Acquired Neurological Speech/Language Disorders In Childhood

Bruce E Murdoch

• Publisher: CRC Press
• Year: 2017
• ISBN:
  9781135479022
• Edition: 1
• Topic: Medicine
• Subtopic: Medical Theory, Practice & Reference

The long-held belief that acquired aphasia in children is primarily of the non-fluent type has been challenged in recent years. This book discusses language problems arising from cerebro-vascular accidents occurring in childhood, and from other

Chapter 1: Acquired Childhood Aphasia: Neuropathology, Linguistic Characteristics and Prognosis

Anne E.Ozanne and Bruce E.Murdoch

Definition of Acquired Childhood Aphasia

Language disorders occurring in childhood are usually divided into developmental and acquired disorders. In general, the term ‘developmental language disorder’ is used to describe those language problems which are apparent from the initial stages of language development. In most cases, developmental language disorders in children have an idiopathic origin, although these disorders may also occur secondary to other conditions such as peripheral hearing loss, mental retardation, cerebral palsy, child autism, or environmental deprivation.

In contrast, acquired aphasia in childhood results from brain damage. A variety of definitions of acquired childhood aphasia have appeared in the literature. Some examples of these definitions are shown in Table 1.1. Despite the minor variations evident in these definitions, two major features of acquired childhood aphasia appear to be consistently identified. First, the onset of acquired childhood aphasia is precipitated by some type of cerebral insult. The cerebral insult, in turn, can result from a variety of causes, including head trauma, cerebrovascular accidents, brain tumours, infections and seizure disorders (Miller et al., 1984). Second, most authors agree that acquired aphasia in childhood follows a period of normal language acquisition during which the child commences learning language normally, though some studies of acquired childhood aphasia have included subjects whose cerebral insult occurred before the development of language. In the present book, the demonstrable presence of a cerebral insult is taken as the major feature and discussion is included of subjects where the lesion occurred both before and after language development.

Table 1.1 Definitions of acquired childhood aphasia

Historical Perspective

Although the first descriptions of acquired aphasia in children were reported in the late 1800s (Bernhardt, 1885; Cotard, 1868, cited in Guttmann, 1942; Freud, 1897), nearly 100 years later, little conclusive information is available to help clinicians in the management of the cases they may find in their caseloads. Little also is understood about the linguistic pathology from which to derive the most effective and efficient treatment strategies.

From the limited number of studies reported in the literature, a traditional description of childhood acquired aphasia has emerged. In the past it has often been stated that acquired childhood aphasia is rare, however, when it does occur it is characterized by an initial period of mutism followed by a non-fluent, motor type of language impairment with no accompanying comprehension deficit or other features of a fluent type of aphasia (e.g. jargon, logorrhea and paraphasia). In addition, acquired childhood aphasia was usually regarded as being transitory in nature, affected individuals making a good recovery. The stated rarity (Cotard, 1868; Denckla, 1979) was in part contributed to by the observation that children who do exhibit aphasia also showed rapid recovery of language skills. Bernhardt (1885) stated that childhood aphasia was not rare but because the aphasia was of a transient nature and rarely permanent it was often not reported. In support of Bernhardt (1885), Nadoreczny (1926, cited in Guttmann, 1942) also noted that most cases of acquired childhood aphasia recover within a few weeks.

The recovery of language in acquired childhood aphasia varies amongst children. Some children go through the normal language development process as they regain their language skills while others skip developmental stages during the recovery process (Basser, 1962; Byers and McLean, 1962). One 8-year-old girl with left hemiplegia, described by Byers and McLean (1962), initially communicated by gestures and within 3 weeks of becoming aphasic was responding verbally to simple sums. Soon after that, with her ability to write letters using her right hand, came the use of automatic speech including counting and reciting poetry. No description, however, was given of her functional language at this time. Within 3 months this child had returned to school, her only reported aphasic symptoms being a word-finding deficit.

Another characteristic of the traditional description of childhood acquired aphasia is a period of mutism immediately post-onset. This has been described as the chief characteristic of childhood aphasia by Branco-Lefèvre (1950) and Alajouanine and Lhermitte (1965). Guttmann (1942) noted an absence of spontaneous speech in 14 of his 16 cases of acquired childhood aphasia, mostly in children less than 10 years of age. Nine of the 15 right hemiplegic subjects (60 per cent) reported by Hécaen (1976) had a period of mutism lasting from 5 days to 3 months. Hécaen (1983) observed that mutism appeared mostly in children with anterior lesions (63 per cent) while only 10 per cent of children with temporal lesions showed mutism.

Some authors have suggested a psychological basis for the initial mutism shown by children with acquired aphasia (Alajouanine and Lhermitte, 1965; Byers and McLean, 1962). Reasons suggested for a psychological basis to the period of mutism include a presence of aspontaneity in written and gestural expression as well as in spoken language. In addition, when speech does return, increased incentives and encouragements are required to get the children to use words they are capable of producing. Furthermore, it has been noted that in general children tend to become silent and isolated at times of conflict or difficulties.

When speech and language do return, the traditional description of the aphasia is of a non-fluent, motor-type (Bernhardt, 1885; Carrow-Woolfolk and Lynch, 1982; Guttmann, 1942). Other features of acquired childhood aphasia reported in the literature include telegraphic speech (Guttmann, 1942) simplified syntax (Alajouanine and Lhermitte, 1965) and hesitation and dysarthria (Byers and McLean, 1962; Guttmann, 1942). Many investigators have noted that paraphasias, logorrhea and jargon are rare, or in the majority of cases, absent (Alajouanine and Lhermitte, 1965; Collignon et al., 1968; Hécaen, 1976). Some authors (Alajouanine and Lhermitte, 1965; Guttmann, 1942; Poetzl, 1926), however, noted that the traditional description of acquired aphasia was most commonly seen in children less than 10 years of age while older children tended to present more like adult aphasics. Hécaen (1976) was unable to confirm this relationship between aphasic type and age, but did, however, postulate a relationship between lesion site and aphasic type. He found that children with acquired aphasia resulting from anterior lesions presented with an initial mutism while thosewith temporal lobe lesions showed comprehension deficits in the acute stages that resolved within 1 year. Alajouanine and Lhermitte (1965) and Hécaen (1983) also noted transitory comprehension deficits in one-third of their subjects.

Another characteristic of acquired childhood aphasia noted to be present, particularly in the acute stages post-onset, is a naming deficit or poverty of lexical stock (Alajouanine and Lhermitte, 1965; Collignon et al., 1968). Hécaen (1976) noted that naming disorders occurred in 7 of 15 of his left hemisphere-lesioned subjects. In three of these cases this deficit persisted long-term and was often noted in school reports.

Satz and Bullard-Bates (1981:405) carried out a comprehensive review of the literature to investigate the three aspects of the traditional description of acquired aphasia in children: its rarity, its clinical description and its rapid recovery. Overall, the findings of their review, which are described below, demonstrated a need to reevaluate the traditional description of acquired childhood aphasia. They took all subjects in published studies who met the following criteria:

1. Some speech reported before the lesion onset
2. Hand preference reported before lesion onset
3. Patient under 16 years of age before lesion onset
4. Evidence that lesion was unilateral only
5. Comparison of presence vs absence of aphasia following unilateral injury

Of 21 studies and 929 reported cases only 68 cases met the above criteria. In many studies handedness data was not provided. In other studies only cases with aphasia were included and therefore could not form part of a review on the incidence of acquired childhood aphasia.

In conclusion, Satz and Bullard-Bates (1981) stated that if the lesion is unilateral and encroaches on the speech areas then childhood aphasias are not rare. They noted, however, a lower prevalence of unilateral vascular disease in children as compared with adults. Furthermore, they concluded that if the left hemisphere is damaged the risk of language impairment is approximately the same in right-handed children as in adults. Regardless of age (at least after infancy), the risk of acquired aphasia is substantially greater following left-sided rather than right-sided lesions. Finally, it was concluded that, although rare, crossed aphasias do exist in left-handed children regardless of age. In particular crossed aphasias are especially rare after 3–5 years of age in right-handed children.

When reviewing the clinical type of aphasia Satz and Bullard-Bates (1981) concluded that the clinical pattern is predominantly non-fluent with rare or absent paraphasias and logorrhea, but disorders of auditory comprehension, naming and writing may coexist. They stipulated that at that time it was unclear how those clinical patterns related to age and maturational effects or to the lesion, its size, cause, type, site or the time after the lesion.

The third aspect of acquired aphasia in children which Satz and Bullard-Bates(1981) reviewed was the apparent rapid recovery of the aphasia. They concluded that: in the majority of cases spontaneous recovery is dramatic (i.e. approximately 75 per cent of cases), 25–50 per cent of cases still present with aphasia within 1 year post-onset, the recovery from aphasia is unrelated to the presence/severity of hemiparesis, and that despite recovery from aphasia, intellectual, cognitive or school achievement may still be impaired. Satz and Bullard-Bates (1981) could not identify the factors affecting recovery but suggested that these may include cause, aphasia type, lesion size or age at the time of the lesion.

Satz and Bullard-Bates (1981) did not believe that their findings supported the equipotentiality hypothesis put forward by Basser (1962) and Lenneberg (1967). These authors did state, however, that their findings were in line with studies which have noted a structural asymmetry of the brain at birth (Chi et al., 1977; Galaburda et al., 1978) as well as those which have noted functional asymmetry in non-aphasics (Hiscock and Kinsbourne, 1978; Molfese et al., 1975). Satz and Bullard-Bates (1981) noted that the results of their study, however, do not explain the dramatic recovery rate seen in children with acquired aphasia.

Since the early 1980s, therefore, it has been recognized that childhood acquired aphasia is not as rare as previously thought and despite the rapid recovery seen in some cases, 25–50 per cent of children who develop acquired aphasia still have aphasic symptoms 1 year post-onset. It is these children to whom we will now turn our attention. Several questions still need to be asked. What are the precise linguistic deficits with which children with acquired aphasia present? Do these linguistic deficits relate to specific causes? Do these deficits differ from linguistic impairments seen in children with developmental language impairment? What assessment and treatment strategies are available to clinicians working with these cases? These issues are addressed in the remainder of this chapter and in Chapter 2.

Neuropathological Substrate of Acquired Childhood Aphasia

Although acquired childhood aphasia can be caused by a similar range of disorders of the nervous system as adult aphasia, the relative importance of each of the different causes to the occurrence of language disturbances in children differs from the situation seen in adults. For instance, although in peacetime cerebrovascular accidents are the most common cause of aphasia in adults, the most common cause of acquired childhood aphasia is traumatic head injury.

Head Injury

In the majority of cases of acquired childhood aphasia reported in the literature thecause is head injury. Head injuries can be divided into two major types: closed head injuries and open head injuries. In a closed head injury the covering of the brain remains intact even though the skull may be fractured. An open head injury differs from a closed head injury in that the brain or meninges are exposed. By far the majority of traumatic head injuries in both children and adults in civilian life are closed head injuries.

Damage to the brain following traumatic head injury may be either focal, multi-focal or diffuse in nature. In general, closed head injuries tend to produce more diffuse pathology while open head injuries are associated with more focal pathology. Brain contusions (bruises), lacerations and haemorrhages can be caused at the time of head injury from either the direct trauma at the site of impact on the skull, acceleration of the brain against the bony shelves of the skull (e.g. the sphenoidal ridge) or from contra-coup trauma that occurs when the brain strikes the skull on the side opposite the point of insult. Brain and Walton (1969) identified three different destructive forces which are applied to the brain at the moment of impact: compression or impression which forces the brain tissue together, tension which pulls the brain apart, and shearing produced by rotational acceleration and which develops primarily at those points where the brain impinges upon bony or ligamentous ridges within the cranial vault. According to Adams et al. (1977), the primary mechanism producing brain injury following closed head injury is diffuse axonal damage in the white matter occurring at the time of impact and caused by a shearing mechanism arising from rotational acceleration.

It has often been reported that children show a striking rate of recovery following closed head injury. Some authors have suggested that one of the reasons for the good prognosis for recovery in childhood is that the degree of brain damage following head injury is less in children than in adults, due in part to the different nature of their head injuries as well as to differences in the basic mechanisms of brain damage following head injury. Most childhood head injuries result from falls or low speed accidents. Consequently many paediatric head injuries are associated with a lesser degree of rotational acceleration and therefore, presumably, with a lesser amount of brain damage (Levin et al., 1982). Jamison and Kaye (1974) noted that persistent neurological deficits were only present in children injured in road traffic accidents which are, by their nature, likely to yield greater diffuse brain injury. Likewise, a study conducted by Moyes (1980) showed road traffic accidents to be the most common cause of long-term morbidity following childhood head injury. In addition, Strich (1969) suggested that the shearing strains produced by rotational acceleration in head trauma are less pronounced in smaller brains.

Although the rate of spontaneous recovery in children following closed head injury is often described as excellent, persistent long-term language disorders have been reported (Gaidolfi and Vignolo, 1980; Jordan et al., 1988; Satz and Bullard-Bates, 1981) and even when specific linguistic symptoms resolve cognitive and academic difficultiesoften remain. The speech/language disorders associated with childhood head injuries together with the mechanisms of head injury are discussed in more detail in Chapter 3.

Cerebrovascular Disorders

Several investigators have documented the occurrence of acquired aphasia with vascular disorders in children (Aram et al., 1983, 1986; Dennis, 1980). Cerebrovascular accidents or strokes are spontaneous interruptions to the blood supply to the brain, arising from either occlusion of the cerebral blood vessels (ischaemic stroke) or in some cases from rupture of one of the cerebral blood vessels (haemorrhagic stroke). Although cerebrovascular accidents are much less common in children than in adults, they occur more frequently than is commonly thought and are a significant cause of morbidity and mortality in the childhood population. Banker (1961) reported that of 555 childhood autopsy cases studied by him, death was due to a cerebrovascular accident in 48 (8.6 per cent).

Virtually all the diseases of blood vessels which affect adults may at some time also occur in children (Bickerstaff, 1972; Salam-Adams and Adams, 1988). Despite this, the causes of vascular diseases of the brain in children differ from those in adults. For instance, degenerative disorders such as atherosclerosis affect primarily the middle-aged and elderly and are rare in childhood (Moosy, 1959). Some vascular diseases of the brain, such as embolism arising from subacute or acute bacterial endocardial valvular disease, occur at all ages while others, such as vascular disorders associated with congenital heart disease, are peculiar to childhood.

Acute hemiplegia of childhood is a term used by many paediatricians and neurologists to describe the sudden onset of hemiplegia in children. A wide variety of vascular diseases of the brain, including both occlusive and haemorrhagic disorders, have been described under this heading.

Idiopathic childhood hemiplegia

The most commonly reported and dramatic syndrome resulting from an ischaemic stroke in childhood is idiopathic childhood hemiplegia. This syndrome involves the sudden onset of hemiplegia as a result of a unilateral brain infarct of unknown origin and can affect children from a few months of age up to 12 years of age (Bickerstaff, 1972). According to Bickerstaff (1972), females are affected more than males in a ratio of about 3:2.

The cause of idiopathic childhood hemiplegia has been argued for many years and a variety of possible causes proposed including: polioencephalitis (Strumpell, 1884), encephalitis (Adams et al., 1949; Bernheim, 1956; Brandt, 1962), venous thrombosis(Bernheim, 1956; Branch, 1962; Norman, 1962), demyelination (Wyllie, 1948), epilepsy (Norman, 1962), and occlusion of the internal carotid artery (Bickerstaff, 1964; Duffey et al., 1957; Goldstein and Burgess, 1958). Although there appears to be some agreement that arterial occlusion is the most common cause of idiopathic childhood hemiplegia the reason for the occlusion is less certain. For reasons indicated above, atheroma cannot be implicated in childhood. Studies using carotid angiograms have demonstrated the presence of thrombosis of either the common or internal carotid arteries in some cases of idiopathic childhood hemiplegia (Salam-Adams and Adams, 1988). Bickerstaff (1964) suggested that roughening of the wall of the internal carotid artery as a result of arteritis secondary to throat, tonsillar or cervical gland infection might be the causal factor in some instances. Further, in some reported cases neither angiography nor post-mortem examination was able to demonstrate the presence of vascular lesions, suggesting that in these cases an embolus may have temporarily blocked a cerebral artery and then later broken up before the angiogram was taken or the postmortem performed (Salam-Adams and Adams, 1988).

Other vascular occlusive disorders in childhood

A number of other vascular occlusive disorders peculiar to childhood can also cause ischaemic strokes in children. These disorders include: vascular disease associated with congenital heart disease, arteritis (inflammation of an artery) of various types, sickle cell anaemia, vascular occlusion associated with irradiation of the base of the brain, moyamoya, and strokes associated with homocystinuria and Fabry’s angiokeratosis.

Ischaemic strokes associated with congenital heart disease occur most frequently in the first 2 years of life, corresponding to the stage when congenital heart disease has its greatest frequency (6 per 1000 live births) (Salam-Adams and Adams, 1988). Banker (1961) reported that of the childhood cerebrovascular accident cases examined by him, 28 per cent were associated with congenital heart disease, making it the single most common cause o...

Table of contents

• Cover Page
• Brain Damage, Behaviour and Cognition: Developments in Clinical Neuropsychology
• Title Page
• Copyright Page
• Series Preface
• Contributors
• Chapter 1: Acquired Childhood Aphasia: Neuropathology, Linguistic Characteristics and Prognosis
• Chapter 2: Acquired Childhood Aphasia: Assessment and Treatment
• Chapter 3: Speech and Language Disorders Following Childhood Closed Head Injury
• Chapter 4: Communicative Disorders in Childhood Infectious Diseases
• Chapter 5: Linguistic Status Following Acute Cerebral Anoxia in Children
• Chapter 6: Linguistic Problems Associated with Childhood Metabolic Disorders
• Chapter 7: Communicative Impairments in Neural Tube Disorders
• Chapter 8: Speech and Language Disorders in Childhood Brain Tumours
• Chapter 9: Effect of CNS Prophylaxis on Speech and Language Function in Children
• Chapter 10: Acquired Childhood Speech Disorders: Dysarthria and Dyspraxia