The neuropsychopedagogue Juan Carlos Cancelado Rey explains in this article the neuropsychology of aphasias from a processing model, focusing on the definition, characteristics, symptoms, and affected processes of Broca’s aphasia and Wernicke’s aphasia.

Neuropsychology of aphasias from a processing model: “I never thought that speaking would be so difficult” – Broca, “What’s wrong with them, why don’t they understand me?” – Wernicke.

Language, although it is a human faculty for communication through articulation and speech, its relevance lies in how it shapes the mind and allows it to express itself to others. Therefore, it would be valid to present language as a cognitive function that operates together with other functions and integrates processes as a whole.

This will help us to understand a little more about what, in clinical practice, is difficult to differentiate in the case of who is usually aphasic and who is not. Since there is no physical trait that can give us a clinical representation of a specific or global aphasic condition, or even be part of its semiology. In a way, although it may seem paradoxical, the way to know it is through the effort of speaking and understanding. If the patient is able to do it correctly or, on the other hand, if their interlocutor finds difficulty in understanding them or knowing what they want to communicate.

What are Aphasias?

Aphasias denote alterations in language as a consequence of acquired brain damage, which affect the capacity for verbal communication at an expressive, receptive, and/or global level (Ardila, 2005).

The Boston school, whose representatives Goodglass and Kaplan (2002) define it as impairments in the articulation, production, and comprehension of language that are not compatible with an incoordination or physiological etiology muscular paralysis.

However, the diagnostic labels of Broca or Wernicke do not specifically describe the patient’s cognitive profile based on processes, due to many overlaps, but they become a tool for communication in daily clinical practice among professionals and to know what to expect. In this way, we can delve deeper into the cognitive deficits that accompany the patient’s primary impairment.

Language processes: anatomopathological relationship and aspects of neuropsychological evaluation

The language processes of Ellis and Young (1992) allow us to differentiate central aspects, such as errors made by patients with acquired brain damage or patients with language disorders of neurodegenerative etiology.

1. Repetition

At birth, we come with a certain orientation towards language. The perceptual systems, such as the auditory system, develop and modulate over time in relation to the environment. This process is responsible for transforming acoustic information into phonological information.

However, we must consider other underlying processes such as the lexical and semantic store, and the relationship with the phonological loop of working memory.

In this sense, the mechanism referred to as acoustic-phonological conversion, from the cognitive model of processes, is of vital importance for language learning.

Following the model of the dual route by Gregory Hickok and David Poeppel (2004), the repetition process has a close anatomopathological relationship with the dorsal or sublexical pathway, with clear lateralization in the left hemisphere. The processed phonological information is sent through this pathway to carry out its articulatory response, starting from areas of sensorimotor integration and leading it through the articulatory network of the angular gyrus, arcuate fasciculus, and Broca’s area for articulatory movement. Additionally, the superior longitudinal fasciculus is important in repetition and phonological aspects, playing a relevant role in relation to the phonological loop of working memory.

The evaluation of the repetition process is usually done:

• Qualitatively during the patient’s anamnesis.
• With tests that evaluate syllables, pairs of syllables, logatoms, pairs of words with phonological relationship, and phrases.

Considering that both the test and clinical observation can help us specify the type of aphasia and its affected process.

2. Comprehension

In the early years of life, comprehension as an expression of language shows exponential growth in the phonological lexicon, acquiring automatism through relations and experiences with the environment. Words and meanings are acquired at a speed that allows the processing of information, such as acoustic-phonological analysis, to be enriched by experience and emotions over time.

Thanks to the formation of a lexical-phonological store, the relationship between the heard word, the acoustic analysis, the incoming phonological lexicon, and the semantic system (Vega, 2012) enables a person to:

• Understand auditory words and codes as text.
• Strengthen the grammatical architecture of their expressive language, preserving an order, intonation, lexicon, and a phonetic, syntactic, and semantic sense when articulating it.

Dual-route model

The dual-route model by Gregory Hickok and David Poeppel (2004) states that the ventral pathway, located in various portions of the temporal lobe, has a special function in lexical and semantic processes. When the uncinate fasciculus (which connects anterior temporal and inferior frontal structures) is affected, the comprehension of complex syntactic structures may be compromised. In contrast, impairments in the arcuate fasciculus may be relevant for signs of an inability to comprehend the meaning of isolated words.

In this sense, qualitative data from a thorough anamnesis and clinical observations contribute to the evaluation process, as well as the appropriate selection of tests that assess visuo-visual, visuo-verbal, and/or verb-verbal aspects.

The objective should be to assess all types of tasks, as this allows us to differentiate whether the comprehension deficit corresponds to a primary alteration or is secondary to other affected processes.

3. Production

The idea of producing language begins with the need to transmit information. The more proficient our phonological and semantic lexicon is, the more articulated language can be generated.

When we talk about production, we emphasize a direct route that lacks meaning, through the mechanism of acoustic-phonological conversion, and another route for the production of semantic content.

This helps us understand the dissociation we observe in some patients between their ability to repeat but not to spontaneously produce language, and vice versa. It also leads to a better understanding of the reasons behind assessing repetition of pseudowords and real words separately since they follow different pathways.

Regarding language production, it is expressed grammatically to adequately communicate its syntactic, phonological, phonetic, lexical, and semantic value. If this is not the case, it can be observed through clinical observations and neuropsychological assessment tests administered to the patient.

The generating pathways are often dorsal routes explained previously in the dual-route processes (Gregory and Poeppel, 2004).

Language assessment tests

However, it should be understood that language evaluation should occur throughout the entire assessment process. The person’s spontaneous language is an important source of information (Lezak et al., 2012). Consequently, we can determine their ability in acoustic-phonological discrimination, comprehension (semantic storage: what information is being conveyed? lexical storage: appropriate word choice, phoneme selection), fluency, and speech production.

For evaluation purposes, three types of tests are commonly used:

• Direct question tests.
• Picture description tests.
• Responses to questions about an exciting historical topic.

In this way, the assessment of articulatory skill, grammatical structure, and melody is usually performed using the Boston Naming Test.

Some authors emphasize the length of the sentence emitted by the person as it allows for better quantification and the establishment of normal ranges with phrases, for example, of nine words in a single expiration without pauses (Helm-Stabrooks and Albert, 2005).

4. Naming

Naming is a central symptom of aphasia. Problems in naming an object become evident depending on the affected processes. This is known as language anomia, which is often considered a difficulty in accessing information, with circumlocutions and some paraphasias.

Types of anomia

In practice, it has been observed and assessed that patients can present three types of anomia (Fernández and Vega, 2006):

1. Access anomia

In this type of anomia, the patient often experiences the “tip of the tongue” phenomenon, being unable to access a word even though they have knowledge of it. However, when given a phonological clue, they are able to recall it completely.

For example, by helping them name a magazine when the evaluator provides the clue:

— Evaluator: It starts with an “m”.

— Patient: Ah, I got it! It’s a magazine, it’s a magazine!

This type of anomia is complicated to locate anatomically, although there could be several causes related to access to the word, such as problems in more frontal processes of evocation and other correlations with white matter.

2. Semantic anomia

In this type of anomia, the patient knows the objects they should name but lacks the word to express it. Thus, when told it is a “chair,” the patient may respond with confusion, for example:

— Evaluator: It’s a chair.

— Patient: Chair? Is this called a chair?

Their confusion corresponds to a reduced vocabulary compared to what is expected.

This type of anomia is often related to anterior temporal regions due to their semantic verbal function.

3. Phonological anomia

In this type of anomia, the patient’s choice of phoneme in verbal expression is often incorrect. They cannot access the word correctly, and their production involves syllabic approximations with errors in the first syllable, for example:

— Patient: It’s a Compi… Comru… Compo… Computer!

The angular gyrus is often related to this type of anomia due to its phonological component.

Anomia assessment is usually performed using the Boston Naming Test (Kaplan et al., 1978) or the DO-80 Oral Naming Test of Images (Deloche and Hannequin, 1997).

Up to this point, it has been necessary to explain the previous processes to facilitate the understanding of Broca’s aphasic condition and Wernicke’s aphasia, without falling into the dichotomy of the lesion model, where Broca is known as the one who cannot speak and Wernicke as the one who does not understand, obviously disregarding the articulatory and verbal errors in Broca and the phonological errors in Wernicke.

In this way, by following the perisylvian aphasic syndromes, that is, language impairments localized around the Sylvian fissure of the left hemisphere, composed of the three main aphasic syndromes (Broca’s, conduction, and Wernicke’s), we will facilitate the understanding of the two syndromes under study, Broca’s and Wernicke’s. This is because their semiology can be varied depending on whether the affected area is more anterior, medial, or posterior to the perisylvian region.

Broca’s Aphasia

“I never thought that speaking would be so difficult.”

Also known as efferent aphasia or kinetic aphasia (Luria,1970), expressive aphasia (Hécaen and Albert, 1978), verbal aphasia (Head, 1926), and Broca’s aphasia (Benson, 1979).

What is Broca’s aphasia?

This syndrome involves alterations in language fluency.

Characteristics of Broca’s aphasia

Broca’s aphasia is characterized by:

• Reduced expressive language.
• Impact on repetition.
• Short and agrammatical expression composition.
• Production problems related to verbs more than nouns.
• It is typically localized in the lower frontal-lateral areas surrounding the Sylvian fissure, in front of the pre-rolandic fissure (Brodmann areas 44 and 45).

Articulatory verbal errors in Broca’s aphasia

• Verbal simplifications: simplifying the syllabic sequence and repetition. For example, the patient says “thee” instead of “three.”
• Anticipation: the patient refers to, for example, pall” instead of “ball.”
• Perseveration: errors with more than one consonant tend to persist. For example, pronouncing “taple” instead of “table.”
• Substitution of fricative phonemes: replacing (f, s, j) with plosives (p, t, k). That is, saying “plower” instead of “flower.”
• Agrammatism: agrammaticality in the production of Broca’s aphasia shows defective understanding of the sentence by altering its grammatical order. Thus, the patient may say “dog garden” instead of “the dogs are in the garden.” Agrammaticality and anomia in Broca’s aphasia are usually the result of subcortical lesions affecting damaged vascular territories that involve the middle cerebral artery or the neocortex in the inferior frontal lobe.

Altered processes in Broca’s aphasia

Regarding the altered processes in Broca’s aphasia:

• Spontaneous speech is not fluent; the patient tends to produce it with effort using single words and short phrases.
• The phonetic and phonological process presents dysarthria, omission of phonemes, reduction of consonant clusters, and use of phonological paraphasias.
• Morphosyntax tends to be agrammatical and with telegraphic speech. It presents aprosody, and verbal auditory comprehension is relatively preserved since the disorganized language, due to the lack of relating grammatical components, does not allow understanding of the sentence.
• Naming is characterized by phonological anomia, which improves with syllabic cues.
• Repetition is altered.
• Reading aloud is defective, with comprehension similar to oral speech, showing agrammatism, bradylalia, interrupted flow, and difficulty.
• Writing has spelling errors, omissions, and substitutions of graphemes.

The signs of language process impairments in Broca’s aphasia can be seen in practice through the presence of patients who can speak and make themselves understood but maintain small errors in verbal articulation or comprehension. As mentioned before, this can also occur in Broca’s aphasia. Other patients, on the other hand, are not very understandable, their language is not fluent, and they have disautomatization in speech articulation. Some patients may present a more pronounced phonological anomia, which can be strengthened with phonetic cues; thus, each of these patients may or may not articulate language and produce sentences (with defects).

Wernicke’s aphasia

“What’s wrong with you that you don’t understand me?”

Also known as receptive, sensory, or central aphasia.

What is Wernicke’s aphasia?

Wernicke’s aphasia is found in posterior lesions of the superior and middle temporal gyrus, an area known as the auditory association cortex.

Alterations in Wernicke’s aphasia

Wernicke’s aphasia encompasses a set of alterations that show:

• Logorrhea: fluent but disorganized speech.
• A significant number of paraphasias:
  • Semantic: substituting terms with others that are related in meaning. An example of this would be replacing “cow” with “milk.”
  • Phonological: substituting one phoneme for another within the same word, for example, “house” becomes “mouse”.
• According to Jakobson (1964), because the patient loses the boundaries of the sentence and does not finish it, the grammatical structure can have an excessive number of elements (a disorder called “paragrammatism”).

Characteristics of Wernicke’s aphasia

1. While Broca’s aphasia shows more impairment in the articulation and praxis of language production, in Wernicke’s aphasia, the characteristic feature is paraphasias, due to an affected input to the access of the semantic store and the lexical store.
2. The auditory discrimination in patients with Wernicke’s aphasia tends to be somewhat defective. This hinders a proper acoustic phonological analysis that enables the adequate construction of sentence grammar and improves the comprehension of oral language.
3. As a result, writing is altered with substitutions, omissions, and letter rotations.
4. In terms of repetition, there is a slight difficulty in performing it. The patient’s receptive capacity is limited to subsequently repeat sufficient words based on the cognitive load of the task. At this point, the patient may experience fatigue, understanding several words, but if the evaluator or therapist adds a cognitive load with a greater number of words, the patient fails to make sense of them.

This can, in turn, lead to a false idea on the part of the therapist or evaluator in determining the severity level or expressive evolution in Wernicke’s aphasia, as long as they do not consider:

• The cognitive load with which my patient performs the fatiguing task.
• The difficulty in improving comprehension.
• Other processes such as naming, writing, or reading.

How do aphasia stages evolve?

It is important to consider the temporal moment when the injury occurs because in most cases, the patient’s hospital-level observations do not correspond to the same semiology after a few months. That is, when specific vascular territory involvement occurs, such as in the middle, internal, carotid, or posterior cerebral arteries, there is a focal lesion, but on a superficial level, there is inflammation affecting some cognitive functions. After a few weeks and due to spontaneous recovery, the condition begins to improve. What was initially a global aphasia has changed, as the patient may articulate slightly better, revealing the type of errors or alterations in processes in their expression. Also, they start to comprehend better, perhaps discerning the acoustics to some extent and making appropriate phonological conversions.

Stages of aphasia

1. The phase in which the sequelae first appear and show global aphasia is called the acute phase. During this phase, the onset of signs can vary until they even disappear.
2. After this acute phase, the patient enters a subacute period. During this time, sequelae are established, which may improve spontaneously due to self-organization in the brain. Some authors give this phase around a year for the brain to recover.
3. Afterwards, we encounter a chronic phase. Patients who are two years past the stroke event and whose sequels manifest as impairments in their expressive and receptive language abilities may show significant improvements as they decide to learn language anew. Therapies can help them compensate for language automatism through new learning. It is worth noting the role played by the brain plasticity of a young brain compared to an adult one or even more so in cases of neurodegenerative or genetically based conditions.

Bibliography

• Ardila, A., Rosselli, M., Márquez Orta, E., & Rodríguez Flores, L. (2007). Neuropsicología clínica. México, D. F.: Manual Moderno. https://colombia.manualmoderno.com/catalogo/neuropsicologia-clinica-9786074488074-9786074488135.html
• Ardila, A. (2005). Las Afasias. México. Universidad de Guadalajara. https://elrincondeaprenderblog.files.wordpress.com/2016/01/libro-las-afasias-alfredo-ardila.pdf
• Helm-Estabrooks, N. y Albert, M. L. (2005). Manual de la afasia y de terapia de la afasia. Editorial Médica Panamericana. https://www.casadellibro.com.co/libro-manual-de-la-afasia-y-de-terapia-de-la-afasia-2-ed/9788479038335/1019320
•  Lezak, M., Howieson, D. y Loring, D. (2012). Neuropsychological assessment. Oxford University Press (5ª ed.). https://global.oup.com/academic/product/neuropsychological-assessment-9780195395525?cc=co&lang=en&
• Nakase-Thompson, R., Manning, E., Sherer, M., Yablon, S. A., Gontkovsky, S. L. T. y Vickery, C. (2005). Brief assessment of severe language impairments: initial validation of the Mississippi aphasia screening test. Brain Injury, 19(9), 685-691. https://pubmed.ncbi.nlm.nih.gov/16195182/

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