Journal of Consulting and Clinical Psychology Copyright 1981 by the American Psychological Association, Inc.

1981, Vol. 49, No. 6, 791-806 0022-006X/81 /4906-0791 $00.75

Effects of Cerebral Dysfunction on

Neurolinguistic Performance in Children
Francis J. Pirozzolo, Debra J. Campanella, Kathy Christensen,
and Kathryn Lawson-Kerr
Minneapolis Veterans Administration Medical Center

This article reviews in broad strokes some of the basic causes of cerebral dys-
function in children. Structural disorders, postnatal trauma, anoxia, ischemia,
infections, congenital arteriovenous malformations, and toxic and metabolic dis-
orders are discussed. The relationship of plasticity of the brain to recovery of
language function and hemispheric specialization is discussed, with evidence that
the left hemisphere may indeed be preprogrammed to carry out language func-
tions. Behavioral descriptions are given for the major forms of speech and lan-
guage disturbances that occur in childhood. Specific learning disabilities are the
final category of disorders presented. This class of language dysfunction is the
most heterogeneous clinical entity and probably accounts for the largest pro-
portion of cases of delayed language acquisition. It is concluded that future
research efforts should be aimed at better neuropsychological descriptions, fur-
ther attempts to uncover the pathophysiology, and better treatments for language
and learning disorders in children.

The purpose of this article is to review
some of the basic causes of cerebral dys-
function in children; to present behavioral
descriptions of various speech, language, and
learning disorders; and to examine the cur-
rent status of efforts being made to under-
stand some of these disorders. Though
considerable progress is being made in
understanding these disorders, the magni-
tude of the problem of childhood language
disorders demands further research into the
causes and consequences of these problems.
Primary or specific speech and language dis-
orders and secondary speech and language
disorders affect approximately 8.5% of all
preschool children (Bliss, Allen, & Walker,
1978). Recent statistics from the U.S. Office
of Education indicate that over 60% of all
children with educational handicaps are re-
ferred for treatment of language or learning
disabilities. Even though a considerable
number of children do overcome these dif-
ficulties and reach a level of communication
skills equivalent to that of their age-mates,
one follow-up study (Wolpaw, Nation, &
Requests for reprints should be sent to Francis J.
Pirozzolo, who is now at the Department of Neurology,
Baylor College of Medicine, Texas Medical Center,
Houston, Texas 77030.
791
Aram, Note 1) showed that 70% of children
who had preschool language disorders con-
tinued to show signs of impairment at age
9, with 60% of these children in special class
placement. It is clear that childhood speech,
language, and learning problems are one of
the greatest challenges facing clinical neu-
ropsychology.
There are many disease states that can
interfere with the acquisition of language or
disrupt that which has already been ac-
quired. Inherent structural disorders, post-
natal trauma, anoxia, ischemia, epilepsy,
infections, congenital arteriovenous malfor-
mations, and toxic or metabolic disorders are
only a few of the conditions that can produce
language disorders. The diseases' discussed
below (for more complete treatment see Pi-
rozzolo, 1981) all can affect a child's cog-
nitive development by producing language
disorders or more generalized mental retar-
dation. In general the severity of the con-
dition determines how severe and how per-
vasive the deficits will be.
Prenatal Trauma
There are primarily three types of lesions
that might be due to mechanical trauma,
anoxia, or vascular abnormalities (Mala-
792 PIROZZOLO, CAMPANELLA, CHRISTENSEN, AND LAWSON-KERR
mud, 1970): (a) sclerosis of the white matter,
usually bilateral and symmetrical—histo-
logic findings include glial proliferation in
the distribution of the draining territory of
the vein of Galen, which may represent the
late stages of periventricular hemorrhages;
(b) microgyria, which may give the appear-
ance of focal areas of atrophy; (c) status
marmoratus—consisting of an increase in
finely medullated fibers and gliosis, which
is usually bilateral and primarily affects the
corpus striatum and the thalamus.
It has been hypothesized that some of
these lesions may be caused by hypoxia.
Myers (1968) has shown a similar distri-
bution of lesions that appeared as sequelae
of neonatal hypoxia in monkeys.
Children with these types of lesions may
have other deficits in addition to communi-
cation disorders. Generalized cognitive dis-
orders (mental retardation) and motor def-
icits may also be present, depending on the
severity of cerebral dysfunction. In addition,
many children may have mild cognitive dis-
orders that may go unrecognized.
Postnatal Trauma
Vascular lesions are not uncommon, par-
ticularly in premature infants. For example,
subdural hematomas are not unusual and
reach a peak incidence at 6 months of age.
Subdurals may be caused by forcep delivery,
other forms of head trauma, bacterial men-
ingitis, and surgical procedures to correct
hydrocephalus. Even after surgical interven-
tion there may be a number of complications
that can produce neurological sequelae (e.g.,
diffuse adhesive arachnoiditis with cerebral
atrophy). In addition, if the hematoma was
due to trauma, the possibility exists that the
clinical picture may be complicated by the
presence of cerebral contusions and lacera-
tions.
Closed head injuries are also not uncom-
mon in children. A number of complications
may occur that can produce permanent neu-
rologic problems. Examples of these include:
posttraumatic communicating hydrocepha-
lus, ventricular dilatation, and meningiocer-
ebral cicatrix. As always the severity of the
cognitive deficits depends on the degree and
type of injury. Generally speaking, if cardiac
massage and/or artificial ventilation are
needed, the prognosis for recovery is not as
favorable.
Ischemia
Malamud (1970) has shown that ischemia
may produce laminar necrosis of the cortical
gray matter, which is usually localized in the
watershed zones between the territories of
supply of two arteries. Arterial blood flow
may be occluded in many ways. Respiratory
or ear infections can occasionally occlude
one of the supraclinoid arteries. Sickle cell
anemia and arteritis due to tuberculosis or
other forms of meningitis may produce oc-
clusion of intracranial vessels. Cardiac val-
vular disease may also be a source of thrombi.
Epilepsy
Childhood epilepsy is not uncommon, al-
though permanent communication disorders
are rarely produced by this disorder. During
severe status epilepticus, however, a child
may become anoxic, which in turn may lead
to significant and irreversible brain damage.
Usually the areas that are affected most fre-
quently include the thalamus, the dentate
nucleus, and the corpus striatum. Similar
lesions have been produced in monkeys after
artificial induction of status epilepticus (Pi-
rozzolo, 1981).
Febrile seizures may also produce struc-
tural damage, and these usually affect the
mesial temporal areas as well as Ammon's
Horn. Falconer, Serafetinides, and Corsellis
(1964) has shown that these are frequently
damaged in patients with complex partial
epilepsy.
Landau and Kleffner (1957) and Victor,
Gascon, and Goodglass (Note 2) have de-
scribed the syndrome of acquired aphasia
and associated electroencephalographic
(EEG) abnormalities with or without con-
vulsive disorders in children. It has been
characterized as a progressive loss of lan-
guage, usually followed by a convulsive dis-
order and EEG abnormalitites of various
types.
Migraine
Migraine is an unusual cause of transient
language disorders that may occur between
 LANGUAGE AND LEARNING DISORDERS
20 minutes and 2 hours prior to the onset
of headache. The disorder is transient in
nature, although on occasion the disabilities
produced by the ischemic period of the at-
tack may become permanent in some indi-
viduals if there are multiple, chronic periods
of ischemia.
Hypoglycemia
Hypoglycemic episodes have been known
to produce language disorders in adults and
children (Dreifuss, 1975). Brain regions that
are most frequently involved are similar to
areas predominately affected by anoxia,
which include laminar necrosis of the cere-
bral cortex, lesions of Ammon's Horn, and
lesions of the striatum (Pirozzolo, 1981).
Purkinje cells are known to be especially sen-
sitive to hypoglycemic episodes.
Prenatal Infections
Rubella is one of the more common in-
fections that can produce mental retarda-
tion, congenital disfigurement, blindness,
deafness, and language disorders. Dreifuss
(1975) has found that rubella can produce
cellular necrosis, gliosis, and retardation or
inhibition of cell growth. In addition, peri-
vascular inflammatory cell changes and low-
grade leptomeningitis can result from this
infection. Other infections that can produce
various neurological deficits include cyto-
megalic inclusions disease and granuloma-
tous meningoencephalitis (toxoplasmosis).
All of these prenatal infections may lead to
occlusion of the aqueduct producing hydro-
cephalus.
Postnatal Infections
Meningitis. There are two forms of men-
ingitis that are more likely to produce neu-
rological sequelae: hemophilus influenzae
meningitis and tuberculous meningitis. Both
forms may also produce obstructive hydro-
cephalus.
Cerebral abscesses. Abscesses may in-
crease intracranial pressure by producing a
mass effect, or they may be the source of
infection and continual irritation, with re-
sulting neurologic problems.
Viral infections. Viral infections can pro-
793
duce encephalitis, which may lead to arter-
itis, demyelination, and hemorrhagic lesions.
Toxic and metabolic disorders. There
are numerous toxins that can produce cog-
nitive disorders in children. Lead is one of
the toxins that has received an increasing
amount of attention during the past several
years. Lead intoxication can produce wide-
spread neurologic abnormalities, learning
disabilities, neuronal degeneration, and in
severe cases, cerebral edema.
There are a wide number of metabolic
diseases that can affect a child's acquisition
of speech and language skills. Some of the
more common metabolic disorders include
diseases of amino-acid metabolism, Wilson's
disease, lipid storage diseases, gangliosi-
doses, and diffuse cerebral white matter de-
generative diseases.
Mild hypoxia secondary to carbon mon-
oxide poisoning can be a cause of nonlocal-
izing cerebral dysfunction. In the most mild
states of hypoxia, children present behav-
ioral disorders such as those commonly seen
in minimal brain dysfunction—or to use the
Diagnostic and Statistical Manual of Men-
tal Disorders (DSM-III; American Psychi-
atric Association, 1980) terminology, atten-
tion deficit disorder. More severe states of
hypoxia can cause drowsiness and distur-
bances of alertness.
Language Disorders
The definition of childhood language dis-
orders has been disputed by various workers
in the field. Bloom and Lahey (1978) re-
viewed the various definitions of childhood
aphasia and concluded that the term is used
to represent a disorder in which impaired
language behavior is judged to be the pri-
mary problem rather than a result of mental
retardation, deafness, or emotional prob-
lems. The etiology is most often presumed
to be pathology in the central nervous sys-
tem. These authors acknowledge that it is
not clear how the term childhood aphasia,
thus used, differs from the use of the term
language disorder.
The American Psychiatric Association
(1980) has distinguished between aphasia
and developmental language disorders on the
basis of whether the impaired language
794 PIROZZOLO, CAMPANELLA, CHRISTENSEN, AND LAWSON-KERR
abilities are acquired or congenital. They use
the term acquired aphasia to refer to a lan-
guage disorder associated with head trauma,
seizures, or EEG abnormalities that has fol-
lowed normal language development. De-
velopmental language disorders, on the other
hand, occur when normal language has
failed to develop. This distinction between
acquired aphasia and developmental lan-
guage disorders is discussed in this article.
The discussion of developmental language
disorders includes syndromes labeled by
other authors as developmental dysphasia
(Benton, 1978), childhood aphasia (Myk-
lebust, 1971), developmental aphasia (Ben-
ton, 1964), and congenital aphasia (Chase,
1972).
Hecacn (1976) has reviewed the various
descriptions of acquired childhood aphasia
appearing in the literature. He concludes
that there are two essential characteristics
noted by all authors: the high frequency of
mutism, and the complete absence of logor-
rhea and rare occurrence of paraphasias.
Writing disorders, articulatory disorders,
reading disorders, naming disorders, and
verbal comprehension disorders have been
present to varying degrees. Since Hecaen's
report, Woods and Teuber (1978) have re-
ported a case of jargon aphasia in a 5-year-
old boy.
Acquired aphasia has been studied for the
information that can be brought to bear on
questions concerning lateralization of speech
functions and plasticity of the human brain.
The study of lateralization of language is
concerned with hemispheric representation
of language functions in normal develop-
ment. The study of plasticity is concerned
with the ability of the brain to compensate
for damage to areas normally involved in the
development of a given function, in this case
language.
Although several lines of evidence drawn
from the study of acquired aphasia in chil-
dren have been brought to bear on questions
of both lateralization and plasticity, close
examination of these arguments suggests
that most are relevant only to the question
of plasticity. That is, studies of acquired
aphasia in children are most instructive with
respect to the brain's ability to compensate
for damage to language areas, but they pro-
vide much less information about the hemi-
spheric representation of language in normal
development. Lenneberg (1967) has re-
viewed data on recovery from acquired
aphasia, incidence of aphasia following left
hemispherectomy in patients with earlier left
hemisphere insult, and incidence of aphasia
in children with right and left hemisphere
lesions. In each case he argues that the data
suggest that early in life the hemispheres are
equipotential for language and that lan-
guage functions are gradually restricted to
the left hemisphere during childhood.
With respect to recovery from acquired
aphasia, Lenneberg reviews published case
material that indicates that the majority of
adults with aphasia have either temporary
aphasias (3 months duration or less) or last-
ing residual aphasic symptoms. He con-
cludes that slow and continuous improve-
ment over the years is extremely rare. In
contrast, he describes the recovery process
in children with acquired aphasia as one in
which improvement may occur steadily over
a period of several years up until puberty,
with most children fully recovering their lan-
guage functioning. He argues that the nature
of this recovery process suggests that in chil-
dren the right hemisphere, as well as the left,
is able to assume language functions. Al-
though this description of recovery from ac-
quired aphasia in childhood may be viewed
as a strong argument for greater plasticity
of language functions in children than in
adults, the relationship of these data to the
question of lateralization of language is ten-
uous at best. Certainly data indicating that
unilateral lesions produced lasting aphasic
symptoms in children would provide evi-
dence for early lateralization of language
functions in normal development. The ab-
sence of such data, however, is not neces-
sarily an argument against early lateraliza-
tion. Lenneberg's argument suffers from a
failure to clearly distinguish between the
potential a given area of the brain may have
to compensate for the loss of language in the
face of damage to other areas and the actual
assumption of language function by a given
area of the brain in normal development. In
other words, the nature of the recovery pro-
cess in children does not rule out the possi-
bility that language function is lateralized
 LANGUAGE AND LEARNING DISORDERS
early in development and that areas of the
brain not normally involved in language as-
sume these functions after brain insult. Gar-
diner and Walter (1977) have called atten-
tion to the dangers inherent in drawing
conclusions about normal development from
studies of development in brain-damaged
children. They note that potent compensat-
ing mechanisms in the damaged brain may
very well obscure evidence of factors asso-
ciated with a normal course of development.
This failure to clearly distinguish between
lateralization and plasticity colors Lenne-
berg's (1967) treatment of Basser's (1962)
data on hemispherectomies subsequent to
lesions acquired early in life. Basser found
an absence of aphasia in patients who ac-
quired a lesion during infancy and later had
the diseased hemisphere removed regardless
of the hemisphere involved. In contrast, pa-
tients who acquired a lesion during later life
and had subsequent hemispherectomy had
permanent aphasia if the operation was done
on the left side and no aphasia if it was done
on the right side. Although these data again
speak to the question of plasticity, the pos-
sibility of compensating mechanisms ob-
scuring the course of normal development
invalidates Lenneberg's interpretation of the
data in terms of equipotentiality of the hemi-
spheres for language.
There remains a significant body of data,
which Lenneberg (1967) has cited, that
bears directly on the question of lateraliza-
tion of language function in normal devel-
opment: the incidence of aphasia in children
with right and left hemisphere brain lesions
acquired early in life. Basser (1962) reported
equal frequencies of acquired aphasia fol-
lowing right and left hemisphere lesions in
children under the age of 2. Between the
ages of 2 and 10, the incidence of aphasia
following right hemisphere lesions was dra-
matically higher than in adults with right
hemisphere lesions. Lenneberg interpreted
these data as a strong argument for gradual
lateralization of language during childhood.
Recently, however, Woods and Teuber
(1978) presented evidence that earlier data
such as Basser's on the incidence of acquired
aphasia in children may be misleading. On
reviewing these early studies, these authors
noted a striking difference between the ob-
795
servations reported before and after the in-
troduction of antibiotics and mass immuni-
zation. Before the 1930s fully one third of
the total childhood aphasias reported in the
studies they examined were associated with
right hemisphere lesions. More recent stud-
ies, including their own study of 65 children
with unilateral lesions (Woods & Teuber,
1978), reported only 5% of the childhood
aphasias occurring after right hemisphere
lesions, if known left handers were excluded.
These authors argued that the high incidence
of crossed aphasia reported in earlier studies
may reflect the much higher incidence of
bilateral pathological damage in patients
who did not have the benefit of antibiotics
or other modern treatment following a uni-
lateral brain insult.
The failure of recent data on childhood
acquired aphasia to support a theory of early
equipotentiality of the hemispheres for lan-
guage is consistent with evidence from stud-
ies of psychometric deficits following unilat-
eral lesions in childhood (Fedio & Mirsky,
1969; McFie, 1961; Rudel & Denckla, 1974;
Rudel, Teuber, & Twitchell, 1974; Woods
& Teuber, 1973), structural asymmetries of
the hemispheres of the planum temporale in
the fetus and newborn (Teszner, Tzavaras,
Graner, & Hecaen, 1972; Wada, Clark, &
Hamm, 1975), evoked potential responses to
auditory stimuli (Molfese, cited in Wada et
al., 1975), language development in children
with right or left hemispherectomies (Dennis
& Whitaker, 1976), and a child with asymp-
tomatic agenesis of the left temporal lobe
(Pirozzolo, Whitaker, Seines, & Homer,
1977).
Similarly, recent studies of recovery from
childhood aphasia suggest that early studies
may have overestimated the plasticity of the
human brain. Hecaen (1976) and Woods
and Teuber (1978) reported that persistent
verbal deficits are not uncommon following
acquired aphasia in childhood; they suggest,
however, that there may be an age threshold
for recovery. A recent study by Woods and
Carey (1979) indicates that left hemisphere
lesions incurred before 1 year of age do not
result in significant impairment on a variety
of language tasks. In contrast, left hemi-
sphere lesions occurring after 1 year, if they
cause initial aphasia, leave significant resid-
796 PIROZZOLO, CAMPANELLA, CHRISTENSEN, AND LAWSON-KERR
ual impairment on most of the same lan-
guage tasks, with the degree of residual
impairment possibly bearing a positive
relationship to age at injury. Pirozzolo and
Kerr (1981) have called attention to the need
for cautious interpretation of the relation-
ship between age at time of injury and de-
gree of recovery. They cite several studies
that call into question the widely held prin-
ciple that the younger the patient at the time
of injury, the greater the eventual recovery.
Drawing on evidence from animal studies,
Schneider (1979) has hypothesized that
early brain lesions in humans may cause
behavioral anomalies, which are not char-
acteristic effects of later injuries.
In summary, current appraisals of the
data on acquired childhood aphasia suggest
that lateralization of language occurs very
early in development, possibly before birth.
Plasticity of language function, as tradition-
ally understood, is probably greater in child-
hood than adulthood but begins to decline
early in the childhood years. Moreover, re-
cent evidence suggests that notions of plas-
ticity and recovery may require redefinition
to account for behavioral anomalies that
may be specific to early lesions.
Developmental Language Disorders
Benton (1964) used the term develop-
mental aphasia to refer to
a condition in which a child shows a relatively specific
failure of the normal growth of language functions. The
failure can manifest itself either in a disability in speak-
ing with near normal speech understanding or in a dis-
ability in both understanding and expression of speech.
The disability is called a "specific" one because it cannot
readily be ascribed to those factors which often provide
the general setting in which failure of language devel-
opment is usually observed, namely, deafness, mental
deficiency, motor disability or severe personality disor-
der, (p. 41)
Benton stressed the variety in the individual
clinical pictures presented by these children.
He noted the steadily growing body of evi-
dence that implicates cerebral damage as an
essential causative factor in developmental
language disorders and suggested that sep-
arate classification of those children who do
not show evidence of cerebral damage does
not seem warranted.
More recently Benton (1978) has differ-
entiated several subgroups represented by
the label developmental dysphasia, which
he defines as "a collective term covering a
variety of conditions involving failure or dis-
tortion in the development of speech and lan-
guage" (p. 43). He notes the widespread
acceptance of two broad categories of dis-
turbance, expressive and receptive-expres-
sive. The child with an expressive disorder
manifests a level of speech production sig-
nificantly below his or her level of speech
comprehension. In contrast, the clinical pic-
ture of the child with a receptive-expressive
disorder is dominated by impairment in
speech comprehension. Distorted or impov-
erished speech production is invariably a
part of the syndrome, but the receptive def-
icit is considered to be primary. He distin-
guishes three conditions within the expres-
sive disorders: (a) dysarthria, in which the
primary problem is defective neuromotor
control of the organs of speech articulation;
(b) inconsistent articulation disturbances, in
which the primary problem is an impairment
of coordination or integration; and (c) lexical
and syntactical impoverishment. In all three
groups language comprehension is relatively
intact. In contrast, the subgroup of children
with receptive-expressive disorders are se-
riously impaired in speech comprehension.
In addition, their defects in speech produc-
tion are qualitatively different from those of
children with a primarily expressive disor-
der. Benton alerts the reader to the difficulty
of interpreting studies of developmental lan-
guage disorders in which the subgroups have
been mixed or inadequately described.
Chase (1972) has reviewed descriptions
of the clinical features of children with con-
genital aphasia. Although the speech of chil-
dren with receptive-expressive disorders
shows substantial individual variation, it is
usually characterized by impaired phonolog-
ical organization, reduced output, and poorly
differentiated grammatical structure. The
omission of prepositions, conjunctions, and
articles may result in a telegraphic style of
speech. In some cases distractibility, short
attention span, emotional lability, and hy-
peractivity accompany the language distur-
bance.
Cromer (1978) and Tallal (1978) have
defined developmental language disorders
 LANGUAGE AND LEARNING DISORDERS
"by exclusion," that is, impairment or delay
of language function of nonspecific etiology.
Tallal and Piercy (1978) identified two
approaches to the study of the origins of
developmental language disorders: examin-
ing either linguistic anomalies or those
"simpler" cognitive capacities believed to
be necessary for speech comprehension and
production. Studies using the linguistic ap-
proach have been reviewed by Menyuk
(1978) and are beyond the scope of this ar-
ticle.
Several types of cognitive impairment
have been studied as potential underlying
causes of developmental language disorders:
impaired auditory perception (e.g., Mark
& Hardy, 1958; McReynolds, 1966; Rosen-
thai, 1972), impairment of the auditory stor-
age system (e.g., Eisenson, 1968; Rosenthal
& Eisenson, Note 3), impairment of rhythmic
ability (e.g., Griffiths, 1972; Kracke, 1975),
and deficits in sequential perception (e.g.,
Lashley, 1951; Lowe & Campbell, 1965;
Monsees, 1961; Poppen, Stark, Eisenson,
Forrest, & Wertheim, 1969).
In general the study of cognitive impair-
ment in developmental language disorders
has been dominated by the conviction that
auditory processing factors underlie these
disorders (Rees, 1973). Recent work has fo-
cused on a possible link between nonverbal
auditory perceptual deficits and speech per-
ceptual deficits at the phoneme level. Tallal
and Piercy (1973a, 1973b) demonstrated
that unlike normals, children with develop-
mental language disorders are incapable of
processing nonverbal auditory stimuli pre-
sented at rapid rates. That this defect was
observed even when perception of sequence
was not required led these authors to suggest
that the sequencing deficit previously ob-
served in children with language disorders
(e.g., Lowe & Campbell, 1965) may be sec-
ondary to their inferior discrimination of
rapidly presented auditory stimuli.
This rate-dependent deficit was also found
in studies involving speech sounds (Tallal
& Piercy, 1974, 1975) and the perception
of syllables in word context (Tallal, Stark,
Kallman, & Mellits, 1980). Further studies
(Stark & Tallal, in press; Tallal, 1976) dem-
onstrated that these subjects' errors in speech
perception were mirrored by their errors in
797
speech production. That is, these children
were most impaired in both perception and
production of speech sounds that rely on
brief temporal cues for their discrimination.
Tallal et al. (1980) proposed that the in-
ability to process rapidly changing acoustic
information results in the inability of chil-
dren with developmental language disorders
to identify and discriminate certain pho-
nemes, such as stop consonants. Tallal and
Piercy (1978) reviewed the ways in which
the presenting disorder of language might
be related to the observations of impaired
auditory perception. The auditory defect
might be viewed as (a) a necessary cause of
developmental language disorders, (b) suf-
ficient but not necessary cause of develop-
mental language disorders, (c) secondary to
a primary linguistic defect, and (d) concom-
itant of the linguistic defect but not causally
related to it. Tallal concluded with her work-
ing hypothesis that in some cases defective
processing of rapidly changing acoustic in-
formation with an associated reduced mem-
ory span for auditory sequence is sufficient
cause for developmental language disorders.
A recent study by Ludlow, Cudahy, Caine,
Brown, and Bassich (Note 4) casts some
doubt on the hypothesized relationship be-
tween impaired processing of rapidly chang-
ing acoustic information and developmental
language disorders. They found that not only
did language impaired children show deficits
in auditory perception of temporal order, but
similar deficits could be found in two groups
with normal language function as well (pa-
tients in the early stages of Huntington's
disease and hyperactive children). The au-
thors suggest that auditory temporal se-
quencing deficits that have previously been
linked to developmental language disorders
may be better understood as reflecting gen-
eral cognitive dysfunction. Though it re-
mains to be seen whether similar results will
be obtained on nonsequencing auditory dis-
crimination tasks and whether similar pro-
cesses account for the deficits across groups,
for example auditory discrimination versus
attention, the study by Ludlow et al. (Note
4) raises an important question about the
specificity of auditory processing deficits to
developmental language disorders.
Other researchers have cautioned against
798 PIROZZOLO, CAMPANELLA, CHRISTENSEN, AND LAWSON-KERR
restricting the study of developmental lan-
guage disorders to single cognitive abilities
such as auditory processing of rapidly pre-
sented information. Benton (1978) sug-
gested that despite useful findings this spe-
cific approach cannot provide a picture of
the constellation of abilities and disabilities
that may be characteristic of different
types of developmental language disorders.
Fletcher (1981) has stressed the importance
of incorporating analyses of developmental
changes into the study of children who fail
to acquire proficiency in some aspect of cog-
nitive functioning. Similarly, Menyuk (1978)
has suggested that the basis of the problem
in developmental language disorders may
change with time. This suggestion implies
a possible integration of linguistic and cog-
nitive deficit approaches to developmental
language disorders, in that with increasing
age, the primary problem in the comprehen-
sion and production of speech may shift from
one of auditory processing, for example, to
one of semantic and syntactic analysis.
Speech Disorders
Speech disorders are generally classified
according to the characteristics of articula-
tion, voice quality, and fluency of speech
output. Abnormalities in any of these cate-
gories can occur in isolation or in combi-
nation with each other. In this section be-
havioral descriptions are provided for each
of the disorders. Following are brief descrip-
tions of specific disease entities that gener-
ally result in distinct patterns and combi-
nations of speech deficits.
Articulation Disorder
Articulation disorder refers to deviant oral
production of speech sounds. Specific types
of articulation errors include (a) substitution
of one sound for another, (b) omission of a
sound, (c) distortion of sounds, and (d) ad-
dition of inappropriate sounds. Prevalence
of an error type is usually dependent on the
underlying cause of the disorder. Distinct
error patterns that emerge with specific or-
ganic deficits such as cleft palate, cerebral
palsy, hearing loss, and mental retardation
are discussed in a later section. Other or-
ganic causes resulting in articulation disor-
ders may be dental abnormalities, tongue
abnormalities, and tongue thrust. Lisping is
a specific term used to describe distorted
articulation of /s/, /z/, /th/, and /sh/.
Dysarthria is a term frequently used to
describe clusters of speech production dif-
ficulties that usually include imprecise ar-
ticulation. Darley, Aronson, and Brown
(1975) refer to dysarthria as "a collective
name for a group of related speech disorders
that are due to disturbances in muscular con-
trol of the speech mechanism resulting in
impairments of any of the basic motor pro-
cesses involved in the execution of speech"
(p. 2). Their term includes extant motor dys-
functions involving respiration, phonation,
articulation, resonance, and prosody.
The majority of school-aged children who
misarticulate do not have obvious organic
deficits. In fact many sound substitutions
and omissions are manifested as part of the
normal developmental sequence of speech
acquisition (Winitz, 1969; Templin, 1957).
Normally developing children are frequently
observed to substitute easy sounds for more
difficult sounds. Most children master cor-
rect articulation of all phonemes by 8 years
of age (Winitz, 1969; Templin, 1957).
Articulation errors that are not due to
obvious organic disorder and are not consid-
ered part of the normal developmental se-
quence are sometimes referred to as dyslalia.
These errors are usually the result of a fail-
ure to learn phonological rules (Van Riper,
1972; Winitz, 1969). It is presumed that
faulty articulation learning is often the result
of poor speech models and lack of stimula-
tion and motivation (Phillips, 1975). Other
factors shown to be related to articulation
proficiency are chronological age, intelli-
gence, mental age, auditory discrimination,
and pitch discrimination (Winitz, 1969).
Locke (1980a, 1980b) provides an excellent
commentary on the role of speech perception
skills in the articulation disordered child.
Studies of defective auditory perceptual
skills reflect the critical importance of the
auditory system to the acquisition of speech.
Chase (1972) stressed this point in his dis-
cussion on the maturational development of
the neural substrates of the auditory system.
 LANGUAGE AND LEARNING DISORDERS
Voice Disorders
Voice disorders are disturbances of oral
production in which the speaker's voice
sounds unpleasant or is inappropriate for the
speaker's age and sex. Voice disorders can
result from either neuromuscular or func-
tional causes (Shanks & Duguay, 1974).
Most voice disorders are described in terms
of deviations in pitch, loudness, or quality
of vocal production. These characteristics
are the acoustic correlates of features of res-
piration, phonation, and resonance.
Deviant voice quality is often described by
a variety of terms: hypernasal, denasal,
breathy, harsh, and hoarse. Hoarseness ap-
pears to be the most common voice disorder
observed in the school-aged child. This dis-
order is often associated with vocal abuse,
sometimes resulting in a nodule or irritation
on the edge of the vocal folds. Excessive use
of the voice, inappropriate loudness, and in-
appropriate pitch are the most common
forms of vocal abuse in children. Hypernas-
ality and denasality, although seen less fre-
quently than hoarse voice quality, are not
uncommon. Hypernasality suggests an in-
adequacy of the soft palate to sufficiently
prevent excess air from travelling through
the nasal passage. It is usually associated
with the structural abnormality of cleft pal-
ate but also can occur after surgical removal
of the adenoids, with diseases causing pa-
ralysis of the soft palate, and sometimes in
the absence of any obvious organic defi-
ciency. Denasality is a term used to describe
a voice quality resulting from occlusion of
the nasal passages. Enlarged adenoids and
abnormal growth in the nasal passage are
the most common causes of denasality in
children.
Pitch deviations occurring in children usu-
ally fall into one of the following categories:
(a) pitch level too high, (b) pitch level too
low, (c) monopitch, and (d) pitch breaks.
Pitch breaks refer to abrupt changes in voice
pitch, generally of an octave or more, that
occur involuntarily in speech. These are par-
ticularly common in boys during puberty.
Other common causes of pitch deviations
may be hearing loss, emotional conflict, hor-
monal problems, tension, or laryngeal ab-
normality (Boone, 1971; Moore, 1971).
799
Loudness disorders can range from com-
plete loss of voice (aphonia) to excessively
loud voice. These are generally the least
common of the voice disorders seen in
school-aged children. Hearing loss is an im-
portant consideration when a child is ob-
served to use an inappropriate loudness level.
Deviations in loudness also may result from
emotional problems, vocal fold paralysis,
and certain neurological deficits.
Stuttering
Stuttering refers to a disruption in the
fluency of speech output. Although no one
specific definition of this disorder has been
universally agreed upon, most authors de-
scribe the symptomatology of stuttering in
similar ways. Characteristics that are usu-
ally included in the description of stuttering
are (a) overt speech behaviors and (b) con-
comitant variables that often appear to be
the result of tension and anxiety in the stut-
terer. Overt speech behaviors seen as fea-
tures of stuttering are repetitions and pro-
longations of sounds, syllables, or words that
interrupt the fluency and rhythm of speech.
The clinical picture of stuttering usually in-
cludes abnormally long pauses or "blocks."
Descriptions of repetitions, prolongations,
and pauses have largely been based on per-
ceptual identification by the listener.
Concomitant or associated behaviors that
have been described in the literature indicate
that a large variety of visible or audible non-
speech events can occur in conjunction with
overt stuttering behavior (Bloodstein, 1969).
These include extraneous muscle activities
such as frowning, contortions of the mouth,
head jerks, eye blinks, tongue protrusion,
movement of the nostrils, and a multitude
of other responses.
The literature also reports less overt phys-
iological changes that often accompany stut-
tering. Contrary to the perceptual identifi-
cation of overt behaviors, detection and
quantification of these physiological pro-
cesses have been accomplished with the use
of a wide assortment of instruments. Studies
have shown alterations in electroencepha-
lographic activity (Freestone, 1942; Sayles,
1971; Travis & Malamud, 1937), dilation
of the pupils (Gardner, 1937), decreases in
800 PIROZZOLO, CAMPANELLA, CHRISTENSEN, AND LAWSON-KERR
blood sugar levels (Moore, 1957), and eye
movement abnormalities (Kopp, 1963). Most
recent research has shown deviations in ar-
ticulatory dynamics of stuttering (Zimmer-
man, 1980a, 1980b), differences in laryngeal
behavior among the various types of stut-
tering (Conture, McCall, & Brewer, 1977),
and variations in regional cerebral blood
flow (Wood, Stump, McKeehan, Sheldon,
& Proctor, 1980).
Many authors have suggested that the fea-
tures of an individual's stuttering are prone
to change over time (Bloodstein, 1969; Blue-
mel, 1932; Froeschels, 1961; Van Riper,
1971). It is reported that in the initial phases
of stuttering in children of 2-6 years of age,
repetitions and prolongations are relatively
effortless, and there is little evidence of con-
cern about the dysfluency of speech. As the
stuttering advances, the frequency of dys-
fluencies increases and specific situation and
word fears arise. Stuttering seen in the late
adolescence and adulthood is often in its
most advanced stages. It is frequently as-
sociated with evidence of speech situations,
fearful anticipation of stuttering, and fre-
quent word substitutions and circumlocu-
tions (Bloodstein, 1969; Van Riper, 1971).
It is in this late stage of stuttering that many
of the previously mentioned concomitant
features, such as extraneous muscle activity,
tend to arise. These are presumed to be the
result of tension and anxiety.
Communication Deficits Associated With
Other Specific Disorders
A variety of speech and language deficits
are usually observed in children with any one
of the following disorders: hearing loss, cleft
palate, cerebral palsy, mental retardation,
and emotional disturbance. In most cases
articulation, language, and voice are all dis-
turbed in varying degrees in each one of
these disorders. Children with hearing loss
are reported to display hypernasality, mo-
notonous pitch, lack of loudness control, and
strident voice quality (Angelocci, Kopp, &
Holbrook, 1964; Carlin, 1968; Colton &
Cooker, 1968). Defective articulation is often
manifested by omission of high frequency
consonants, confusion of vowels, and un-
voicing of consonants (Penn, 1955). Lan-
guage impairments of hearing-impaired chil-
dren have been shown to vary greatly,
depending on the age of onset of hearing loss
and the child's stage of language acquisition.
Cleft palate refers to congenital abnor-
malities of the peripheral speech structures,
including the lip, soft palate, and hard pal-
ate. The oral production disorders of chil-
dren with cleft palate are frequently ob-
served to be gross sound-substitution errors
(Westlake & Rutherford, 1961) and hyper-
nasal voice quality (Bzoch, 1979). In terms
of language expression, Bzoch (1979) has
reported delays in first use of words, ex-
pressive vocabulary, first use of sentences,
and level of syntactic development.
Cerebral palsy is a nonprogressive brain
disorder that occurs in the perinatal period.
Voice characteristics that may accompany
cerebral palsy are breathiness, aspirate voice
quality, abnormal pitch, and loudness dis-
order (Lencione, 1976). Fluency abnormal-
ities such as short bursts of speech, exces-
sively fast rate, or delay in initiation of
voicing have also been reported. The lan-
guage problems sometimes associated with
cerebral palsy include retardation of lan-
guage development, grammatical confu-
sions, substantial lag in oral expression as
compared to comprehension, and verbal per-
severation (Mysak, 1971).
Mentally retarded children have been re-
ported to show significant delays in language
development (Graham & Graham, 1971;
Lackner, 1968; Ryan, 1975). Specific char-
acteristics have indicated that the mentally
retarded are apt to have reduced vocabulary
size, simplified sentence structure, and delay
in use of verbal mediation (Naremore &
Denver, 1975). Other authors have shown
that there are qualitative differences be-
tween normal and retarded children in terms
of morpheme usage (Menyuk, 1971) and
word associations (Semmel, Barritt, & Ben-
nett, 1970). Defective articulation has been
shown to be of higher incidence in the men-
tally retarded than in the normal population,
but the nature of the errors of these two
groups are quite similar (Matthews, 1971;
Schiefelbusch, 1972).
Emotional disturbances in children, par-
ticularly autism and psychosis, have been
shown to result in a variety of language dif-
 LANGUAGE AND LEARNING DISORDERS 801

faculties. Autistic children use little or no clinical populations of dyslexics (e.g., Boder,
spontaneous speech for the purpose of inter- 1973; Denckla & Rudel, 1976; Mattis,
personal communication. When speech is French, & Rapin, 1975; Pirozzolo, 1979;
emitted it is usually parrotlike or echolalic Pirozzolo & Hess, Note 5) have shown that
and lacking in normal prosody (Kanner, the largest subgroups of dyslexics have more
1964; Kessler, 1966). Confusion of pronouns general disturbances of language function in
and other errors of syntax and semantics, as addition to the reading disabilities for which
determined by analysis of spontaneous the children were referred for assessment.
speech, are sometimes observed (Baltaxe The relationship between language and
& Simmons, 1977; Rutter, 1965). Some of reading is an intimate, complex, and obscure
the characteristics associated with childhood one. Speech comprehension is the historical
schizophrenia are use of speech full of emo- and logical precursor to the written language
tional content, symbolic use of words, and system. In alphabetic languages reading and
wide variation of meaningfulness of speech, writing depend on an association between a
ranging from realistic speech to auditory unit of visual information (i.e., a letter) and
hallucinations. Accompanying nonverbal a unit of phonological information. This vi-
communication behaviors may be facial sual information is comprised of distinctive
expressions that are void of emotion, staring features, and these features are arranged
eyes, and catatonic reactions. Other types into certain combinations that are redundant
of psychoses may result in speech charac- in their orthographic regularity and pho-
terized by neologisms, logorrhea, and per- nemic translations of letter combinations. In
severation. Bizarre irrelevance, deviant voice addition to these characteristics, further pat-
quality, and increased variability in the use terns of redundancy are imposed by the syn-
of nouns, prepositions, and pronouns has also tactic and semantic elements of the lan-
been reported. guage. Thus reading, the so-called "language
by eye," is highly dependent on its derivation
from speech. It is definitely not an autono-
Specific Learning Disabilities mous and equal language system (to speech),
since it depends so heavily on spoken lan-
The final category in the present treat- guage. The deficits observed in the congen-
ment of language disorders in children cov- itally blind and congenitally deaf are evi-
ers specific learning disabilities. Children dence of this. Furth (1966) has shown that
with learning disorders probably account for profoundly deaf children have very severe
the greatest proportion of children who pres- language deficiencies even under the most
ent some form of linguistic disturbance. The favorable conditions, whereas it is widely
prevalence of learning disabilities is largely accepted that blind children can acquire spo-
unknown, due in part to the inability of au- ken language normally and learn to read
thorities to agree on an operational defini- through the substitution of the somesthetic
tion (Gaddes, 1976). Most researchers now system for the visual.
agree that subtle neuropsychological dys- If reading is dependent on oral language,
functions underlie these disorders. There is it is not surprising that many authorities
also substantial agreement on the notion that consider linguistic deficits to be causal fac-
learning disability is not a single, homoge- tors in developmental reading disability.
neous clinical entity (Benton, 1978; Mattis, Numerous studies have shown that good
1981; Pirozzolo, 1979; Satz & Morris, 1981). readers are superior to poor readers on a
Though some children have cognitive dis- variety of linguistic tasks. Early reading
abilities that do not affect either oral or achievement has been found to be strongly
written language, the most common defects associated with phonemic segmentation
in reading and learning disabilities affect (Liberman, Shankweiler, Liberman, Fowler,
linguistic performance. A study by Satz and & Fischer, 1977). Poor readers are noto-
Morris (1981) showed that at least 60% of riously deficient in these and other phono-
a population of learning-disabled children logical skills (Liberman & Shankweiler,
had marked language disabilities. Studies of 1976). Young children lack phonemic
802 PIROZZOLO, CAMPANELLA, CHRISTENSEN, AND LAWSON-KERR
awareness when they begin to learn to read,
but disabled readers may continue to be de-
layed in these skills, which may in fact be
the cause of their reading failure.
Older children with developmental read-
ing disability have also been shown to differ
from normal readers on a variety of linguis-
tic tasks. Although reading achievement at
younger ages is not associated with syntactic
deficits (Falk, 1977; Taylor, 1977), recent
data from studies of older children (Fletcher,
Satz, & Scholes, 1981) strongly suggest that
poor readers differ from good readers in
higher order syntactic comprehension. Ad-
ditional data suggest that older poor readers
are also deficient in semantic knowledge
skills such as semantic categorization (Per-
fetti, Note 6).
Numerous other linguistic disturbances
have been reported in children with devel-
opmental reading disability. Table 1 de-
scribes some of the language disorders re-
vealed in neuropsychological evaluations of
these children.
Conclusion and Future Directions
In the area of childhood acquired aphasia,
we have begun to conceive lateralization of
language as occurring early in development,
possibly before birth. Notions of plasticity
of language function have been revised to
reflect an earlier decline in plasticity in
childhood and the possibility of behavioral
anomalies specific to early lesions. The study
Table 1
Neurolinguistic Disturbances in Children with Developmental Reading Disorders
Disorder
Anomia
Auditory comprehension deficits
Repetition defects
Speech sound discrimination
Phonemic sequencing disorders
Agrammatism
Articulation disorders
Bucco-lingual dyspraxia
Sound blending difficulty
Phoneme-to-grapheme correspondence errors
Poor general verbal performance
of developmental language disorders contin-
ues to reflect a search for underlying deficits,
although future studies may emphasize de-
velopmental rather than deficit models.
In the area of speech disorders, there has
been a striking increase in interest in clinical
work with children with speech disorders,
although this increase in clinical interest has
not been matched by an increase in research
interest (Tower, 1979). Nevertheless the
past two decades have seen major advances
being made in our understanding of human
speech and language, with electromyo-
graphic, spectrographic, and computer-based
methods being applied to the study of speech
production.
In the area of learning disabilities, efforts
aimed at describing the neuropsychological
features, that is, the behavioral symptom-
atology and associated clinical findings, are
resulting in increased agreement about the
nature of these disorders. The etiology of
developmental learning disabilities remains
hopelessly obscure, yet some recent progress
has been made in the possible discovery of
an underlying pathophysiology. Educational
treatment (e.g., remedial reading) remains
the only successful intervention strategy, but
encouraging results are being achieved
through the use of special pharmacological
agents (Wilshire, Atkins, & Manfield, 1979;
Pirozzolo & Maletta, Note 8).
Perhaps because most children proceed
through the stages of language acquisition
without apparent delay, few researchers
Study
Mattis, French, & Rapin (1975), Denckla & Rudel
(1976), Pirozzolo, Rayner, & Whitaker (Note 7)
Kinsbourne & Warrington (1963)
Mattis (1981)
Wepman (1960)
Denckla (1977)
Pirozzolo (1979)
Mattis (1981)
Mattis (1981)
Mattis (1981)
Pirozzolo & Rayner (1979), Boder (1973), Mattis,
French, & Rapin (1975)
Kinsbourne & Warrington (1963)
 LANGUAGE AND LEARNING DISORDERS
have devoted much attention to the processes
of normal language acquisition. Due in part
to the rejection of dogmatic behaviorism, the
past 20 years have seen some advances in
the study of language and mental processes.
This progress has been made in virtually all
areas of linguistic behavior, and slowly this
theoretical knowledge is being translated
into practical rules of speech, language, and
learning behavior in children. If the impetus
to gain a more precise understanding of chil-
dren's language and learning abilities does
not come from the advances in empirical
knowledge about child development, then it
will most certainly come from an interest in
those children who do not follow the normal
sequence of stages of development but who,
instead, manifest deviations from the norms
that developmental psycholinguists have so
carefully denned.
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Received May 8, 1981 •