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Assessing Speech and Landuage

Assessing Speech and Landuage

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Speech and Language D
i
sturbances255255
From
:
Current Cl
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cal Neurology: Atyp
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, Totowa, NJ
16
Character
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z
i
ng and Assess
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ng Speech and LanguageD
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sturbances
Carol Frattal
i
and Joseph R
.
Duffy
INTRODUCTION
Speech and language disturbances in atypical parkinsonian disorders often present as initial symp-toms or prominent neurobehavioral sequelae that worsen as the disease progresses. These disorders,even in their early stages, can have profound effects on communicative functioning and, by exten-sion, psychosocial well-being. In the face of neurodegenerative disease, the downward course of theability to communicate mirrors a loss considered elemental to the human condition; it unavoidablyrobs the individual of a primary mode of expression of thoughts and ideas and, in its most severeform, basic needs.We draw a distinction between
speech
and
language
for purposes of clarity throughout this chap-ter. These terms, sometimes used interchangeably or in combination by clinicians and researchers,can be defined and distinguished in a hierarchical representational framework 
(1)
:
Language represents high-order cortico-cortical and cortical-subcortical network activity as a componentof cognitive-linguistic processes. These processes represent thoughts, feelings, and emotions that gener-ate intent to communicate. They are next converted to verbal symbols that follow psycholinguistic rules(e.g., phonology, morphology, syntax, semantics, pragmatics) as ordered meaningfully by propositionalelements (units of meaning). Language processes can be divided broadly as those that link thought (mean-ing) to word forms (lexical-semantic) and those that sequence words and word endings to convey relation-ships among words (syntactic)
(2)
. In its disordered state, a breakdown of language, either atlexical-semantic or syntactic process levels, is called aphasia.Speech represents cortical-subcortical and brain stem activity via neuromuscular and central and periph-eral nervous system activity involving two processes: motor speech programming and neuromuscularexecution. In motor speech programming, selection and organization of sensorimotor plans activate thespeech musculature at appropriate coarticulated times, durations, and intensities. During speech produc-tion, the neuromuscular transmissions that involve respiration, phonation, resonation, articulation, andprosody generate muscle contractions and finely coordinated movements of oral/motor structures thatgenerate an identifiable acoustic signal. In their disordered states, breakdowns of motor speech program-ming and related neuromuscular activity are known as apraxia (nonverbal orofacial or buccofacial apraxia,apraxia of speech) and dysarthria respectively.
Overview of Neuroanatomical Correlates
If approached from the perspective of classical neuroanatomical correlates, damage to portions of the auditory and visual association areas of the cortex can result in comprehension deficits of thespoken or written word. Damage to Wernicke’s area (Brodmann area 22), in the posterior portion of 
 
256Frattal
i
and Duffy
the superior temporal gyrus of the dominant hemisphere, can result in a type of aphasia generallycalled Wernicke’s aphasia. Wernicke’s aphasia is marked by reduced comprehension and fluent butoften paragrammatic verbal output characterized by word or nonword substitutions (paraphasias)sometimes to the extent of producing fluent streams of non-English or neologistic jargon. In contrast,damage to Broca’s area (Brodmann areas 44–45), in the third convolution or inferior gyrus of thefrontal lobe of the dominant hemisphere can result in a type of aphasia generally called Broca’saphasia. Broca’s aphasia, in contrast to Wernicke’s aphasia, is marked by relatively spared compre-hension but sparse, effortful, nonfluent, and agrammatic verbal output. Along the parameters of flu-ency, comprehension, repetition, and naming, other classic aphasia syndromes have been identifiedincluding conduction, transcortical motor, transcortical sensory, and global aphasia.The nondominant hemisphere is also increasingly implicated in its role in language functions,particularly for global and thematic processing of narratives, pragmatics (relation between languagebehavior and context in which it is used or interpreted), and prosody (elements of speech melody,rate, stress, juncture, and duration) of language, and inferencing, coherence, and topic maintenanceduring discourse processing and production
(3,4)
.Skilled motor programs for control of the larynx, lips, mouth, respiratory system, and other acces-sory muscles of articulation are thought to be initiated from Broca’s area. Damage to this area, orwithin other parts of the left hemisphere’s network of structures involved in the planning and pro-gramming of speech, results in apraxia of speech. Once these programs are activated via the premotorzone of Broca’s area, thus mediating orofacial and speech praxis, the facial and laryngeal regions of the motor cortex (bilaterally) activate the speech musculature for actual emission of sound. The neu-ral substrates of neuromuscular execution originate in the primary motor cortex (Brodmann area 4)with pathways descending either directly or indirectly via the pyramidal or extrapyramidal tracts.The pyramidal tract consists of upper motoneurons in the cerebral cortex with axons coursing throughthe pyramidal tract in the medulla and terminating on anterior horn cells or interneurons in the spinalcord. The pyramidal tract is composed of the corticospinal tract and the corticobulbar tract that influ-ences cranial nerve activity. Types of dysarthria that could result (e.g., spastic dysarthria) would havefeatures of spasticity, increased muscle stretch reflexes, and clonus. In contrast, damage to lowermotoneurons from spinal and cranial nerves results in loss of voluntary and reflex responses of muscles. The result would be hypotonia and absence of muscle stretch reflexes. Paralysis and atrophywould occur, with the early stages of atrophy resulting in fibrillations and fasciculations. Dysarthriaswith damage to lower motoneurons would have characteristics of flaccidity (e.g., flaccid dysarthria)
(5)
. Other pathways that, if interrupted, would result in dysarthria, include extrapyramidal (coursingthrough structures of the basal ganglia) and cerebellar motor pathways, which could result in hyper-kinetic or hypokinetic components following extrapyramidal damage, or ataxic dysarthria followingcerebellar damage (
see
Appendix A for descriptions of aphasia syndromes, apraxias, and dysarthriatypes; Appendix B for case descriptions and test stimuli used for audio samples of speech and lan-guage disorders that accompany this chapter).With advances in neuroimaging techniques, a dynamic systems rather than localization view of speech and language functions is being adopted. Neuroimaging findings have shown that languageprocessing extends beyond the classical perisylvian region containing Broca’s and Wernicke’s areasand depends on many neural sites linked as systems. For example, both left temporal and prefrontal/ premotor cortices have been found to be activated by language processing, and do so selectively.Neuroimaging studies have also shown that structures in the basal ganglia, thalamus, and supplemen-tary motor area are engaged in language processing
(6)
. Adding to the evidence of functional connec-tivity, a recent study suggests that the anatomical and functional organization of the human auditorycortical system points to multiple, parallel, hierarchically organized processing pathways involvingtemporal, parietal, and frontal cortices
(7)
. Computational mapping methods, which can combine
 
Speech and Language D
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sturbances257
probabilistic maps of cytoarchitectonically defined regions with functional imaging data, hold prom-ise for further elucidating brain region specialization. For example, Horwitz et al.
(8)
. found that BA45, not BA 44, is activated by oral or signed language production, implicating BA 45 as the part of Broca’s area that is fundamental to the modality-independent aspects of language generation.
Overview of Clinical Assessment Procedures
In order to clinically assess or scientifically examine aspects of speech and language, the clinicianor researcher employs a battery of instrumental and behavioral tests or experimental tasks that tapboth isolated and integrated components of speech and language. This approach is intended to deter-mine relative strengths and weaknesses necessary for differential diagnosis, and to assess the conse-quential effects of specific disturbances on functional communication in daily life contexts. Therefore,a clinical battery is best composed of diagnostic instruments that measure the fine-grained features of speech or language, and functional measures of communication that address speech or language as anintegrative construct in the context of daily life activities. In line with contemporary models of healthand disability that encompass both biophysical and psychosocial aspects of medical intervention(e.g., World Health Organization International Classification of Functioning, Disability and Health;
see
ref.
9
). Clinicians and researchers are also extending clinical measurement to aspects of generalwellness or quality of life in order to determine the effect of an impairment or activity limitation onsocial participation, autonomy, and self-worth.Specific to language, behavioral measurement (online automated tasks that capture aspects of processing or production as they occur in real time; standardized paper-and-pencil tests) typicallyincludes assessment of aspects of spontaneous speech, comprehension of oral and written language,repetition of words and phrases of increasing length, naming of objects and actions, and writing.Assessment of these parameters allows differential diagnosis of aphasia, either as a classical syn-drome or as a constellation of deficits that point to specific neuropathological processes.Assessment of speech typically is conducted via a combination of perceptual, acoustic, and physi-ologic methods
(1)
. Perceptual methods are based primarily on auditory-perceptual attributes that allowclinical differential diagnosis. Acoustic methods contribute to acoustic quantification and description of clinically perceived impaired speech and confirm perceptual judgments of, for example, slow speechrate, breathy or tremulous voice quality, vocal pitch and loudness variations, hypernasal resonance,and imprecise articulation. Their ability to make visible and quantify the speech signal can be used asbaseline data or as an index of stability or change. Physiologic methods focus on characterizing themovements of speech structures and respiratory function, muscle contractions that generate move-ment, temporal parameters and relationships among central and peripheral neural activity and biome-chanical activity, and temporal relationships among active CNS (central nervous system) structuresduring the planning and execution of speech (for comprehensive reviews of assessment methods,
see
ref.
1
for motor speech disorders; refs.
10
and
11
for aphasia and related neurologic language disor-ders; refs.
4
and
12
for right-hemisphere communication disorders; ref.
13
for functional communica-tion and psychosocial consequences of neurologic communication disorders).Our purposes here are to characterize the atypical Parkinsonian disorders of corticobasal degen-eration (CBD), progressive supranuclear palsy (PSP), multiple systems atrophy (MSA), and demen-tia with Lewy Body disease (DLB) from the perspectives of speech and language. For each diagnosticgroup, we: (a) describe the neuroanatomical correlates of speech and language disorders, (b) identifytheir clinically common and differentiating features on the bases of clinical assessment and clinicalresearch findings, and (c) offer some clinical management suggestions. We end by suggesting somedirections for future research. Table 1 abstracts the common and distinctive features of speech andlanguage disturbances across diagnostic groups.

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