brintellex
ValprolBanner
Annals of Indian Academy of Neurology
  Users Online: 3428 Home | About the Journal | InstructionsCurrent Issue | Back IssuesLogin      Print this page Email this page  Small font size Default font size Increase font size

Table of Contents
ORIGINAL ARTICLE
Year : 2015  |  Volume : 18  |  Issue : 4  |  Page : 424-429
 

Clinicoanatomical correlation in stroke related aphasia


1 Department of Neurology, Govind Ballabh Pant Hospital and Maulana Azad Medical College, New Delhi, India
2 Department of Audiology and Speech Therapy, Govind Ballabh Pant Hospital and Maulana Azad Medical College, New Delhi, India

Date of Submission01-Mar-2015
Date of Decision09-Mar-2015
Date of Acceptance04-Apr-2015
Date of Web Publication17-Nov-2015

Correspondence Address:
Vikram Bohra
118/250, Vikramaditya Marg, Mansarovar, Jaipur - 302 020, Rajasthan
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-2327.165469

Rights and Permissions

 

   Abstract 

Context: With advances in neuroimaging, traditional views regarding the clinicoanatomic correlation in stroke patients with aphasia are being challenged and it has been observed that lesions at a given cortical or subcortical site may manifest with different aphasia profiles. Aims: To study as to whether there is a strict clinicoanatomical correlation between the type of aphasia and lesion site in patients with first ever stroke. Settings and Design: Observational study, based in a tertiary care center. Materials and Methods: Stroke patient's ≥18 years of age were screened and those with first ever stroke and aphasia were subjected to a detailed stroke workup and language assessment using the Hindi version of Western Aphasia Battery (WAB). Statistical analysis was done with χ2 test with Yates correction and Kruskal-Wallis test. The level of significance was set at P < 0.05. Results: Overall aphasia was detected in 27.9% of the 260 screened cases with stroke. Amongst 60 cases with first ever stroke and aphasia, the aphasia type was: Global (33.33%), Broca's (28.3%), transcortical motor (13.33%), transcortical sensory (10%), Wernicke's (8.33%), anomic (5%), and conduction (1.67%) aphasia. A definite correlation between the lesion site and the type of aphasia as per the traditional classification was observed in 35% cases only. Conclusions: No absolute correlation exists between the lesion site and the type of clinical aphasia syndrome in majority of the patients with cortical and subcortical stroke.


Keywords: Aphasia, clinico-anatomic correlation, clinico-topographic correlation, stroke


How to cite this article:
Bohra V, Khwaja GA, Jain S, Duggal A, Ghuge VV, Srivastava A. Clinicoanatomical correlation in stroke related aphasia. Ann Indian Acad Neurol 2015;18:424-9

How to cite this URL:
Bohra V, Khwaja GA, Jain S, Duggal A, Ghuge VV, Srivastava A. Clinicoanatomical correlation in stroke related aphasia. Ann Indian Acad Neurol [serial online] 2015 [cited 2020 Sep 19];18:424-9. Available from: http://www.annalsofian.org/text.asp?2015/18/4/424/165469



   Introduction Top


Stroke is among the leading causes of the disability worldwide and aphasia is one of the common presentations of stroke. The frequency of aphasics among stroke patients ranges from 21 to 38% (Pedersen et al., 1995; Wade et al., 1986; Kauhanen et al., 2000; Brust et al., 1976; Siirtola et al, 1977). [1] Aphasia is defined as a disorder of language that is acquired secondary to brain damage (Alexander and Benson, 1997). [2] It was one of the first higher cortical functions to be used for localization of brain lesions. Various studies have been done to validate if there is strict clinicotopographic correlation seen between the aphasia type and location of the brain lesion in stroke patients. While some studies have concluded that lesion location is the main determinant of the aphasic syndrome encountered in a stroke patient (Hayward et al., Kreisler et al., Yang et al.), other studies have opined against such a definite localization concept (Peychinska et al., Joseph et al.). [18] For subcortical aphasias also, most of the studies have opined against any definite association between classical aphasic syndromes and subcortical lesions (Colombo et al., D'Esposito and Alexander). This study was undertaken with the aim of studying the validity of correlating the clinical aphasia profile with lesion site and comparing aphasia profiles in cortical versus subcortical insults. As the aphasia profile changes over time, we also planned to study the clinical aphasia profile in acute, subacute, and chronic insults with regards to a given lesion site.


   Materials and Methods Top


The study was carried out at a tertiary healthcare center in Central India (Govind Ballabh Pant Hospital, New Delhi). Stroke patients reporting to the hospital over a 1-year period from March 2012 to March 2013 were screened for the presence of aphasia. Patients with mental obtundation, dementia, or recent head injury were excluded. Aphasia was detected in 72 (27.69%) out of 260 screened stroke patients. Aphasics with recurrent stroke were excluded and 60 aphasic patients ≥18 years of age with first ever stroke (ischemic/hemorrhagic) were included in the study. Ischemic stroke cases were classified as per the trial of ORG 10172 in acute stroke treatment (TOAST) classification. Detailed aphasia assessment was done with the help of the Hindi version of Western Aphasia Battery (WAB) and classified into different types of fluent (Wernicke's, transcortical sensory, conduction, and anomic aphasia) or nonfluent (Broca's, global, transcortical motor, transcortical mixed, or isolation) aphasia based on their scores for fluency, comprehension, repetition, and naming subtests. All patients were also investigated for stroke-related risk factors and subjected to neuroimaging (computed tomography (CT) or magnetic resonance imaging (MRI) brain) for localization of the lesion. Data was fed on excel sheet and analyzed using SPSS software version 20.χ2 test with Yates correction and Kruskal-Wallis test, when appropriate, were used. The level of significance was set at P < 0.05.


   Results Top


Out of 260 stroke patients screened for aphasia, there were 160 (61.5 %) males and 100 (38.5 %) females. Ischemic stroke accounted for 85.36% and hemorrhagic stroke for 14.62% of the cases. Aphasia was detected in 27.69% of the cases. There was no statistically significant difference in the occurrence of aphasia in ischemic (27.9% cases) vs hemorrhagic stroke (26.3% cases) and gender had no impact on the occurrence of aphasia. Aphasia was observed in 48.4% cases with left and 8.8% cases with right hemispheric involvement, confirming the statistically significant association between left hemispheric lesions and aphasia (P < 0.001).

Overall, 60 stroke patients with aphasia were included in the study [Table 1]. Age of the patients ranged from 21 to 80 years (median age-60 years). Around 43.3% (26/60) of these cases had young onset (<50 years) stroke. Majority (95%) of the patients were right-handed and literate (66.7%) and crossed aphasia was seen in four (6.67%) cases among the study group. Around 68.33% of the cases hailed from an urban, while 31.67% belonged to a rural background. The most common risk factor for stroke was hypertension (40%), followed by smoking (35%), alcoholism (25%), coronary artery diseases (11.67%), atrial fibrillation (AF; 11.7%%), diabetes mellitus (10%), valvular heart diseases (10%), and dilated cardiomyopathy (3.37%).
Table 1: Master sheet showing the lesion location and aphasia type among the study group

Click here to view


Echocardiographic abnormalities were detected in 45% cases and included left ventricular hypertrophy with diastolic dysfunction (18.3%); valvular heart disease (6.67%); left auricular/left ventricular (LA/LV) thrombus (6.67%); dilated cardiomyopathy (3.3%); and regional wall motion abnormalities and systolic dysfunction due to coronary artery disease (10%). On carotid Doppler study, internal or common carotid artery stenosis was detected in 26 (43.3%) patients.

Lesion localization was based on MRI brain in 46 (76.67%) and CT head in 14 (23.3%) patients. Majority of the patients (n = 53, 88.3%) had either a single infarct or hemorrhage, but seven (11.67%) patients, despite no history of stroke in the past, revealed multiple infarcts on imaging. Overall, 47 (78.33%) patients had ischemic infarcts; 11 (18.33%) had hemorrhagic infarcts, while two (3.33%) had intracerebral hemorrhage. Location of the infarct/hemorrhage was purely cortical in two (3.33%), subcortical in 10 (16.67%), and corticosubcortical in 48 (80%) cases.

Etiology or cause of ischemic stroke was: Atherothrombotic large vessel disease in 24 (40%); cryptogenic in 19 (31.67%); cardioembolic in 11 (18.3%); artery to artery embolism in three (5 %), and lacunar stroke/small vessel disease in one (1.67%).

Aphasia assessment was done in the acute stroke phase (<2 weeks post stroke) in 22 (36.67%), in the subacute stroke phase (2 weeks-3 months) in 23 (38.33%), and in the chronic stroke phase (>3 months) in 15 (25%) cases. Post stroke duration for assessment of aphasia varied from 3 days to 1 year. Nonfluent aphasia was seen in 77.3% cases in the acute stroke phase, 56.2% cases in the subacute stroke phase, and all the cases in the chronic stroke phase.

The most common type of aphasia in our study group was global aphasia (33.33%) followed by Broca's (28.3%), transcortical motor (13.33%), transcortical sensory (10%), Wernicke's (8.33%), and anomic (5%) aphasia. Conduction aphasia was seen in one case only, while there was no case of isolation or transcortical mixed aphasia. Behavioral change at stroke onset was observed in 66.67% cases with aphasia. Behavior was agitated in 33.33%; apathetic in 25%, and depressed in 8.33% cases. Aphasia was accompanied by hemiplegia in 73.33% and faciobrachial paresis in 16.67%, but 10% cases had only aphasia. Among patients with only aphasia, three had transcortical motor, while one each had Wernicke's, transcortical sensory, and anomic aphasia. Aphasia severity, as determined by the aphasia quotient (AQ) derived from the WAB, was mild (AQ 75-93.8) in five (8.33%), moderate (AQ 50-74) in 13 (21.67%), and severe (AQ < 50) in 40 (70%) cases.

Based on the history, the pattern of aphasia at stroke onset and at the time of assessment remained unchanged in 44 (73.33%) cases. However in 16 (26.67 %) cases with a global aphasia profile at stroke onset, the pattern of aphasia changed over a period ranging from 3 days to 6 months. Majority (68.7%) of these cases evolved into other nonfluent types of aphasia (Broca's - 43.75% and transcortical motor - 25%). Evolution to Wernicke's aphasia was seen in 12.5%, while one case each (6.25%) evolved into transcortical sensory, conduction, and anomic aphasia.

In two cases with pure cortical lesions, global aphasia was seen in one and anomic aphasia in the other. In 10 cases with pure subcortical lesion, 50% had Broca's aphasia, 30% had global aphasia, and 20% had Wernicke's aphasia. In 48 cases with corticosubcortical lesions, 33.3% had global aphasia, 25% had Broca's aphasia, 16.7% had transcortical motor aphasia, 12.5% had transcortical sensory aphasia, 6.2% had Wernicke's aphasia, 6.2% had anomic aphasia, and 2.1% had conduction aphasia.

Conformity between lesion location and the type of aphasia as per the traditional localizationist model was observed in 21 (35 %) patients only. Majority (65%) of the patients failed to show any conformity between the location of the brain lesion and the type of aphasia. Frontal lesions were accompanied by more severe impairment of fluency (P = 0.189) and naming (P = 0.26); parietal by comprehension (P = 0.42) and naming (P = 0.28); temporal by naming (P = 0.17), comprehension (P = 0.18), and repetition (P = 0.28); while no significant effect was observed with occipital lesions. In the setting of subcortical lesions, lentiform nucleus lesions were accompanied by significant impairment in comprehension (P = 0.05) and repetition (P = 0.03). Lesions of the caudate nucleus caused less severe impairment of fluency (P = 0.196), comprehension (P = 0.127), repetition (P = 0.116), and naming (P = 0.869) [Figure 1],[Figure 2],[Figure 3],[Figure 4],[Figure 5],[Figure 6],[Figure 7],[Figure 8] and [Figure 9].
Figure 1: Distribution of aphasia types in patients with parietal lobe lesions

Click here to view
Figure 2: Distribution of aphasia types in patients with frontal lobe lesions

Click here to view
Figure 3: Distribution of aphasia types with temporal lobe lesion *All patients had associated lentiform nucleus involvement

Click here to view
Figure 4: Distribution of aphasia types with frontoparietal lesions

Click here to view
Figure 5: Distribution of aphasia types with parietotemporal lesions

Click here to view
Figure 6: Distribution of aphasia types with frontoparietotemporal lesions

Click here to view
Figure 7: Distribution of aphasia types with frontoparietal with basal ganglia (caudate and/or lentiform) lesions

Click here to view
Figure 8: Distribution of aphasia types in patients with parietooccipital lesion. Those with Broca's aphasia had additional involvement of frontal lobe, while those with global aphasia had additional involvement of caudate nucleus

Click here to view
Figure 9: Distribution of aphasia types among those with different subcortical lesion sites

Click here to view



   Discussion Top


Ischemic stroke occurred in 85.36% and hemorrhagic stroke in 14.62% of our cases and this matches the stroke incidence mentioned in other Indian studies [1] as well as the Harvard Stroke Registry. [2] Young stroke (<50 year) constituted 43.3% of cases. Various studies in past have documented aphasia in 22.7-67.6% of the stroke cases. [2],[3],[4],[5] In our study, aphasia was present in 27.69% of the cases and stroke type or gender had no impact on the occurrence of aphasia. In previous studies, crossed aphasia has been reported in 1-4% of the stroke cases. [6],[7] In our study, 95% of patients were right-handed and crossed aphasia was seen in 6.67% of the cases.

The three most common risk factors for stroke, as documented in earlier studies, include hypertension, diabetes, and AF. [7],[8] In our study also hypertension was the most common risk factor (40%), but other modifiable stroke risk factors like smoking (35%), alcoholism (25%), and cardiac disorders (25%) were more common as compared to AF (11.7%) and diabetes (10%). Cardioembolic stroke has been reported as one of the most common cause of stroke in previous studies (48-62%), but was seen in 18.3% of our cases only. [7],[8] Atherothrombotic large vessel disease (40%) emerged as the most common cause, while the etiology remained cryptogenic in 31.67% of the cases.

A preponderance of nonfluent aphasia was seen in our study group, the most common type being global (33.33%) followed by Broca's (28.3%), transcortical motor (13.33%), transcortical sensory (10%), Wernicke's (8.33%), anomic (5%), and conduction aphasia (1.7%). Overall, nonfluent aphasia was seen in 77.3% of the cases with acute, 56.2% cases with subacute, and all the cases with chronic post stroke aphasia. Earlier studies [3],[5],[8],[9],[10] have also reported a higher incidence of nonfluent aphasia with global and Broca's aphasia being the major subtypes. However, anomic aphasia which has been reported with a frequency of 16-25% in previous studies [3],[9],[10] was seen in 5% of our cases only. Pure subcortical lesions were seen in 16.67% of our cases. In one study by Colombo et al., the incidence of fluent and nonfluent aphasia was similar in patients with subcortical lesions. [11] In contrast, 80% of our cases with subcortical lesions had nonfluent aphasia.

In a study by Pedersen et al., [9] it was observed that stroke related aphasia usually evolves to a less severe form over time. In our study, a change in aphasia profile over time was observed in 16 (26.67%) cases only. Majority (68.75%) of these cases with global aphasia evolved into other nonfluent aphasia types, while the rest evolved into fluent aphasia (e. g., global to Wernicke's and Broca's to anomic). The overall aphasia pattern remained unchanged in cases presenting with a fluent aphasia at the outset. Aphasia was accompanied by hemiplegia or faciobrachial paresis in 90% of our cases. Aphasia as the only manifestation of stroke has been reported in around 5.1% cases in a study by Fennis et al., [12] but was seen in 10% of our cases.

While some previous studies favor [10],[13],[14],[15] the concept of a definite correlation between the aphasia type and lesion location in patients with stroke, other studies negate it; [11],[16],[17],[18] and the debate continues. Majority (65%) of our patients failed to show any conformity between the lesion site and the type of aphasia as per the traditional localizationist aphasia model. A definite correlation between the lesion site and the type of aphasia was observed in 35% cases only. Frontal lesions were more frequently associated with impairment of fluency and naming; parietal with impairment of naming and comprehension and temporal with impairment of comprehension, naming, and repetition. Occipital and caudate lesions did not have any significant effect on fluency, comprehension, repetition, or naming. Lesions of the lentiform nucleus showed severe impairment of comprehension and repetition. In conclusion, clinicotopographical correlation is not seen in the majority of stroke patients with aphasia and lesions at different sites may produce a similar clinical aphasic profile.

 
   References Top

1.
Nadamuni S. Researchers identify stroke subtypes in India. Lancet 2002;359:500.  Back to cited text no. 1
    
2.
Alexander MP, Benson DF. The aphasias and related disturbances, in clinical neurology, vol 1, edited by R. J. Joynt, Lippincott, Philadelphia, 1997. pp. 1-58.  Back to cited text no. 2
    
3.
Godefroy O, Dubois C, Debachy B, Leclerc M, Kreisler A; Lille Stroke Program. Vascular aphasias: Main characteristics of patients hospitalized in acute stroke units. Stroke 2002;33: 702-5.  Back to cited text no. 3
    
4.
Kyrozis A, Potagas C, Ghika A, Tsimpouris PK, Virvidaki ES, Vemmos KN. Incidence and predictors of post-stroke aphasia: The Arcadia Stroke Registry. Eur J Neurol 2009;16:733-9.  Back to cited text no. 4
    
5.
Croquelois A, Bogousslavsky J. Stroke aphasia: 1,500 consecutive cases. Cerebrovasc Dis 2011;31:392-9.  Back to cited text no. 5
    
6.
Campbell WW, DeJong RN, Haerer AF. DeJong′s the neurologic examination. 6 th edition. Philadelphia, PA: Lippincott Williams & Wilkins: 2005. p.79-87.  Back to cited text no. 6
    
7.
Inatomi Y, Yonehara T, Omiya S, Hashimoto Y, Hirano T, Uchino M. Aphasia during the acute phase in ischemic stroke. Cerebrovasc Dis 2008;25:316-23.  Back to cited text no. 7
    
8.
Engelter ST, Gostynski M, Papa S, Frei M, Born C, Ajdacic-Gross V, et al. Epidemiology of aphasia attributable to first ischemic stroke: Incidence, severity, fluency, etiology, and thrombolysis. Stroke 2006;37:1379-84.  Back to cited text no. 8
    
9.
Pedersen PM, Vinter K, Olsen TS. Aphasia after stroke: Type, severity and prognosis. The Copenhagen aphasia study. Cerebrovasc Dis 2004;17:35-43.  Back to cited text no. 9
    
10.
Yang ZH, Zhao XQ, Wang CX, Chen HY, Zhang YM. Neuroanatomic correlation of the post-stroke aphasias studied with imaging. Neurol Res 2008;30:356-60.  Back to cited text no. 10
    
11.
Colombo A, Sorgato P, Scarpa M. Language disturbances following vascular lesions restricted to the left basal ganglia, thalamus and white matter. Neuropsychology 1989;3:75-80.  Back to cited text no. 11
    
12.
Fennis TF, Compter A, van den Broek MW, Koudstaal PJ, Algra A, Koehler PJ. Is isolated aphasia a typical presentation of presumed cardioembolic transient ischemic attack or stroke? Cerebrovasc Dis 2013;35:337-40.  Back to cited text no. 12
    
13.
Hayward RW, Naeser MA, Zatz LM. Cranial computed tomography in aphasia. Correlation of anatomical lesions with functional deficits. Radiology 1977;123:653-60.  Back to cited text no. 13
    
14.
Mazzocchi F, Vignolo LA. Localisation of lesions in aphasia: Clinical-CT scan correlations on stroke patients. Cortex 1979;15:627-53.  Back to cited text no. 14
    
15.
Kreisler A, Godefroy O, Delmaire C, Debachy B, Leclercq M, Pruvo JP, et al. The anatomy of aphasia revisited. Neurology 2000;54:1117-23.  Back to cited text no. 15
    
16.
Peychinska D, Danovska M, Chakarov D, Simeonova V, Lilovski C. Dynamic follow up of aphasic disorders in patients with ischemic stroke in acute stage. J IMAB 2004;10:19-20.  Back to cited text no. 16
    
17.
D′Esposito M, Alexander MP. Subcortical aphasia: Distinct profiles following left putaminal hemorrhage. Neurology 1995;45:38-41.  Back to cited text no. 17
    
18.
Joseph KA, Joseph RD, Strand EA, Whitwell JL, Layton KF, Joseph EP, et al. Clinicopathological and imaging correlates of progressive aphasia and apraxia of speech. Brain 2006;129:1385-98.  Back to cited text no. 18
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]
 
 
    Tables

  [Table 1]



 

Top
Print this article  Email this article

    

 
   Search
 
  
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Article in PDF (778 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  


    Abstract
   Introduction
    Materials and Me...
   Results
   Discussion
    References
    Article Figures
    Article Tables

 Article Access Statistics
    Viewed4241    
    Printed52    
    Emailed0    
    PDF Downloaded152    
    Comments [Add]    

Recommend this journal