comments on the manuscript, and Judy Benson
for her suggestions.
References
1 Brandt T, Bötzel K, Yousry T, Dieterich M, Schulze S: Rotational vertigo
in embolic stroke of the vestibular and auditory cortices. Neurology 1995;
45:42–44.
2 Brandt T, Dieterich M: Vestibular syndromes in the roll plane: topographic
diagnosis from brainstem to cortex. Ann Neurol 1994;36:337–347.
3 Sans A, Raymond J, Marty R: Réponses thalamiques et corticales à la stimulation électrique du nerf vestibulaire chez le chat. Exp Brain Res 1970;
10:265–275.
4 Büttner U, Henn V: Thalamic unit activity in the alert monkey during natural vestibular stimulation. Brain Res 1976;103:127–132.
5 Grüsser OJ, Pause M, Schreiter U: Localization and responses of neurons
in the parietoinsular vestibular cortex of awake monkeys (Macaca fascicularis). J Physiol 1990;430:537–557.
6 Grüsser O-J, Pause M, Schreiter U: Vestibular neurons in the parietoinsular cortex of monkeys (Macaca fascicularis). J Physiol 1990;430:559–583.
7 Penfield W, Jasper H: Epilepsy and the functional anatomy of the human
brain. Boston, Little, Brown, 1954.
8 Friberg L, Olsen TS, Roland PE, et al: Focal increase of blood-flow in the
cerebral cortex of man during vestibular stimulation. Brain 1985;108:609–
623.
9 Brandt T, Dieterich M: The vestibular cortex. Its locations, functions, and
disorders. Ann NY Acad Sci 1999;871:293–312.
10 Dieterich M, Brandt T: Thalamic infarctions: differential effects on vestibular function in the roll plane (35 patients). Neurology 1993;43:1732–
1740.

Case Reports
Downloaded by:
Stockholms Universitet
198.143.54.1 - 8/14/2015 12:06:33 PM

98