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PubMed1998

Localisation of a gene implicated in a severe speech and language disorder.

Between 2 and 5% of children who are otherwise unimpaired have significant difficulties in acquiring expressive and/or receptive language, despite adequate intelligence and opportunity. While twin studies indicate a significant role for genetic factors in developmental disorders of speech and language, the majority of families segregating such disorders show complex patterns of inheritance, and are thus not amenable for conventional linkage analysis. A rare exception is the KE family, a large three-generation pedigree in which approximately half of the members are affected with a severe speech and language disorder which appears to be transmitted as an autosomal dominant monogenic trait. This family has been widely publicised as suffering primarily from a defect in the use of grammatical suffixation rules, thus supposedly supporting the existence of genes specific to grammar. The phenotype, however, is broader in nature, with virtually every aspect of grammar and of language affected. In addition, affected members have a severe orofacial dyspraxia, and their speech is largely incomprehensible to the naive listener. We initiated a genome-wide search for linkage in the KE family and have identified a region on chromosome 7 which co-segregates with the speech and language disorder (maximum lod score = 6.62 at theta = 0.0), confirming autosomal dominant inheritance with full penetrance. Further analysis of microsatellites from within the region enabled us to fine map the locus responsible (designated SPCH1) to a 5.6-cM interval in 7q31, thus providing an important step towards its identification. Isolation of SPCH1 may offer the first insight into the molecular genetics of the developmental process that culminates in speech and language.

Chromosome Mapping↗
PubMed2004

[Early diagnosis of language disorders].

Talking is normal and not talking is not. In case of developmental language delay, "wait and see" is not a good medical practice. In many cases, this delay is secondary to conditions such as hearing loss, mental retardation, brain damage, pervasive developmental disorder, environmental deprivation... In other cases, it is a specific language delay or a specific language disorder (dysphasia). Specific speech assessment and speech therapy are indicated to prevent behavioural problems, and learning disabilities.

Child, Preschool↗
PubMed1996

Management of speech and language disorders in a mental illness unit.

Few speech and language therapists work with psychiatric patients. This study investigates how the specific communication problems of this population are addressed by care staff. Following a survey to determine the prevalence of speech and language problems in a psychiatric population, subjects assessed as having moderate or severe difficulties were selected for further study in order to investigate how they were currently being managed by the people responsible for their care. Key workers or charge nurses were interviewed, and ward and department nursing care plans were examined for mentions of speech and language problems, for aims in connection with these problems and for strategies to achieve these aims. Speech and language problems were not mentioned in 40% of the nursing care plans inspected. Where speech and language problems were mentioned there were aims in connection with half of these and strategies to achieve the aims in only 10% of the sample. The reasons for failure to mention speech and language in nursing care plans and for discrepancies between the results of speech and language therapy assessment and assessments of ward and department staff are discussed.

Adolescent↗
PubMed2006

Effects of alternative communication on the communicative effectiveness of an individual with a progressive language disorder.

This study was designed to investigate the effects of two different modes of communication on the communicative output of an individual who is no longer able to communicate verbally, presenting with a primary progressive aphasia and apraxia of speech. The two treatment approaches included training the patient with a text-to-speech alternative communication device and with American sign language. An alternating treatment design was used to compare two communicative approaches (an alternative communication device and American sign language) on the subject's communicative effectiveness. Communicative effectiveness was measured in terms of number of words, correct information units and percentage correct information units, using a protocol that was adapted to quantify the output generated by the alternative communication device and American sign language. Increases across all three measures resulted for both the alternative communication device and American sign language. The clinical implications are explored, and the results add to existing studies regarding treatment possibilities using alternative communication for individuals who present with a progressive speech and language disorder, without concomitant cognitive deficits.

Aphasia, Primary Progressive↗
PubMed1990

The relationship between psychopathology and speech and language disorders in neurologic patients.

Depression, anxiety, and conversion reaction are common in neurologic patients. These disorders can produce neurologic-like symptoms that either mask or intensify those produced by the neurologic disease. This paper reviews clinical and research findings relating psychopathology to the formation and remediation of speech and language disorders in neurologic patients. The need to consider the psychosocial and psychopathological aspects of neurologic communicative disorders, and the link between emotional and communicative processes, are emphasized. Diagnostic criteria for the identification of psychogenic communicative disorders are outlined.

Communication Disorders↗
PubMed1984

Brain-stem, middle latency and late cortical evoked potentials in children with speech and language disorders.

The topography of the brain-stem (ABR), middle latency (MLR) and cortical (ACR) evoked responses was investigated in children with normal speech and language development and those with either a language or motor speech disorder. The aim was to determine whether it is possible to discriminate between the groups of children in terms of the evoked potential characteristics. There were significant inter-group differences, particularly relating to the amplitude of the different responses. The ABR in both the language and motor speech groups exhibited smaller amplitudes for waves I, III and V than the control group, with no change in latency. Two explanations were suggested; firstly abnormal functioning of the peripheral hearing mechanism even though the hearing thresholds were normal which could be a secondary effect due to deprivation of normal speech and language development; and secondly far-field recording effects due to differences in the electrical conductivity of tissue and the distance separating the generator site and recording electrodes. The MLR in the motor speech group was significantly larger at the mastoid and temporal electrode sites than either the control or language groups. This was considered to be an enhanced myogenic response like the other exaggerated brain-stem reflexes seen in congenital suprabulbar paresis. Significantly larger amplitudes of the ACR were also recorded from the motor speech group at the Cz electrode site. This was thought to be due to underactivity of some normal cortical inhibitory system and not a direct result of increased MLR amplitude. The ACR in the language disordered children exhibited an abnormal left temporal hemispheric dominance and a more inverted or 'dissimilar' wave form at the T3 electrode site on the correlation analysis. These findings suggest impaired functioning of the left temporal cortex in our children who have failed to develop language normally. We feel that this has more significance for the language abnormality than the low amplitude ABRs which were observed in both the language and motor speech disordered children.

Brain Mapping↗
PubMed1992

Linguistic trade-offs in school-age children with and without language disorders.

Factors influencing the occurrence of trade-off effects among linguistic components were examined. Several linguistic measures were used to represent syntactic and phonological production in order to determine whether interrelationship patterns would vary across measures. Linguistic interactions present in imitated speech were compared to those from spontaneous speech. Group effects were explored by comparing data from children with language-learning disabilities, children with reading disabilities, and normally developing children. Results indicated trade-offs between some linguistic measures and positive relationships among others. More trade-offs were present in imitated speech than in spontaneous utterances. In general, interrelationship patterns were similar across groups. Interpretation of these results in reference to current models of sentence production is offered.

Child↗
PubMed2003

Maternal neuronal antibodies associated with autism and a language disorder.

Neurodevelopmental disorders could be caused by maternal antibodies or other serum factors. We detected serum antibodies binding to rodent Purkinje cells and other neurons in a mother of three children: the first normal, the second with autism, and the third with a severe specific language disorder. We injected the serum (0.5-1.0 ml/day) into pregnant mice during gestation and found altered exploration and motor coordination and changes in cerebellar magnetic resonance spectroscopy in the mouse offspring, comparing with offspring of mice injected with sera from mothers of healthy children. This evidence supports a role for maternal antibodies in some forms of neurodevelopmental disorder.

Adult↗