Disorders of communication and swallowing occur across the lifespan and may result from disruption of neurologic function and anatomical abnormalities of the head, neck, and respiratory system. Effective assessment and treatment involves collaboration across medical and rehabilitation disciplines. A discussion of normal function, incidence and prevalence, etiology, categories of impairment and treatment options is provided for each group of disorders.

Introduction

Speech refers to motor acts that result in the production of sounds through the coordination of respiration, phonation, resonance, articulation, and prosody. Language is the symbolic organization of sounds into purposeful words and sentences to represent thought and includes linguistic elements such as morphology and syntax and paralinguistic elements of prosody.¹ Cognition refers to mental processes and systems, such as attention, perception, memory, organization, and executive function.²

Successful communication requires intact neural pathways and peripheral structures to plan, modify, and process speech, language, and cognition. Neural activation patterns of communication and cognition are widespread and include structures and circuits of the cerebrum, the brainstem, the limbic system, and the cerebellum (Table 57–1).

For example, in spoken language, humans require the temporal lobe for comprehension, the frontal lobe for production, the occipital lobe to visualize gestures and facial expression, and the parietal lobe for sensorimotor integration.³ The cerebellum and basal ganglia refine and coordinate speech movements, and the brainstem relays and receives the neural signals to and from the anatomy of speech and hearing^4,5 (Table 57–2).

Disorders of speech, language, and cognition exist in isolation or in combination with one another and may be congenital or acquired. Speech disorders include dysarthria, apraxia of speech, voice disorders, and stuttering. Language disorders include impairments in auditory comprehension, reading comprehension, verbal expression, and written expression, as in child language disorders or aphasia. Cognitive communication disorders affect attention, memory, problem solving, reasoning, organizing, planning, and insight.

Epidemiology

According to the National Institute of Deafness and Communication Disorders, one in six Americans has a disorder of communication. Apraxia of speech (AOS) was found in approximately 8% of a cohort of patients with neurogenic motor speech disorders; AOS typically co-occurs with aphasia.^6–8 Childhood apraxia of speech (CAS) is estimated to occur in 1 to 2 per 1,000 members of the general population.^9,10 Stuttering is present in an estimated 1% to 2.4% of children and 1% of adults.^11–13 Voice disorders are reported by 7.5 million of Americans (National Institute on Deafness and Other Communication Disorders 2010a) and are more common in occupations that require frequent use of voice such as teachers.¹⁴

Language disorders of neurogenic origin occur in approximately 1 million individuals in the United States and are related to dementia in 2 million people.¹⁵ It has been reported that 8% of children in America present with developmental language disorders, and 10% have at least a moderate speech disorder.¹⁶ Disorders of cognitive communication occur in 1.4 million Americans annually following stroke; between 1 and 2 million trauma-related cases are seen in children.^17,18

Disorders

Dysarthria involves impairment of articulation, volume and pitch control, vocal quality (e.g., vocal hoarseness), resonance (e.g., hyper- or hyponasality), rate, or rhythm resulting from weakness, slowness, incoordination, and alteration in muscle tone.¹⁹ Dysarthria is classified by etiology, anticipated course, age at onset, and the speech process and/or functional component that is impaired.²⁰ A widely used classification system of dysarthria based on perceptual characteristics and types of etiologies was developed at the Mayo Clinic^21,22 (Table 57–3).

AOS is an articulatory programming disorder with impairment of the positioning and sequencing of speech musculature, absent weakness, slowness, or incoordination.^22,23 The hallmarks of AOS include effortful groping with attempted self-correction, persistent dysprosody (abnormal rhythm, stress, and/or intonation), articulatory inconsistency on repeated productions, and difficulty initiating utterances.²⁴ Stuttering is a disorder of fluency and typically manifests in repetition, prolongation, or blockage of speech sounds.¹² A person who stutters may also develop secondary behaviors in response to dysfluency, such as extraneous facial or head and neck movements.²⁵ A voice disorder is characterized by constrained vocal quality, loudness, pitch, or loss of voice along with maladaptive compensatory strategies. Perceptual voice deviations may also be present in dysarthria.

Aphasia is a language disorder characterized by impairments in auditory comprehension, verbal expression, reading comprehension, and/or written expression. The nature and extent of aphasia depend on the site and size of the lesion. The classic stroke-aphasia syndromes are defined by locus of damage and frequently co-occurring clusters of impairments in fluency, auditory comprehension, repetition, and naming²⁶ (Table 57–4).

The classification of aphasias is therefore based on a thorough evaluation that assesses the fluency, comprehensions, and repetition of language (Fig. 57–1).

Subtypes of aphasia are further characterized by fluency, word-finding ability, auditory comprehension, and speech fluency. These clinical assessments are also helpful in localizing the lesion of injury (Table 57–5).

The taxonomy of symptoms associated with each syndrome is thought to be related to the disruption of vascular supply to structures in the immediate locus of the infarct as well as hypoperfusion in the surrounding areas.²⁷ In fluent aphasia, prosody is preserved, whereas in nonfluent aphasia, speech output is effortful and limited.²⁸ Preserved repetition is a defining characteristic of the transcortical aphasias.^29,30 In addition to the classic aphasia syndromes, other diagnostic entities include the subcortical aphasias and primary progressive aphasia, a neurodegenerative language condition.^31–33

Pathophysiology

Speech disorders can be due to neurologic or structural etiologies. Dysarthria may be caused by disorders of or damage to the central or peripheral nervous system, the neuromuscular junction, or the muscular system.^21,22,34 AOS occurs most frequently after left hemisphere stroke,^35–37 although it may also result from progressive neurologic disease.^38–40 Childhood apraxia of speech (CAS) is present from birth and is thought to include a genetic component.^41,42 Developmental stuttering typically results from a combination of genetic and environmental factors.⁴³ In rare cases, acquired stuttering may be a symptom of brain injury, such as stroke or tumor.^44,45 Voice disorders may result from damage to the central or peripheral nervous system as well as congenital or acquired structural deficits.

The most common cause of aphasia is stroke in the lateral aspects of the left cerebral hemisphere, such as a middle cerebral artery infarct affecting Broca’s or Wernicke’s area.^46,47 Although rare, cases of aphasia subsequent to right hemisphere stroke have been reported.^48,49 Aphasia may also present when a stroke originating in a subcortical structure is related to hypoperfusion in the cerebral cortex⁵⁰ (Fig. 57–2).

Cognitive communicative disorders may result from discrete or diffuse brain damage. Progressive neurologic diseases such as dementia and primary progressive aphasia involve gradual deterioration of cognitive functions, whereas TBI is associated with variable severity and presentation.^51–53

Speech, language, and cognitive communication disorders may result from iatrogenic causes, as in the case of voice disorders subsequent to chemoradiation or surgery for head and neck cancer.⁵⁴ Cognitive communication impairments may also be related to substance abuse or exposure to environmental toxins.^55–57 On occasion, the etiology of speech, language, and cognitive communication impairments remains unknown.

Diagnosis

Clinical Examination

Speech-language pathologists administer screening and formal tests to elicit signs of communication impairments, such as imprecise speech articulation during sentence repetition, trouble following complex instructions, or difficulty naming pictured objects. Patient-reported symptoms inform the diagnosis; for example, an acute onset of speech or language deficits is characteristic of stroke, whereas a gradual onset suggests progressive neurologic disease (Table 57–6).

Differential Diagnosis

Disorders of speech and language are distinct diagnostic entities, although they do co-occur.²⁰ Dysarthria is a neurogenic speech disorder, whereas other speech disorders are due to structural etiologies, such as head and neck cancer or cleft palate. Voice disorders, including abnormalities of vocal quality due to vocal fold lesions or vocal fold motion impairments (e.g., hoarseness, roughness) are also separate diagnostic entities. However, perceptual voice deviations (e.g., vocal hoarseness, strain, low volume) may be considered within the realm of dysarthria and may even be pathognomonic of certain etiologies.

Furthermore, dysarthria is characterized by predictable speech sound errors resulting from weakness, slowness, incoordination, or abnormal muscle tone, in contrast to irregular articulatory breakdowns in apraxia of speech in the setting of intact muscle function^20,22,58,59 (Table 57–7). Finally, the content of a person’s message is generally preserved in the motor speech disorders of dysarthria and apraxia of speech but is impaired in cases of aphasia.

Diagnostic Studies

Speech-language pathologists perform speech/oral motor examinations to assess the respiratory mechanism, laryngeal mechanism, velum/pharynx, tongue, lips/face/teeth, and jaw. Formal tests, such as the Frenchay Dysarthria Test or the Apraxia Battery for Adults-2 are often used.^60,61 Speech intelligibility measures include the Assessment of Intelligibility of Dysarthric Speech.⁶² Perceptual scales, such as the Consensus Auditory-Perceptual Evaluation of Voice (CAPE-V), may be used to rate voice characteristics.⁶³ Objective acoustic measurements may be obtained using specialized equipment and software. Voice function is assessed by endoscopic viewing of the larynx and surrounding structures during speech and nonspeech tasks; the vibration of the vocal folds is assessed under rapid pulses of light, or stroboscopy.

Comprehensive language batteries, such as the Western Aphasia Battery and the Boston Diagnostic Aphasia Examination, provide a survey of all language modalities.^64,65 Supplementary tests, such as the Boston Naming Test-2 and the Reading Comprehension Battery for Aphasia, may be administered to probe specific deficit areas.^66,67 The Montreal Cognitive Assessment, a brief screening assessment, or the Ross Information Processing Assessment, a more extensive battery, can be administered to examine orientation, attention, short-term memory, and reasoning.^68,69 Specialized questionnaires, such as the Communication Confidence Rating Scale for Aphasia and the Quality of Communication Life Scale, probe the impact of communication disorders on quality of life.^70,71 The clinical assessment of communication and cognition is supplemented by reports from other disciplines, including neurology, radiology, neuropsychology, and otolaryngology, among others.

Treatment

Management goals are individualized and based on test performance and patient-family goals. Therapy can be delivered in individual and/or group sessions and focuses on restoration, compensation, or a combination of the two. Many standardized therapy protocols are available, such as Melodic Intonation Therapy for Broca’s aphasia and the Lee Silverman Voice Treatment for dysarthria in Parkinson’s disease.^72–74 In cases of severe impairment, oral/verbal communication is supplemented or replaced by augmentative and alternative communication (AAC) in the form of electronic devices or communication boards.⁷⁵

In conjunction with behavioral therapy, medical interventions have been shown to improve communication.⁷⁶ Protocols employing repetitive transcranial magnetic stimulation (rTMS) may improve naming in individuals with nonfluent aphasia by suppression of the overactive right hemisphere homologues.^77–79 Additionally, medical therapies to restore perfusion to ischemic tissue, such as carotid stenting, endarterectomy, endovascular therapy, thrombolysis, and temporarily induced blood pressure elevation, result in improvements on cognitive-language tasks.^80–82

Conclusion

Speech, language, and cognition are fundamental to the production and comprehension of communication. Any disruption in the neurophysiology and anatomy underlying these processes may result in a communication disorder. Several methods of treatment are available to target the specific deficits documented by clinical evaluation and patient report.

Introduction

Swallowing is a highly complex neuromuscular sequence of events that requires precise coordination of structures in the aerodigestive tract to safely propel a bolus from the oral cavity into the stomach while protecting the airway. This process can be divided into four stages, demarcated by the location of the bolus, and varies depending on bolus consistency⁸³ (Fig. 57–3).

During drinking, the bolus is held in the anterior oral cavity while the posterior tongue and soft palate prevent premature spillage into the pharynx (oral preparatory stage). Then, at the onset of the oral propulsive stage, the anterior tongue contacts the hard palate and moves posteriorly, propelling the bolus past the fauces and into the oropharynx.

In the case of a solid bolus, there are two distinct oral stages. During stage 1 transport, coordinated motions of the tongue and cheek move the bolus to the lower teeth. The bolus is then broken down by saliva and mastication in preparation for the pharyngeal stage. Stage 2 transport is initiated by the lingual transfer of the prepared bolus to the oropharynx by the same process as delineated in the oral propulsive state for liquids (Fig. 57–4).

The pharyngeal stage involves four valves that direct the bolus through the pharynx and prevent it from entering the airway.⁸⁴ The first valve, the velopharynx, is composed of the soft palate and pharyngeal walls; it seals the nasopharynx and enables generation of adequate pressures to propel the bolus. The second valve, the larynx, has three levels of protection that prevent the bolus from entering the airway: the closure of the true vocal folds, the approximation of the false vocal folds, and epiglottic inversion. The third valve, the hypopharynx, generates the pressure that drives the bolus through the pharynx. The fourth and final valve is the upper esophageal sphincter, which relaxes during the swallow, allowing the passage of the bolus into the esophagus. During the esophageal stage, peristalsis and gravity move the bolus through the lower esophageal sphincter into the stomach (Table 57–8).