Handedness and Language

The human brain is highly specialized regarding language and cognitive functions. In addition to the complexities of site, magnitude, and type of neurologic insult, the relationship between handedness and the side of the brain that is injured determines the characteristics of the communication disorder. For most right-handed and left-handed individuals, the language association areas are in the left hemisphere. In a small percentage of left-handed individuals, the language centers might be in the right hemisphere or bilaterally represented. The left hemisphere is specialized for speech and language functions in the vast majority of people (approximately 96%), regardless of handedness. The right hemisphere is specialized for constructional, visual spatial, and attentional functions.

Types of Communication Disorders Caused by Nervous System Pathology

Cognitive-communicative disorders as a result of brain injury, disease, or pathology might include aphasia and related neurobehavioral disorders; communicative-cognitive disorders secondary to right hemisphere stroke, traumatic brain injury, and dementia; and the motor speech disorders including the dysarthrias and apraxia of speech. Table 3-1 presents the major neurogenic communication disorders, neurologic diagnosis or disease, and salient speech-language and cognitive characteristics.

Table 3-1 Major Neurogenic Communication Disorders, Neurologic Diagnosis, and Language and Cognitive Characteristics

Brain Plasticity and Neurorehabilitation

Research in the basic neurosciences over the past 30 years has provided strong evidence regarding the dynamic aspects of the brain to change. While most of the research to date has been in animal models, human translational studies have begun to emerge. The term brain plasticity refers to the capacity and resiliency of the brain to undergo structural and functional changes.¹⁹ The ability of the brain to adapt and restructure is particularly evident after injury and has important implications for rehabilitation and recovery of function. Ideally, the rehabilitation team will work collaboratively to determine the best intervention at the optimal time to take advantage of the brain’s malleability. For an individual patient this can include the selection of the type and intensity of behavioral treatment (the external stimulation). At times this might be paired with administration of adjunctive brain stimulation such as a neuropharmacologic agent, electrical cortical stimulation, and/or transcortical magnetic stimulation.

In animals, the type of the external stimulation has been shown to be very important. A large body of research demonstrates that the type of input affects brain reorganization.^36,^51,⁵⁷ This has been termed use-dependent,⁵¹ or more recently learning-dependent, activity.⁵⁷ This refers to the specificity of the experience after brain injury being critical in determining what brain and behavioral changes will occur. Nudo et al.⁵⁷ found that motor maps are altered by motor skill acquisition versus repetitive use alone, and brain plasticity coincided with the reacquisition of motor skills in lesioned animals and the acquisition of new motor skills in intact animals. These data imply that at critical recovery periods in humans, restorative treatments should target the most complex behaviors that a patient can produce. It could be that focusing only on compensatory activities rather than restorative functions has costs in terms of ultimate recovery of function.

Neuromodulation can be done with certain pharmacologic agents. When paired with behavioral treatment, some agents, particularly those affecting the catecholamine system (dextroamphetamine, methylphenidate, levodopa), have been found to enhance outcome after both focal ^6,^22,^35,⁶⁹ and diffuse^46,⁷¹ cortical experimental injury. It should be noted that this does not extend to all behaviors.⁶⁶ Explorations of pharmacologic modulation have been done in humans to facilitate recovery from poststroke deficits such as aphasia and hemiplegia^30,^65,^77,⁷⁸ and to enhance recovery of cognitive deficits subsequent to traumatic brain injury.^38,⁸¹ Physiologic events after brain injury can complicate the timing for administration of various agents. Drugs that are effective in the very acute or subacute period after injury may be ineffective or even detrimental at later recovery periods.²⁸ Our experiences and that of others are encouraging regarding the use of certain agents to accelerate recovery; however, not all clinical studies report positive findings.^26,⁵⁹

Aphasia and Related Neurobehavioral Disorders

Aphasia

Aphasia in adults occurs as a result of acquired brain damage to the language-dominant hemisphere, usually the left, and shares common neurophysiologic features with other stroke consequences. Chapey and Hallowell ¹⁶ provide a straightforward definition: “Aphasia is an acquired communication disorder caused by brain damage, characterized by an impairment of language modalities: speaking, listening, reading, and writing; it is not the result of a sensory deficit, a general intellectual deficit, or a psychiatric disorder.” The language impairments can range from mild with some word-finding problems (anomic aphasia) to severe with very little ability to speak, understand, read, or write (global aphasia). In the United States today, more than 1 million people are living with aphasia,⁴⁵ and 80,000 new patients with aphasia will be treated each year.⁵⁶

Since the time of Broca,¹¹ aphasia has probably been the most studied neurogenic communication disorder. Because of the nature of the injury and the critical left hemisphere language association areas (Figure 3-1), aphasia has been classified in terms of the characteristics of the linguistic deficits and the location of the lesion.

FIGURE 3-1 Language-related areas in the brain. Simplified lateral view of the left hemisphere showing primary language areas of the brain. The central sulcus provides an arbitrary division between anterior and posterior brain regions. Broca’s area is adjacent to the precentral gyrus (motor strip) that controls the movements of facial expression, articulation, and phonation. Wernicke’s area is in the posterior part of the superior temporal gyrus adjacent to the primary auditory cortex (superior temporal gyrus). The arcuate fasciculus is a pathway that connects Broca’s and Wernicke’s areas. Many of the cortical language association areas lie close to the Sylvian fissure and participate in a complex network of areas that contribute to language processing.

The traditional aphasia classification system ^9,⁴³ is based on clusters of language symptoms and contrasts the characteristics of verbal output, auditory comprehension, and repetition ability (Table 3-2). This framework forms the basis for two of the most frequently employed formal assessments used by speech-language pathologists: the Boston Diagnostic Aphasia Exam²⁹ and the Western Aphasia Battery.⁴²

Table 3-2 The Aphasias: Comparisons of Verbal Output, Repetition, Auditory Comprehension, Associated Signs, and Region Affected

Modern imaging studies and research in psycholinguistics have shown limitations with the traditional classification scheme. In particular, the roles of Wernicke’s and Broca’s area are not as clear as they first appeared.¹⁸ A variety of other left hemisphere regions, both cortical and subcortical, have been found to be involved in language processing. While it is now recognized that the processing of language requires a large network of interacting brain areas, it is also the case that certain linguistic behaviors group together and are often predictable depending on the anterior or posterior location of the lesion. Anterior aphasias include Broca’s and transcortical motor aphasia. Posterior aphasias include Wernicke’s, conduction, and transcortical sensory aphasias. Global and anomic aphasias are not as localized. Aphasias limited to strictly subcortical pathology have also been described.⁵⁵ Whether speech output is nonfluent versus fluent, the degree of auditory comprehension deficit, and the ability to repeat can be checked by the physiatrist at the bedside (Figure 3-2) to get an estimate of the type of aphasia.

FIGURE 3-2 Flow chart to assess aphasia types. This flow chart characterizes fluency of speech output, auditory comprehension, and repetition ability for brief bedside screening of patients with aphasia. The plus symbol (+) indicates that the specific function is intact or at least fairly good. The minus symbol (–) indicates the specific function is relatively impaired. Note that a plus symbol does not necessarily indicate that the function is normal, and a minus symbol does not necessarily indicate that a function is completely defective.

(From Canter GJ: Syndromes of aphasia in relation to cerebral connectionism, South Bend, IN, 1979, Short course presented to the Indiana Speech and Hearing Association, with permission.)

Primary Progressive Aphasia

A specific primary progressive aphasia (PPA) is now recognized.^21,^44,⁵⁰ This disorder blurs the lines between focal and diffuse disease. In contrast to aphasia caused by an acute event such as a stroke, PPA has an insidious onset. Although the family or patient might claim there was a specific event, careful history will reveal a progressive onset with the patient being aware of the language deficits before family members. The most frequent presenting complaint is word-finding difficulty. During the first 2 years, the patient with PPA often has symptoms that appear to be localized, similar to those of an aphasia subsequent to a stroke. After the early course of the disease, PPA usually progresses to dementia with the characteristic cognitive disorders of other dementias. A diagnosis of PPA requires a minimum 2-year history of language decline, relative sparing of other mental functions, independence in activities of daily living, a neurologic workup excluding other causes of aphasia, and a neuropsychological workup that supports the complaints.⁵⁰

Management of Aphasia

All aphasias evolve over time, allowing probable prognoses to be made based on careful baseline assessment (3 to 4 weeks after onset). For example, the condition of a patient with severe nonfluent (global) aphasia at baseline with adequate speech-language treatment is likely to evolve to a chronic Broca-type aphasia. The condition of a patient who has severe fluent (Wernicke’s) aphasia at baseline with adequate treatment has a good probability of evolving to a conduction or anomic aphasia.

Treatment by the speech-language pathologist is based on a careful assessment of all communication modalities: speaking, listening, reading, and writing. The patient’s deficit areas and relative strengths and weaknesses are determined. Assessments of both impairment and activity/participation levels are ideally done as defined by the World Health Organization.⁸³ The focus of speech-language treatment in the acute and subacute recovery period is restoration of speech and language abilities, and treatment is individualized. Education and counseling with the family are also important.⁵

Numerous therapy approaches specific to the complex speech-language behaviors exhibited by patients with aphasia are available and have been demonstrated to be effective.²³ Metaanalyses^63,⁶⁴ of the outcomes of therapy for aphasia have shown that language therapy for aphasia has a significant positive impact on recovery in the acute and chronic phases, and the amount of speech-language treatment is a critical factor for establishing effective and long-lasting improvements.^7,^10,^17,⁵² Intensive aphasia therapy (on average 98 hours) appeared to be a requirement for positive outcomes,^10,⁷² and shorter amounts of treatment (on average 44 hours or less) are not effective.^7,^10,⁷³ Evidence-based practice is not the least expensive use of rehabilitation dollars but is the better investment of resources if significant improvement is expected.

Related Neurobehavioral Disorders

Often co-occurring with aphasia are a number of related neurobehavioral disorders, and it is important to differentiate them from the communication disorder. Only apraxia and agnosia are reviewed here. The physiatrist should consult a more detailed mental status examination such as Strub and Black ⁷⁰ and/or a neuropsychologist for a differential diagnosis of these higher-order motor and sensory processing disorders.

Apraxia

Apraxia is an acquired disorder of learned skilled, sequential motor movements that cannot be accounted for by elementary disturbances of strength, coordination, sensation, or lack of comprehension or attention.²⁵ Apraxia is not a low-level motor disturbance but a deficit in motor planning that involves the integrative steps that precede skilled or learned movements.⁷⁰ Apraxias occur more often as a result of left hemisphere lesions. Because adequate verbal comprehension is a prerequisite to valid praxis (motor integration needed for execution of complex learned movements) testing, it is important for the speech-language pathologist to be consulted regarding auditory comprehension abilities when a motor planning problem is suspected. It is also important that patients with a motor planning deficit not receive a diagnosis of comprehension difficulties, because the motor planning disorder prevents their making an adequate response to comprehension testing.

Ideamotor apraxia is the most common type of apraxia. Patients with this form of apraxia fail to perform previously learned motor acts accurately. Impairments can be seen in buccofacial, limb, or whole-body musculature. Ideational apraxia is a disturbance of complex motor planning of a higher order than is seen in ideamotor apraxia. It is a breakdown in the performance of a task that involves a series of related steps.⁷⁰ Brief screening by commands can help the physiatrist to differentiate a motor planning disorder from a true language disorder (Table 3-4).

Table 3-4 Evaluation of Ideamotor Apraxia

Commands	Errors
Buccofacial
“Show me how to—”:
1. “Blow out a match.”	Difficulty giving short, controlled exhalation; saying “blow”; inhaling; difficulty maintaining appropriate mouth posture
2. “Protrude your tongue.”	Inability to stick out tongue; tongue moving in mouth but tending to push against front teeth and not protruding
3. “Drink through a straw.”	Inability to sustain a pucker; blowing instead of drawing through the straw; random mouthing movements
Limb
“Show me how to—”:
1. “Salute.”	Hand over head; hand waving; improper position of hand
2. “Use a toothbrush.”	Failure to show any proper grip; failure to open mouth; grossly missing the mouth; using finger to pick teeth; not allowing adequate distance for shaft of toothbrush; using the finger as a toothbrush
3. “Flip a coin.”	Movements miming tossing the coin into the air with an open hand; supinating or pronating the hand as though turning a doorknob; flexing the arm without flipping thumb against finger
4. “Hammer a nail.”	Moving hand back and forth horizontally; pounding with fist
5. “Comb your hair.”	Using fingers as teeth of comb; smoothing the hair; making inexact hand movements
6. “Snap your fingers.”	Extension of fingers with patting movements; tapping of finger on thumb; sliding finger off thumb with insufficient force
7. “Kick a ball.”	Stamping foot; pushing foot along floor; moving foot laterally
8. “Crush out a cigarette.”	Stamping foot; kicking foot on floor
Whole body
“Show me how to—”:
1. “Stand like a boxer.”	Awkward arm position; hands at side
2. “Swing a baseball bat.”	Difficulty in placing both hands together; chopping movements
3. “Bow” (for a man) or “Curtsy” (for a woman)	Any inappropriate truncal movement