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Insular ischemic stroke: clinical presentation and outcome.
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PMID:  23139684     Owner:  NLM     Status:  PubMed-not-MEDLINE    
BACKGROUND: The insula is a small but complex structure located in the depth of the sylvian fissure, covered by the frontal, parietal and temporal operculum. Ischemic strokes limited to the insula are rare and have not been well studied. Our objective is to better define the clinical presentation and outcome of insular ischemic strokes (IIS).
METHODS: We reviewed the institutional prospective, consecutive stroke database from two centers to identify patients with IIS seen between 2008 and 2010. We also searched the Medline database using the keywords insula(r), infarction and stroke to identify previously published IIS cases confirmed by MRI. Minimal extension to an adjacent operculum or subinsular area was accepted. Clinicoradiological correlation was performed by distinguishing IIS involving the anterior (AIC) or posterior insular cortex (PIC). We collected clinical, demographic and radiological data. The outcome was determined using the modified Rankin Scale (mRS).
RESULTS: We identified 7 patients from our institutions and 16 previously published cases of IIS. Infarcts were limited to the AIC (n = 4) or the PIC (n = 12) or affected both (n = 7). The five most frequent symptoms were somatosensory deficits (n = 10), aphasia (n = 10), dysarthria (n = 10), a vestibular-like syndrome (n = 8) and motor deficits (n = 6). A significant correlation was found between involvement of the PIC and somatosensory manifestations (p = 0.04). No other statistically significant associations were found. IIS presentation resembled a partial anterior circulation infarct (n = 9), a lacunar infarct (n = 2) or a posterior circulation infarct (n = 2). However, most cases presented findings that did not fit with these classical patterns (n = 10). At the 6 month follow up, mRS was 0 in 8/23 (35%) patients, 1-2 in 7/23 (30%) and unknown in 8/23 (35%).
CONCLUSIONS: IIS presentation is variable. Due to the confluence of functions in a restricted region, it results in multimodal deficits. It should be suspected when vestibular-like or motor but especially somatosensory, speech or language disturbances are combined in the same patient. The outcome of IIS is often favorable. Larger prospective studies are needed to better define the clinical presentation and outcome of IIS.
F Lemieux; S Lanthier; M-C Chevrier; L Gioia; I Rouleau; C Cereda; D K Nguyen
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Publication Detail:
Type:  Journal Article     Date:  2012-10-18
Journal Detail:
Title:  Cerebrovascular diseases extra     Volume:  2     ISSN:  1664-5456     ISO Abbreviation:  Cerebrovasc Dis Extra     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-11-09     Completed Date:  2012-11-12     Revised Date:  2013-05-30    
Medline Journal Info:
Nlm Unique ID:  101577885     Medline TA:  Cerebrovasc Dis Extra     Country:  Switzerland    
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Languages:  eng     Pagination:  80-7     Citation Subset:  -    
Service de Neurologie, Hôpital Notre-Dame, Centre Hospitalier de l'Université de Montréal, Montréal, Qué., Canada.
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Journal ID (nlm-ta): Cerebrovasc Dis Extra
Journal ID (iso-abbrev): Cerebrovasc Dis Extra
Journal ID (publisher-id): CEE
ISSN: 1664-5456
ISSN: 1664-5456
Publisher: S. Karger AG, Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34,
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Copyright © 2012 by S. Karger AG, Basel
collection publication date: Season: Jan-Dec Year: 2012
Electronic publication date: Day: 18 Month: 10 Year: 2012
pmc-release publication date: Day: 18 Month: 10 Year: 2012
Volume: 2 Issue: 1
First Page: 80 Last Page: 87
PubMed Id: 23139684
ID: 3492997
DOI: 10.1159/000343177
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Insular Ischemic Stroke: Clinical Presentation and Outcome
F. Lemieuxa
S. Lanthiera
M.-C. Chevriera
L. Gioiaa
I. Rouleaua
C. Ceredab
D.K. Nguyena*
aService de Neurologie, Hôpital Notre-Dame, Centre Hospitalier de l'Université de Montréal, Montréal, Qué., Canada
bNeurocenter (EOC) of Southern Switzerland, Department of Neurology, Ospedale Civico, Lugano, Switzerland
Correspondence: *Dang K. Nguyen, Service de Neurologie, Hôpital Notre-Dame, Centre Hospitalier de l'Université de Montréal, 1560 Sherbrooke Est, Montréal, QC H2L 4M1 (Canada), E-Mail
[equal] C. Cereda and D.K. Nguyen contributed equally to this work.


Hidden by the frontal, temporal and parietal opercula, deep in the sylvian fissure, the insular lobe is thought to play multiple roles including visceromotor, viscerosensory and limbic functions, as well as roles in gustatory, pain and other somatosensory processing, volitional swallowing, speech and language [1]. In addition, recent studies suggested that the insula is a convergence zone implicated in the coordination between internal and external information through emotional subjective awareness [2]. The insula may facilitate motor recovery in stroke [3,4]. The role of the insula in stroke survival has been subject to controversy [5].

The clinical presentation and outcome of insular ischemic strokes (IIS) have not been well described, mainly due to its relative rarity [2]. In this study, we review 16 published cases of IIS and report 7 additional ones.


Consecutive stroke patients hospitalized at the Stroke Unit of the Centre Hospitalier de l'Université de Montréal (CHUM) and the Neurocenter of Southern Switzerland are prospectively registered in databases. We reviewed medical charts and neuroimaging studies of the last 200 patients of each database with middle cerebral artery (MCA) stroke. Those with infarcts predominantly affecting the insular cortex were eligible. Extension to the adjacent operculae or subinsular area (extreme capsule, claustrum, external capsule) was accepted as long as it accounted for <50% of the total infarct volume. Using the keywords insula(r), infarction and stroke, we searched the Medline database to identify published cases of IIS corresponding to our inclusion criteria. Patients from both sources without brain MRI or with confounding neurological conditions (e.g., other structural brain lesions) were excluded, as were studies that presented cases without patient-specific information. We retrospectively collected clinicodemographic and neuroimaging data at presentation and at follow-up. The reported presenting signs and symptoms were reviewed by a stroke neurologist with 12 years of experience and a senior resident in neurology to classify the pattern of presentation using the Oxfordshire classification. The clinical outcome at 6 months was defined using the modified Rankin Scale (mRS) [6]. The central insular sulcus delimited infarct of the anterior insular cortex (AIC; short gyri A1, A2 and A3), posterior insular cortex (PIC; long gyri B1 and B2) or both locations. Relative risk estimates were computed to assess the association between each clinical manifestation and IIS location.

These associations were tested using z tests applied to the natural log of the relative risks. The study was approved by our institutional ethics committee.

Study Group

We identified 7 patients from our databases who fitted our inclusion criteria. No patient was excluded. Of the 50 articles describing IIS cases, we excluded 21 (53%) with incomplete data, 11 (33%) because the ischemic lesion was deemed too extensive and 6 (15%) without brain MRI. In the end, 12 articles that presented a total of 16 cases were included for analysis. Table 1 summarizes the clinicodemographic data and outcome by infarct location of the 23 patients forming the entire study group. For a detailed description of individual cases from the literature and from our institutions, please refer to the online supplementary material (for all online suppl. material, see In the following sections, patients A–G refer to those patients seen at our institutes.

Clinical Manifestations

Somatosensory manifestations were reported in 10 patients (43%; 6 patients from the literature and patients A, B, E and G from our institutes) [7,8,9,10]. Symptoms included numbness (n = 2), dysesthesia (n = 2) and paresthesia (n = 2). At examination, sensory deficits were limited to pain (n = 6), temperature (n = 1) or both (n = 1), or affected all elementary and discriminative modalities (n = 2). The deficit was contralateral to the lesion in all cases. It affected a hemibody with (n = 1) or without facial sparing (n = 3), or was limited to one or two limbs (n = 6).

Aphasia was reported in 10 patients (43%; patients B, C, D and E) [7,10,11,12,13]. Non-fluent aphasia with anomia and phonemic paraphasia was the most frequently reported clinical picture (n = 8), combined with mild comprehension impairment with normal (n = 1) or poor repetition (n = 1). Wernicke's aphasia (n = 2) and a mild receptive aphasia (n = 1) were also reported. In general, language deficits were transient. However, in one case, speech initiation and verbal fluency were still impaired 5 months after stroke [13]. Interestingly, transient resolution of aphasia during an emotional outburst was reported (patient C) [13].

Dysarthria (n = 10, 43%; patients A, F and G) [7,11,12,13,14,15], a vestibular-like syndrome variably described as vertigo, dizziness, unsteadiness or instability (n = 8, 35%; patients A, F and G) [7,16,17] and weakness contralateral to the lesion (n = 6, 26%; patients B and F) [11,12,13] were also frequently reported. Weakness was either brachial, brachiofacial, proportional, combined with hemiataxia (n = 1 each) or limited to the lower face (n = 2). Dysautonomic disorders were also reported (n = 4), characterized by hypertension bursts [7], T-wave inversion [12], syncope [17] or lipothymia (patient G). Gustatory disturbances (n = 3; patient E) [7,8] somatoparaphrenia (n = 3; patients A and E) [7], speech and oral-buccal apraxia (n = 1) [18], auditory processing deficit (n = 1) [14], movement disorder (n = 1) [17] and hypersalivation (n = 1) [8] were rarely reported.

Clinical Syndromes

Using the Oxfordshire classification [19], the partial anterior cerebral infarct (PACI) was the most frequent pattern (n = 9; patients B, C and D) [7,10,11,13,15,18] followed by the lacunar infarct (LACI; n = 2) [9,11] and posterior cerebral infarct (POCI; n = 2) [7,16]. However, most cases (n = 10; patients A, E, F, G and H) had manifestations that did not fit exactly with these classical patterns or presented unusual clinical patterns rarely encountered in stroke [7,8,12,14,17]. We consider those findings as unusual. Four patients with a non-POCI pattern presented with vestibular-like symptoms (patients A and F) [7,17]. Unusual stroke manifestations were dysautonomic disorders (n = 3; patient G) [7,12,17], somatoparaphrenia (n = 3; patients A and E) [7], gustatory disturbances (n = 3; patient E) [7,8], auditory processing deficit (n = 1) [14] and hypersalivation (n = 1) [8].

Infarct Location

The infarct involved the dominant hemisphere in 14 patients (61%). It affected the AIC only (n = 4, 17%; patients D and G) [13,16,18], the PIC only (n = 12, 52%; patients A, B and E) [7,9,10,11,15,17] or both (n = 7, 30%; patients C and F) [7,8,11,12,14]. Limited extension to the adjacent structures was present in 17 cases (74%), involving the subinsular area (n = 11, 48%), the frontal (n = 4, 17%), temporal (n = 5, 22%) and/or parietal opercula (n = 3, 13%) (fig. 1, 2). Table 1 shows that involvement of the PIC was significantly associated with somatosensory manifestations (p = 0.04). However, no other statistically significant associations were found.


Among the 15 patients with known outcome, most (n = 9, 60%) were asymptomatic or had minimal clinical deficit within 48 h of symptom onset. Among the 7 patients evaluated at our centers, 3 had a normal neurological examination (patients C, E and D) and 2 had only mild sensory findings (patients A and G) within 24 h of symptom onset. Among the patients with known outcome, at 6 months, mRS was 0 in 8 patients (35%; patients C, D, E, F and G) [7,17] and 1 or 2 in 7 patients (30%; patients A and B) [7,8,13,15,18].


Our study shows that IIS can result in a vast array of deficits, the most frequent being somatosensory, language, speech, vestibular-like and motor symptoms. These deficits are in line with known functions of the insula, based on previous electrophysiological, functional and lesional studies [1,20]. For example, Penfield and others [21,22,23,24] have consistently reported somatosensory-but also language-, speech-, vestibular- and motor-evoked responses during stimulation of the insular cortex. While a combination of somatosensory, speech, language and motor disturbances may suggest a larger MCA stroke, certain unusual concomitant symptoms should raise suspicion of a smaller stroke in the multimodal insular area and include vestibular, gustatory and auditory deficits or somatoparaphrenia, as well as a rapid improvement of deficits. Furthermore, although IIS may sometimes result in proportional motor or sensory deficits, mimicking a lacunar infarct (pure motor, sensory, ataxic hemiparesis), concomitant language, vestibular, gustatory or auditory processing deficits should raise the suspicion of an IIS. Less commonly, IIS can also present as a posterior circulation stroke, with acute vertigo, nausea and/or ataxia.

The functional prognosis of IIS appears to be excellent as more than half of the patients were asymptomatic or had minimal deficits within 48 h, and all had a mRS inferior or equal to 2 at 6 months. This is somewhat not surprising considering that IIS are small by definition. Our group and others [25,26] have also previously observed rapid and complete recovery of hemiparesis and dysphasia following insular resection in the context of tumor resection and epilepsy surgery. This suggests that surrounding or distant structures can generally compensate limited insular damage.

A statistically significant association between somatosensory deficit and IIS involving the PIC was observed, consistent with findings from most stimulation studies in which somatosensory responses were more frequently located in the posterior part of the insula [2,27]. However, there were no clear correlations between the localization of the ischemic infarct and the other most common symptoms mentioned above. This is most likely due to the small number of patients. Nonetheless, converging evidence from anatomical and functional studies in humans and non-human primates indicates a functional differentiation exist in the insula [28].

The arterial supply of the insula arises solely from the MCA, mainly from the M2 segment. The insular arteries arising from the M2 segment supply the insular cortex, the capsula extrema and sometimes the claustrum and capsula externa [29,30]. Most likely, IIS are secondary to embolic occlusion of an M2-MCA division or its branches, with good collateral flow protecting the more distal cortex; thus, the insula becomes the terminal perfusion area [31].

The main limitation of our study relies on its partial retrospective nature including a non-systematic and incomplete evaluation of clinical and neuropsychological deficits at presentation, and biased reports of certain symptoms of interest or outcome. For instance, the association between the insular cortex and autonomic control has been eluded by several authors [32]. In our study, the low number of reported autonomic disturbances, their heterogeneity and the presence of confounding factors did not allow for further interpretation. Such disturbances can only be assessed using a standardized quantitative approach in a prospective manner. In addition, although this is the largest series of IIS cases reported in the literature to our knowledge, the sample size remains modest.


Due to the confluence of functions in a restricted region, IIS results in multimodal deficits combining in descending order somatosensory, speech or language, vestibular-like, motor, gustatory and somatoparaphrenic disturbances. Recuperation is generally rapid and the outcome excellent. Larger prospective studies are needed to better define the clinical presentation and outcome of IIS.

Disclosure Statement

The authors have no conflicts of interest to declare.

Supplementary Material

Supplemental Tables

1. Augustine JR. Circuitry and functional aspects of the insular lobe in primates including humansBrain Res Brain Res RevYear: 1996222292448957561
2. Ibañez A,Gleichgerrcht E,Manes F. Clinical effects of insular damage in humansBrain Struct FunctYear: 201021439741020512375
3. Chollet F,DiPiero V,Wise RJ,Brooks DJ,Dolan RJ,Frackowiak RS. The functional anatomy of motor recovery after stroke in humans: a study with positron emission tomographyAnn NeurolYear: 19912963711996881
4. Weiller C,Chollet F,Friston KJ,Wise RJ,Frackowiak RS. Functional reorganization of the brain in recovery from striatocapsular infarction in manAnn NeurolYear: 1992314634721596081
5. Borsody M,Warner Gargano J,Reeves M,Jacobs B,MASCOTS Insula-Stroke Substudy GroupInfarction involving the insula and risk of mortality after strokeCerebrovasc DisYear: 20092756457119390182
6. Quinn TJ,Dawson J,Walters MR,Lees KR. Functional outcome measures in contemporary stroke trialsInt J StrokeYear: 2009420020519659822
7. Cereda C,Ghika J,Maeder P,Bogousslavsky J. Strokes restricted to the insular cortexNeurologyYear: 2002591950195512499489
8. Metin B,Melda B,Birsen I. Unusual clinical manifestation of a cerebral infarction restricted to the insulate cortexNeurocaseYear: 200713949617566941
9. Cattaneo L,Chierici E,Cucurachi L,Cobelli R,Pavesi G. Posterior insular stroke causing selective loss of contralateral nonpainful thermal sensationNeurologyYear: 20076823717224581
10. Birklein F,Rolke R,Müller-Forell W. Isolated insular infarction eliminates contralateral cold, cold pain, and pinprick perceptionNeurologyYear: 200565138116275823
11. Mejdoubi M,Calviere L,Boot B. Isolated insular infarction following successful intravenous thrombolysis of middle cerebral artery strokesEur NeurolYear: 20096130831019295219
12. Mandrioli J,Zini A,Cavazzuti M,Panzetti P. Neurogenic T wave inversion in pure left insular stroke associated with hyperhomocysteinaemiaJ Neurol Neurosurg PsychiatryYear: 2004751788178915548512
13. Shuren J. Insula and aphasiaJ NeurolYear: 19932402162188496709
14. Bamiou DE,Musiek FE,Stow I,Stevens J,Cipolotti L,Brown MM,Luxon LM. Auditory temporal processing deficits in patients with insular strokeNeurologyYear: 20066761461916924014
15. Hiraga A,Tanaka S,Kamitsukasa I. Pure dysarthria due to an insular infarctionJ Clin NeurosciYear: 20101781281320400317
16. Liou LM,Guo YC,Lai CL,Tsai CL,Khor GT. Isolated ataxia after pure left insular cortex infarctionNeurol SciYear: 201031899119806312
17. Etgen T,Winbeck K,Conrad B,Sander D. Hemiballism with insular infarction as first manifestation of Takayasu's arteritis in association with chronic hepatitis BJ NeurolYear: 200325022622912574956
18. Nagao M,Takeda K,Komori T,Isozaki E,Hirai S. Apraxia of speech associated with an infarct in the precentral gyrus of the insulaNeuroradiologyYear: 19994135635710379594
19. Bamford J,Sandercock P,Dennis M,Burn J,Warlow C. Classification and natural history of clinically identifiable subtypes of cerebral infarctionLancetYear: 1991337152115261675378
20. Kumral E,Calli C. External and extreme capsular stroke: clinical, topographical and etiological patternsCerebrovasc DisYear: 20062121722216446533
21. Nguyen DK,Nguyen DB,Malak R,Leroux JM,Carmant L,Saint-Hilaire JM,Giard M,Cossette P,Bouthillier A. Revisiting the role of the insula in refractory partial epilepsyEpilepsiaYear: 20095051052018717706
22. Guenot M,Isnard J,Sindou M. Surgical anatomy of the insulaAdv Tech Stand NeurosurgYear: 20042926528815035341
23. Ostrowsky K,Magnin M,Ryvlin P,Isnard J,Guenot M,Mauguière F. Representation of pain and somatic sensation in the human insula: a study of responses to direct electrical cortical stimulationCereb CortexYear: 20021237638511884353
24. Penfield W,Faulk ME Jr. The insula; further observations on its functionBrainYear: 19557844547013293263
25. Malak R,Bouthillier A,Carmant L,Cossette P,Giard N,Saint-Hilaire JM,Nguyen DB,Nguyen DK. Microsurgery of epileptic foci in the insular regionJ NeurosurgYear: 20091101153116319249926
26. Duffau H,Taillandier L,Gatignol P,Capelle L. The insular lobe and brain plasticity: lessons from tumor surgeryClin Neurol NeurosurgYear: 200610854354816213653
27. Mazzola L,Isnard J,Peyron R,Mauguière F. Stimulation of the human cortex and the experience of pain: Wilder Penfield's observations revisitedBrainYear: 201213563164022036962
28. Kurth F,Zilles K,Fox PT,Laird AR,Eickhoff SB. A link between the systems: functional differentiation and integration within the human insula revealed by meta-analysisBrain Struct FunctYear: 201021451953420512376
29. Varnavas GG,Grand W. The insular cortex: morphological and vascular anatomic characteristicsNeurosurgeryYear: 199944127136 discussion 36–38. 9894973
30. Ture U,Yasargil MG,Al-Mefty O,Yasargil DC. Arteries of the insulaJ NeurosurgYear: 20009267668710761659
31. Fink JN,Selim MH,Kumar S,Voetsch B,Fong WC,Caplan LR. Insular cortex infarction in acute middle cerebral artery territory stroke: predictor of stroke severity and vascular lesionArch NeurolYear: 2005621081108516009763
32. Soros P,Hachinski V. Cardiovascular and neurological causes of sudden death after ischaemic strokeLancet NeurolYear: 20121117918822265213

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Keywords: Key Words Stroke, Insular cortex, Clinical presentation.

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