Language as a stressor in aphasia

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Language as a stressor in aphasiaDalia Cahana-Amitay a , Martin L. Albert a , Sung-Bom Pyun b ,Andrew Westwood a , Theodore Jenkins c , Sarah Wolford d &Mallory Finley aa Harold Goodglass Aphasia Research Center, VA HealthcareSystem, Boston, Department of Neurology, Boston University ,MA, USAb Department of Physical Medicine and Rehabilitation , KoreaUniversity College of Medicine , Seoul, Koreac Department of Slavic and Eastern Languages , BostonCollege, Chestnut Hill , MA, USAd Department of Communication Sciences & Disorders ,Emerson College , Boston, MA, USAPublished online: 19 Apr 2011.

To cite this article: Dalia Cahana-Amitay , Martin L. Albert , Sung-Bom Pyun , AndrewWestwood , Theodore Jenkins , Sarah Wolford & Mallory Finley (2011) Language as a stressor inaphasia, Aphasiology, 25:5, 593-614

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APHASIOLOGY, 2011, 25 (5), 593–614

Language as a stressor in aphasia

Dalia Cahana-Amitay1, Martin L. Albert1, Sung-Bom Pyun2, AndrewWestwood1, Theodore Jenkins3, Sarah Wolford4, and Mallory Finley1

1Harold Goodglass Aphasia Research Center, VA Healthcare System, Boston,Department of Neurology, Boston University, MA, USA2Department of Physical Medicine and Rehabilitation, Korea University Collegeof Medicine, Seoul, Korea3Department of Slavic and Eastern Languages, Boston College, Chestnut Hill,MA, USA4Department of Communication Sciences & Disorders, Emerson College, Boston,MA, USA

Background: Persons with aphasia often report feeling anxious when using language whilecommunicating. While many patients, caregivers, clinicians, and researchers would agreethat language might be a stressor for persons with aphasia, systematic empirical studiesof stress and/or anxiety in aphasia remain scarce.Aim: The aim of this paper is to review the existing literature discussing languageas a stressor in aphasia, identify key issues, highlight important gaps, and propose aprogramme for future study. In doing so we hope to underscore the importance of under-standing aspects of the emotional aftermath of aphasia, which plays a critical role in theprocess of recovery and rehabilitation.Main Contribution: Post stroke emotional changes in persons with chronic aphasia clearlyhas adverse effects for language performance and prospects of recovery. However, thespecific role anxiety might play in aphasia has yet to be determined. As a starting point,we propose to view language in aphasia as a stressor, linked to an emotional state weterm “linguistic anxiety”. Specifically, a person with linguistic anxiety is one in whomthe deliberate, effortful production of language involves anticipation of an error, with theimminence of linguistic failure serving as the threat. Since anticipation is psychologicallylinked to anxiety and also plays an important role in the allostatic system, we suggestthat examining physiologic stress responses in persons with aphasia when they are askedto perform a linguistic task would be a productive tool for assessing the potential relationof stress to “linguistic anxiety”.

Address correspondence to: Dalia Cahana-Amitay PhD, Boston University, Department of Neurology,Harold Goodglass Aphasia Research Center, VA Healthcare System, 150 South Huntington AvenueBoston, MA 02130, USA. E-mail: [email protected]

Our thanks to Mira Goral, Jacqueline Laures-Gore, Kristine Lundgren, Loraine Obler, and CarolePalumbo for their insightful comments on this manuscript. We would also like to thank Danny Kaloupekand our anonymous reviewers for their extremely valuable comments. Support for this research was pro-vided by the National Institutes of Health, NIDCD grant 5P30DC005207, Boston University, Departmentof Neurology, Harold Goodglass Aphasia Research Center and VA Healthcare System, 150 SouthHuntington Avenue, Boston, MA 02130, and NIA grant 2R01AG14345 Boston University, Department ofNeurology, Language in the Ageing Brain, VA Healthcare System, 150 South Huntington Avenue, Boston,MA 02130.

© 2011 Psychology Press, an imprint of the Taylor & Francis Group, an Informa businesshttp://www.psypress.com/aphasiology DOI: 10.1080/02687038.2010.541469

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mailto:[email protected]

http://www.psypress.com/aphasiology

594 CAHANA-AMITAY ET AL.

Conclusions: Exploring the putative relationship between anxiety and language in apha-sia, through the study of physiologic stress responses, could establish a platform forinvestigating language changes in the brain in other clinical populations, such as in indi-viduals with Alzheimer’s disease or persons with post-traumatic stress disorder, or evenwith healthy ageing persons, in whom “linguistic anxiety” might be at work when theyhave trouble finding words.

Keywords: Aphasia; Anxiety; Language; Stress.

Persons with aphasia often report feeling anxious when using language while commu-nicating. The experience of language as a stressor is described in the excerpt below,written by a woman who acquired aphasia as a young adult (Newborn, 1998, p. 196):

. . . the net effect of this behavioral impairment is that the aphasic is especially consciousof and deliberate in language production . . . speech is a matter of special concern, anx-iety, and labor. The aphasic always has to worry about what to say, how to say it, andhow to keep command of that which has already been planned . . . the aphasic mustdeliberately choose words and then attend to planning how to form, arrange, and speakthem.

By her account, the compromised linguistic skills in aphasia force patients into a stateof extreme concern about the clarity and accuracy of their verbal communication,even in the face of the simplest verbal exchange. It could be argued, then, that personswith aphasia are preoccupied with the increased risk of breakdown in communicationas a result of the language disorder, which results in a state of “linguistic anxiety”. Wecontend that the cumulative stress associated with language use brings about a stateof anxiety in (some) persons with aphasia, where anxiety is taken to be “a state of self-preoccupation in which evaluation of one’s (inadequate) capabilities to deal with thethreat is prominent. Accompanying this negative affective state is a strong physiolog-ical or somatic component . . . This somatic state may be the physiological substrateof “readiness,” which may underlie a state of preparation to counteract helplessness”(Barlow, 2004, p. 64). While we construe stress and anxiety as two related but inde-pendent constructs, we found the use of these terms in the literature to be, at times,inconsistent, vague, and ambiguous. As a result, throughout this paper we make aconscious effort to keep these concepts distinct, as far as possible.

The notion that aphasia involves anxiety is not new and dates at least as far back asGoldstein (1942, 1948, 1959) and Luria (1970) who maintained that aphasic patients“avoid the frustration, humiliation, anxiety, and catastrophic reaction that may beotherwise induced by the prospect of speaking defectively” (Sapir & Aronson, 1990,p. 504). Consequently, language breakdown in neurologic patients cannot be viewedin isolation from the potential effects anxiety might have on it, a stance that we adoptin this review.

While many patients, caregivers, clinicians, and researchers would agree that lan-guage may be a stressor that could bring about anxiety in persons with aphasia,systematic empirical studies of anxiety in aphasia remain scarce. The aim of thispaper is to review the existing literature, identify key issues, highlight important gaps,and propose a programme for future study. In doing so we hope to underscore theimportance of understanding aspects of the emotional aftermath of aphasia, whichplays a critical role in the process of recovery and success of rehabilitation (Code,2010).

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LANGUAGE AS A STRESSOR IN APHASIA 595

EMOTIONAL CHANGES AMONG STROKE SURVIVORS

The study of emotional changes following stroke, such as depression and anxi-ety, is fraught with methodological issues that make the interpretation of reportedfindings difficult. There is little agreement among researchers about what symp-toms are diagnostically valid for detecting post stroke depression and anxiety(Chemerinski & Levine, 2006). Many rely on definitions provided by the Diagnosticand Statistic Manual of Mental Disorders, 4th edition, text revision (AmericanPsychiatric Association, 2000). However, these criteria have been disputed becausethey include signs or symptoms that may be found in a broad range of neuro-logic disorders that are not necessarily related to depression or anxiety, such asweight loss, diminished appetite, or insomnia, and are thus diagnostically question-able (Chemerinski & Levine, 2006; Herrmann & Wallesch, 1993). In addition, somecommon post stroke neurological signs or symptoms, such as altered facial expres-sions and problems in motor speech and prosody, could mistakenly be taken to reflecta depressive state (Code & Herrmann, 2003; Code & Muller, 1992; Stern, 1999).Exacerbating the methodological problems, studies rarely use the same assessmentbatteries, scales, questionnaires, and baseline measures in their experimental studies(Code & Herrmann, 2003; Frankel, 2008;Herrmann & Wallesch, 1993; Robinson,2006). Furthermore, researchers often do not consider the possible consequencesthat premorbid personality traits, coping styles, and responses to loss might have forchanges in patients’ emotional state following stroke, and do not control for them intheir research design (Cohen, 1998; Greenop, Almeida, Hankey, van Bockxmeer, &Lautenschlager, 2009).

Nonetheless, studies of post stroke depression and anxiety are important in thatthey consider the emotional wellbeing of stroke survivors, which is as elemental totheir human experience as it is for healthy individuals (Code & Herrmann, 2003).An important component of emotional wellbeing is anchored in a person’s capacity toengage in human interaction (Code, Hemsley, & Herrmann, 1999; Code & Herrmann,2003), which is certainly changed in persons with aphasia (Tanner, 2003). Those stud-ies that have explored the consequences of emotional dysregulation in persons withaphasia have mostly focused on post stroke depression (Code & Herrmann, 2003;Hemsley & Code, 1996), with little attention to the incidence and effects of anxiety,the study of which seems to have been neglected in the general stroke population aswell (Sagen et al., 2010).

Changes in stroke survivors’ emotional states are not uncommon, and may includea wide range of emotional states, such as depression, anxiety, anger, mania, euphoria,psychosis, denial, catastrophic reaction, apathy, irritability, aggression, and patholog-ical laughing/crying (Chemerinski & Levine, 2006; Cohen, 1998; Robinson, 2006).Of these, the most common is depression, defined, according to the Diagnostic andStatistic Manual of Mental Disorders, 4th edition, text revision, as a “mood dis-order due to stroke with depressive features for two weeks or more, including atleast four of the following depressed mood features: changed appetite/weight, dis-rupted sleep, decreased interest or pleasure, psychomotor agitation or retardation,poor energy, feelings of worthlessness or inappropriate guilt, concentration prob-lems, and suicidal thoughts” (American Psychiatric Association, 2000). However, theexact incidence of this clinical state remains controversial, with considerable variabilityreported, ranging from 5% to 60% (Barker-Collo, 2007; Chemerinski & Levine, 2006;Code & Herrmann, 2003; De Wit et al., 2008; Hackett, Yapa, Parag, & Anderson,

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2005; House, Dennis, Warlow, Hawton, & Molyneaux, 1990; Kauhanen et al., 1999;Lipsey, Robinson, Pearlson, Rao, & Price, 1985; Small & Llano, 2009; Starkstein& Robinson, 1988; Townend, Whyte, et al., 2007). A commonly accepted estimatefor the development of depression stands at approximately one-third of stroke sur-vivors (Hackett, Yapa, Patag, & Anderson, 2005; Hilari, Northcott, Roy, & Marshall,2010). Post stroke anxiety, defined according to the Diagnostic and Statistic Manualof Mental Disorders, 4th edition, text revision as a “state of excessive worrying presentfor a period of at least 6 months, accompanied by at least three of the followingsymptoms: restlessness, irritability, low energy, poor concentration, increased mus-cle tension, poor sleep”, shows slightly different and less variable figures than thosereported for depression, with 14–21% of stroke patients exhibiting post stroke anxi-ety (Åström, 1996; Barker-Collo, 2007; Burvill et al., 1995; Leppavouri, Pohjasvaara,Vataja, Kaste, & Erkinjuntti, 2003; Sagen et al., 2010).

In spite of the high likelihood of their occurrence, depression and anxiety areoften overlooked and/or misdiagnosed in the acute stage (Bogousslavsky, 2003;Chemerinski & Levine, 2006; Paolucci, 2008; Sagen et al., 2009, 2010) and carry over,untreated, into the chronic phases (Åström, Adolefsson, & Asplund, 1993; De Witet al., 2008; Clarke & Currie, 2009; Sagen et al., 2009). Åström et al. (1993), for exam-ple, found a rise in the incidence of post stroke depression over the span of three yearsfrom 3 months post onset through 3 years post stroke, with a dip at 12 months (25%at the acute stage, 31% at 3 months, 16% at 12 months, and 29% at 24 months), coin-cident with diminished life satisfaction and reduced participation in daily activities.However, those patients who suffer depression in the acute stage are not necessarilythe same as those who end up experiencing depression chronically (Staub, Carota,Karapanayiotides, Berney, & Bogousslavsky, 2001). Symptoms observed in the acuteand chronic stages are somewhat different, possibly because of the distinct patho-physiology associated with each (Small & Llano, 2009). Acutely, patients often showpseudodepressive symptoms, such as emotionalism, catastrophic reaction, patholog-ical crying, anxiety, apathy, and loss of psychic self-activation, often misclassified asdepression (Bogousslavsky, 2003), whereas subacutely, patients mostly exhibit signs ofminor depression typically manifested as loss of interest or pleasure (Small & Llano,2009).

Depressed or anxious stroke survivors have been found to suffer adverse effectson their self-agency, volition, identity, personality, drive, motivation, and physical andcognitive functioning (Berg, Palomaki, Lehtihalmes, Longvist, & Kaste, 2001; Carota,Rossetti, Karapanayiotides, & Bogousslavsky, 2001; Herrmann, Black, Lawrence,Szekely, & Szalai, 1998; Kauhanen et al., 1999; Mukheriee, Levin, & Heller, 2006,Robinson, 2006; Sagen et al., 2010; Santos, Caeiro, Ferro, Albuquerque, & Figueira,2006; Sharpe et al., 1994). Impaired cognitive functions include verbal logical think-ing, comprehension, nonverbal problem solving, verbal memory, visual memory,attention, executive functions, and psychomotor speed, which seem to persist wellinto the first year post stroke (Kauhanen et al., 1999; Robinson, 2006). These changeshave been attributed to neurological, psychological, and psychosocial factors (Cohen,1998; Code & Hermann, 2003; Gainotti, 1997; Thomas & Lincoln, 2008), wherethe post stroke altered emotional state is considered to be either a primary con-sequence of damage to particular neural networks in the left hemisphere (Beblo,Wallesch, & Herrmann, 1999; Castillo, Starkstein, Fedoroff, Thomas, & Robinson,1993; Herrmann, Bartels, Schumacher, & Wallesch, 1995; Herrmann, Bartels, &Wallesch, 1993; House et al., 1990; Lauterbach, Jackson, Wilson, Dever, & Kirsh,

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1997; Robinson, 2003, 2006; Starkstein et al., 1990; Starkstein & Robinson, 1988),or a secondary response to the need to adjust to a life with disability (Code &Herrmann, 2003; Herrmann & Wallesch, 1993; Robinson, 2006). Patients who fail toadapt have been found to experience difficulties engaging in social interactions, puttingthem at risk of increased social isolation, stigmatisation, and marginalisation (Code& Herrmann, 2003; Herrmann & Wallesch, 1993; Mukheriee et al., 2006), impedingtheir physical, cognitive and functional recovery (Bogousslavsky, 2003; Chemerinski &Levine, 2006; Chemerinski, Robinson, & Koiser, 2001; Clarke & Currie, 2009; Gusev& Bogolepova, 2009; Masskulpan, Riewthong, Diapratham, & Kiptniratsaikul, 2008;Neau et al., 1998; Pohjasvaara, Erkinjutti, Vataja, & Kaste, 1998; Pohjasvaara, Vataja,Leppavouri, Kaste, & Erkinjutti, 2001; Singh et al., 2000;), and possibly even increas-ing their risk of mortality (Morris, Robinson, Andrzejerski, Samuels, & Price, 1993;Shimoda & Robinson, 1998; Gainotti, Azzoni, & Marra, 1999; Bogousslavsky, 2003;Linden, Bloomstand, & Skoog, 2007; Townend, Brady, & McLaughlan, 2007).

An important factor affecting the long-term prognosis of stroke survivors is theco-morbidity of depression with anxiety (Castillo et al., 1993; Leppavuori et al., 2003;Mukheriee et al., 2006; Shimoda & Robinson, 1998; Starkstein et al., 1990). Anxietyhas been found to have consequences for the onset, duration, severity, and efficacy oftreatment of post stroke depression (Coplan & Gorman, 1990; Coryell, Zimmermann,& Pfohl, 1985; Liebowitz et al., 1990; Shores et al., 1992). However, it has been arguedthat post stroke depression and anxiety are, in fact, independent of one another anddo not share the same aetiology (Shimoda & Robinson, 1998). While not preciselymapped as yet, the neural architecture associated with each condition may be differ-ent (Castillo et al., 1993; Starkstein et al., 1990). There is also some evidence thatanxiety selectively affects activities of daily living (ADL) while depression influencescognitive functioning (Shimoda & Robinson, 1998). However, this observation is ques-tionable since it is based on a study with methodological shortcomings, which theauthors themselves list, including use of insufficiently sensitive cognitive assessmenttools, bias in population selection (exclusion of patients with severe comprehensionproblems and inclusion of mostly black participants), and lack of control of patients’pharmacotherapy regimens. Moreover, other researchers have found that depressionis associated with low ADL scores (Åström et al., 1993; Fure, Wyller, Engedal, &Thmmessen, 2006; Kotila, Numminen, Waltimo, & Kaste, 1998; Neau et al., 1998;Parikh, Lipsey, Robinson, & Price, 1987; Primeau, 1988; Sinyor et al., 1986).

ANXIETY IN APHASIA

The consequences of anxiety for speech or language capacity have typically beendiscussed in relation to a range of voice and speech disorders, such as developmen-tal stuttering and psychogenic and neurogenic stuttering (for a recent review, seeLundgren, Helm-Estabrooks, & Klein, 2010. See also Alm, 2004; Aronson, 1985;Caruso, Chodzko-Zajko, Bidinger, & Sommers, 1994; Cox, 1986; Doruk et al., 2008;Ezrati-Vinacour & Levin, 2004; Ozdemir et al., 2010; Palasik, Irani, & Goberman,2009; Peters & Hulstijn, 1984; Sapir & Aronson, 1990; Weber & Smith, 1990). Asmall group of studies examined the consequences of anxiety for motor speech inaphasia and found problems, such as dysphonia, in patients with Broca’s apha-sia but not Wernicke’s aphasia, which have been attributed to psychological stress(Heeschen, Ryalls, & Hagoort, 1988; Luchsinger & Arnold, 1965; Masdeu, Schoene,& Funkenstein, 1978; Ryalls, 1984; Sapir & Aronson, 1990). However the study of

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anxiety, as it might relate specifically to the language component in aphasia, hasreceived far less attention (Carota et al., 2001; Cohen, 1998; Gainotti, 1972, 1997;Sapir & Aronson, 1990; Starkstein, Fedoroff, Price, & Robinson, 1993). In these fewstudies descriptions of how language performance is compromised in the face of anx-iety are typically based on imprecise linguistic measures, such as “subjective verbalexpression”, that provide little insight into what aspects of language might be vulner-able to breakdown in an anxious patient with aphasia (Carota et al., 2001; Starksteinet al., 1993).

APHASIA AND PHYSIOLOGIC STRESS RESPONSES TOLANGUAGE USE

If persons with aphasia in fact experience language as a stressor, with the cumulativeeffect of stress resulting in an anxious state, then they should perceive language use asa threat, entailing certain behavioural and physiologic responses to situations in whichthey are required to speak. An intricate subcortical and cortical network is involvedin the interpretation and regulation of stress, including the brain stem reticular sys-tem, limbic structures, and frontal lobes, with activation of the autonomic nervoussystem and hypothalamo-pituitary-adrenal axis (HPA) being a characteristic stressresponse (Abreu et al., 2009; McEwen & Gianaros, 2010; Seeman, Epel, Gruenewald,Karlamangla, & McEwen, 2010). Allostatic systems (sympathetic, neuroendocrine,and immune systems) modulate the response and adaptation to stress, producingincreased arousal (McEwen, 2007; Ursin & Ericksen, 2004). Optimal responses ofthe stress system are critical for wellbeing, successful task performance, and engage-ment in appropriate social interactions (Chrousos, 2009). The protective benefits ofallostasis come with a cost to adaptation, commonly referred to as allostatic load(McEwen, 2007; McEwen & Stellar, 1993), “the wear-and-tear on the body and brainresulting from chronic dysregulation (i.e., over-activity or inactivity) of physiologi-cal systems that are normally involved in adaptation to environmental challenge”(McEwen & Gianaros, 2010, p. 194). In the general stroke population such dysreg-ulation adversely affects motor skills, cognitive function, prognosis, and mortalityrate (e.g., Christensen, Boysen, & Johannsen, 2004; Franceshini, Teneconi, Zoppoli,& Barreca, 2001; Marklund, Peltonen, Nilsson, & Olsson, 2004). Researchers haveused different biomarkers to measure allostatic load in persons under stressful andstress-free situations to determine their physiologic stress responses, including mea-sures of cortisol in saliva, urine, and blood, epinephrine, norepinephrine, dopamine,and growth factors, as well as measures of cardiovascular function, such as bloodpressure (Abreu et al., 2009).

With rare exception, there are virtually no studies that directly examine thephysiologic stress responses in persons with aphasia, in relation to their language per-formance. The one exception that we could find is the series of studies by Laures-Goreand colleagues, which measured salivary cortisol levels in persons with aphasia and inhealthy controls in relation to performance on linguistic tasks (Laures, Odell, & Coe,2003; Laures-Gore, Heim, & Hsu, 2007; Laures-Gore, DuBay, Duff, & Buchanan,2010). Laures-Gore, Heim, et al. (2007) hypothesised that persons with aphasia wouldshow hypercortisolaemia in response to the stressfulness of the linguistic demand,stemming from chronic HPA dysregulation. For the linguistic task the investigatorsused an adaptation of the Trier Social Stress Test: A 5-minute speech, during whichparticipants were asked to tell an unfamiliar listener about their occupation, followed

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by questions. For persons with aphasia this referred to their job before their stroke; forcontrols, to their current job or their job before retirement. Of the 15 aphasic partici-pants, 5 required prompting to complete this task. A non-linguistic task administeredto all participants was the Mirror Drawing Test, in which participants were asked totrace the picture of a star, where indirect visual contact with their hand was madethrough a mirror placed in front of their hand. In addition to obtaining physiologicalmeasurements of stress, the investigators also measured participants’ self-perceivedlevel of stress at the conclusion of the initial 30-minute baseline waiting period andthen again at the end of each task.

Profiles of cortisol levels sampled throughout the testing period differed betweenaphasic patients and controls, but differences between the linguistic and the non-linguistic tests were not statistically significant. On the self-evaluative perception ofstress test, a clear difference between the two groups emerged, with persons with apha-sia rating the linguistic test as being much more stressful than the non-linguistic task.However, the differences in cortisol profiles between the two groups did not lend them-selves to easy analysis. Laures-Gore, Heim, et al. (2007) proposed that patients withaphasia consistently experience language as a repetitive stressor and, as a result, sufferfrom chronic HPA hypoactivity, commonly found in a range of stress related disorders(e.g., Fries, Hesse, Hellhammer, & Hellhammer, 2005; Heim, Ehlert, & Hellhammer,2000). Nonetheless, this explanation needs to be reconciled with evidence cited inCarota et al. (2001), according to which patients with left hemisphere damage showincreased autonomic responses that have been claimed to inhibit the arousal systemmodulated by the right hemisphere, leading to decreased arousal overall.

Decreased arousal in persons with aphasia has consequences for their attentionalsystems (Laures et al., 2003; Hula & McNeil, 2008; McNeil, Matthews, Hula, Doyle,& Fossett, 2006; McNeil, Odell & Tseng, 1991; McNeil & Pratt, 2001; Murray, 2002;Tseng, McNeil, & Milenkovic, 1993). Problems in attention allocation have beenreported for aphasic patients, in terms of slower reaction times and poorer accuracy indual-task paradigms, where linguistic stimuli are simultaneously presented with othercompeting input (e.g., Hula & McNeil, 2008; Hula, McNeil, & Sung, 2007; Laures,2005; McNeil, Matthews, Hula, Doyle, & Fossett, 2006; Tseng et al., 1993; Murray,2002, 2004; Murray, Holland, & Beeson, 1997a, 1997b, 1998; Murray, Keeton, &Karcher, 2006). It is not implausible to propose that linguistic anxiety feeds into thisattentional dysfunction, where the patient’s hyperfocus on area of worry, i.e., concernabout impaired language performance, reduces his/her ability to attend to the lan-guage task at hand, a problem continually reinforced by aroused physiologic stressresponses. The suppression of these negatively laden thoughts and feelings competesfor the same attention resources available for processing task-relevant information,and so might lead to suboptimal performance.

Studies exploring arousal in aphasia have not directly focused on patients’ phys-iologic responses such as galvanic skin response (Heilman, Schwartz, & Watson,1978), blood pressure, and cortisol levels (Laures et al., 2003) in high stress situa-tions. However, Laures et al. (2003) assumed that increased arousal would be observedwith increased task demand. Whether such increased demand is, in fact, stress-relatedis hard to say, since it is ultimately the brain that determines what is stressful foran individual (McEwen & Gianaros, 2010). It does so by “supporting consciousand unconscious appraisal processes; it determines the health-damaging or healthpromoting behaviors that result from this appraisal; and it regulates peripheral allody-namic control systems that feed back to the brain to affect functional and structural

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neuroplasticity” (McEwen & Gianaros 2010, p. 210). Findings from Laures et al.(2003) paint a mixed picture, with mild changes in blood pressure but no cortisolreactivity in persons with aphasia in response to performance on linguistic and non-linguistic auditory vigilance tasks. To account for this dissociation the investigatorssuggested considering the distinct temporal dynamics of the two physiologic sys-tems examined (the immediacy of the cardiovascular reactivity vis-à-vis the delayedreactivity of cortisol) as a source for this difference. They also speculated that the non-threatening nature of the experimental design was insufficiently challenging to arousethe patients. Laures-Gore, Heim, et al. (2007) made similar arguments, even thoughthe experimental methods used in the 2007 study were designed to increase threat and,so, arousal. Since the patients in this study once again failed to show cortisol reactiv-ity, the investigators conjectured that persons with aphasia are habituated to languagetasks, which are frequently administered to them while in treatment. Under such anaccount, though, patients would not have been expected to show heightened levelsof cortisol at the onset of testing. As Laures-Gore, Heim, et al. (2007) themselvesacknowledge, since no other measures of physiologic stress responses were examinedin the patients, it is quite possible that effects in other physiologic systems (e.g., bloodpressure, skin conductance, heart rate) may have been overlooked.

A potential drawback of this study concerns the imprecision of the language mea-sures selected for analysis. The authors do not report the number or types of errorsthe patients made while producing the elicited discourse sample discussing their occu-pation. In determining the possible consequences that anxiety might have for thelanguage produced by persons with aphasia, the well-formedness of their linguisticoutput should be scored. Such analyses might include measures of communicativeeffectiveness (Menn, Ramsberger, & Helm-Estabrooks, 1994), lexical productivity,syntactic architecture, and discourse organisation (Coelho, 2007; Sherratt, 2007),which take into account the number of elements produced, the appropriateness of thestructures chosen, omissions, substitutions, and other types of errors.i Such an analy-sis would have perhaps helped account for why 5 of the 15 patients required promptingto complete the task.

In a subsequent study using the Laures-Gore, Heim, et al. (2007) experimentalparadigm, Laures-Gore et al. (2010) made an attempt to address this issue, mea-suring cortisol reactivity before and after the same discourse task, and correlatingcortisol levels with behavioural measures of word productivity (Cherney, Shadden, &Coelho, 1998) and error frequency (Docherty, DeRosa, & Andreasen, 1996) in theelicited discourse speech samples. While this attempt is a step in the right direction,the fact that the discourse samples elicited were of different types—narrative vs con-versation guided by open-ended questions—poses a problem for the interpretation ofthe findings. These discourse types have different textual features with distinct pro-cessing demands that call for specific linguistic structures (Berman, 2008; Ulatowska& Olness, 2007), and so might involve word productivity and error frequency, whichare not comparable to one another. Thus it is not clear to us what it would meanfor a patient to have a low or high index of word productivity or error frequency, if

iGoral and Kempler (2008), who performed a treatment study examining changes in patterns of verbproduction in chronic aphasia, used the number of verbs and nouns per text, and the verb–noun ratio asoutcome measures. These measures might be particularly useful, since the task they used to elicit discoursesamples in their study is similar to the one Laures-Gore, Heim, et al. (2007) used in that it required thepatient to talk about his job before the stroke.

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these measures are calculated across these two text types. Despite these methodolog-ical quibbles, we note the pioneering work of Laures-Gore and her colleagues in thiscomplicated and important but understudied domain.

Laures-Gore et al. (2010) predicted that lower levels of cortisol would be associatedwith lesser word productivity, but found the opposite in some of their patients (lessthan half): a moderate association between word productivity and cortisol levels inpersons with aphasia, where increased levels were linked to greater word productivity.They offer several possible explanations, linking cortisol reactivity to task persistence,effort exerted during task performance, or the involvement of psychosocial variables,such as ego, unpredictability, evaluative threat, and lack of control. To this list we pro-pose adding motivation, which in early studies of aphasia has been linked to anxiety(Shill, 1979), where it has been claimed that appropriate levels of anxiety optimallychallenge patients inducing better performance (for related comments, see the sec-tion below). At present these accounts remain speculative in nature, especially giventhe small sample size on which the observations are based. Nonetheless, this find-ing underscores the importance of using sensitive language measures in studying theputative relationship between anxiety and language in aphasia.

A potential measure of interest is filled pauses (ums), the occurrence of which inneurologically intact individuals has been linked to high anxiety, evaluation, apprehen-sion, and self consciousness, with more pauses produced as a function of greater self-consciousness about speech and focused attention on linguistic output (Christenfeld& Creager, 1996). Extending this account to persons with aphasia, Christenfeld andCreager (1996) have proposed that the higher number of ums observed in the speechof Broca’s patients, in comparison with Wernicke’s patients, is associated with theirheightened awareness of their impairment and deliberation in speaking, which dis-rupts the automaticity of speech production. Measuring changes in the distributionof filled pauses in the speech of anxious persons with aphasia over time can serve asa behavioural marker of stress and/or anxiety, much like Laures-Gore et al.’s (2010)index of word productivity, allowing for long term follow-up of patients’ anxiety andso improving their rehabilitative prognosis.ii

Reducing anxiety in aphasia

Reducing anxiety in aphasia is of clinical importance, given the presumed link betweenincreased levels of stress and patients’ poor adaptation skills (Pachalska, Knapik,Smolak, & Pytel, 1987) and paucity of coping resources (Laures-Gore, Hamilton,& Matheny, 2007a; Laures-Gore et al., 2010). In early studies of aphasia recovery,level of anxiety has been identified as key to patients’ motivation to perform well,and hence was linked to successful rehabilitation (Darley 1972, 1975; Luria, 1963,1970; Shill, 1979; Wepman, 1951, 1953). Excessive anxiety may delay or even blockrecovery; lack of anxiety promotes it; and sufficiently heightened anxiety enables it(Shill, 1979). This claim is consistent with the well-established Yerkes-Dodson Law(1908), linking level of performance to level of mental and physiological arousal, fol-lowing an inverted U-shaped curve, with poorest performance observed at both ends

iiInterestingly, in a recent study assessing cognitive and emotional functionality in neurologically intactelderly participants over a period of 6 months, the occurrence of filled pauses (“ums”) in phone interviewshas been found to be a reliable marker for monitoring changes in mood and executive functions over time(Penard et al., 2009).

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of the arousal curve (lowest and highest). Of course, determining what level of anxietyis ideal for recovery is difficult. Degree of anxiety has been associated with aware-ness of disorder/disability, expectations of recovery, acceptance and lack thereof fromfriends and family, type of feedback from the various caregivers, clinicians, and otherpersons involved in the rehabilitation process (Darley, 1975). Skelly (1975) has identi-fied four main areas of concern that patients typically report, based on data collectedfrom 50 stroke patients: (i) difficulty comprehending incoming speech, especially fromprofessional staff, (ii) observing nonverbal negative reactions from caregivers and clin-icians, (iii) information being withheld about interventions, on the assumption thatthey cannot understand the explanations provided, and (iv) feeling lack of respect ofpersonhood, through intrusive questions or requests to perform certain tasks in treat-ment. In the current aphasiology literature the relevance of motivation for restitutionof disturbed functions in aphasia continues to be discussed in the context of psychoso-cial studies investigating social participation (e.g., Dalemans, De Witte, Beurskens,Van Den Heuvel, & Wade, 2010) and patient resilience (Cyr, 2010), and in somepharmacotherapy studies where changes in patients’ motivation have been found inresponse to the administration of a dopaminergic agent (L-dopa) (Seniow, Litwin,Litwin, Lesiak, & Czlonkowska, 2009).

The potential benefit of reducing anxiety to improve language performance inpatients with aphasia has been discussed in a small number of studies exploring theeffects of stress reduction on persons with aphasia treated with complementary alter-native medicine (CAM) therapies such as acupuncture (Jianfei, Meifang, & Jia, 1988;Zhajun, 1989), hypnosis (Magnaniello, 1986; Thompson, Hall, & Sison, 1986), relax-ation training (Ince, 1968; Marshall & Watts, 1976; Murray & Ray, 2001; Yesavage& Jacob, 1984), biofeedback (Katz, Bhardawaj, & Carstens, 1999; McNeil, Prescott,& Lemme, 1976), and nature-based therapy (NBT) (reviewed in Lundgren, 2004).Findings from these studies are, for the most part, inconclusive or difficult to interpret,since they lack methodological rigor, are based on small sample size, and include fewor no quantitative language/speech and cognitive measures (Laures & Shisler, 2004).More solid results come from mindfulness and relaxation studies, the most frequentlyused CAM therapy to date (Lundgren, 2006; Marshall & Laures-Gore, 2008; Murray& Kim, 2004), whose benefits for adult neurogenic communication disorders have beenfound in stroke survivors, patients with traumatic brain injury (TBI), and patientswith dementia (Laures & Shisler, 2004; Murray & Kim, 2004). This technique involvesmaintaining attentional focus on stimulus or muscle activity while inhibiting compet-ing thoughts or sensory input, the result of which is physiologic changes opposite tothose associated with stress (Murray & Kim, 2004). Such relaxation treatment hasbeen shown to be efficacious when given in conjunction with other conventional lan-guage therapies (Murray, 2008; Murray & Kim, 2004; Murray & Ray, 2001). Murrayand Ray (2001), for example, found that a patient with chronic aphasia who receivedrelaxation therapy prior to syntactic stimulation improved on testing in number ofgrammatical utterances, correct information units (CIUs), and successful utterancesproduced.

Additional evidence suggesting that reducing anxiety in patients with aphasia mightpromote their language performance has been found in a small number of pharma-cotherapy studies, where the administration of the beta blocking agent propranololwas associated with improved naming in both nonfluent and fluent aphasic patients(Beversdorf et al., 2007; Tanaka et al., 2009; Tanaka, Albert, Fujita, Nonaka, &Oka, 2006). Tanaka et al. (2006) and Tanaka et al. (2009) were interested in deter-mining whether improved language performance might be correlated with measurable

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changes in the function of the autonomic nervous system. They used an open labeldesign to measure patients’ language performance (Boston Naming Test and auditorycomprehension), heart rate, and mood, at baseline, before, during, and following treat-ment, and found that propranolol indeed improved language performance in personswith aphasia, and did so by selectively affecting a physiological expression of anxi-ety (reduction in heart rate was observed while scores on the visual analogue moodscale remained unchanged). Although these findings are limited, at best, for method-ological reasons (open label, small sample size, no placebo condition), they suggestthat the physiological aspects of autonomic nervous system (ANS) function mightbe more important to language function in aphasia than has been previously consid-ered. Beversdorf et al. (2007), who also found significant improvement in naming inpatients with aphasia after administration of propranolol, linked the observed beta-adrenergic effects to the modulation of signal-to-noise ratio in the cortex (Hasselmo,Linster, Patil, Ma, & Cekic, 1997; Heilman, Nadeau, & Beversdorf, 2003). Futurestudies with more power, distinguishing peripheral and central autonomic effects inpersons with and without aphasia, will be helpful as research develops into the relationof autonomic system function to aphasia.

Targeting patients’ anxiety by regulating their ANS responses might result in anincreased ability to attend to a given language task. It is also possible that providingpatients with attention training could bring about a reduction in their level of anx-iety. There is an emerging body of evidence suggesting that in neurologically intactbut anxious individuals, attention training away from “threat” alleviates their anxiety(Eldar & Bar-Haim, 2010). How this might be applied to the treatment of persons withaphasia is a project for further development, especially if the source of their anxietyis language itself. Perhaps the incorporation of nonverbal elements into therapy couldserve as a means to shift the patients’ attention away from that which might be overlythreatening. The question of whether drugs targeting attention, e.g., noradrenaline,dopamine, and acetylcholine (ant)agonists (for a recent review, see Sivan, Neumann,Kent, Stroud, & Bhakta, 2010) can also be used to reduce anxiety opens yet anotheravenue for future research. Indeed, the efficacy of different drugs for language per-formance in aphasia (for a review see Small & Llano, 2009) might very well have anattention component that is indirectly modulated.

LANGUAGE AS A STRESSOR IN APHASIA

As detailed in this review, post stroke emotional changes in persons with chronic apha-sia clearly have adverse effects for language performance and prospects of recovery.However, the specific role anxiety might play in aphasia has yet to be determined.As a starting point, we propose to view language in aphasia as a stressor, linked toan emotional state we term “linguistic anxiety”. Specifically, a person with linguisticanxiety is one in whom the deliberate, effortful production of language involves antic-ipation of an error, with the imminence of linguistic failure serving as the threat. Sucha proposal would not only offer an extension to the earliest speculations about therole of anxiety in aphasia (e.g., Goldstein, 1942, 1948, 1959), it could also be incor-porated into a speech production model (e.g., Caramazza, 1997; Levelt, 1992, 2001),where anticipation of error might work in tandem with mechanisms of error detection,repair, and speech planning.

The notion of anticipation of error does not imply that patients would necessar-ily perceive themselves as stressed and/or anxious prior to completion of a linguistic

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task. Behavioural measures of stress and/or anxiety need not map onto perceptionsof stress and/or anxiety (Laures-Gore et al., 2010). Self-ratings of stress and/or anxi-ety could very well follow a task (as in Laures, Heim, et al., 2007), or even be deniedaltogether (as in Tanaka et al., 2009) as a function of a repressive coping style (Myers,2010). Since anticipation is psychologically linked to anxiety and also plays an impor-tant role in the allostatic system (McEwen & Gianaros, 2010), measuring allostaticload in persons with aphasia when they are asked to perform a linguistic task, mightprovide a useful tool for assessing the relation of stress to “linguistic anxiety”. Such astudy would reflect an eclectic approach to psychological changes observed in aphasia,which ties together post-stroke biochemical brain alterations, psychological copingstyles, and reaction to loss (Tanner, 2003).

IMPLICATIONS FOR RESEARCH

From a methodological standpoint, the use of physiologic stress responses in the studyof aphasia and language performance might offer a means to identify whether or nota person with aphasia might be experiencing language as a stressor, pointing to thepossible presence of linguistic anxiety, without having to rely only on linguisticallydemanding questionnaires (Laures, Heim, et al., 2007) or on subjective self reports ofstress and/or anxiety, which often provide a misleading picture of a patient’s emotionalstate. In an extensive review of 146 studies examining autonomic nervous activity inemotions of healthy individuals, Kreibig (2010) found several reliable cardiovascu-lar, electrodermal, and respiratory measures of anxiety. In these studies anxiety wasinduced by an anticipatory experimental condition, such as threat of shock or speechpreparation, and manifested itself by increased heart rate, higher diastolic blood pres-sure, increased nonspecific skin conductance rate, higher respiratory rate, and otherphysiologic measures. These changes reflect “sympathetic activation, vagal deactiva-tion, and a pattern of reciprocal inhibition”. Whether such changes would also beobserved in persons with aphasia is uncertain, given that their neural architectureis clearly not equivalent to that of neurologically intact individuals (for a relatedcomment, see Laures-Gore, Heim, et al., 2007).

A range of physiologic measures could be used to examine physiologic stressresponses and language performance in persons with aphasia, to determine whichsystem might be activated in response to an anxiety-inducing stimulus. While the effi-cacy of cortisol reactivity as an appropriate measure of physiologic stress responsesin persons with aphasia is currently being examined (Laures-Gore, Heim, et al.,2007; Laures-Gore et al., 2010), alternative (or additional) biomarkers such as heartrate, skin conductance, or pupillometry might be used to allow for continuous mea-surement and offer insight into the potential patterns of language-based anxietypeaks.

To induce anxiety in persons with aphasia, the experimental design would have tobe sufficiently threatening to generate a stress response sufficiently similar to the stressinduced in real-life communicative situations that are perceived as threatening to peo-ple with aphasia. Laures-Gore, Heim, et al. (2007) emphasised the need to includea social-evaluative component in the experimental design, where participants mightperceive judgement of their performance as “costly” enough to induce anxiety. Theycited previous research where such experimental methods were associated with HPAresponsiveness. We would agree that such a component of research design would be

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relevant, given the literature investigating effects of “stereotype threat” on task per-formance, where social stigma is used as a means to increase the threat of failing ona task. In such studies members of a social group are introduced to a domain-specificnegative stereotype stigmatising their group (Steele, 1997; Steele & Aronson, 1995),adversely affecting their task performance for fear of confirming that social stigma(e.g., women’s suboptimal performance on complex maths problems when told thatmaths solving abilities are linked to gender differences). This component of researchdesign increases the stakes of the assigned tasks by influencing a patient’s perceptionof either the relevance of the task to the study, as in “only some of your scores will beimportant to study, but we will not tell you which ones count”; or the tasks’ difficulty,as in “the tasks you will be given will become increasingly difficult”.

To determine whether persons with aphasia have linguistic anxiety or are generallyanxious, their performance on both linguistic and non-linguistic tasks should be anal-ysed. Patients might show variability in terms of levels of anxiety associated with theproduction of language in a constrained task vs. a naturalistic setting. Thus it wouldbe appropriate to include in such a study both standardized confrontation tests, suchas the Boston Naming Test (Kaplan, Goodglass, & Weintraub, 1983), as well as dis-course elicitation tasks, such as picture descriptions or narrative production. It wouldalso be useful to include both production and comprehension tasks, so as to minimisethe potential effects of body movement on the physiologic stress response, which mightbe more noticeable in language production. Patients’ performance on tasks involvingcompeting stimuli would be helpful in demonstrating the potential consequences of“linguistic anxiety” in aphasia, given the relationship between heightened anxiety andcompromised attention.

Interestingly, inducing stress by degrading the quality of the auditory stimulus(Dick, Bates, & Ferstl, 2003; Kilborn, 1991), increasing the speed of stimulus pre-sentation (Miyake, Carpenter, & Just, 1994), and introducing a competing stimulus(Blackwell & Bates, 1995) has been shown to generate transient aphasia-like speechpatterns in neurologically unimpaired individuals, suggesting that ANS dysregulation,indeed, interferes with intact language function. If such physiologic changes, directlymeasured through cardiovascular, electrodermal, and respiratory measures of anxi-ety (see Kreibig, 2010), mediate language variability in what might be described asa “normal-to-aphasic continuum” (Silkes, McNeil, & Drton, 2004), identifying thosephysiologic indices could help explain aspects of adaptation and neural reorganisationinvolved in aphasia recovery (Hula & McNeil, 2008).

CLINICAL IMPLICATIONS

Understanding the impact of emotional changes following stroke in persons withaphasia continues to pose a challenge for persons facilitating aphasia therapy (Code,2003, 2010). Adequate treatment of patients must involve precise and explicit specifica-tion of all therapy components (Byng & Black, 1995; Horton & Byng, 2000), includingexamination of the potential role anxiety might have in language function in apha-sia. While most clinicians would agree that level of anxiety in persons with aphasia isone of the important psychosocial factors linked to patients’ quality of life, only fewaddress its management in the context of the therapy they provide, mostly for fear ofoffering an imbalanced impairment-focused therapy (Dembowski, 2006).

To this end, measuring physiologic stress responses in patients with aphasia mightoffer an unbiased window into determining the extent to which anxiety needs to be

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regulated in a patient, if at all, and so enable the tailoring of specific therapeuticinterventions to his/her particular needs. For example, measuring blood pressure inpatients might help identify cases of “white coat effect”, which has been reportedin some persons with mild aphasia when placed in a clinical setting controlled bya speech therapist (Sakamoto, Sakamaki, Tani, Sugai, & Kurabayashi, 2002). Suchpatients might enjoy self-guided sessions (Sakamoto et al., 2002) or group therapy(Kovarsky, Curran, & Zobel Nichols, 2009; Simmons-Mackie & Damico, 2009), whereclinician involvement can be kept to a minimum and might be perceived by the patientas less anxiety inducing. While group therapy is not directly designed to reduce anx-iety, it might offer patients a supportive and relaxed environment, where they canconsistently show psychosocial and speech-language gains (Elman, 2007; Elman &Bernstein-Ellis, 1999; Ross, Winslow, Merchant, & Brumfitt, 2006; Simons-Mackie,Elman, Holland, & Damico, 2007). Similarly, patients could be placed in mindful-ness or relaxation therapy programmes (Murray, 2008; Murray & Kim, 2004; Murray& Ray, 2001) or a pharmacotherapy regimen, as an adjunct to any standard speech-language therapy they might be receiving, to help manage their stress, reduce theiranxiety and enhance their rehabilitation outcome. Preliminary evidence suggests thatsuch interventions hold promise, but studies exploring this idea are still few and farbetween.

BEYOND APHASIA

Exploring the putative relationship between anxiety and language in aphasia, throughthe study of physiologic stress responses, could establish a platform for investigatinglanguage changes in the brain in other clinical populations, such as in individualswith Alzheimer’s disease or persons with post-traumatic stress disorder, or even withhealthy ageing persons, in whom “linguistic anxiety” might be at work when theyhave trouble finding words. Findings from such studies would fit within the broaderpsychosocial debates linking anxiety and language function in neurologically intactindividuals, including second language learners, public speakers, and stutterers, shed-ding light on the yet to be determined role that the autonomic nervous system mighthave for language function in the anxious brain.

Manuscript received 11 August 2010Manuscript accepted 14 November 2010

REFERENCESAbreau, B. C., Zgaljardic, D., Borod, J. C., Seale, G., Temple, R. O. Ostir, G. V., et al. (2009). Emotional

regulation, processing, and recovery after acquired brain injury. In K. Matsuka & C. Christiansen (Eds.),Life balance: Multidisciplinary theories and research (pp. 223–240). Thorofare, NJ: Slack Incorporated,and Bethesda, MD: AOTA Press.

Alm, P. A. (2004). Stuttering, emotions, and heart rate during anticipatory anxiety: A critical review. Journalof Fluency Disorders, 29, 123–133.

American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., textrevision). Washington, DC: American Psychiatric Association.

Aronson, A. (1985). Clinical voice disorders. New York, NY: Thieme.Åström, M. (1996). Generalized anxiety disorder in stroke patients: A 3-year longitudinal study. Stroke, 27,

270–275.Åström, M., Adolefsson, R., & Asplund, K. (1993). Major depression in stroke patients: A 3-year

longitudinal study. Stroke, 24, 976–982.

Dow

nloa

ded

by [

Mon

ash

Uni

vers

ity L

ibra

ry]

at 1

3:52

05

Oct

ober

201

4


Barker-Collo, S. L. (2007). Depression and anxiety 3 months post stroke: Prevalence and correlates. Archivesof Clinical Neuropsychology, 22, 519–531.

Barlow, D. (2004). Anxiety and its disorders: The nature and treatment of anxiety and panic (pp. 64–65). NewYork, NY: Guilford Press.

Beblo, Th., Wallesch, C. W., & Herrmann, M. (1999). The crucial role of frontostriatal circuits for depres-sive disorders in the post-acute stage after stroke. Neuropsychiatry, Neuropsychology, and BehavioralNeurology, 12, 234–246.

Berg, A., Palomaki, H., Lehtihalmes, M., Lonqvist, J., & Kaste, M. (2001). Post stroke depression in acutephase after stroke. Cerebrovascular Disease, 12, 14–20.

Berman, R. (2008). The psycholinguistics of developing text construction. Journal of Child Language, 35,735–771.

Beversdorf, D. Q.,Sharma, U. K., Phillips, N. N.,Notestine, M. A.,Slivka, A. P.Friedman, N. M., et al.(2007). Effect of propranolol on naming in chronic Broca’s aphasia with anomia. Neurocase, 13, 256–259.

Blackwell, A., & Bates, E. (1995). Inducing agrammatic profiles in normals: Evidence for the selectivevulnerability of morphology under cognitive resource limitation. Journal of Cognitive Neuroscience, 7,228–257.

Bogousslavsky, J. (2003). William Feinberg lecture 2002: Emotions, mood and behavior after stroke. Stroke,34, 1046–1050.

Burvill, P. W., Johnson, G. A., Jamrozik, K. D., Anderson, C. S., Stewart-Wynne, E. G., Byng, S., et al.(1995). What makes a therapy? Some parameters of therapeutic intervention in aphasia. EuropeanJournal of Disorders of Communication, 30(3), 303–316.

Caramazza, A. (1997). How many levels of processing are there in lexical access? Cognitive Neuropsychology,14(1), 177–208.

Carota, A., Rossetti, A. O., Karapanayiotides, T., & Bogousslavsky, J. (2001). Catastrophic reaction in acutestroke: A reflex behavior in aphasic patients. Neurology, 57, 1902–1905.

Caruso, A. J., Chodzko-Zajko, W. J., Bidinger, D. A., Sommers, R. K. (1994). Adults who stutter: Responsesto cognitive stress. Journal of Speech and Hearing Research, 37, 746–754.

Castillo, C. S., Starkstein, S., Fedoroff, P. J., Thomas, T. R., & Robinson, R. G. (1993). Generalized anxietydisorder after stroke. The Journal of Nervous Mental Disease, 181, 2.

Chakera, T. M. (1995). Prevalence of depression after stroke: The Perth Community Stroke Study. BritishJournal of Psychiatry, 166, 320–327.

Chemerinski, E., & Levine, S. R. (2006). Neuropsychiatric disorders following vascular brain injury.Vascular Brain Injury, 73(7), 1006–1014.

Chemerinski, E., Robinson, R. G., & Kosier, J. T. (2001). Improved recovery in activities of daily livingassociated with remission of poststroke depression. Stroke, 32, 113–117.

Cherney, L. R., Shadden, B. B., & Coelho, C. A. (Eds.). (1998). Analyzing discourse in communicativelyimpaired adults. Gaithersburg, MD: Aspen Publishers.

Christenfeld, N., & Creager, B. (1996). Anxiety, alcohol, aphasia, and ums. Journal of Personality and SocialPsychology, 70(3), 451–460.

Christensen, H., Boysen, G., & Johannsen, H. H. (2004). Serum-cortisol reflects severity and mortality inacute stroke. Journal of Neurological Sciences, 217, 175–180.

Chrousos, G. P. (2009). Stress and disorders of the stress system. Nature Reviews Endocrinology, 5(7), 374–381.

Clarke, D. M., & Currie, K. C. (2009). Depression, anxiety and their relationship with chronic diseases:A review of the epidemiology, risk, and treatment evidence. The Medical Journal of Australia, 190(7),S54–S60.

Code, C. (2003). The quantity of life for people with chronic aphasia. Neuropsychological Rehabilitation,13, 365–378.

Code, C. (2010). Aphasia. In J. Damico, N. Muller, & M. J. Ball (Eds.), The handbook of language and speechdisorders (pp. 317–336). Oxford, UK: Wiley-Blackwell.

Code, C., Hemsley, G., & Herrmann, M. (1999). The emotional impact of aphasia. Seminars in Speech andLanguage, 20, 19–31.

Code, C., & Herrmann, M. (2003). The relevance of emotional and psychosocial factors in aphasia torehabilitation. Neuropsychological Rehabilitation, 13(1/2), 109–132.

Code, C., & Muller, D. J. (1992). The Code-Muller protocols: Assessing perceptions of psychosocialadjustment to aphasia and related disorders. London, UK: Whurr.

Dow

nloa

ded

by [

Mon

ash

Uni

vers

ity L

ibra

ry]

at 1

3:52

05

Oct

ober

201

4


Coelho, C. A. (2007). Management of discourse deficits following traumatic brain injury: Progress, caveats,and needs. Seminars in Speech and Language, 28(2), 122–135.

Cohen, M. R. (1998). Expression of anxiety and depression in a case of subcortical motor aphasia.Neurorehabilitation, 11(3), 255–260.

Coplan, J. D., & Gorman, J. M. (1990). Treatment of anxiety disorder in patients with mood disorders.Journal of Clinical Psychiatry, 51(suppl), 9–13; discussion 14–17.

Coryell, W., Zimmermann, M., & Pfohl, B. (1985). Short term prognosis in primary and secondary majordepression. Journal of Affective Disorders, 9, 265–270.

Cox, M. (1986). The psychologically maladjusted stutterer. In K. St. Louis (Ed.), The atypical stutterer:Principles and practices of rehabilitation (pp. 93–122). Orlando, FL: Academic Press.

Cyr, R. (2010). Resilience in aphasia: Perspectives of stroke survivors and their families. DoctoralDissertation, University of Alberta. URL: http://hdl.handle.net/10048/917

Dalemans, R. J., De Witte, L. P., Beurskens, A. J., Van Den Heuvel, W. J., & Wade, D. T. (2010). Aninvestigation into the social participation of stroke survivors with aphasia. Disability & Rehabilitation,32(20), 1678–1685. doi: 10.3109/09638281003649938.

Darley, F. L. (1972). The efficacy of language rehabilitation in aphasia. Journal of Speech and HearingDisorders, 37, 3–21.

Darley, F. L. (1975). Treatment of acquired aphasia. In W. J. Friedlander (Ed.), Advances in neurology,Vol. 7. New York, NY: Raven Press.

De Wit, L. Putman, K., Baert, I., Lincoln, N. B., Angst, F., Bevens, H., et al. (2008). Anxiety and depressionin the first six months after stroke: A longitudinal multicentre study. Disability & Rehabilitation, 30(24),1858–1866.

Dembowski, J. S. (2006). Speech-language pathologists respond to psychological aspects of aphasia withvarying degrees of clinical attention. [In S. Brumfitt, Psychological aspects of aphasia: Speech andlanguage therapists’ view on professional practice.] Disability and Rehabilitation, 28, 523–534.

Dick, F., Bates, E., & Ferstl, E. C. (2003). Spectral and temporal degradation of speech as a simulation ofmorphosyntactic deficits in English and German. Brain & Language, 85, 535–542.

Docherty, N., DeRosa, M., Andreasen, N. (1996). Communication disturbances in schizophrenia andmania. Archives of General Psychiatry, 53(4), 358–364.

Doruk, A., Turkbay, T., Yelboga, Z., Ciyiltepe, M., Iyisoy A., Sutcigil, L., et al. (2008). Autonomicnervous system imbalance in young adults with developmental stuttering. Bulletin of ClinicalPsychopharmacology, 18, 274–281.

Eldar, S., & Bar-Hiam, Y. (2010). Neural plasticity in response to attention training in anxiety. PsychologicalMedicine, 40, 667–677.

Elman, R.J. (2007). The importance of aphasia group treatment for rebuilding community and health.Topics in Language Disorders, 27(4), 300–308.

Elman, R. J., & Bernstein-Ellis, E. (1999). The efficacy of group communication treatment in adults withchronic aphasia. Journal of Speech Language and Hearing Research, 42, 411–419.

Ezrati-Vinacour, R., & Levin, I. (2004). The relationship between anxiety and stuttering: A multidimen-sional approach. Journal of Fluency Disorders, 29, 135–148.

Franceshini, R., Teneconi, G., Zoppoli, F., & Barreca, T. (2001). Endocrine abnormalities and outcome ofischemic stroke. Biomedical Pharmacotherapy, 55, 458–465.

Frankel, T. (2008). Conversation intelligence after stroke: A drug trial. Doctoral Dissertation,University of Witwatersrand, Johannesburg, South Africa. URL: witsetd.wits.ac.za:8080/dspace/.../1/

PhD%20introductory%20pages.pdfFries, E., Hesse, J., Hellhammer, J., & Hellhammer, D.H. (2005). A new view on hypocortisolism.

Psychoneuroendocrinology, 30, 1010–1016.Fure, B., Wyller, T. B., Engedal, K., & Thmmessen, B. (2006). Emotional symptoms in acute ischemic

stroke. International Journal of Geriatric Psychiatry, 21(4), 382–387.Gainotti, G. (1972). Emotional behavior and hemispheric side of the lesion. Cortex, 8, 41–55.Gainotti, G. (1997). Emotional, psychological, and psychosocial problems of aphasic patients: An intro-

duction. Aphasiology, 11, 635–650.Gainotti G., Azzoni, A., Marra, C. (1999). Frequency, phenomenology and anatomical-clinical correlates

of major post-stroke depression. British Journal of Psychiatry, 175, 163–167.Goldstein, K. (1942). After effects of brain injuries in war: Their evaluation and treatment. New York, NY:

Grune & Stratton.Goldstein, K. (1948). Language and language disturbances: Aphasic symptom complexes and their signifi-

cance for medicine and theory of language. New York, NY: Grune & Stratton.

Dow

nloa

ded

by [

Mon

ash

Uni

vers

ity L

ibra

ry]

at 1

3:52

05

Oct

ober

201

4

http://hdl.handle.net/10048/917


Goldstein, K. (1959). Functional disturbances in brain damage. In S. Arieti (Ed.), American handbook ofpsychiatry (pp. 770–794). New York, NY: Basic Books.

Goral, M., & Kempler, D. (2008). Training verb production in communicative context: Evidence from aperson with chronic non-fluent aphasia. Aphasiology, 22(7–8), 707–717.

Greenop, K. R., Almeida, O. P., Hankey, G. J., van Bockxmeer, F., & Lautenschlager, N. T. (2009).Premorbid personality traits are associated with post-stroke behavioral and psychological symptoms: Athree-month follow-up study in Perth, Western Australia. International Psychogeriatrics, 21, 1063–1071.

Gusev. E. I., & Bogolepova, A. N. (2009). Depressive disorders in stroke patients. Neuroscience andBehavioral Physiology, 39(7), 639–643.

Hackett, M. L., Yapa, C., Parag, V., & Anderson, C. S. (2005). Frequency of depression after stroke: Asystematic review of observational studies. Stroke, 36, 1340.

Hasselmo, M. E., Linster, C., Patil, M., Ma, D., & Cekic, M. (1997). Noradrenergic suppression of synaptictransmission may influence cortical signal-to-noise ratio. Journal of Neurophysiology, 77, 3326–3339.

Heeschen, C., Ryalls, J., & Hagoort, P. (1988). Psychological stress in Broca’s versus Wernicke’s aphasia.Clinical Linguistics & Phonetics, 2, 309–316.

Heilman, K. M., Nadeau, S. E., & Beversdorf, D. Q. (2003). Creative innovation: Possible brain mecha-nisms. Neurocase, 9, 369–379.

Heilman, K., Schwartz, H., & Watson, R. (1978). Hypoarousal in patients with the neglect syndrome andemotional indifference. Neurology, 28, 229–232.

Heim, C., Ehlert, U., & Hellhammer, D. (2000). The potential role of hypocortisolism in the pathophysiol-ogy of stress-related bodily disorders. Psychoneuroendocrinology, 25, 1–35.

Hemsley, G., & Code, C. (1996). Interactions between recovery in aphasia, emotional and psychoso-cial factors in subjects with aphasia, their significant others and speech pathologists. Disability andRehabilitation, 18(11), 567–584.

Herrmann, M. (1997). Studying psychosocial problems in aphasia: Some conceptual and methodologicalconsiderations. Aphasiology, 11, 717–725.

Herrmann, M., Bartels, C., Schumacher, M., & Wallesch, C. W. (1995). Poststroke depression: Is there apatho-anatomical correlate for depression following the post-acute stage of stroke? Stroke, 26, 850–856.

Herrmann, M., Bartels, C., & Wallesch, C. W. (1993). Depression in acute and chronic aphasia: Symptoms,pathoanatomico-clinical correlations, and clinical implications. Journal of Neurology, Neurosurgery, andPsychiatry, 56, 672–678.

Herrmann, N., Black, S. F., Lawrence, J., Szekely, C., & Szalai, J. P. (1998). The Sunnybrook stroke study:A prospective study of depressive symptoms and functional outcomes. Stroke, 29, 618–624.

Hermann, M., & Wallesch, C. W. (1993). Depressive changes in stroke patients. Disability andRehabilitation, 15, 55–66.

Hilari, K., Northcott, S., Roy, P., & Marshall, J. (2010). Psychological distress after stroke and aphasia: Thefirst six months. Clinical Rehabilitation, 24, 181–190.

Horton, S., & Byng, S. (2000). Examining interaction in language therapy. International Journal of Language& Communication Disorders, 35(3), 355–375.

House, A., Dennis, M., Warlow, C., Hawton, K., & Molyneaux, A. (1990). Mood disorders after strokeand their relation to lesion location: A CT scan study. Brain, 113, 1113–1129.

Hula, W., McNeil, M. R., & Sung, J. E. (2007). Is there an impairment of language-specific processing inaphasia? Brain and Language, 103, 240–241.

Hula, W. D., & McNeil, M. R. (2008). Models of attention and dual-task performance as explanatoryconstructs in aphasia. Seminars in Speech and Language, 29(3), 169–187; quiz C 3–4.

Ince, L. (1968). Desensitization with an aphasic patient. Behavioral Research and Therapy, 6, 235–237.Jianfei, C., Meifang, Y., & Jia, W. (1988). Hemorrheological study on the effect of acupuncture in treating

cerebral infarction. Journal of Traditional Chinese Medicine, 8(3), 167–172.Kaplan, E., Goodglass, H., & Weintraub, S. (1983). Boston Naming Test. Baltimore, MD: Lippincott

Williams & Wilkins.Katz, W., Bhardawaj, S., & Carstens, B. (1999). Electromagnetic articulatography treatment for an adult

with Broca’s aphasia and apraxia of speech. Journal of Speech, Language, and Hearing Research, 42(6),1355–1366.

Kauhanen, M. L., Korpelainen, J. T., Hiltunen, P., Brusin, E., Mononen, H., Maatta, R., et al. (1999).Poststroke depression correlates with cognitive impairment and neurological deficits. Stroke, 30,1875–1880.

Kilborn K. (1991). Selective impairment of grammatical morphology due to induced stress in normallisteners: Implications for aphasia. Brain & Language, 41, 275–288.

Dow

nloa

ded

by [

Mon

ash

Uni

vers

ity L

ibra

ry]

at 1

3:52

05

Oct

ober

201

4


Kotila, M., Numminen, H., Waltimo, O., & Kaste, M. (1998). Depression after stroke: Results from theFinnstroke Study. Stroke, 29, 368–372.

Kovarsky, D., Curran, M., & Zobel Nichols, N. (2009). Laughter and communicative engagement ininteraction. Seminars in Speech and Language, 30(1), 27–36.

Kreibig, S. D. (2010). Autonomic nervous system activity in emotion: A review. Biological Psychology, 84,394–421. doi:10.1016/j.biopsycho.2010.03.010.

Laures-Gore, J., DuBay, M., Duff, M., & Buchanan, T. (2010). Identifying behavioral measures of stress inindividuals with aphasia. Journal of Speech, Language, and Hearing Research, 53(5), 1394–1400.

Laures-Gores, J., Hamilton, A., & Matheny, K. (2007a). Coping resources, perceived stress, and recent lifeexperiences in individuals with aphasia. Journal of Medical Speech-Language Pathology, 15(4), 423–431.

Laures-Gore, J., Heim, C., & Hsu, Y. (2007). Assessing cortisol reactivity to a linguistic task as a marker ofstress in individuals with left-hemisphere stroke and aphasia. Journal of Speech Language, and hearingResearch, 50, 493–507.

Laures, J., & Shisler, R. (2004). Complementary and alternative medical approaches to treating adultneurogenic communication disorders: A review. Disability and Rehabilitation, 26(6), 315–325.

Laures, J. S. (2005). Reaction time and accuracy in individuals with aphasia during auditory vigilance tasks.Brain and Language, 95(2), 353–357.

Laures, J. S., Odell, K. H., & Coe, C., (2003). Arousal and auditory vigilance in individuals with aphasiaduring a linguistic and a non-linguistic vigilance task. Aphasiology, 17, 1133–1152.

Lauterbach, E. C., Jackson, J. G., Wilson, A. N., Dever, G. E., & Kirsh, A. D. (1997). Major depressionafter left posterior globus pallidus lesions. Neuropsychiatry, Neuropsychology, and Behavioral Neurology,10, 9–16.

Leppavuori, A., Pohjasvaara, T., Vataja, R., Kaste, M., & Erkinjuntti, T. (2003). Generalized anxietydisorders three to four months after ischemic stroke. Cerebrovascular Diseases, 16(3), 257–264.

Levelt, W. J. (1992). Accessing words in speech production: Stages, processes, and representations. Cognition,42, 1–22.

Levelt, W. J. M. (2001). Spoken word production: A theory of lexical access. Proceedings of the NationalAcademy of Sciences, 98(23), 13464–13471.

Liebowitz, M. R., Hollander, E., Schneider F., Campeas, R., Fallon, B., Welkowitz, L., et al. (1990). Anxietyand depression: Discrete diagnostic entities? Journal of Clinical Pharmacology, 10(suppl 3), 61S–66S.

Linden, T., Bloomstand, C., & Skoog, I. (2007). Depressive disorders after 20 months in elderly strokepatients: A case control study. Stroke, 38(6), 1860–1863.

Lipsey, J. R., Robinson, R. G., Pearlson, G. D., Rao, K., & Price, T. R. (1985). The dexamethasonesuppression test and mood following stroke. American Journal of Psychiatry, 142, 318–323.

Luchsinger, R., & Arnold, G. E. (1965). Voice, speech, and language. Clinical communicology: Its physiologyand pathology. Belmont, CA: Wadsworth.

Lundgren, K. (2004). Nature-based therapy: Its potential as a complementary approach to treatingcommunication disorders. Seminars in Speech and Language, 25(2), 121–131.

Lundgren, K. (2006). Complementary and alternative treatment of aphasia. Presented at the CanadianAssociation of Speech-Language Pathologists and Audiologists. Winnipeg, Manitoba, May.

Lundgren, K., Helm-Estabrooks, N., & Klein, R. (2010). Stuttering following acquired brain damage:A review of the literature. Journal of Neurolinguistics, 23(5), 447–454. doi:10.1016/j.jneuroling.2009.08.008, 1–8.

Luria, A. (1963). Restoration of function after brain injury. New York, NY: MacMillan.Luria, A. (1970). Traumatic aphasia: Its syndromes, psychology, and treatment. The Hague, The Netherlands:

Mouton.Magnaniello, A. (1986). Hypnotherapy in the rehabilitation of a stroke victim: A case study. American

Journal of Clinical Hypnosis, 29, 64–68.Marklund, N., Peltonen, M., Nilsson, T. K., & Olsson, T. (2004). Low and high circulating cortisol levels

predict mortality and cognitive dysfunction early after stroke. Journal of Internal Medicine, 256, 15–21.Marshall, R., & Watts, M. (1976). Relaxation training: Effects of communicative ability of aphasic adults.

Archives of Physical Medicine and Rehabilitation, 57, 464–467.Marshall, R. J. S., & Laures-Gore, J. (2008). A single subject study of unilateral nostril breathing in aphasia.

Poster presented at the Annual Meeting of the International Neuropsychological Society, Hawaii.Masdeu, J. C., Schoene, W. C., & Funkenstein, H. (1978). Aphasia following infarction of the left

supplementary motor area. Neurology, 28, 1220.

Dow

nloa

ded

by [

Mon

ash

Uni

vers

ity L

ibra

ry]

at 1

3:52

05

Oct

ober

201

4


Masskulpan, P., Riewthong, K., Diapratham, P., & Kiptniratsaikul, V. (2008). Anxiety and depressivesymptoms after stroke in nine rehabilitation centers. Journal of Medical Association Thailand, 91(10),1595–1602.

McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation: Central role of the brain.Physiological Reviews, 87, 873–904.

McEwen, B. S., & Gianaros, P. J. (2010). Central role of the brain in stress and adaptation: Links tosocioeconomic status, health, and disease. Annals of the New York Academy of Sciences, 1186, 190–222.

McEwen, B. S., & Stellar, E. (1993). Stress and the individual: Mechanisms leading to disease. Archives ofInternal Medicine, 153, 2093–2101.

McNeil, M., Prescott, T., & Lemme, M. (1976). An application of electromygraphic biofeedback toaphasia/apraxia treatment. Clinical Aphasiology Conference Proceedings, 151–171.

McNeil, M. R., Matthews, C. T., Hula, W. D., Doyle, P. J., & Fossett, R. D. (2006). Effects of visual-manualtracking under dual-task conditions on auditory language comprehension and story retelling in personswith aphasia. Aphasiology, 20, 167–174.

McNeil, M. R., Odell, K., & Tseng, C. H. (1991). Toward the integration of resource allocation into ageneral theory of aphasia. In T. E. Prescott (Ed.), Clinical aphasiology (pp. 21–39). Austin, TX: Pro-Ed.

McNeil M. R., & Pratt S. R. (2001). A standard definition of aphasia: Toward a general theory of aphasia.Aphasiology, 15, 901–911.

Menn, L., Ramsberger, G., & Helm-Estabrooks, N. (1994). A linguistic communication measure for aphasicnarratives. Aphasiology, 8(4), 343–359.

Miyake A., Carpenter P. A., & Just M. A. (1994). A capacity approach to syntactic comprehensiondisorders: Making normal adults perform like aphasic patients. Cognitive Neuropsychology, 11, 671–717.

Morris, P. L. P., Robinson, R. G., Andrzejewski, P., Samuels, J., & Price, T. R. (1993). Association ofdepression with 10 year poststroke mortality. American Journal of Psychiatry, 150, 124–129.

Mukheriee, D., Levin, R. L., & Heller, W. (2006). The cognitive, emotional, and social sequelae of stroke:Psychological and ethical concerns in post-stroke adaptation. Topics in Stroke Rehabilitation, 13(4),26–35.

Murray, L. (2004). Cognitive treatments for aphasia: Should we and can we help attention and workingmemory problems? Journal of Medical Speech Language Pathology, 12(3), xxxv–xl.

Murray, L., & Ray, H., (2001). A comparison of relaxation training and syntax stimulation for chronicnonfluent aphasia. Journal of Communication Disorders, 34, 87–113.

Murray, L. L. (2002). Attention deficits in aphasia: Presence, nature, assessment, and treatment. Seminarsin Speech and Language, 23(2), 107–116.

Murray, L. L. (2008). The application of relaxation training approaches to patients with neurogenic dis-orders and their caregivers. Perspectives on Neurophysiology and Neurogenic Speech and LanguageDisorders, 18, 90–98.

Murray, L. L., Holland, A. L., & Beeson, P. M. (1997a). Grammaticality judgments of mildly aphasicindividuals under dual-task conditions. Aphasiology, 11(10), 993–1016.

Murray, L. L., Holland, A. L., & Beeson, P. M. (1997b). Auditory processing in individuals with mildaphasia: A study of resource allocation. Journal of Speech, Language, and Hearing Research, 40(4), 792–808.

Murray L. L., Holland A. L., & Beeson P. M. (1998). Spoken language of individuals with mild fluent apha-sia under focused and divided-attention conditions. Journal of Speech, Language, and Hearing Research,41, 213–227.

Murray, L. L., Keeton, J., & Karcher, L. (2006). Treating attention in mild aphasia: Evaluation of attentionprocess training-II. Journal of Communication Disorders, 39, 37–61.

Murray, L. L., & Kim, H. Y. (2004). A review of select alternative treatment approaches for acquiredneurogenic disorders: Relaxation therapy and acupuncture. Seminars in Speech and Language, 25(2),133–149.

Myers, L. B. (2010). The importance of the repressive coping style: Findings from 30 years of research.Anxiety, Stress & Coping, 23(1), 3–17.

Neau, J. P., Ingrand, P., Mouille-Brachet, C., Rosier, M. P., Couderq, C. Alvarez, A., et al. (1998).Functional recovery and social outcome after cerebral infarction in young adults. CerebrovascularDisease, 8, 296–302.

Newborn, B. (1998). Self-portrait of an aphasic (from a personal and professional viewpoint). In W. Sife(Ed.), After stroke: Enhancing quality of life [co-published simultaneously as Loss, grief, and care, Vol.8(1/2).] Binghamton, NY: Harworth Press.

Dow

nloa

ded

by [

Mon

ash

Uni

vers

ity L

ibra

ry]

at 1

3:52

05

Oct

ober

201

4


Ozdemir, B., Doruk, A., Celik, C., Amasyali, B., Ciyiltepe, M., & Ozcan, C. (2010). Evaluation of auto-nomic nervous system function with tilt table testing in young adults with persistent developmentalstuttering. Bulletin of Clinical Psychopharmacology, 20(1), 45–49.

Pachalska, M., Knapik, H., Smolak, M., & Pytel, T. (1987). The dynamics of anxiety in the process ofnon-verbal psychotherapy for patients with aphasia. Aphasiology, 1(3), 283–285.

Palasik, S., Irani, F., & Goberman, A. M. (2009). Trait and state anxiety in people who stutter and peoplewho do not stutter. Perspectives on Fluency and Fluency Disorders, 19, 99–105.

Paolucci, S. (2008). Epidemiology and treatment of post-stroke depression. Neuropsychiatric Disease andTreatment, 4(1), 145–154.

Parikh, R. M., Lipsey, J. R., Robinson, R. G., & Price, T. R. (1987). A two-year longitudinal study of post-stroke mood disorders: Dynamic changes in correlates of depression at one and two years. Stroke, 18,579–584.

Penard, N., Counihan, S. U. E., D’arcy, S., Rapcan, V., Reilly, R. B., & Robertson, I. H. (2009). Investigatingspeech as a source of biomarkers for changes in cognition, executive function, and mood. Poster presentedat the Academy of Aphasia, Boston, October.

Peters, H. F., & Hulstijn, W. (1984). Stuttering and anxiety: The difference between stutterers and nonstut-terers in verbal apprehension and physiologic arousal during the anticipation of speech and nonspeechtasks. Journal of Fluency Disorders, 9, 67–84.

Pohjasvaara, T., Erkinjuntti, T., Vataja, R., & Kaste, M. (1998). Correlates of dependent living 3 monthsafter ischemic stroke. Cerebrovascular Disease, 8, 259–266.

Pohjasvaara, T., Vataja, R., Leppavuori, A., Kaste, M., & Erkinjuntti, T. (2001). Depression is an inde-pendent predictor of poor long-term functional outcome post-stroke. European Journal of Neurology, 8,315–319.

Primeau, F. (1988). Post-stroke depression: A critical review of the literature. Canadian Journal ofPsychiatry, 33, 757–765.

Robinson, R. G. (2003). Poststroke depression: Prevalence, diagnosis, treatment, and disease progression.Biological Psychiatry, 54, 376–587.

Robinson, R. G. (2006). The clinical neuropsychiatry of stroke (2nd ed). New York, NY: CambridgeUniversity Press.

Ross, A., Winslow, I., Merchant, P., & Brumfitt, S. (2006). Evaluation of communication, life participa-tion, and psychological well-being in chronic aphasia: The influence of group intervention. Aphasiology,20(5), 427–448.

Ryalls, J. (1984). Some acoustic aspects of CVC utterances in aphasia. Phonetica, 41, 103–111.Sagen, U., Arnstein, F., Moum, T., Morland, T., Gunnar Vik, T., Nagy, T., & Dammen, T. (2010). Early

detection of patients at risk for anxiety, depression, and apathy after stroke. General Hospital Psychiatry,32, 80–58.

Sagen, U., Vik, T. G., Moum, T., Morland, T., Finset, A., & Dammen, T. (2009). Screening for anxiety anddepression after stroke: Comparison of the hospital anxiety and depression scale and the Montgomeryand Asberg depression rating scale. Journal of Psychosomatic Research, 67(4), 325–332.

Sakamoto, H., Sakamaki, T., Tani, T., Sugai, Y., & Kurabayashi, M. (2002). White-coat effect inducedby therapist’s presence during speech therapy. American Journal of Physical Medicine & Rehabilitation,81(12), 929–935.

Santos, C. O., Caeiro, L., Ferro, J. M., Albuquerque, R., & Figueira, M. L. (2006). Anger, hostility, andaggression in the first days of acute stroke. European Journal of Neurology, 13(4), 351–358.

Sapir, S., & Aronson, A. (1990). The relationship between psychopathology and speech and languagedisorders in neurogenic patients. Journal of Speech and Hearing Disorders, 55, 503–509.

Seeman, T., Epel, E., Gruenewald, T., Karlamangla, A., & McEwen, B. S. (2010). Socio-economic differ-entials in peripheral biology: Cumulative allostatic load. Annals of the New York Academy of Sciences,1186, 223–239.

Seniow, J., Litwin, M., Litwin, T., Lesniak, M., & Czlonkowska, A. (2009). New approaches to the rehabil-itation of post-stroke focal cognitive syndrome: Effect of levodopa combined with speech and languagetherapy on functional recovery from aphasia. Journal of the Neurological Sciences, 283, 214–218.

Sharpe, M., Hawton, K., Seagroatt, V., Bamford, J., House, A., Molyneux, A., et al. (1994). Depressivedisorders in long-term survivors of stroke: Associations with demographic and social factors, functionalstatus, and brain lesion volume. The British Journal of Psychiatry, 164, 380–386.

Sherratt, S. (2007). Multilevel discourse analysis: A feasible approach. Aphasiology, 21(3/4), 375–393.Shill, M. (1979). Motivational factors in aphasia therapy: Research suggestions. Journal of Communication

Disorders, 12, 503–517.

Dow

nloa

ded

by [

Mon

ash

Uni

vers

ity L

ibra

ry]

at 1

3:52

05

Oct

ober

201

4


Shimoda, K., & Robinson, R. G. (1998). Effect of Anxiety disorder on impairment and recovery fromstroke. The Journal of Neuropsychiatry and Clinical Neurosciences, 10, 34–40.

Shores, M. M., Glubin, T., Cowley, D. S., Dager, S. R., Roy-Byrne, P. P., & Dunner, D. L. (1992). Therelationship between anxiety and depression: A clinical comparison of generalized anxiety, dysthymicdisorder, panic disorder, and major depressive disorder. Comprehensive Psychiatry, 33, 237–234.

Silkes, J. P., McNeil, M. R., & Drton, M. (2004). Simulation of aphasic naming performance in non-brain-damaged adults. Journal of Speech, Language, and Hearing Research, 47, 610–623.

Simmons-Mackie, N., & Damico, J.S. (2009). Engagement in group therapy for aphasia. Seminars in Speechand Language, 30, 18–26.

Simmons-Mackie, N., Elman, R. J., Holland, A., & Damico, J. S. (2007). Management of discourse in grouptherapy for aphasia. Topics in Language Disorders, 27, 5–23.

Singh, A., Black, S. E., Hermann, N., Leibovitch, F. S., Ebert, P. L., Lawrence, J., et al. (2000). Functionaland neuroanatomical correlations in post stroke depression: The Sunnybrook Stroke Study. Stroke, 31,637–644.

Sinyor, D., Amato, P., Kaloupek, D. G., Becker, R., Goldenberg, M., & Coopersmith H. (1986). Post-strokedepression: Relationships to functional impairment, coping strategies, and rehabilitation outcome.Stroke, 17, 1102–1107.

Sivan, M., Neumann, V., Kent, R., Stroud, A., & Bhakta, B. B. (2010). Pharmacotherapy for treat-ment of attention deficits after non-progressive acquired brain injury: A systematic review. ClinicalRehabilitation, 24(2), 110–121.

Skelly, M. (1975). Aphasia patients talk back. American Journal of Nursing, 75, 1140–1142.Small, S., & Llano, D. (2009). Biological approaches to aphasia treatment. Current Neurology and

Neuroscience Reports, 9, 443–450.Starkstein, S. E., Cohen, B. S., Fedoroff, P., Parikh, P. M., Price, T. R., & Robinson, R. G. (1990).

Relationship between anxiety disorders and depressive disorders in patients with cerebrovascular injury.Archives of General Psychiatry, 47(3), 246–251.

Starkstein, S. E., Fedoroff, J. P., Price, T. R., Leiguarda, R., & Robinson, R. G. (1993). Catastrophic reactionafter cerebrovascular lesions: Frequency, correlates, and validation of a scale. Journal of Neuropsychiatry& Clinical Neurosciences, 5, 189–194.

Starkstein, S. E., & Robinson, R. G. (1988) Aphasia and depression. Aphasiology, 2, 1–20.Staub, F., Carota, A., Karapanayiotides, T., Berney, A., & Bogousslavsky, J. (2001). Observed behavioral

changes and postsroke depression. Cerebrovascular Disease, 11(4), 9.Steele, C. M. (1997). A threat in the air: How stereotypes shape the intellectual identities and performance

of women and African-Americans. American Psychologist, 52, 613–629.Steele, C. M., & Aronson, J. (1995). Stereotype threat and the intellectual test performance of African-

Americans. Journal of Personality and Social Psychology, 69, 797–811.Stern, R. A. (1999). Assessment of mood states in aphasia. Seminars in Speech & Language, 20, 33–51.Tanaka,Y., Albert, M. L., Fujita, K., Nonaka, C., Miyazaki, M., & Yokoyama, E. (2009). Autonomic ner-

vous system and aphasia. Presented at the Neurobiology of Language Conference, Chicago, October2009.

Tanaka Y., Albert M. L., Hujita F., Nonaka C., & Oka T. (2006). Beta-blocker improves language output inaphasia. Presented at American Neurological Association 131st Annual Meeting, 9 October, Chicago.

Tanner, D. (2003). Eclectic perspectives on the psychology of aphasia. Journal of Allied Health, 32(4), 256–260.

Thomas, S. A., & Lincoln, N. B. (2008). Predictors of emotional distress after stroke. Stroke, 39, 1240–1245.Thompson, C., Hall, H., & Sison, C. (1986). Effects of hypnosis on imagery training on naming behavior in

aphasia. Brain & Language, 28, 141–153.Townend, B. S., Whyte, S., Desborough, T., Crimmins D., Markus, R., Levi, C., et al. (2007). Longitudinal

prevalence and determinants of early mood disorder post-stroke. Journal of Clinical Neuroscience, 14,429–434.

Townend, E., Brady, M., & McLaughlan, K. (2007a). A systematic evaluation of the adaptation ofdepression diagnostic methods for stroke survivors who have aphasia. Stroke, 38, 3076–3083.

Tseng, C. H., McNeil, M. R., & Milenkovic, P. (1993). An investigation of attention allocation deficits inaphasia. Brain & Language, 45(2), 276–296.

Ulatowska, H. K., & Olness, G. S. (2007). Pragmatics in discourse performance: Insights from aphasiology.Seminars in Speech and Language, 28, 148–157.

Ursin, H., & Eriksen, H. R. (2004). Review: The cognitive activation theory of stress.Psychoneuroendocrinology, 29, 567–592.

Dow

nloa

ded

by [

Mon

ash

Uni

vers

ity L

ibra

ry]

at 1

3:52

05

Oct

ober

201

4


Weber, C. M., & Smith, A. (1990). Autonomic correlates of stuttering and speech assessed in a range ofexperimental tasks. Journal of Speech and Hearing Research, 33, 690–706.

Wepman, J. M. (1951). Recovery from aphasia. New York, NY: Ronald.Wepman, J. M. (1953). A conceptual model for the processes involved in recovery from aphasia. Journal of

Speech and Hearing Disorders, 18, 4–13.Yerkes R. M., & Dodson J. D. (1908). The relation of strength of stimulus to rapidity of habit-formation.

Journal of Comparative Neurology and Psychology, 18, 459–482.Yesavage, J., & Jacob, R. (1984). Effects of relaxation and mnemonics on memory, attention, and anxiety in

the elderly. Experimental Ageing Research, 10(4), 211–214.Zhanjun, Z. (1989). Efficacy of acupuncture in the treatment of post stroke aphasia. Journal of Traditional

Chinese Medicine, 9(2), 87–89.

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Language as a stressor in aphasia