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Aphasia: Prognosis and treatment

Aphasia: Prognosis and treatment
Literature review current through: Jan 2024.
This topic last updated: Oct 06, 2021.

INTRODUCTION — Aphasia is a loss of ability to produce or understand language. The most common cause of aphasia is cerebrovascular disease, particularly cerebral infarction. Aphasia complicates 15 to 38 percent of ischemic strokes [1-4]. Other structural pathologies (infection, trauma, neoplasm) and certain neurodegenerative diseases (primary progressive aphasia) can also cause aphasia.

Aphasia can be a devastating condition and is one of the most feared consequences of cerebral infarction and other brain injuries [5]. Although quality of life in patients with aphasia is difficult to measure directly, the disruption in communication with its likely effects on employment status and social networks suggests that its impact can be profound [6-8]. Caregivers of stroke survivors are likely to experience more stress when caring for a family member with, rather than without, aphasia [9,10]. Comprehension deficits can also limit rehabilitation efforts targeting other poststroke deficits such as hemiparesis [11,12]. Patients with poststroke aphasia have greater morbidity and mortality than stroke patients without aphasia [13]. While most, if not all, patients with poststroke aphasia have some functional recovery, residual deficits are common. Unfortunately, there is limited evidence that therapeutic interventions are effective.

This topic reviews the prognosis and management of aphasia, focusing on poststroke aphasia, which is the most common etiology. The evaluation of aphasia, the management of primary progressive aphasia, and other aspects of stroke prognosis and management are discussed separately. (See "Approach to the patient with aphasia" and "Initial assessment and management of acute stroke" and "Frontotemporal dementia: Clinical features and diagnosis".)

PROGNOSIS — Recovery from aphasia is influenced by lesion location and type of aphasia. As an example, large lesions in the left hemisphere with global aphasia have a much poorer recovery than small, subcortical lesions with anomia.

The prognosis for aphasia recovery depends in large part upon the underlying etiology. This has been best studied in cerebrovascular disease. Most patients with poststroke aphasia improve to some extent [1-4,14,15]. Most improvement occurs within the first few months and plateaus after one year. The severity of the initial aphasia strongly correlates with the long-term deficit; those with milder degrees of aphasia at onset are the most likely to recover completely [16-18]. In one study of poststroke aphasia, baseline phonology was the linguistic component that was most predictive of recovery at one year; other factors associated with good one-year outcomes were younger age, higher Barthel Index, higher educational level, and hemorrhagic (as opposed to ischemic) stroke [19]. Patients with significant aphasia may benefit from intensive treatment regimens even after the period of spontaneous recovery [20,21]. Smaller studies in patients with aphasia resulting from traumatic brain injury indicate that the clinical course is similar to poststroke aphasia [11].

Diffusion and perfusion magnetic resonance imaging (MRI) studies demonstrate that early recovery after stroke (in the first few days and weeks) is related to reperfusion of language areas [2,22]. Functional neuroimaging studies suggest that subsequent improvement is associated with increased activation of contiguous areas in the perisylvian language areas as well as homologous brain regions in the right hemisphere [22-32].

Patients with aphasia resulting from right-hemisphere lesions often have less severe permanent language deficits, likely as a consequence of incomplete language lateralization in these individuals (see "Approach to the patient with aphasia", section on 'Cerebral dominance'). While there is some evidence to suggest that left-handed individuals with left-hemisphere stroke and women have less complete lateralization of language dominance than right-handed individuals and men, neither handedness nor sex have consistently been shown to impact recovery from poststroke aphasia [4,15,16,33]. Similarly, increased age has not been consistently shown to influence prognosis [31].

MANAGEMENT — The underlying cause of the aphasia should be treated specifically, whether it is degenerative, vascular, inflammatory, neoplastic, or epileptic (see appropriate topic reviews).

Aphasia resulting from an intraparenchymal mass or hematoma, or from an extra-axial mass or fluid collection, may improve dramatically with removal of the offending mass. In the case of central nervous system (CNS) tumors, treatment of edema with steroids may result in rapid improvement, but worsening of the neoplastic disease is likely to be accompanied by recurrence of aphasia.

Episodes of aphasia resulting from epileptic seizures should resolve with adequate anticonvulsant therapy. The treatment of acquired epileptic aphasia (Landau-Kleffner syndrome) is problematic, and children with this disease may be left with permanent linguistic dysfunction, particularly auditory comprehension defects [34]. (See "Epilepsy syndromes in children", section on 'Developmental and epileptic encephalopathy with spike-wave activation in sleep (DEE-SWAS)'.)

Speech and language therapy — Aphasia may resolve spontaneously, especially when it is caused by a small ischemic lesion, but in most cases, a speech-language pathologist is consulted to assist the patient in recovering linguistic abilities and to train the patient and family members in alternative strategies for communication. The available data from clinical trials offer weak support for this approach, but no single technique has emerged as more effective than others [30,35,36]. Challenges in studying the use of speech and language therapy include the heterogeneity of aphasia syndromes, the wide variety and lack of standardized techniques employed in speech and language therapy, as well as the fact that many patients improve spontaneously [37]. The actual speech-language rehabilitation technique may not matter as much as the actual number of sessions and intensity of therapy.

One review of 10 studies of 864 patients with poststroke aphasia found that intense (in excess of two hours per week) speech and language therapy over a short period of time was more effective than less intense therapy provided over a longer period of time [37,38]. However, a subsequent randomized study in 116 patients found that in the subacute setting, patients who received two hours of therapy per week had similar recoveries compared with those who received five hours of therapy a week [39].

Study results have also differed as to whether similar or disparate benefits are expected from professional therapists versus community-based programs or trained family members [39,40]. While some have found that language therapy works best when administered early after stroke, others have found that, after adjusting for the effects of early spontaneous recovery, similar gains can be attained when speech therapy is administered in more chronic stages [37,41,42].

Newer language therapy techniques that are being studied include the use of computer-assisted techniques, as well as so-called constraint-induced aphasia therapy (CIAT; high-intensity therapy that restricts the use of nonverbal communication) [43-46]. In one study of 27 patients with chronic poststroke aphasia, CIAT produced benefits both when used alone and when combined with memantine (see 'Pharmacologic approaches' below) [47]. Developments are also being made in the application of augmentative and alternative communication devices. The recent development of smartphones, tablet computers, and similar devices has led to the availability of downloadable applications for therapy and communication.

Pharmacologic approaches — The rationale behind pharmacologic treatment of aphasia involves replacing depleted neurotransmitters, enhancing neuroplasticity, and improving cerebral blood flow [22]. No pharmacologic intervention has been proven to result unequivocally in long-term benefit [48]. Examples of clinical trials of medications in patients with poststroke aphasia include the following:

Bromocriptine was studied in a randomized, double-blind trial in 38 patients with a poststroke nonfluent aphasia [14]. After 16 weeks of treatment, there was no difference in the recovery of language function between active and placebo-treated groups. This negative result was concurrent with the results of a previous randomized study [49].

Amphetamine in conjunction with speech/language therapy (10 sessions over five weeks) appeared to improve language more than therapy alone in a randomized, double-blind study in 21 poststroke aphasia patients [50]. The between-group differences appeared to be maintained at the six-week and six-month assessments but were no longer significant after six months. A 2003 systematic review of the use of amphetamines in poststroke rehabilitation concluded that the aggregated results of small studies supported future research of this treatment approach, but not their use in routine clinical practice [51].

Piracetam was studied in 24 stroke patients with aphasia [52]. After six weeks of treatment, the piracetam-treated group appeared to make greater gains in language function on certain subtest areas compared with the placebo-treated group. A meta-analysis of prior studies of piracetam in acute stroke concluded that there was weak evidence of piracetam's efficacy in the treatment of poststroke aphasia [48].

The acetylcholinesterase inhibitors donepezil and galantamine have shown promise in open-label studies in patients with poststroke aphasia [2,53,54]. There is some evidence that donepezil and other acetylcholinesterase inhibitors may be efficacious in vascular dementia and also in aphasia resulting from neurodegenerative dementia. (See "Treatment of vascular cognitive impairment and dementia" and "Cholinesterase inhibitors in the treatment of dementia".)

Memantine (10 mg twice daily) was studied along with CIAT in 27 patients with chronic poststroke aphasia in a randomized, controlled, parallel-group study [47]. Memantine treatment was associated with a sustained benefit at 48 weeks on measures of aphasia and communication. The benefit of drug treatment appeared to be augmented by CIAT.

Depression often develops in patients with chronic or progressive aphasias and may impair aphasia recovery [55-57]. Psychotherapy or pharmacologic management may improve the outcome in these patients. However, a six-month clinical trial of the monoamine oxidase inhibitor, moclobemide, in 90 unselected patients with poststroke aphasia did not find that treatment was associated with greater improvement of the aphasia compared with placebo treatment [58]. The use of prophylactic antidepressant medications is not supported in patients with poststroke aphasia or aphasia of other etiologies. It seems reasonable, however, to monitor such patients for the development of depression and institute treatment if depression does emerge. (See "Unipolar depression in adults: Assessment and diagnosis" and "Diagnosis and management of late-life unipolar depression" and "Unipolar major depression in adults: Choosing initial treatment".)

Transcranial magnetic or electrical stimulation — These modalities hold promise for treatment but are not currently used in clinical practice.

Transcranial magnetic stimulation – Applied to the contralateral, unaffected cerebral hemisphere, transcranial magnetic stimulation (TMS) is believed to suppress its activity, and as a result, the tonic inhibition of the affected hemisphere [22]. While uncontrolled reports in a small number of patients with poststroke aphasia and a limited number of small controlled trials report evidence of efficacy, further study of this modality is required [59-62]. A small, placebo-controlled study of TMS in 10 patients with Alzheimer disease suggested a benefit from treatment in auditory sentence comprehension but not other test measures [63]. Another randomized study of 24 patients with subacute poststroke aphasia found that 10 sessions of repetitive TMS followed by 45 minutes of speech and language therapy was associated with improved language recovery compared with sham-treated patients [64]. Persistent benefit at three months as measured by the Concise Chinese Aphasia test score was found in a subsequent randomized study in 45 poststroke aphasia patients [65].

Transcranial direct current stimulation – In an alternative approach, transcranial direct current stimulation (tDCS), the cortex is stimulated by a weak polarizing electric current using electrodes applied to the scalp [66]. In one study, this modality was applied to 10 patients with chronic stroke-induced aphasia and appeared to induce enhanced naming accuracy [67]. In another nonrandomized study in eight patients with chronic poststroke aphasia, cortical stimulation applied via surgically implanted electrodes appeared to augment the effect of speech and language therapy [42]. A futility study of anodal transcranial direct stimulation in 74 aphasic patients indicated nonfutility of treatment versus sham treatment and paves the way for further research on the technique [68]. A meta-analysis of studies applying tDCS failed to find evidence that tDCS improves functional communication, although it did find evidence that tDCS improves object-naming (noun-generation) [69].

This treatment is also being evaluated in patients with primary progressive aphasia [70,71].

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Aphasia (The Basics)" and "Patient education: Recovery after stroke (The Basics)")

SUMMARY AND RECOMMENDATIONS

Prognosis for recovery after stroke Aphasia is a common complication of cerebrovascular disease and is associated with significant disability. Patients with poststroke aphasia are likely to experience some improvement after the initial event. The prognosis for full recovery is greatest when patients have milder degrees of aphasia at the onset. (See 'Prognosis' above.)

Role of speech therapy We suggest speech and language therapy for patients with poststroke aphasia (Grade 2C). The available data from clinical trials offer weak support for this approach, but no single technique has emerged as more effective than others. The use of speech and language therapy has become the standard of care and has value in helping patients and families compensate for the devastating loss in the patient's communication skills. (See 'Speech and language therapy' above.)

Poststroke depression – Patients with aphasia are at risk of developing depression, which is likely to interfere with recovery and rehabilitation efforts. Patients should be monitored for the development of depression. (See 'Pharmacologic approaches' above.)

Pharmacologic treatments – There is insufficient evidence to recommend other pharmacologic interventions to improve patients' recovery from aphasia. (See 'Management' above.)

  1. Inatomi Y, Yonehara T, Omiya S, et al. Aphasia during the acute phase in ischemic stroke. Cerebrovasc Dis 2008; 25:316.
  2. Berthier ML. Poststroke aphasia : epidemiology, pathophysiology and treatment. Drugs Aging 2005; 22:163.
  3. Wade DT, Hewer RL, David RM, Enderby PM. Aphasia after stroke: natural history and associated deficits. J Neurol Neurosurg Psychiatry 1986; 49:11.
  4. Pedersen PM, Jørgensen HS, Nakayama H, et al. Aphasia in acute stroke: incidence, determinants, and recovery. Ann Neurol 1995; 38:659.
  5. Solomon NA, Glick HA, Russo CJ, et al. Patient preferences for stroke outcomes. Stroke 1994; 25:1721.
  6. Davidson B, Howe T, Worrall L, et al. Social participation for older people with aphasia: the impact of communication disability on friendships. Top Stroke Rehabil 2008; 15:325.
  7. Isaki E, Turkstra L. Communication abilities and work re-entry following traumatic brain injury. Brain Inj 2000; 14:441.
  8. Hilari K, Byng S. Health-related quality of life in people with severe aphasia. Int J Lang Commun Disord 2009; 44:193.
  9. Bakas T, Kroenke K, Plue LD, et al. Outcomes among family caregivers of aphasic versus nonaphasic stroke survivors. Rehabil Nurs 2006; 31:33.
  10. Choi-Kwon S, Kim HS, Kwon SU, Kim JS. Factors affecting the burden on caregivers of stroke survivors in South Korea. Arch Phys Med Rehabil 2005; 86:1043.
  11. Demir SO, Altinok N, Aydin G, Köseoğlu F. Functional and cognitive progress in aphasic patients with traumatic brain injury during post-acute phase. Brain Inj 2006; 20:1383.
  12. Paolucci S, Matano A, Bragoni M, et al. Rehabilitation of left brain-damaged ischemic stroke patients: the role of comprehension language deficits. A matched comparison. Cerebrovasc Dis 2005; 20:400.
  13. Ellis C, Simpson AN, Bonilha H, et al. The one-year attributable cost of poststroke aphasia. Stroke 2012; 43:1429.
  14. Ashtary F, Janghorbani M, Chitsaz A, et al. A randomized, double-blind trial of bromocriptine efficacy in nonfluent aphasia after stroke. Neurology 2006; 66:914.
  15. Laska AC, Hellblom A, Murray V, et al. Aphasia in acute stroke and relation to outcome. J Intern Med 2001; 249:413.
  16. Pedersen PM, Vinter K, Olsen TS. Aphasia after stroke: type, severity and prognosis. The Copenhagen aphasia study. Cerebrovasc Dis 2004; 17:35.
  17. Bakheit AM, Shaw S, Carrington S, Griffiths S. The rate and extent of improvement with therapy from the different types of aphasia in the first year after stroke. Clin Rehabil 2007; 21:941.
  18. Lazar RM, Minzer B, Antoniello D, et al. Improvement in aphasia scores after stroke is well predicted by initial severity. Stroke 2010; 41:1485.
  19. El Hachioui H, Lingsma HF, van de Sandt-Koenderman MW, et al. Long-term prognosis of aphasia after stroke. J Neurol Neurosurg Psychiatry 2013; 84:310.
  20. Poeck K, Huber W, Willmes K. Outcome of intensive language treatment in aphasia. J Speech Hear Disord 1989; 54:471.
  21. Moss A, Nicholas M. Language rehabilitation in chronic aphasia and time postonset: a review of single-subject data. Stroke 2006; 37:3043.
  22. Jordan LC, Hillis AE. Disorders of speech and language: aphasia, apraxia and dysarthria. Curr Opin Neurol 2006; 19:580.
  23. Richter M, Miltner WH, Straube T. Association between therapy outcome and right-hemispheric activation in chronic aphasia. Brain 2008; 131:1391.
  24. Saur D, Lange R, Baumgaertner A, et al. Dynamics of language reorganization after stroke. Brain 2006; 129:1371.
  25. de Boissezon X, Démonet JF, Puel M, et al. Subcortical aphasia: a longitudinal PET study. Stroke 2005; 36:1467.
  26. Price CJ, Crinion J. The latest on functional imaging studies of aphasic stroke. Curr Opin Neurol 2005; 18:429.
  27. Warren JE, Crinion JT, Lambon Ralph MA, Wise RJ. Anterior temporal lobe connectivity correlates with functional outcome after aphasic stroke. Brain 2009; 132:3428.
  28. Turkeltaub PE, Messing S, Norise C, Hamilton RH. Are networks for residual language function and recovery consistent across aphasic patients? Neurology 2011; 76:1726.
  29. Lidzba K, Staudt M, Zieske F, et al. Prestroke/poststroke fMRI in aphasia: perilesional hemodynamic activation and language recovery. Neurology 2012; 78:289.
  30. Mattioli F, Ambrosi C, Mascaro L, et al. Early aphasia rehabilitation is associated with functional reactivation of the left inferior frontal gyrus: a pilot study. Stroke 2014; 45:545.
  31. Forkel SJ, Thiebaut de Schotten M, Dell'Acqua F, et al. Anatomical predictors of aphasia recovery: a tractography study of bilateral perisylvian language networks. Brain 2014; 137:2027.
  32. Robson H, Zahn R, Keidel JL, et al. The anterior temporal lobes support residual comprehension in Wernicke's aphasia. Brain 2014; 137:931.
  33. Hagmann P, Cammoun L, Martuzzi R, et al. Hand preference and sex shape the architecture of language networks. Hum Brain Mapp 2006; 27:828.
  34. Nieuwenhuis L, Nicolai J. The pathophysiological mechanisms of cognitive and behavioral disturbances in children with Landau-Kleffner syndrome or epilepsy with continuous spike-and-waves during slow-wave sleep. Seizure 2006; 15:249.
  35. Kelly H, Brady MC, Enderby P. Speech and language therapy for aphasia following stroke. Cochrane Database Syst Rev 2010; :CD000425.
  36. de Jong-Hagelstein M, van de Sandt-Koenderman WM, Prins ND, et al. Efficacy of early cognitive-linguistic treatment and communicative treatment in aphasia after stroke: a randomised controlled trial (RATS-2). J Neurol Neurosurg Psychiatry 2011; 82:399.
  37. Robey RR. A meta-analysis of clinical outcomes in the treatment of aphasia. J Speech Lang Hear Res 1998; 41:172.
  38. Bhogal SK, Teasell R, Speechley M. Intensity of aphasia therapy, impact on recovery. Stroke 2003; 34:987.
  39. Bakheit AM, Shaw S, Barrett L, et al. A prospective, randomized, parallel group, controlled study of the effect of intensity of speech and language therapy on early recovery from poststroke aphasia. Clin Rehabil 2007; 21:885.
  40. Meinzer M, Streiftau S, Rockstroh B. Intensive language training in the rehabilitation of chronic aphasia: efficient training by laypersons. J Int Neuropsychol Soc 2007; 13:846.
  41. Aftonomos LB, Appelbaum JS, Steele RD. Improving outcomes for persons with aphasia in advanced community-based treatment programs. Stroke 1999; 30:1370.
  42. Cherney LR, Erickson RK, Small SL. Epidural cortical stimulation as adjunctive treatment for non-fluent aphasia: preliminary findings. J Neurol Neurosurg Psychiatry 2010; 81:1014.
  43. Szaflarski JP, Ball A, Grether S, et al. Constraint-induced aphasia therapy stimulates language recovery in patients with chronic aphasia after ischemic stroke. Med Sci Monit 2008; 14:CR243.
  44. Cherney LR, Patterson JP, Raymer A, et al. Evidence-based systematic review: effects of intensity of treatment and constraint-induced language therapy for individuals with stroke-induced aphasia. J Speech Lang Hear Res 2008; 51:1282.
  45. Meinzer M, Djundja D, Barthel G, et al. Long-term stability of improved language functions in chronic aphasia after constraint-induced aphasia therapy. Stroke 2005; 36:1462.
  46. Palmer R, Enderby P, Cooper C, et al. Computer therapy compared with usual care for people with long-standing aphasia poststroke: a pilot randomized controlled trial. Stroke 2012; 43:1904.
  47. Berthier ML, Green C, Lara JP, et al. Memantine and constraint-induced aphasia therapy in chronic poststroke aphasia. Ann Neurol 2009; 65:577.
  48. Greener J, Enderby P, Whurr R. Pharmacological treatment for aphasia following stroke. Cochrane Database Syst Rev 2001; :CD000424.
  49. Sabe L, Salvarezza F, García Cuerva A, et al. A randomized, double-blind, placebo-controlled study of bromocriptine in nonfluent aphasia. Neurology 1995; 45:2272.
  50. Walker-Batson D, Curtis S, Natarajan R, et al. A double-blind, placebo-controlled study of the use of amphetamine in the treatment of aphasia. Stroke 2001; 32:2093.
  51. Martinsson L, Hårdemark HG, Wahlgren NG. Amphetamines for improving stroke recovery: a systematic cochrane review. Stroke 2003; 34:2766.
  52. Kessler J, Thiel A, Karbe H, Heiss WD. Piracetam improves activated blood flow and facilitates rehabilitation of poststroke aphasic patients. Stroke 2000; 31:2112.
  53. Berthier ML, Hinojosa J, Martín Mdel C, Fernández I. Open-label study of donepezil in chronic poststroke aphasia. Neurology 2003; 60:1218.
  54. Hong JM, Shin DH, Lim TS, et al. Galantamine administration in chronic post-stroke aphasia. J Neurol Neurosurg Psychiatry 2012; 83:675.
  55. Code C, Hemsley G, Herrmann M. The emotional impact of aphasia. Semin Speech Lang 1999; 20:19.
  56. Kauhanen ML, Korpelainen JT, Hiltunen P, et al. Aphasia, depression, and non-verbal cognitive impairment in ischaemic stroke. Cerebrovasc Dis 2000; 10:455.
  57. Thomas SA, Lincoln NB. Factors relating to depression after stroke. Br J Clin Psychol 2006; 45:49.
  58. Laska AC, von Arbin M, Kahan T, et al. Long-term antidepressant treatment with moclobemide for aphasia in acute stroke patients: a randomised, double-blind, placebo-controlled study. Cerebrovasc Dis 2005; 19:125.
  59. Martin PI, Naeser MA, Theoret H, et al. Transcranial magnetic stimulation as a complementary treatment for aphasia. Semin Speech Lang 2004; 25:181.
  60. Naeser MA, Martin PI, Nicholas M, et al. Improved picture naming in chronic aphasia after TMS to part of right Broca's area: an open-protocol study. Brain Lang 2005; 93:95.
  61. Mottaghy FM, Sparing R, Töpper R. Enhancing picture naming with transcranial magnetic stimulation. Behav Neurol 2006; 17:177.
  62. Elsner B, Kugler J, Pohl M, Mehrholz J. Transcranial direct current stimulation (tDCS) for improving aphasia in patients with aphasia after stroke. Cochrane Database Syst Rev 2015; :CD009760.
  63. Cotelli M, Calabria M, Manenti R, et al. Improved language performance in Alzheimer disease following brain stimulation. J Neurol Neurosurg Psychiatry 2011; 82:794.
  64. Thiel A, Hartmann A, Rubi-Fessen I, et al. Effects of noninvasive brain stimulation on language networks and recovery in early poststroke aphasia. Stroke 2013; 44:2240.
  65. Wang CP, Hsieh CY, Tsai PY, et al. Efficacy of synchronous verbal training during repetitive transcranial magnetic stimulation in patients with chronic aphasia. Stroke 2014; 45:3656.
  66. Monti A, Ferrucci R, Fumagalli M, et al. Transcranial direct current stimulation (tDCS) and language. J Neurol Neurosurg Psychiatry 2013; 84:832.
  67. Baker JM, Rorden C, Fridriksson J. Using transcranial direct-current stimulation to treat stroke patients with aphasia. Stroke 2010; 41:1229.
  68. Fridriksson J, Rorden C, Elm J, et al. Transcranial Direct Current Stimulation vs Sham Stimulation to Treat Aphasia After Stroke: A Randomized Clinical Trial. JAMA Neurol 2018; 75:1470.
  69. Elsner B, Kugler J, Pohl M, Mehrholz J. Transcranial direct current stimulation (tDCS) for improving aphasia in adults with aphasia after stroke. Cochrane Database Syst Rev 2019; 5:CD009760.
  70. Tsapkini K, Frangakis C, Gomez Y, et al. Augmentation of spelling therapy with transcranial direct current stimulation in primary progressive aphasia: Preliminary results and challenges. Aphasiology 2014; 28:1112.
  71. Tippett DC, Hillis AE, Tsapkini K. Treatment of Primary Progressive Aphasia. Curr Treat Options Neurol 2015; 17:362.
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