Prosody represents a precocious, universal and resilient domain of spoken language. However, the extensive array of prosodic features, encompassing both linguistic and paralinguistic aspects, is susceptible to a multitude of alterations in the context of linguistic disorders. These changes manifest themselves in different ways, depending on the nature and extent of the underlying speech disorder. These alterations can impact various aspects of language, including the adequacy of rhythm and intonation structure (both form and function), the interfaces that prosody establishes with the other levels of language, fluency and the transmission of emotions.

In this regard, it is noteworthy that in 1981, Crystal distinguished between the broader phonetic concept of ‘dysprosody’ and the phonological concept of ‘prosodic disability’. In the first case, there is a phonetic difficulty in the use of pitch, duration, loudness and rhythmic patterns, whereas in the second case there is a phonological impairment that causes a prosodic deviation of the aforementioned features, due to an inability to select, retrieve and plan prosodic processes. This is also the basis for the distinction between ‘speech disorders’ and more complex ‘language disorders’. The former category encompasses dysarthria, apraxia, voice and fluency disorders, which pertain to the act of speaking, incorporating its articulatory, bio-anatomical and oral-motor components. The latter category, which includes aphasia, phonological disorder, autism and dementia, is closely related to the components of the language system (the grammar) in its productive and receptive sides.

In a more general sense, the term ‘prosodic impairment’ is now employed to refer to a range of prosodic deficiencies observed in clinical populations. A variety of pathologies may give rise to a state of prosodic impairment, which can manifest in different ways. It is essential to differentiate between congenital and acquired conditions, as well as between neurological diseases that also affect the cognitive system (both left and right hemisphere damage) and those that preserve it (Wymer et al. 2002). In addition, there are speech disorders due to a motor control disorder that severely affects intelligibility and comprehension (for a review, see Hargrove & McGarr 1994; Shriberg 1994; Stojanovik & Setter 2011).

One fundamental premise is that in the majority of disorders, alterations in prosody typically occur in conjunction with other language deficits affecting its interfaces, such as syntax, semantics or pragmatics. This is due to the comorbidity of other functional, neurological or motor factors. Moreover, in many pathologies, prosody is not the domain of speech that is most impaired; for instance, children with primary specific disorders or developmental dyslexia tend to show greater difficulties in grammatical processes than in prosody. The situation is different when the disorder involves phonological damage, even in conjunction with a cognitive delay, or when the individual presents motor difficulties, with or without cognitive impairment, resulting in reduced intelligibility, dysarthria, apraxia, voice quality deviation and stuttering.

It should be noted that prosodic deficits do not always manifest in the same way. It is essential to differentiate between those that impact the linguistic functions of prosody (grammatical prosody) such as prosodic contrasts, focus, phrasing, information structure (Ladd 2008) and those that, conversely, affect the paralinguistic, non-verbal functions (affective prosody), such as the expression of emotions and states of mind (Pell 2006; Mitchell & Ross 2013). The descriptive picture becomes more complex in view of the fact that in some disorders both grammatical and expressive prosodic changes may be present. Furthermore, a deficit in prosody is evident in both the production and the comprehension of speech, encompassing aspects such as phonation and articulation.

A substantial corpus of literature has been published on this topic, although not all speech disorders have received equal attention over time. Researchers have generally concentrated on pathologies affecting language development in children, including primary language disorder, autism spectrum disorder, childhood apraxia of speech, and those occurring in adults, such as Parkinson's disease, dementia and aphasia. Additionally, there are also specific research areas dedicated to the investigation of prosody in genetic diseases such as Down syndrome or Williams syndrome, as well as in individuals with sensorial disabilities, including hearing impairment, with or without cochlear implants.

With regard to prosody, despite the specific characteristics of each pathological condition, it is evident that the majority of disorders exhibit alterations in rhythm and intonation, resulting in atypical patterns when compared to those observed in control subjects. The existing literature on this subject is now extensive and includes studies of an interdisciplinary nature, ranging from the analysis of articulatory to intonation coefficients. It is not feasible to provide a comprehensive account of the different research directions pertaining to each speech disorder: the subsequent sections will therefore attempt to present some pivotal findings derived from the most extensively investigated pathologies to date.

Aphasia is a prevalent neuropathological condition associated with language dysfunction. Aphasics subjects show a compromised and ineffective state of communication. The various forms of aphasia are associated with specific language impairments, arising from damage to the brain regions responsible for language production (Broca's aphasia) or language comprehension (Wernicke's aphasia). Specifically, Broca's aphasia is the result of damage to the anterior inferior region of the left hemisphere, leading to a state of agrammatism that impairs language production. This impairment is characterised by slow, disjointed speech which is typified by the absence of functional words and grammatical connections. From a prosodic perspective, individuals diagnosed with Broca's aphasia exhibit intonational, rhythmic and temporal alterations (Gandour et al. 1989). However, the results of different studies are often conflicting (for a detailed review, see Zipse & Gallée 2023). In general, it appears that in agrammatic aphasics, the pitch contour and amplitude tend to be preserved, although there are notable alterations in timing, resulting in an increased overall rate, pauses, and a difficulty in adapting syllable duration to the lexical or sentence context. According to Danly & Shapiro (1982), individuals diagnosed with Broca's aphasia do not have the typical prepausal lengthening and f0 declination observed in long utterances. This is likely attributed to the frequent f0 resetting resulting from the inherent difficulty of planning and executing longer syntactic units. However, in a condition of severe aphasia, individuals seem to use prosody as a compensatory mechanism for pragmatic meanings and also for some syntactic functions (Rhys et al. 2013).

The situation is distinct for Alzheimer's disease, a chronic and progressive neurological pathology that induces dementia in the elderly as a consequence of substantial alterations in motor and cognitive control. In this case, the memory deficit, in conjunction with progressive neurocognitive impairment, causes a significant language deficit, which documents a state of difficulty in the controlling, planning and remembering aspects of the past life. This leads to a series of linguistic alterations, including broken utterances, repetitions, pauses, hesitations and filler sounds. In this manifestation of incoherent and disordered speech, there is also a semantic impairment and frequent phonological errors. As the disease progresses, the periods of silence increase until a state of global aphasia is reached, so that the silence and the hesitation ratios increase progressively. Prosodic impairment show a changes in timing, rhythm and intonation (Roberts et al. 1996; Tosto et al. 2011; Meilàn et al. 2014; Misiewicz et al. 2018). However, the most severely affected domain appears to be the production and the comprehension of emotional prosody (Amrelova et al. 2022).

The majority of motor speech disorders entail a compromise of phonation and speech rate. Consequently, these disorders are characterised by a deviation in fluency, including articulation and speech rate, pauses, and deviations in voice quality characteristics. This situation also has consequences at the prosodic level, resulting in an altered intonation and phrasing. In this vein, Parkinson's disease (PD) represents one of the most prevalent neurodegenerative diseases that manifests in adulthood, characterised by motor impairments in speech. The majority of Parkinson's patients show marked hypokinetic dysarthria which affects phonation, articulation and prosody. A hallmark of PD is the occurence of disfluent and hypoarticulated speech, typified by a high frequency of pauses and a concomitant reduction in speech rate. Furthermore, the speech of individuals with PD shows monotonous intonation patterns due to reduced variation in fundamental frequency (f0), intensity, pitch range and the production of nuclear intonation configurations that differ from those observed in control subjects (Darkins et al. 1988; Mennen et al. 2008; Thies et al. 2020). A recent study of 30 Portuguese-speaking subjects (Frota et al. 2021) demonstrated that pharmacological treatment enhances the selection of pitch accents in accordance with sentence modality. However, the study also demonstrated that pharmacological treatment does not facilitate phrasing, which remains impaired. The duration of the disease does not appear to impact the quality of prosodic performance, although it does result in a gradual slowing of speech rate. Recent research has identified a novel point of interest in the context of Italian PD patients (Gili Fivela et al., 2020). The analysis of acoustic and articulatory data has revealed that, in contrast to prevailing expectations, speech gesture amplitude and articulation rate do not invariably decrease. Instead, there is the possibility of an increase, which would suggest that compensatory strategies may be involved.

The findings of studies conducted on genetic syndromes have yielded a more varied array of results. Among the full spectrum of genetic conditions, Down syndrome is the most prevalent pathology associated with a significant deficit in cognitive abilities. The diverse range of language difficulties encountered by individuals with Down syndrome can be ascribed to a multitude of underlying causes. Some are associated with anatomical and biological factors, while others are linked to cognitive delay. In terms of prosody, individuals with Down syndrome exhibit a range of vocal characteristics, including frequent interruptions, prolonged sounds, a slower speech rate, unstable intensity and pitch (among all, Nadel 1988; Law & Bishop 2004; Sorianello 2012). The presence of a small oral cavity and a general hypotonia of the facial muscles, coupled with difficulties in motor skills, oral planning and maintaining intraoral pressure, results in a significant degree of dysarthria, frequently accompanied by stuttering. This causes phonetic errors, a reduced vowel space and altered vibration of the vocal folds. The intonation contours are typically characterised by a narrow pitch range and a lack of variation, while the mean fundamental frequency (F0) is higher compared to control subjects.

In addition to its linguistic implications, prosody also provides insight into the emotional and affective state of the speaker. Expressive prosody serves to supplement the meaning of a spoken message with non-linguistic cues. This is based on the activation of a range of non-verbal paralinguistic indices, including facial expressions, gestures and eye gaze. In addition, acoustic modifications of the voice are also involved, such as pitch, sound energy and duration (Pell 2006).

Affective prosody has been demonstrated to impact on both speech production and comprehension (Pell & Baum 1997; Ross & Monnot 2008). In its undamaged state, it requires a functioning and active brain system, which is why it appears so fragile. Affective prosody disorders may have a variety of underlying causes, including a range of aetiologies. As is evidenced by the extensive literature on the subject, the most frequently referenced causes are stroke (both left and right hemisphere damage), neurodegenerative diseases such as Parkinson's and Alzheimer's, multiple sclerosis, progressive aphasia, traumatic brain injury, surgical removal of brain tissue due to the presence of tumours (for a discussion, see Coulombe et al. 2023).

In such instances, the production of prosodic features tends to be monotonous and devoid of the emotional expressions that characterise spoken language. This can establish the groundwork for subsequent social interaction difficulties. At the level of comprehension, there is a reduction in the capacity to decode the message and an inability to recognise the non-verbal prosodic features associated with the production of emotions. However, the broad spectrum of disorders with diverse aetiologies that can manifest affective dysprosody does not always facilitate a coherent interpretative framework that would enable the association of a prosodic symptom with a specific pathological condition. This difficulty can be attributed to the multifunctional nature of affective prosody, which engages a number of regions within the brain thereby establishing different connections. In addition, changes in the domain of expressive prosody are infrequently addressed within clinical settings, thus impeding the adequate rehabilitation of patients suffering from affective dysprosody.

Prosody refers to a range of linguistic and paralinguistic processes and functions. Consequently, studies of prosodic impairment employ a variety of theoretical and methodological approaches, as well as a number of assessment protocols and instruments.

In accordance with this objective, the aim is twofold. Firstly, the construction of a valid assessment instrument will facilitate a fine-grained evaluation of how prosodic features deviate in different clinical settings. Secondly, a more profound understanding of the nature of prosodic deficits in atypical populations is crucial for the development of diagnostic and treatment protocols that most effectively address the prosodic deficits arising from both speech and language disorders. Nevertheless, achieving this objective is challenging, due to the multifaceted role of prosody in speech, a topic which has also been the subject of scientific debate (Peppé 2009). The fundamental question concerns the distinction between prosodic variations that are indicative of a clinical condition and those that are merely sociolinguistic manifestations. Additionally, it is challenging to ascertain whether a change is attributable to a prosodic impairment or an alternative deficit at a different level of language (e.g. syntactic or semantic), given that prosody is a pervasive component that can be influenced by all linguistic structures and patterns.

A variety of methods for the identification and categorisation of prosodic difficulties have been developed over time, with a significant number of these methodologies having their origins in the field of computer science. In this regard, the Prosody-Voice Profiles (PROP) tool, initially developed by Shriberg & Widder (1990) and subsequently revised by Shriberg (1993), is primary employed in the assessment of developmental disorders in children. It encompasses seven distinct categories, ranging from pitch and loudness to phrasing and voice quality, to quantify the extent of a speech delay. In 2001, Wells and Peppé proposed the prosodic battery known as PEPS-C (Profiling Elements of Prosodic Systems-Child version). This battery comprises the Input/Output and Form/Function categories, and enables the assessment of children’s ability to produce and to comprehend prosody in comparison with typically developing controls.

A variety of diagnostic instruments are available for the purpose of evaluating aphasia and other neurogenic disorders. These include the Fluency, Grammatical Competence and Paraphasia Scale of the Western Aphasia Battery (Kertesz 2006), although it should be noted that these tools do not exclusively focus on the assessment of prosody abilities.

With regard to affective prosody, at least the Aprosodia Battery (Ross et al. 1997) and the Comprehensive Affect Testing System (Froming et al. 2022) are worth mentioning.

In the following years, various authors have argued on the necessity for the establishment of prosodic assessment batteries founded upon normative and standardised data, empirical evidence and ecological tasks, in addition to clinical utility (Diehl & Rhea 2009). Concurrently, the necessity for automated protocols to overcome the challenges inherent to auditory, and often subjective assessment, has also been emphasised (van Santen et al. 2009).

In this direction, the methods currently employed for the analysis and assessment of prosody in clinical populations are numerous. These include techniques such as the elicitation of intonation contrasts using prosodic minimal pairs, imitation of intonation contours, and the utilisation of descriptive, narrative and pragmatic tasks. In terms of perceptual methodology, listening experiments have employed both discrimination and identification tasks.

Furthermore, there is a pressing need within the domain of clinical linguistics for the establishment of standardised and annotated large corpora, which are indispensable instruments for the community to conduct research, encompassing comparative and predictive studies.

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