Pure dysarthria due to an insular infarction

Cortical infarction presenting with pure dysarthria is rarely reported. Previous studies have reported pure dysarthria due to cortical stroke at the precentral gyrus or middle frontal gyrus. We report a 72-year-old man who developed pure dysarthria caused by an acute cortical infarction in the insular cortex. The role of the insula in language has been difficult to assess clinically because of the rarity of pure insular strokes. Our patient showed pure dysarthria without aphasia, indicating that pure dysarthria can be the sole manifestation of insular infarctions.     

Lesions to the posterior insular cortex cause dysarthria

Background: Up to now, there are few systematic studies in a sufficient number of patients with lesions involving the insular cortex (IC) examining whether damage of the IC is directly related to dysarthria. Thus, this is the first study applying modern voxel‐lesion behaviour mapping (VLBM) aimed to examine whether the IC is involved in dysarthria – and if so – which part of the IC is involved. Methods: Twenty‐five patients with acute stroke lesions affecting the IC and peri‐insular region were investigated employing VLBM analysis. Results: Present data indicated that dysarthria is associated with stroke lesions affecting the right‐ and left‐sided posterior IC. Conclusions: Owing to the known extensive spectrum of cortical and subcortical somatosensory and motor connections, it seems that the IC might be one region involved in the generation of speech motor execution.     

Neuropsychiatric effects of insular stroke

The neuropsychiatric effects of insular damage in humans have not previously been examined. We therefore examined the neuropsychiatric impairment in seven patients with left insular stroke, six patients with right insular stroke, six patients with left hemisphere noninsular stroke, and six patients with right hemisphere noninsular stroke. Between 4 and 8 weeks after acute stroke, patients were administered a neuropsychiatric battery. Patients with right insular lesions had a greater frequency of subjective anergia and underactivity (Fisher's exact p = .002) as well as tiredness (Fisher's exact p < .002) compared with patients with non-insular lesions or left insular lesions. Subjective feelings of impaired energy or drive after right insular damage may result from disconnection between the insula and the frontal lobe or the anterior cingulate cortex, structures that have been associated with willed action and motor behavior.     

Clinical study of 39 patients with atypical lacunar syndrome

The aim of this study was to describe the clinical characteristics of atypical lacunar syndrome (ALS) based on data collected from a prospective acute stroke registry. In total, 2500 acute stroke patients were included in a hospital based prospective stroke registry over a 12 year period, of whom 39 were identified as having ALS and radiologically proven (by computed tomography or magnetic resonance imaging) lacunes. ALS accounted for 1.8% of all acute stroke patients, 2.1% of acute ischaemic stroke, and 6.8% of lacunar syndromes. ALS included dysarthria facial paresis (n = 12) or isolate dysarthria (n = 9), isolated hemiataxia (n = 4), pure motor hemiparesis with transient internuclear ophthalmoplegia (n = 4), pure motor hemiparesis with transient subcortical aphasia (n = 3), unilateral (n = 2) or bilateral (n = 3) paramedian thalamic infarct syndrome, and hemichorea hemiballismus (n = 2). Atypical lacunar syndromes were due to small vessel disease in 96% of patients. Atherothrombotic infarction occurred in one patient and cardioembolic infarct in another, both presenting pure dysarthria. Outcome was good (in hospital mortality 0%, symptom free at discharge 28.2%). After multivariate analysis, the variables of speech disturbances, nausea/vomiting, ischaemic heart disease, and sensory symptoms were found to be significantly associated with ALS. In conclusion, atypical lacunar syndrome is an infrequent stroke subtype (one of each 14 lacunar strokes). ALS occurred in 6.8% of lacunar strokes. Isolated dysarthria or dysarthria facial paresis were the most frequent presenting forms. The prognosis of this infrequent non-classic lacunar syndrome is good.     

Effects of stroke localization on cardiac autonomic balance and sudden death.

BACKGROUND AND PURPOSE: Stroke has been shown to alter autonomic function. The purpose of this study was to show the differential effects of stroke localization on autonomic function parameters assessed by heart rate variability (HRV). METHODS: To determine the differential effect of ischemic stroke localization on autonomic cardiac innervation, we evaluated 62 patients with ischemic stroke and 62 age- and sex-matched controls. The localization of the infarct was determined by CT and MRI. Power spectrum analysis of HRV was performed. Myocardial necrosis was ruled out by echocardiography and creatine kinase myocardial isoenzymes measurements. RESULTS: All stroke patients had significantly decreased low frequency, high frequency, and standard deviation of all relative risk intervals values (P<0.001). However, patients with right-middle cerebral artery (R-MCA) and insula lesions had significantly lower power spectrum analysis values compared with all other localizations (P<0.001). In addition, 5 patients with R-MCA insular lesions died suddenly compared with 2 patients with left-middle cerebral artery insular lesions during hospitalization. Both sympathetic- and parasympathetic-controlled HRV were decreased in patients with ischemic stroke. The most pronounced decrease was found in the territory of R-MCA insular cortex, which suggests that cardiac autonomic tone may be regulated by insula and that these patients are more prone to cardiac complications such as arrhythmias and sudden death due to autonomic imbalance. CONCLUSION: We conclude that stroke in the region of insula (especially the right) leads to decreased HRV and to increased incidence of sudden death.     

Insular cortex lesions alter baroreceptor sensitivity in the urethane-anesthetized rat

Cardiovascular representation has been demonstrated within the insular cortex and lateralization has been previously inferred. In this study, baroreceptor gain was investigated in response to the systemic injection of the pressor agent phenylephrine (PE) and the depressor agent sodium nitroprusside (SNP) in 57 urethane-anesthetized, male Sprague–Dawley rats before and after single lesion placement. Lesions mainly confined to the anterior insula (left or right) or the adjacent cortex were without significant effect on baroreceptor gain. Left posterior insular lesions, however, significantly increased baroreceptor gain (p<0.0001) whereas right posterior insular lesions had no effect on baroreceptor gain although heart rate and blood pressure were both significantly increased after lesion placement (p<0.05). These data suggest that: (1) the posterior insula (and not surrounding cortex or anterior insula) is primarily involved in cardiovascular control; (2) the left insular cortex may be chiefly concerned with parasympathetic cardiac regulation. Conversely, the right posterior insular cortex may regulate both cardiac and vasomotor sympathetic tone, as has been suggested in other species.     

Neurogenic cardiac outcome in patients after acute ischemic stroke: The brain and heart connection

BackgroundNeurogenic cardiac impairment can occur after acute ischemic stroke (AIS), but the mapping of the neuroanatomic correlation of stroke-related myocardial injury remains uncertain. This study aims to identify the association between cardiac outcomes and middle cerebral artery (MCA) ischemic stroke, with or without insular cortex involvement, as well as the impact of new-onset atrial fibrillation (AF) after AIS on recurrent stroke.MethodsSerial measurements of high sensitivity troponin T (TnT), brain natriuretic peptide (BNP), electrocardiography (ECG), echocardiogram, and cardiac monitoring were performed on 415 patients with imaging confirmed MCA stroke, with or without insular involvement. Patients with renal failure, recent cardiovascular events, or congestive heart failure were excluded.ResultsOne hundred fifteen patients (28%) had left MCA infarcts with insular involvement, 122 (29%) had right MCA infarcts involving insular cortex, and 178 (43%) had no insular involvement. Patients with left MCA stroke with insular involvement tended to exhibit higher BNP and TnI, and transient cardiac dysfunction, which mimicked Takotsubo cardiomyopathy in 10 patients with left ventricular ejection fraction (LVEF) of 20-40%. Incidence of new-onset AF was higher in right MCA stroke involving insula (39%) than left MCA involving insula (4%). Nine out of fifty-three patients with new-onset AF were not on anticoagulant therapy due to various reasons; none of them experienced recurrent AF or stroke during up to a 3-year follow-up period. Statistically significant correlations between BNP or TnT elevation and left insular infarcts, as well as the incidence of AF and right insular infarcts, were revealed using linear regression analysis.ConclusionsThe present study demonstrated that acute left MCA stroke with insular involvement could cause transient cardiac dysfunction and elevated cardiac enzymes without persistent negative outcomes in the setting of health baseline cardiac condition. The incidence of new-onset AF was significantly higher in patients with right MCA stroke involving the insula. There was no increased risk of recurrent ischemic stroke in nine patients with newly developed AF who were not on anticoagulant therapy, which indicated a need for further research on presumed neurogenic AF and its management.     

Neglect after right insular cortex infarction

BACKGROUND AND PURPOSE: Case reports have shown an association between right insular damage and neglect. The aim of this study was to examine the incidence of neglect among patient groups with right or left insular infarction. METHODS: We examined neglect in 9 right-handed subjects with insular stroke as evidenced by CT and/or MRI scans (4 with right insular and 5 with left insular cerebrovascular accident) between 4 and 8 weeks after acute stroke with tests of visual, tactile, and auditory perception. RESULTS: Compared with patients with left insular lesions, patients with right insular lesions showed significant neglect in the tactile, auditory, and visual modalities. CONCLUSIONS: The right insular cortex seems to have a role in awareness of external stimuli, and infarction in this area may lead to neglect in multisensory modalities.     

Insular lesions, ECG abnormalities, and outcome in acute stroke

It has been suggested that lesions in the insula may result in abnormal electrocardiographic (ECG) findings and increase the risk of sudden death. We investigated if computed tomography (CT) detected insular lesions due to acute stroke were related to ECG abnormalities and mortality at three months. Acute insular lesions were diagnosed in 43/179 patients (left insular = 25; right insular = 17; bilateral = 1) with acute stroke (cerebral infarcts = 62 and intracerebral haemorrhage = 17) based on CT scans from 5-8 days after stroke onset; 12 lead ECGs were recorded on admission and ECG telemetry was done in the first 12-24 hours after admission. Information regarding mortality at three months was obtained. Insular lesions were related to sinus tachycardia with heart rate >120 bpm (p = 0.001), ectopic beats >10% (p = 0.032), and ST elevation (p = 0.011). Right insular lesions were related to atrial fibrillation (p = 0.009), atrioventricular block (p = 0.029), ectopic beats >10% (p = 0.016), and inverted T wave (p = 0.040). Right insular lesions, compared with left or no insular lesions, increased the odds of death within three months (OR 6.2, 95% CI 1.5 to 25.2) independent of stroke severity, lesion volume, and age. As the number of patients in the present study is relatively small, our findings need to be confirmed in studies on other populations of stroke patients.     

Isolated ataxia after pure left insular cortex infarction

Acute insular infarction, due to its anatomic and functional complexity and wide connections, may present with various clinical presentations, such as somatosensory deficits, gustatory disorder, vestibular-like syndrome, cardiovascular disturbances, neuropsychological disorders, movement disorders, autonomic dysfunction and empathy impairment. However, there was no mention of the symptoms involving the cerebellar system in the related literature. We present a case of pure left insular cortex infarction with isolated truncal ataxia and demonstrate a crucial relationship between the left insular cortex and the cerebellar system. The possible connections are through the spinocerebellar and dentatorubrothalamic pathway. In conclusions, left insular cortex lesions should be considered in the differential diagnosis of isolated truncal ataxia.     

Laterality does not influence early mortality in MCA ischemic stroke

OBJECTIVES: There is clinical and experimental evidence involving the insula in the control of the autonomic system and cardiac function, with differential participation of right and left brain hemispheres, and these differences could influence mortality in the acute phase of brain hemisphere ischemic infarcts. METHODS: We have analyzed retrospectively the mortality during initial hospitalization in a series of 504 consecutive, unselected patients with middle cerebral artery (MCA) ischemic infarcts to detect potential differences between right (220 patients) and left (284 patients) lesions. RESULTS: Factors associated with a higher mortality were the infarct size, the occurrence of nosocomial respiratory infection, age and a history of diabetes mellitus or chronic obstructive pulmonary disease. CONCLUSIONS: The laterality of the infarct did not have a significant influence on stroke mortality during the admission period for the acute stage.     

Agrammatic primary progressive aphasia in two dextral patients with right hemispheric involvement

Agrammatic primary progressive aphasia (PPA-G) has been known to be associated with focal brain atrophy involving the left posterior frontal and anterior insular regions. However, aphasia can also rarely result from right hemispheric lesions in right-handed patients, so-called crossed aphasia in dextrals (CAD). We report two right-handed patients with PPA-G whose 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) showed hypometabolism predominantly in the right hemisphere, implicating “crossed PPA-G.”     

Dichotic-listening evidence of right-hemisphere involvement in recovery from aphasia following stroke

A dichotic-listening procedure was used to investigate the role of the right hemisphere in recovery from aphasia following left-hemisphere stroke. Thirty-one stroke patients were divided into three groups: (a) patients who were recovering from aphasia (Aphasic group, n = 11), (b) patients who had experienced mild strokes with only transient dysarthria (Dysarthric group, n = 10), and (c) patients who had sustained right-hemisphere stroke with no language disturbance (Nonaphasic group, n = 10). In addition, a group of normal, healthy volunteers served as a control group (n = 11). Results show that, like the Control subjects, the Dysarthrics and Nonaphasics showed a strong right-ear advantage (REA) for dichotically presented consonant-vowel (CV) syllables. This is usually thought to be an indication of left-hemisphere dominance (Kimura, 1961). By contrast, the Aphasic group showed left-ear advantage (LEA) suggesting a shift in cerebral dominance for language. The possibility that the results were due to sensory degradation of the auditory messages (lesion effect) was explored. This idea was rejected in favor of an explanation based on increased right-hemisphere mediation of language following left-hemisphere aphasiogenic lesions.     

Aphasia type, age and cerebral infarct localisation

Stroke patients with non-fluent aphasia tend to be younger than fluent aphasics. We investigated whether this difference was due to an age-related change in the anatomico-functional organisation of language areas or to an age-dependent variation on the distribution of infarct localisation. From a hospital prospective stroke database we selected those patients who suffered an ischaemic stroke with at least one non-lacunar infarct demonstrated by computed tomography (n = 423 patients). We retrieved information on language disturbance in the acute phase (no aphasia, non-fluent aphasia, fluent aphasia) and on infarct localisation by CT. Non-fluent aphasia predominated in young (aged < 51 years) patients while in elderly patients (aged > 70 years) the opposite was found (χ² = 8.03; P = 0.005). Posterior infarcts were also more frequent in elderly patients (χ² = 9.9; P = 0.002). There were 27 atypical cases (patients with lesions on language areas without aphasia) and 14 aphasics with atypical infarct localisation (9 fluent aphasics with anterior lesions and 5 non-fluent aphasics with posterior lesions). The proportions of atypical cases, their infarct location or fluency type were not influenced by age. It was concluded that the predominance of fluent aphasia in older patients was related to the higher proportion of posterior infarcts in these patients. The hypothesis of age-related changes in the anatomico-functional organisation of language areas was not supported by the present data. Received: 14 January 1997 Received in revised form: 28 April 1997 Accepted: 26 May 1997     

Diffusion-weighted magnetic resonance imagings at the acute stage in two patients with spectacular shrinking deficit due to cardioembolic stroke]

We report diffusion-weighted magnetic resonance imagings (DWI) at the acute stage of two patients with spectacular shrinking deficit (SSD) due to cardioembolic stroke. Patient 1 was a 74-year-old woman with atrial fibrillation (Af) who had been admitted for acute cholecystitis. She abruptly developed consciousness disturbance, global aphasia and right hemiparesis. Her neurological symptoms rapidly improved 30 minutes after onset, and completely disappeared in four hours. Patient 2 was a 84-year-old woman with Af who had been on medication of warfarin potassium for three years. She abruptly developed consciousness disturbance and left hemiplegia. Her neurological symptoms rapidly improved 90 minutes after onset, and almost completely disappeared in ten hours. Their conditions were consistent with SSD in acute cardioembolic stroke. DWI of Patient 1 taken 27 hours after onset showed hyperintense signal areas in the insular and temporal cortices of the left middle cerebral artery territory, and in the parietal cortex corresponding to the border zone between the territories of the left middle cerebral artery and posterior cerebral artery. DWI of Patient 2 taken 39 hours after onset showed hyperintense signal areas in the insular and frontal cortices of the right middle cerebral artery territory, and in the parietal cortex corresponding to the border zone between the territories of the right middle cerebral artery and posterior cerebral artery. They indicated multifocal ischemic injuries at the acute stage. The T2-weighted MRI of Patient 2 showed a slight hyperintense signal area only in the right parietal cortex, but the fluid-attenuated inversion recovery (FLAIR) in both patients showed no abnormal signals in the corresponding areas. To our knowledge, ischemic lesions in DWI of SSD at the acute stage after rapid recovery have not been reported previously. DWI is useful in SSD for detecting ischemic injuries of cardioembolic origin at the early stage.     

Binswanger's subcortical encephalopathy. Study of a case with predominant left hemispheric lesion (author's transl)

We report the clinical and pathological study of a patient with vascular leucoencephalopathy almost restricted to the left posterior hemisphere. A 65 year--old right handed hypertensive woman has presented with a neuropsychological symptomatology of transcortical sensorial aphasia. We discuss the following points: 1) the patient's disease must be considered as Binswanger's subcortical encephalopathy despite the asymetric topography of the lesions ; 2) particular hemodynamic cerebral factors has possibly determined the asymetric nature of the disease ; 3) a lesion of the left temporo-parieto-occipital area that was strictly sub-cortical, with complete destruction of the posterior part of the arcuate fasciculus has presented with the clinical picture of a transcortical sensorial aphasia.     

Racial differences in stroke recurrence rate following initial lacunar infarct.

One-hundred fourteen black patients and 50 white patients who had suffered an initial lacunar infarct were retrospectively analyzed to determine the incidence of clinical stroke recurrence within 12 months of the initial stroke. Of the 114 black patients, 35 had recurrent stroke (31%). Of the recurrent stroke, 27 were lacunar infarcts and eight were nonlacunar. Utilization of aspirin at a maximal dose of 325 mg/d did not reduce stroke recurrence. Of the 50 white patients, four had recurrent strokes (8%). Of these, only one represented lacunar infarct and three were nonlacunar. All the black (35) and white (four) lacunar stroke patients who suffered stroke recurrence were hypertensive and had been hypertensive for more than 8 years; they also had evidence of end-organ damage consisting of hypertensive retinopathy and left ventricular hypertrophy or had episodes of congestive heart failure.     

Left pseudothalamic cortical syndrome and pain asymbolia]

We report a case of left pseudothalamic cortical syndrome associated with asymbolia for pain in a right-handed male patient. The responsible lesion, detected at both CT and MRI, was infarction of the superficial territory of the middle cerebral artery, restricted to the posterior insula, the superior aspect of T1, the parietal operculum and the supramarginal gyrus. The ascending parietal gyrus and the thalamus were spared. This case, together with data from the literature, suggest that the somatosensory area II was responsible for the pseudothalamic syndrome. This interpretation is concordant with the hypothesis that S II plays the principal role in passive somatosensory discrimination, whereas S I plays the principal role in active discrimination implying stimulus exploration. The location of lesions that were responsible for asymbolia for pain is discussed. This case and those reported by Berthier et al. (1988), provide arguments in favour of Geschwind's hypothesis which attributes asymbolia for pain to sensory-limbic disconnection due to damage of the insula.     

Lateralization of Insular Ischemic Stroke is Not Associated With Any Stroke Clinical Outcomes: The Athens Stroke Registry

Background: Controversial evidence suggests that right insular stroke may be associated with worse outcomes compared to the left insular ischemic lesion. Objectives: We investigated whether lateralization of insular stroke is associated with early and late outcome in terms of in-hospital complications, stroke recurrence, cardiovascular events, and death. Methods: Data were prospectively collected from the Athens Stroke Registry. Insular cortex involvement was identified based on brain CT scans or MRI images. Patients were followed up prospectively at 1, 3, 6 months after hospital discharge and yearly thereafter up to 5-years or until death. The assessed outcomes were in-hospital complications, functional outcome assessed by the modified Rankin Scale, stroke recurrence, cardiovascular events, and death. Cox-regression analysis was performed to estimate the cumulative probability of each outcome according to the lateralization of insular strokes. Results: Among the 1212 patients, 650 had left insular stroke involvement and 562 had right. New onset of in-hospital atrial fibrillation was similar between right and left insular strokes (11.6% versus 12.9%, P = .484). During the 5-year follow-up sudden death occurred in 21 (3.7%) patients with right insular compared to 30 (4.6%) with left insular stroke (P = .476). There was no difference between left and right insular strokes regarding mortality (adjusted odds ratio [OR]: .92, 95% confidence interval [CI]: .80-1.06), stroke recurrence (4.3% versus 4.9%; adjusted OR: .81 95% CI: .58-1.13), cardiovascular events, and sudden death (adjusted OR: .99, 95% CI: .76-1.29) and on death and dependency (adjusted OR: .88, 95% CI: .75-1.02) during a 5-year follow up. Conclusions: Lateralization of insular ischemic stroke involvement is not associated with stroke outcomes.     

Neurogenic ST depression in stroke.

BACKGROUND: Stroke is occasionally associated with ECG repolarization changes including ST depression. Recent evidence suggests a neurogenic contribution to these abnormalities in stroke patients. Animal studies implicate the insular cortex in cardiovascular control. We describe a patient with a left insular infarct and without cardiac or coronary artery disease, who developed ST depression indicating a neurogenic etiology. CASE DESCRIPTION: A 48 year-old female, with no risk factors for stroke, developed sudden expressive aphasia. MRI brain showed an infarct in the left insular cortex. Twenty-four hour Holter monitoring on the third day revealed transient ST depression more than 1.5 mm, which was not reproducible on subsequent monitoring. Transesophageal echo-cardiography (TEE) was normal. She had no cardiac symptoms and serial ECGs, cardiac enzymes (CKMB) and adenosine thallium scan were normal. To-date, there had been no cardiac events like congestive heart failure or myocardial ischemia. CONCLUSION: These findings suggest neurogenic ST depression is related to the left insular infarct in view of the normal adenosine thallium scan, non-reproducibility and evanescence of the ST segment changes and lack of associated cardiac symptoms. When neurogenic ST depression is combined with underlying coronary artery disease, it may adversely influence cardiac outcome after stroke.