THE ELECTRICAL ACTIVITY OF THE BRAIN IN SOME DISORDERS RELATED TO COMMUNICATION G . K. NELSON Chief Research Officer and Head of the Division of Neuropsychology at the National Institute for Personnel Research, a consLiluenL of the South African Council for Scientific and Industrial Research, Johannes- burg Few developments in the field of medicine and particularly of psychiatry have been attended with more initial enthusiasm than the discovery of the electrical activity of the brain. Although Caton's revelation in 1870 that it was possible to record electrical impulses from the brain received little attention, the painstaking research of Berger4 provided the impetus for the sudden and rapid development of electroencephalography from the early thirties. Berger was a psychiatrist and his profession had very high hopes of the electroencephalogram (EEG) especially when it was finally accepted as a genuine phenomenon. Yet it is neurology and neurosurgery that received the more spectacular benefits of the tech- nique which revolutionized the practical and theoretical problems of epilepsy and greatly facilitated the detection of cranial neoplasms and the assessment of head injuries. Meanwhile the specific problems of psychiatry were only partly clarified by ths E E G which has shown itself to be of value mainly in the differential diagnosis of organic, epileptic and so- called functional disorders such as schizophrenia. Nevertheless certain findings in the psychoses do hold promise of ultimately assisting in the understanding of these conditions. While this field is beyond the scope of the present paper, it is important to take note of the application of the E E G in the related field of psychology, in both clinical appraisal and basic research on the determinants of behaviour. T h e purpose of this paper is to review briefly the general significance of the E E G and to evaluate its specific contribution in the field of disorders of communi- cation. General Significance of the EEG T h e normal E E G comprises complex signals of approximately sine- wave form, these waves being recorded at the scalp (Fig. 1) at frequen- cies up to about 30 c / s e c and voltages of a few microvolts. E E G characteristics are defined in terms of frequency, amplitude, wave-form, location, persistence and responsiveness. T h e r e are 4 main r h y t h m s : Tydskrif van die Suid-Afrikaanse Logopediese Vereniging, Vol. 13, Nr. : Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G. Κ. Nelson ι. Alpha. A rhythm at 8-13 c/sec from the parieto-occipital regions of normal adults (Fig. 2). It is present only when the person is awake, is maximal during relaxation and disappears when the eyes are opened. This is known as the blocking response of the alpha rhythm and implies an important role of the functions reflected by this activity in the processes of visual perception and imagery, since alpha blocking may also be seen during visual imagery. While other perceptual modalities such as hearing may also show such changes in the alpha rhythm, the blocking response is most consistent in association with visual processes, providing the basis for the hypothesis that this electrical oscillation represents a scanning system in the visual projection area of the cerebral cortex, which is employed in the integration and coding of information received from the eyes. T h e frequency of the alpha rhythm varies from person to person, and there is some evidence that individual mean frequency is a measure of central nervous speed reflected in temperament, such that relatively rapid reaction, impulsiveness, a wide span of attention and distractibility are associated with higher alpha frequencies, while individuals with lower mean alpha frequencies tend to be cautious, methodical and systematic (Mundy-Castle4 3). Amplitude of the alpha rhvthm is related to level of arousal in a curvi- linear manner, being maximal during relaxed wakefulness and minimal at the two extremes of sleep and hyperexcitation. Characteristic imagery mode is reflected in the index or percent-time of alpha rhythm, i.e. the number of seconds in a ioo-second sample of E E G during which alpha rhythms are apparent. While most--persons have indices of 30-90, low indices are associated with predominantly visual imagery, while high indices, and even alpha rhythms that do not block at all, are found in persons who make use mostly of verbal, kinesthetic or other types of non-verbal imagery. More recently positive correlations of alpha frequency with intelligence test performance have been reported by Mundy-Castle4 4 and Mundy- Castle and Nelson.4 5 2. Beta. These are rhythms of 14-30 c/sec, generally of lower amplitude than alpha and not specifically characteristic of any part of the brain. Fig. 1. Placement of E E G Elec- trodes: Electrode positions a n d names are in accordance with t h e recommendations of t h e I n t e r n a - tional Federation of Societies for E l e c t r o e n c e p h a l o g r a p h y a n d Clinical Neurophysiology. Recor- dings may be bipolar (connecting electrodes in serial chains, e.g. F P 1 - F 3 , F 3 - C 3 ) C 3 - P 3 ) P 3 - O I , etc.) or unipolar, referring each cortical electrode t o a " n e u t r a l " or reference electrode. Unless otherwise stated, all E E G figures in this paper show bipolar recor- dings. A1 C 4 O J O A ; Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders 7 Beta rhythms are associated with cortical activation, but are also found in light sleep. When more prominent than alpha activity, beta rhythms are regarded as a non-specific E E G abnormality. 3· Theta. Theta activity, at 4-7 c/sec is predominant in the E E G ' s of young children, and in sleep in persons of all ages. In a waking adult diffuse theta rhythms are abnormal and suggestive of epilepsy, organic brain disease or severe immaturity of the cortex. Focal theta rhythms are found in head injury and focal epilepsy and may indicate sub-cortical disturbance. 4. Delta. Delta activity comprises any potential fluctuation of c/sec or slower. It is abnormal except in very young children and in deep sleep at all ages. Otherwise focal or diffuse delta activity is generally an accom- paniment of organic pathology. In addition to these main rhythms, other E E G features are of great clinical significance. These include such abnormal features as spikes, sharp waves, and the distinctive wave-and-spike pattern. In general such phenomena are linked with the epilepsies, but are also sometimes found in behaviour disorders. Abnormalities in the E E G are seen in the E E G ' s of 5 to 15 % of the normal population. T h e rough classification of E E G abnormalities and their clinical cor- relates shown in T a b h 1 is a convenient although very inadequate summary. TABLE I : E E G ABNORMALITIES AND T H E I R M A I N C L I N I C A L CORRELATES Type/Location Diffuse or Generalized Localized or Focal Episodic or Pa- Centrencephalic epilepsy Focal epilepsy roxysmal Non-Episodic or Organic pathology Organic lesions non-Paroxysmal Epilepsy Epilepsy Immaturity Maturation defects Developmental Aspects. T h e E E G appears to be the result of largely hereditary factors as shown by the similarity in general pattern in identical twins. Nevertheless the brain rhythm record is a highly in- dividual trait, as unique as the fingerprints. Environmental factors may however bring about temporary or permanent alterations. Temporary changes are produced, by drugs such as alcohol, and by mild head injury, while severe head injury, disease, malnutrition and toxic agents such as lead may cause permanent changes. Apart from the effects of such hazards, the record remains relatively stable from early adulthood to old age. Rhythmic activity is first seen in the infant at the age of about 2 months at a frequency of 2 to 3 c/sec. This frequency increases with age (Fig. 3) until the adult (usually alpha-dominant) pattern becomes established at between 18 and 25 years of age. It is known that this Tydskrif van die Suid-Afrikaanse Logopediese Vereniging, Vol. 13, Nr. 1: Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G. Κ. Nelson development can be adversely affected by such disorders as protein deficiency (Nelson1 0). Activation Methods. Routine clinical E E G examination includes a com- prehensive recording of the brain waves in the resting state. In order to reveal possible latent abnormalities two activation methods are generally used to supplement this recording: (a) Photic stimulation (by means of a special stroboscope directed at the closed eyes); (b) Hyperventilation (deep breathing for three minutes). These techniques are described in full elsewhere (Nelson4 7). Main Areas of the Brain Concerned with Communication Vision and hearing are the two primary sensory modalities involved in the development of ordinary human communication. Disturbances of a sensory and motor kind related to these functions form the main theme of this account of the significance of the E E G . A brief consideration of the representation of these functions in the brain is a necessary pre- liminary to the survey of E E G findings. For reasons of brevity, almost exclusive attention is given to cerebral cortical representation. 1. Vision. Reference has already been made to the apparent role in visual perception of a cerebral neural process giving rise to the alpha rhythm of the E E G . T h e alpha rhythm originates in or near to the calcarine cortex of Area 17 at the occipital pole, but may also arise from the more anterior visual association regions in Areas 18 and 19 of the parietal lobe. Lesions in the more posterior regions tend to produce complete blindness if they are bilateral, or hemianopsia if unilateral. More anterior regions are implicated in binocular vision, while there is evidence that" both frontal and temporal areas are involved in visuo-motor co-ordination. A full account of the neuro-anatomical relations is given by Humphries.2 4 2. Hearing. T h e area of cortex primarily concerned with the reception of auditory signals lies in the temporal lobe, in Area 41 on the upper surface of this lobe which forms the lower bank of the Sylvian fissure. Auditory perception is mediated by the surrounding Area 42, covering most of the middle part of the upper surface of the temporal lobe. 3. Speech. Broca's area (Brodmann's area) is often considered to be of utmost importance in speech, but Jefferson2" considers it to be a highly overrated localized functional area since excision of it in man leads to only transient aphasia, while stimulation of the region results in movements of the larynx and crude vocalization without words. Penfield and Jasper4 9 point out that vocalization has representation of equal value in the dominant and non-dominant hemispheres and that either of the two areas may be removed without interference with speech. On the other hand these authors emphasize that stimulation of a speech area produces aphasia, and that such speech areas are in the left hemisphere in right-handed persons, while in left-handed persons they may be in either hemisphere. When the left hemisphere is severely injured in a right-handed child, speech may be lost for a period of months and is eventually re-established in the cortex Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders 9 of the right hemisphere. Otherwise the "speech" areas of the non-dominant hemisphere are functionally "silent". Four speech areas in the dominant hemisphere were described by Penfield and Jasper4 9 and Penfield and Roberts,5 0 in the frontal, parietal and temporal regions. Kriegf describes Area 40 as a semantic area, because obstruction of this region results in loss of "the highest level of speech". Area 22 is a syntactic area where injury may result in interference with the understanding of speech, or merely the distortion of sounds. A lesion in Area 39 produces nominal aphasia, the inability to assign names to common objects. Fulton 1 5 found that unilateral lesions of the 3rd left frontal convolution in monkeys and chimpanzees led to no apparent impairment of their capacity to vocalize. On the other hand, bilateral lesions in these cortical areas led to confusion and inability to carry out complex motor manouevres, a defect comparable to apraxia in right-handed. humans with lesions in Broca's area. Electrical stimulation of the cingular gyrus in monkeys produces vocali- zation responses identical to those that the animal might be expected to make under normal conditions (Smith5 0). Yet Penfield and Jasper4 9 found that stimulation of a cortical speech area in humans produces aphasia. These observations should not be allowed to obscure the role of subcortical mechanisms in speech; for example the subtle effects of stimulation of some areas around the 3rd ventricle were described by Sem-Jacobsen.54 T h e present paper is nevertheless primarily concerned with cortical manifestations as detected by the E E G . The Contribution of the EEG in Communication Disorders This brief report of E E G findings is based on data obtained from t h e ' following samples (Table 2). Most of these cases were referred to the N.I.P.R. for clinical E E G examination but a number were tested in the course of unrelated research projects. T A B L E 2 Disorder No. of Cases Visual 15 Auditory 2 Delayed speech 21 Aphasia 10 Dyslexia 3 Stuttering 5 Total: 56 Each defect will be considered separately in the light of concomitant clinical syndromes, with evaluation of the E E G findings. T h e nature of many of these cases necessitates a detailed individual description. Tydskrif van die Suid-Afrikaanse Logopediese Vereniging, Vol. 13, Nr. 1: Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) ΙΟ G. Κ. Nelson S E N S O R Y D E F E C T S Vision. T h e question is often asked: I n view of the apparently intricate involvement of the alpha rhythm in the process of visual perception, what are the E E G findings in blind persons? One of the earlier studies was carried out on Helen Keller (Still57). As most people know, Helen Keller became blind and deaf after a sud- den brief illness at the age of 19 months. An E E G recorded when she was 64 showed relatively low-amplitude occipital alpha rhythms, while "alpha" activity was prominent in the more anterior areas. This, it was suggested reflected changes in the functional organization of the cortex corresponding to the emphasis on the sense of touch or tactile discri- mination which she developed. T h e E E G findings in six cases of left occipital lobectomy were described by Masland et al.4" Sharp waves and beta activity were seen, in the temporal, central and frontal areas, and "overactivity" of the left temporal lobe was striking—alpha-like waves and high-voltage "sleep waves" were prominent in this region. T h e E E G in amblyopia was studied by Parsons-Smith4 8 who found abnormal records in 31 out of 50 cases, beta activity being particularly common. Bergman's7 account of unilateral loss of alpha rhythms in hemianopia was criticized by Cobb 9 who believed that in Bergman's cases the lesion responsible for hemianopia almost certainly extended beyond the primary visual system. In 30 blind and partially blind 8 to 9 year old children with retrolental fibroplasia, Metcalf41 found a 9 0 % incidence of E E G abnormality which was not related to intellectual or other characteristics, but was characterized by the unusual prominence of focal disturbances, generally maximal in the occipital regions. In five cases of retinitis pigmentosa associated with juvenile cerebral lipoidosis (Spielmeyer-Vogt disease) uniformly abnormal records with diffuse paroxysmal disturbances and runs at 2.5 to 4 c / s e c as well as waves- and-spikes and occasional variable interhemispheric asynchrony are -described by Ellingson and Schain.1 1 Other recent studies include that of Subirana and Oller-Daurella5 9 who obtained E E G ' s from two anophthalmic children, whose parents were first cousins. T h e records showed a badly organized background with diffuse fast activity. Both cases also showed occipital spikes and wave- and-spike activity. It was suggested that this reflected neurological lesions a n d / o r "functional" focal activity in the cortical visual areas. Jeannerod and Courjon 2 5 describe similar abnormalities ' in five blind children, proposing that occipital spikes in this context represent neural degeneration of the cortex. Lairy et al.3i studied partially sighted and blind children of school-going age, finding occipital spike foci on the left side in 2 5 % and on the right side in 4 % . It was concluded that cases of dyspraxia with sight occipital spikes are more or less reversible with re-education of the psycho-motor difficulty. EEG Findings in the Present Series. Results from 15 cases of visual defect are given in Table 3. T w o of the three cases with a clinical diag- Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders nosis of brain damage ( i , 2, 3) had abnormal E E G ' s , raising the possibility of post-traumatic epilepsy in both cases. Cases 4, 5, 6 and 7 had a clinical diagnosis of athetosis, quadriplegia and hemiplegia. All but one had abnormal E E G ' s suggestive of localized cerebral abnormalities, in each case involving the parietal area (Fig. 4). Case 7 had a normal record. T h e following three patients, Cases 8, 9 and 10 were epileptics and all had abnormal E E G ' s ; although the record of Case 8 did not show any E E G sign of the t u m o u r , the E E G revealed localized epileptogenic abnormalities in both Case 9 and Case 10 (Fig. 5). T h e remaining five miscellaneous disorders with accompanying visual defects are of interest: while it is not surprising that the patient with Riley's disease had a normal E E G (this is a transient disorder of child- hood) the findings were of positive value in the r e m a i n d e r : Case 12, diagnosis unknown, had a remarkable E E G in that occipital beta r h y t h m s seemed to have supplanted alpha activity; the record of Case 13 pointed to clear brain damage with post-operative epilepsy appearing as a disorder of concentration and memory; in Case 14 the E E G confirmed the presence of an organic abnormality in the right parietal area; Case 15 provided an opportunity for the application of another electrophysiological technique, namely electroretinography ( E R G ) , the measurement of the electrical activity of the retina (Fig. 6). T h e E E G , including the response to photic stimulation, was normal, but the E R G , although showing a normal wave- form on both sides, had an amplitude reduction of 50 p : r cent on the right. Evoked responses in the cerebral cortex showed a corresponding inequality when the eyes were independently stimulated by a flashing light, but both occipital lobes appeared capable of responses of equal amplitude. It was therefore concluded that the disturbance was peripheral and not central, but that the right eye was not totally inactive. Comment. T h e incidence of E E G abnormality in these 15 cases was extremely high, 11 cases having abnormal records ( 7 3 % ) , but this should be viewed in the light of the major clinical features, especially brain damage and epilepsy. F r o m the point of view of visual perception, useful diagnostic information was nevertheless supplied by the E E G in 7 instances, viz.: Cases 2, 9 and 10, in whom visual disturbances were shown to be of epileptic origin or at least related to epilepsy*; cases 4, 13 and 14 in whom a localized brain disturbance was demonstrated; case 15, in whom the combination of E E G and E R G resolved the problem of central or peripheral locus of a disturbance resulting in a visual defect. T h u s the E E G was of positive value in 4 7 % of these cases. Hearing. T h e E E G has been held to be of value in the investigation of hearing disorders related to speech difficulties. Abnormal E E G ' s were found *A case described by Strauss 5 8 is called to mind here—an 11-year-old boy suffered attacks of complete blindness, with preservation of consciousness, lasting from 2 to 3 minutes; the E E G showed almost continuous high-voltage 1.5-3 c/sec occipital, temporal and more rarely parietal wave-and-spikes; although neurological examination revealed no abnormality, the interpretation was of a centrencephalic disturbance with maximal effect in the occipital regions; the E E G abnormalities and clinical phenomena were promptly controlled by anticonvul- sant drugs. Tydskrif van die Suid-Afrikaanse Logopediese Vereniging, Vol. 13, Nr. 1: Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G. Κ. Nelson in 19 of 53 children with severe hearing loss (Marcus3 9). Disturbances had a predilection for the temporal lobes. Marcus held that the E E G arousal response (desynchronization of alpha activity) was an adequate index of hearing. T h e use of " E E G audiometry" (to be described in relation to case 17) is considered by Fisch1 2 and Gordon and Taylor 1 9 to be of great assistance in differentiating between peripheral and central deafness. T h e findings of Marcus and of Gottlieb et al.20 support the hypothesis that the cerebral mechanisms relevant to speech acquisition are simplified, facilitated and less prone to interference when control of speech, hand and eye is localized primarily in one hemisphere of the brain. Generally speaking the alpha rhythm shows a reduced amplitude in the dominant hemisphere, so that the consistency a n d / o r degree of inter hemispheric difference in ampli- tude of the alpha rhythms might well form a profitable basis for a systematic study of communicative disorders. EEG Findings in the Present Series. T w o cases of hearing defects are detailed in Table 2. T h e first of these (Case 16) was reported by the speech therapist to have a fluctuating ability to speak. T h e patient was intelligent and it was felt that deafness was not the whole trouble. T h e E E G was suggestive of a localized organic abnormality. T h e second patient, Case 17, who was apparently deaf, had an E E G suggestive of epilepsy associated with a brain abnormality in the left frontal area. T w o months later he was given a "hearing E E G " , signals at a variety of frequencies and intensities being applied to each ear independently in an attempt to assess cortical responsiveness. On this occasion averaging techniques were not used, but an apparent attenuation or augmentation of spontaneous electrical activity was seen in response to 81 of the 142 stimuli presented. T h e range of frequencies covered by these 81 stimuli suggested that, if the cortical responses were genuine, there was little if any hearing loss in this case. Although the findings are similar to those of Lesny and Odvarkova3 5 in normal children and adults, the results of such simple tests are to be treated with considerable reserve owing to the variability of the spontaneous E E G pattern, especially in children. A series of studies utilizing automatic averaging and integrating techniques has been planned to deter- mine more precisely the contribution to be expected from the E E G in this area. Preliminary experiments by Appleby et al} have yielded promising results. Comment. In only one of these patients with suspected hearing defects was an electrical abnormality demonstrated in an area approximating the auditory reception region in the superior portion of the temporal lobe. This was Case 16, where a left parieto-temporal abnormality was-'detected. How- ever, it must be stressed that such focal E E G signs should not lightly be invested with specificity, since they may occur in a variety of syndromes such as epilepsy, psychopathy and delinquency, and their aetiology may be found in head injury, malnutrition (Nelson4 6) or genetic factors (Mundy- Castle45). Nevertheless Gervasio and, Marenzi's studies17 have shown the value of the E E G in differentiating defects in structures and functions up to and including the cochlea from those more centrally located. In a series Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders 13 of 165 deaf-mute children E E G abnormalities were found in 7 4 % ; the results suggested that spreading or localized E E G disturbances indicated deafness consequent on brain injury caused by infective, toxic or traumatic factors; excessive, beta activity was suggestive of congenital deafness (hereditary or otherwise) or inflammatory ear disease. Furthermore, inde- pendently of the nature of the injury, deafness due to cochlear lesions was characterized by a high incidence of normal or mildly abnormal EEG's, while interruption of the auditory fibres at the post-cochlear or cortical levels was associated with irritative abnormalities in the form of "slow spikes" or bursts of beta, theta or delta activity. T h e possible relationship of hearing difficulties to epileptic disorders should not be overlooked, particularly if there is any apparent fluctuation in auditory efficiency. Gowers2 1 described auditory loss before seizures in 6 patients, in one of whom there was concomitant temporary loss of vision. More specifically the frequent association of apparent hearing defects with more general behavioural problems deserves attention in view of the functions of the temporal lobe, which, besides containing the primary receptive area for auditory sensation, also plays a profound role in the behavioural and emotional life of the individual (Chatfield8). This very brief survey of E E G findings in visual and auditory anomalies should serve as a cautionary introduction to a consideration of the E E G in communicative disorders proper. Only if the excessive optimism asso- ciated with the initial enthusiasm that generally surrounds the application of a technique such as the E E G in such a highly specialised field is first dispelled are the actual electro-clinical correlations likely to emerge. T h e following is a brief survey of some types of communicative disorder, representing the more common syndromes of, delayed speech, aphasia and stuttering in relation to the electrical activity of the brain. D E L A Y E D S P E E C H Speech usually develops between the ages of 1 year and 18 months, otherwise deafness is usually suspected. If this cannot be demonstrated the possibility of a mental defect is raised, or failing this, in the words of Adams1, "some psychic disturbance or special neurological defect", but he goes on to point out that there is often no evidence of brain injury. In a group of 41 children with severe speech retardation Webb and Lawson114 found that 13 had generalized and 11 focal E E G abnormalities. A high incidence of E E G abnormality was also reported by Berges et al." in 45 children including cases of delayed speech, stuttering and difficulties in articulation: nearly 50% showed an inter-hemispheric asynchrony, with or without a spike focus, while an equivalent propor- tion had paroxysmal E E G disturbances during hyperventilation and photic stimulation. Most of these signs were found to disappear with the normalization of speech. An interesting interference was that a normal E E G in a child with delayed speech connoted an unfavourable progno- sis, a view reminiscent of that of Hill2 2 in relation to psychopathy. Tydskri van die Suid-Afrikaanse Logopediese Vereniging, Vol. , Nr. 1: Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G. Κ. Nelson EEG Findings in the Present Series. E E G ' s were obtained from 21 patients aged 20 months to 10 years (Table 4). T h e overall incidence of abnormality was 17 out of 21 (81%), the E E G being severely ab- normal in one case (spastic quadriplegia), moderately, abnormal in 11, mildly abnormal in one and doubtful in the remaining four. T h e four patients with normal E E G ' s comprised: behaviour problem, aged 7; mental defect, aged 5 years 11 months; post meningitis, aged 2 years 8 months; an otherwise normal child aged 6 years 9 months T h e most common abnormality w.as excessive parieto-occipital or diffuse slow activity, suggestive of cortical immaturity, found in 5 patients. Focal disturbances were seen in 8 patients, in the right parietal area in 3, and in the right post-temporal, right fronto-centro-temporal, left frontal, left temporal and left parieto-temporo-occipital regions in one patient each. T w o children had marked inter-hemispheric asynchronies in their EEG's. It is perhaps not surprising that five of these patients showed E E G evi- dence of delayed cortical development. In such cases little of prognostic value can be gained from the E E G without repeated studies at intervals of 3 to 6 months. T h e focal disturbances had no consistent location, either in a lobe or hemisphere. While some of these perhaps reflected localized maturation defects, three were of the type usually associated with epilepsy ( F i g · 7)· Only one of these (Case 28) had any history of a disorder related to epilepsy, yet all three showed types of E E G abnormality usually associated with epilepsy. In this connection Adams1 observed that if external electrical stimulation of the cortex is followed by inability to speak, it is logical to assume that spontaneous electrical dysrhythmia may be responsible for de- layed speech in children. Another two cases were brother and sister. Although the E E G abnor- mality was posterior in Case 19 and anterior in Case 20, the right temporal lobe was implicated in each, and the possibility is raised of a genetic contribution to a localized maturation defect in these two children. Comment. Although the incidence of E E G abnormality in these patients with delayed speech must also be viewed against the background of their more general disorders, the E E G provided valuable information in almost all cases, either confirming dysfunction of the brain or differentiating be- tween possible brain lesions and immaturity. A P H A S I A It is accepted that aphasia is often a manifestation of a localized dysfunc- tion of the brain, although evidence for this may be absent in many cases. T h e r e is also reason to suspect that aphasia may at least be triggered by psychogenic factors in some cases. From the neurophysiological standpoint, Adams1 showed that electrical stimulation of a speech area of the cortex was accompanied by aphasia for the duration of the stimulus. T h e role of epileptic discharges in the brain was. considered by Volterra63 who concluded that there are critical and "paracritical" speech changes of a definitely epileptic nature, but also Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders 15 "non-critical" disturbances with no manifest epileptic, other neurological, intellectual or sensory defect, although the E E G shows a "grave irritative epileptic dysrhythmia", generally localized in the brain regions concerned with speech. Kreindler et al:'J found marked interhemispheric asymmetries in the blocking response of the alpha rhythm in 19 of 25 aphasic patients. It was inferred that the absence of alpha rhythm blocking in the dominant hemi- sphere might be attributed to a unilateral alteration of reticulo-cortical interrelations. Nevertheless severe aphasia of various types is commonly associated with " a normal E E G (Gibbs and Gibbs 1 8 ), but where the record is abnormal, these authors claim a frequent association with mid-temporal slow wave foci. E E G ' s were obtained by Liberson"' from 18 aphasic patients, 13 of whom had abnormal records. Of these 10 showed depression or suppression of evoked potentials in the affected hemisphere (all 10 suffering from middle cerebral artery thrombosis), while 3 had bilaterally abnormal EEG's. These findings revealed a high degree of concordance with the evaluation of the speech therapist. EEG Findings in the Present Series. E E G ' s were obtained from 10 patients with aphasia, aged 3 to 37 years. There was a history of epilepsy in two cases, while the remainder comprised one case each of spastic quadriplegia, surgical anoxia, head injury, behaviour disorder, mental re- tardation, "bad home environment", uncomplicated speech and spatial difficulty, and febrile illness. T h e E E G was normal in only two of these patients: an 8 i year old child with a bad home environment and a 3 year old child with a history of convulsions. T h e incidence of E E G abnormality was thus 8 0 % in this small sample, the record being severely abnormal in three cases (quadri- plegia, behaviour disorder and surgical anoxia), moderately abnormal in three (speech and spatial difficulty, febrile illness and mental retardation), and doubtful in two (head injury, epilepsy). T h e types of abnormality were, as in the group with delayed speech, varied: excessive non-paroxysmal slow activity was seen occipitally in the case of speech and spatial difficulty, in the left temporal area in surgical anoxia, and in the right hemisphere in head injury. Focal bursts at various frequencies a n d / o r spikes a n d / o r waves-and-spikes were seen in spastic quadriplegia (right-frontal), febrile illness (temporal and generalized), behaviour disturbance (right hemisphere), and mental retardation (left frontal and fronto-temporal). Although there was again no consistent pattern of abnormality, the E E G was of positive value in 8 of these 10 cases: Case 39: An 8-year-old right-handed boy had speech and spatial difficulty, with no other symptom. T h e E E G suggested a severe cortical maturation defect, or organic pathology, involving the left occipital area in particular (Fig. 8), Case 40: A 3-year-old boy with spastic quadriplegia and aphasia had no epi- leptic manifestation but his E E G showed numerous runs of high-voltage delta Tydskrif van die Suid-Afrikaanse Logopediese Vereniging, Vol. 13, Nr. 1: Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G . Κ. Nelson activity and waves-and-spikes, sometimes generalized but with a focus in the right frontal area. Case 41: An 81-year-old boy with expressive aphasia had a bad home environ- ment. Since he had tried to formulate words his defect was regarded as probably not psychogenic. However, his E E G showed no evidence of either organic patho- logy or delayed maturation. Case 42: A 4-year-old boy had had' a febrile illness months previously, after which he stopped talking and walking. An organic brain lesion was suspected but the E E G showed generalized wave-and-spike outbursts indicative of epi- lepsy, with no sign of a focal disturbance (Fig. 9). Case 43: A 30-year-old woman had a heart operation 3 years prior to her E E G . D u r i n g the operation she suffered a cerebral haemorrhage with consequent total right paralysis and inability to speak, read or write. Speech therapy had been success- ful to a limited d e g r e e : while she was able to speak slowly b u t with some echo- lalia, her E E G (Fig. 10) showed a clear focus of delta, theta and alphoid r h y t h m s in the left temporal area. H a d it been possible to carry out repeat E E G ' s the patient's progress might have been more precisely charted and even predicted. Case 44: A 23-month-old child had fallen off a table at the age of 17 m o n t h s and ceased to speak, although he was able to convey information by signs. His behaviour deteriorated and he was reported to be losing his memory. T h e E E G was doubtful due to a persistent slight asymmetry between the hemispheres, delta activity arising chiefly from the right temporal area. T h i s could reflect a matura- tion defect or an organic lesion. A repeat E E G at the age of 31 m o n t h s resolved the problem. T h i s record was normal, suggesting that the previous record had reflected maturation processes. H e had meanwhile recovered the ability to speak. Case 45: A 7-year-old boy was referred because of a speech defect which had appeared at an early age and resisted therapy. H e was an illegitimate child, ill- treated- by his mother and admitted to an orphanage. T h e first E E G was doubt- ful showing various disturbances of quite obscure significance. T h e second E E G , 3 weeks later, was similar, b u t raised the question of a left-sided cerebral abnor- mality. T h e third E E G , after a further 6 i m o n t h s was unequivocally abnormal, showing r u n s and bursts of theta activity, chiefly of temporal origin, with bursts of delta waves often confined to the left temporal area. His speech had improved b u t his general behaviour had shown marked deterioration. T h e E E G abnorma- lities were interpreted as reflecting a severe maturation defect underlying the behavioural deviation. Case 46: A 3-2-year-old boy gave the impression of being retarded and aphasic. A neurological examination led to the provisional diagnosis of anterior cerebral abnormality. T h i s was confirmed by the E E G which showed a clear left fronto- temporal focus of spikes and sharp waves. C o m m e n t . G o w e r s 2 1 a n d P e n f i e l d a n d J a s p e r 4 9 d e s c r i b e d a p h a s i a i n e p i l e p t i c s , o f t e n f o r m i n g t h e m o s t i m p o r t a n t s i g n of t h e s e i z u r e , b u t a l w a y s a s s o c i a t e d w i t h a n a b n o r m a l d i s c h a r g e i n t h e d o m i n a n t h e m i s p h e r e . T h e l a t t e r a u t h o r s s t r e s s t h a t w h i l e a n e p i l e p t i c d i s c h a r g e p r o d u c e s a c t i v a t i o n a n d i n t e r f e r e n c e , t h e effect o n s p e e c h is c o n f i n e d t o i n t e r f e r e n c e . T h e y q u o t e a c a s e i n w h i c h t h e E E G c o n t a i n e d s p i k e s f r o m t h e left i n f e r i o r t e m p o r a l l o b e . A s A d a m s 1 p u t s it, " e p i l e p s y i n a s p e e c h c e n t r e " d o e s n o t p r o d u c e a " p o u r i n g o u t of w o r d s " d u r i n g t h e a t t a c k , b u t i n s t e a d t h e r e is a n i n a b i l i t y t o s p e a k ; i n s p i t e of t h e fact t h a t s t i m u l a t i o n of a c o r t i c a l s p e e c h a r e a c a u s e s m o v e m e n t of t h e p e r i p h e r a l s p e e c h a p o a r a t u s , t h e r e is n o e x t e r n a l v o c a l i z a t i o n . T y p i c a l of s u c h a n effect is a c a s e d e s c r i b e d b y Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders 17 Gastaut ei al."' of a man with seizures accompanied by rhythmic left tem- poral and post-temporal spikes, during which he had expressive aphasia. T h e potential contribution of the E E G in cases where a psychogenic factor is in question is well exemplified by a case cited by Bagchi et al*: a highly intelligent girl with no personal or familial history of epilepsy developed sibling rivalry and stopped talking. T h e r e were no other behavioural changes. T h e E E G showed severe abnormality in the form of generalized wave-and-spike discharges. N o follow-up data are available, but such a record is strongly suggestive of epilepsy and would provide a strong basis for therapy based on anticonvulsants even though overt epilep- tic symptoms are absent. D Y S L E X I A T h e concept of cerebral dominance has received much attention in the literature relating to reading difficulties, but Hughes et alP and Kennard and Rabinovitch" found no correlation between E E G abnormalities and either reading difficulty or cerebral dominance. T h e study of Webb and Lawson" previously cited was undertaken because of the frequent obser- vation that degree of efficiency in reading in a given child often varies from day to day or even from hour to hour, "as though the deficit were intermittent or paroxysmal." T h e y describe a case of a 13-year-old child with severe dyslexia whose E E G was abnormal due to left temporal spikes. An identical twin had a similar E E G but no other defect. In the opinion of these authors this suggests the possibility of an organic defect underlying dyslexia in the one twin which was demonstrable by the E E G alone. A recent investigation by Knott et aV of 50 children with reading dis- abilities revealed abnormal E E G ' s in 31 (84%), of whom 15 had 14 and 6 per sec positive spikes in their sleeping EEG's. Three groups were dis- tinguished : (a) Normal E E G ' s ; (b) Abnormal E E G ' s with no spikes; (c) Abnormal E E G ' s with spikes. There was however no significant difference in reading disability or any other characteristic between these groups. Of the 31 abnormal records 41% contained positive spikes while 50% showed posterior slow dys- rhythmia. T h r e e patients were studied. From the first of these only one E E G was obtained, but the other 2 were intensively investigated. Case 47: A 21-year-old male mill-hand was stated to have congenital alexia. H e could understand written and spoken speech very well but was unable to read or write. T h e r e were no clinical abnormalities and he gave the impression of having a good I.Q. H e was right-eyed and right-footed. T h e E E G was normal but very unusual in that alpha rhythms at 9-10 c/sec were more prominent frontally than parieto-occipitally, amplitudes being 20 and 15 microvolt respec- tively (Fig. 11). Phase relationships showed that the anterior rhythms were iden- tical with those of more orthodox location, and were thus not independent alphoid rhythms. Case 48: A 12-year-old boy was referred because of dyslexia. His first E E G was moderately abnormal due to a number of medium-high voltage 2 c/sec runs Tydskri van die Suid-Arikaanse Logopediese Vereniging, Vol. 13, Nr. 1: Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G. Κ. Nelson from the left parieto-occipital area, and some asynchrony of the alpha rhythms. At this stage the interpretation was of a maturation defect or organic abnormality in the left parieto-occipital area. A second E E G 5 ϊ months later showed a reduc- tion of slow activity which was now more prominent on the right side, although still of parieto-occipital origin. A third E E G after a further 8 i months showed little change, except that parieto-occipital slow activity appeared independently on both left and right sides, giving some evidence of sub-cortical involvement. T h e final interpretation can only be made with confidence after further E E G ' s have been' obtained. T h e r e has been little change in the dyslexia. Case 49: A 3-year-old boy with a fluctuating behaviour pattern and mild right hemiplegia following surgery for a left cerebral haemorrhage caused by a fall at the age of i o months. His E E G showed several focal paroxysmal 1-2 per second wave-and-spike discharges from the right parieto-temporal region, being suggestive of an epileptogenic abnormality in this area (Fig. 12). His second E E G a year later was more abnormal due to an increase in number and voltage of the focal dis- turbances which had spread to the fronto-central areas as well. After another year the E E G was improved in that wave-and-spike disturbances were less prominent and confined to the right parietal area. A fourth E E G after another i o months, at the age of 5 years 8 months, was still abnormal but showed further improvement due to reduced amplitude of abnormalities and dissociation of spikes and slow waves. j And this time dyslexia became apparent. T h e r e was some improvement in this respect, followed by a relapse prior to the fifth E E G at the age of 7 years. T h e record had changed, containing numerous isolated spikes and larval waves-and- spikes, especially from the left frontal area. After a further one and a half months isolated spikes were seen in the left temporal, fronto-temporal and parietal areas, with some slow activity in the homologous regions of the right hemisphere. Read- ing difficulties continue. A t n o s t a g e h a s t h i s p a t i e n t g i v e n a n y sign of e p i l e p s y , yet t h e E E G a b n o r m a l i t i e s a r e t h o s e m o s t c o m m o n l y a s s o c i a t e d w i t h e p i l e p s y . W h e t h e r o r n o t t h i s is a c a s e of l a t e n t e p i l e p s y , it is s t r i k i n g t h a t t h e E E G a n o m a l i e s a p p e a r t o a r i s e i n t h e r e g i o n s of t h e d o m i n a n t h e m i s p h e r e c o n c e r n e d w i t h r e a d i n g . I t is h o w e v e r i m p o r t a n t t o n o t e t h e fluctuating n a t u r e of his d i s - o r d e r , c h a r a c t e r i z e d b y i n t e r m i t t e n t d i s t r a c t i b i l i t y a n d r e d u c e d s t a m i n a . C o m m e n t . T h e s e t h r e e cases i l l u s t r a t e o n c e m o r e t h e v a r i e t y of E E G a b n o r m a l i t i e s a s s o c i a t e d w i t h d i s o r d e r s of t h e a p h a s i c v a r i e t y . T h e y a l s o s e r v e t o u n d e r l i n e t h e i m p o r t a n c e of serial s t u d i e s t o t a k e a c c o u n t of c h a n g e s d u e t o m a t u r a t i o n . S T U T T E R I N G A n e a r l y p a p e r b y T r a v i s a n d K n o t t 6 0 r e p o r t e d n o difference i n E E G f r e q u e n c y b e t w e e n n o r m a l s p e a k e r s a n d s t u t t e r e r s , b u t in t w o s t u t t e r e r s t o n i c s p a s m s w i t h o u t v o c a l i z a t i o n w e r e a c c o m p a n i e d b y h i g h v o l t a g e s p i k e s i n t h e E E G , s u g g e s t i v e of e p i l e p t i c i n v o l v e m e n t . I n 1 9 3 7 a f u r t h e r r e p o r t b y T r a v i s a n d M a l a m u d 6 2 a g a i n i n d i c a t e d n o difference i n E E G f r e q u e n c y b e t w e e n s t u t t e r e r s a n d c o n t r o l s , a n d a t h i r d p a p e r ( T r a v i s a n d K n o t t 6 1 ) s u p p o r t e d t h e s e r e s u l t s . A s u b s e q u e n t i n v e s t i g a t i o n ( L i n d s l e y 3 7 ) d i d h o w e v e r r e v e a l i n t e r h e m i - s p h e r i c differences in b r a i n p o t e n t i a l s i n s t u t t e r e r s , a n d F r e e s t o n e 1 3 · 1 4 f o u n d t h a t s t u t t e r e r s h a d a h i g h e r a l p h a a n d b e t a a m p l i t u d e t h a n n o r m a l Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders 19 speakers and that this increased further during stuttering. In addition there was relatively little amplitude difference between the hemispheres in stutterers, who also showed less alpha blocking with speech. These features would suggest a diminished focus of attention in stutterers, but Freestone's view was not that the neurological differences suggested by the E E G results were the cause of stuttering but that they acted "as potential sub- soils in which stuttering may arise". In 1943 Douglass1 0 reported that, in silence, normal speakers showed more alpha blocking in the right hemisphere, stutterers in the left. During speech this difference did not appear. His sample of 20 stutterers showed more bilateral alpha blocking during speech than in silence and he con- cluded that speech has a greater attention value for stutterers. In the same year Knott and Tjossen'1 published data supporting the view of Douglass and interpreted these as favouring the lateral dominance theory of stutter- ing. In 1954 Knott and Correll2 8 in a study of the E E G ' s of 14 stutterers found "no very striking difference" between these and the records of non- stutterers, although the former had a slightly higher alpha amplitude. Although Rheinberger et al:'' were also unable to find any significant differ- ence in the E E G ' s of 10 stutterers and 10 non-stutterers, and Scarborough's5 3 study accorded with this, Pierce and Lipcon 5 1 found abnor- mal records in 2 2 % of stutterers and only 8% of a control group. Other differences relating to clinical history and psychological assessment led Pierce and Lipcon to the conclusion that stuttering as a habit is attribut- able to interrelated psychic, social and organic factors. In line with this hypothesis is the recent report by Berges et al.6 already cited in connection with delayed speech. Morin 4 2 investigated 30 young stutterers before and after speech therapy which was successful in 9 cases, produced an improvement in 14 and failed in the remaining 7. Morin claims that the E E G has a prognostic value since all 7 failures had normal E E G ' s while most of the others had abnor- mal records with "slow paroxysmal discharges". Where the E E G was most abnormal success was spectacular and rapid. In addition to these implications concerning the relationship between brain function and stuttering, there is no doubt that some cases of stutter- ing are associated with frank but unusual epileptic patterns. T w o such cases are described by Anastopoulos et al.2 Furthermore, assessments of capillary blood oxygen saturation in stutterers during stress resemble those of paranoid and epileptic patients rather than those of neurotics (Levett Doust3 8). EEG Findings in the Present Series. E E G ' s were obtained from five male stutterers aged 8 to 29. In four patients the E E G was abnormal, and the remaining case had an unusual record: - Case 50: An 8-year-old boy was classified as brain damaged because of marked difficulty in conceptualization, mirror-writing and a history of seizures. His mother had resented her pregnancy and he was born after a five-day labour. H e started to stutter not long before the E E G which was grossly abnormal due to Tydskri van die Suid-Afrikaanse Logopediese Vereniging, Vol. 13, Nr. 1: Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G. Κ. Nelson a focus of slow activity in the left parietal region suggestive of an organic dis- turbance. A repeat E E G i o months later showed little change. Case 51: A 13-year-old boy was referred because of stuttering and a tic. N o history was available. His E E G was of doubtful normality owing to excessive theta activity, raising the question of cortical immaturity. Case 52: A 19-year-old army recruit was normal except for a marked stutter. His E E G was severely abnormal due to an almost continuous focus of slow activi- ty in the right post-temporal area, and severe slowing with hyperventilation (Fig. 13). Case S3- A 19-year-old toolmaker had a history of sudden onset of stuttering at the age of 8 years, following the divorce of his parents and subsequent remar- riage of his father. His E E G was moderately abnormal due to excessive sometimes paroxysmal theta and beta activity from the right post-temporal region. When asked to read aloud, verbal blocking was accompanied by brief bursts of temporo- occipital 6-7 c / s e c activity. Case 54: A 29-year-old man, normal in all respects except for his stutter, had a normal but unusual E E G . During reading there was marked lambda variant activity at 5-7 c/sec. At halts due to stuttering the following phenomena were seen : (a) Brief bursts of occipital 12-14 c / s e c activity (Fig. 14). (b) Suppression of lambda variant activity. (3) Traces of irregular occipital beta rhythms. T h e first of these (12-14 c / s e c bursts) preceded the halts slightly, while sup- pression of lambda activity generally followed them. Lambda activity is often seen during successful reading and has been reported to disappear during stutter- ing. T h e clear augmentation of alpha activity during stuttering is suggestive of fluctuating attention. Comment. In these five cases the only abnormality of any apparent con- sistency is the temporal or post-temporal disturbance in three patients. All were right-handed, yet the focus was in the left, or presumably domi- nant, hemisphere in only one case. T h e significance of such localized abnormalities and of E E G changes accompanying stuttering will be dealt with in a subsequent report of an experimental study of stutterers. Conclusions T h e data presented here provide little reason for optimism on the part of those seeking straightforward correlations between communicative disorders generally and the electrical activity of the brain. In spite of the high inci- dence of E E G abnormality in these patients, this would appear to relate more directly to an underlying clinical syndrome such as epilepsy which need not necessarily be accompanied by any disorder of a sensory or motor kind concerned with communication. Although some of these cases, particularly those with aphasia and stuttering, demonstrate focal abnormalities, such abnormalities may occur in the dominant or sub-dominant hemispheres, although the main speech centres are to be found in the dominant hemisphere. Such cases merely serve to support what is known of the significance of speech and other centres in the dominant hemisphere. On the other hand an actively abnor- mal discharge in the sub-dominant hemisphere can disturb the operation Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders 21 of the crucial centres in the dominant half of the brain. Such an abnormal discharge could have its origin in an injured portion of brain tissue, in an epileptogenic focus or even in a region which has failed to mature at the same rate as the remainder of the brain. Research in this field must however constantly take account of the recent warning of Stern5 5 that the assumption that the brain is a "master organ" controlling other physiological systems, can not exclude the effect of these other systems on the activity of the central nervous system. In the following paper the question is raised of the relative contribution of brain dysfunction (as reflected in the E E G ) to stuttering, and the effect of stuttering oh concomitant brain activity. It is the detection and localization of sites of abnormal brain function giving rise to a variety of clinical symptoms amongst which may be a disorder of communication, that the main practical benefit is to be derived from E E G examination at the present time. Concomitantly the common problem of the relative contribution .of organic and psychogenic factors to the development of a communication disorder can often be resolved with the assistance of an EEG. It remains to be discovered whether refinements of the basic approach to the E E G , such as the study of evoked responses and the analytical tech- niques of auto- and cross-correlation, will throw more light on the precise role of the electrical activity of the brain in the determination of the efficiency of man's communication with his world. Summary A general introduction to electroencephalography (EEG) is given, followed by a brief outline of the main brain areas concerned with vision, hearing and speech. Previous E E G findings in sensory defects, delayed speech, aphasia, dyslexia and stuttering are considered and discussed in the light of E E G ' s from representative cases. Finally the value of the E E G in the diagnosis and study of communication disorders is appraised. Opsomming 'n Algemene inleiding tot elektroenkefalografie (EEG) word aangebied. Daarop volg 'n kort oorsig van die vernaamste breingebiede wat by gesig, gehoor en spraak betrokke is. Vorige EEG-bevindings by waarnemings- gebreke, vertraagde spraakontwikkeling, afasia, disleksia en gehakkel word beskryf en in die lig van E E G ' s van verteenwoordigende gevalle bespreek. Laastens word die waarde van die E E G in die diagnose en studie van kommunikasiesteurings oorweeg. T h e assistance and co-operation of the following is greatly appreciated: Forest T o w n School for Spasties, Johannesburg; Miss .Ina van Wyk and Miss Barbara Pethnick, of the Division of Neuropsychology, National Institute for Personnel Research, Johannesburg. Tydskrif van die Suid-Afrikaanse Logopediese Vereniging, Vol. , Nr. : Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G. Κ. Nelson REFERENCES Ι . Adams, J. (1958): EEG findings in children with delayed speech, Electro- enceph. clin. Neurophysiol., 10, 358. 2. Anastasopoulos, G., Diacoyannis, Α., and Routsonis, K . (1958): Begaiment et epilepsie temporale. Rev. 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Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders 23 29. Knott, J. R., Correll, R. E. and Shepperd, J. N . (1959): Frequency analysis of electroencephalograms of stutterers and non-stutterers. J. Speech Hearing Res., 2, 74-80. 30. Knott, J.· R., Muehl, S. and Benton, A. L . (1965): Electroencephalograms in children with reading disabilities. Electroenceph. clin. Neurophysiol., 18, 513. 31. Knott, J. R. and Tjossem, T . D. (1943): Bilateral electroencephalograms from normal speakers and stutterers. J. exp. Psychol., 32, 357. 32. Kreindler, Α., Crighel, E., Poilici, I. and Rzeznicka, S. (1962) : EEG and vasomotor reactivity in aphasia. Electroenceph. clin. Neurophysiol., 14, 567. 33. Krieg, W. J. S. (1957): Brain Mechanisms in Diachrome, 2nd edition, Evans- ton, 111., Brain Books. 34. Lairy, G. C., Harrison, A. and Leger, Ε. M . (1965): Asynchronous bi-occipital EEG foci of spikes in partially sighted and blind children of school age. Electroenceph. clin. Neurophysiol., 18, 723. 35. Lesny, I. and Odvarkova, J. (1959): The influence of sonic stimulation of a constant tone of different frequencies on human electroencephalogram especi- ally in children. Electroenceph. clin. Neurophysiol., 11, 178. 36. Liberson, W. T . (1965): The study of evoked potentials in aphasics. Electro- enceph. clin. Neurophysiol., 18, 515. 37. Lindsley, D. B. (1940): Bilateral differences in brain potentials from two cerebral hemispheres in relation to laterality and stuttering. J. exp. Psychol., 26, 211-225. 38. Lovett Doust, J. W. (1956): Stress and psychopathology in stutterers. Canad. J. Psycol., 10, 31-37. 39. Marcus, R. E. (1951): Hearing and speech problems in children. Observa- tions and use of electroencephalography. Arch. Otolaryng., 53, 134-146. 40. Masland, R. L., Austin, G. and Grant, F. C. ( i 9 4 9 ) : The electroencephalo- gram following occipital lobectomy. Electroenceph. clin. Neurophysiol., 1, 273- 282. 41. Metcalf, D. R. (1959·): Electroencephalographic findings in ex-premature in- fants with partial and complete blindness due to retrolental fibroplasia. Elec- troenceph. clin. Neurophysiol., 11, 182. 42. Morin, S. (1965): EEG correlates of stuttering. Electroenceph. clin. Neuro- physiol., 18, 425. 43. Mundy-Castle, A. C. (1955): The relationship between primary-secondary function and the alpha rhythm of the electroencephalogram. J. Nat. Inst. Per- sonnel Res., 6, 95-102. 44. Mundy-Castle, A. C. (1958): Electrophysiological correlates of intelligence. J. Personality, 26, 184-199. 45. Mundy-Castle, A. C. and Nelson, G. K. C1962): A neuropsychological study of the Knysna forest workers. Psychol. Afr., 9, 240 : 272. 46. Nelson, G. K. (1959): The electroencephalogram in kwashiorkor. Electro- enceph. clin. Neurophysiol., 11, 73-84. 47. Nelson, G. K. ( i 9 6 0 ) : The measurement and significance of brain rhythms. Trans. S. Afr. Inst. Elect. Eng., 51, 2-17. 48. Parsons-Smith, G. (1953): Activity of the cerebral cortex in amblyopia. Brit. J. Ophth., 37, 359. 49. Penfield, W. and Jasper, Η. H. ( i 9 5 4 ) : Epilepsy and the Functional Anatomy of the Human Brain. Boston, Little. 50. Penfield, W. and Roberts, L. (1959): Speech and Brain Mechanisms. Prince- ton, N.J., Princeton Univ. Press. 51. Pierce, C. M . and Lipcon. Η. H . (1959·): Stuttering: clinical and .electro- encephalographic findings. Mil. Med., 124, 511-519. 52. Rheinberger, Μ . B., Karlin, I. W. and Bertram, A. B. (i943~>: Electro- encephalographic and laterality studies of stuttering and non-stuttering chil- dren. Nervous child, 2, 117-133. 53. Scarbrough, Η. E. (1943): Quantitative and qualitative analysis of EEG's of stutterers and non-stutterers. J. Exp. Psychol., 32, 156-167. 54. Sem-Jacobsen, C. W. (1962): Electrical stimulation-effects on speech in some areas around the third ventricle. Electroenceph. clin. Neurophvsiol., 14. 956. 55. Stern, J. A. (1965): Relationship between the EEG and other physiological measures in man. In: Applications of Electroencephalography in Psychiatry. Wilson, W. P. (Ed.), Durham, N. C., Duke Univ. Press. 56. Smith, W. K. (1Q45): The functional significance of the rastral cin^ular cor- tex as revealed by its responses to electrical excitation. J. Neurophysiol., 8. 241-255. Tydskrif van die Suid-Afrikaanse Logopediese Vereniging, Vol. 13, Nr. 1: Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G . Κ. Nelson 57. Still, W . C. (1947): An electroencephalographic study of Helen Keller. Arch. Neurol. Psychiat., 57, 629-632. 58. Strauss, H . (1963): Paroxysmal blindness. Electroenceph. clin. Neuro-physiol., 15, 921. 59. S u b i r a n a , A. a n d Oller-Daurella, L . (1965): EEG study of two cases of anophthalmia. Electroenceph. clin Neurophysiol., 18, 723. 60. Travis, L . E. and K n o t t , J. R . (1936): Brain potentials from normal speakers and stutterers. J. Psychol., 2, 239. 61. T r a v i s , L . E. and K n o t t , J. R. (1937): Bilaterally recorded brain potentials from normal speakers and stutterers. J. Speech. Dis., 2, 239. 62. T r a v i s , L . E. and M a l a m u d , W . (1937): Brain potentials from normal sub- jects, stutterers and schizophrenic patients. Amer. J. Psychiat., 93, 929. 63. Volterra, V. (1961): Speech disturbances as an expression of critical or. latent epilepsy. Clinical and EEG aspects. Electroenceph. clin. Neurophysiol., 13. 135- 64. W e b b , Ε. M . a n d L a w s o n , L . (1956): The EEG in severe speech and reading disabilities of childhood. Electroenceph. clin. Neurophysiol., 7, 168. APPENDIX C 4 . - P 4 TA- - OA FFl-Fi -01 Τtoo \uV EYES t OPENEFT e y w t ^ ' ' " Λ Γ CLOSE» ^ Fig. 2. N o r m a l Adult E E G : Alpha r h y t h m s , most p r o m i n e n t in t h e parieto-occipital leads, disappear or block w i t h eye-opening. T h e large deflections in channels F P 2 - F 4 a n d F P 1 - F 3 are arti- facts d u e t o eye-movement. Voltage calibration is in microvolts as in succeeding figures. ' Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders 25 / S/85/c C3-P3 „ Y . 1 co«. θ FP2-F4- ZZOZc CJ -ΛΙ τ ίοσ © Fig. 3. Normal E E G from a Child Aged 9 Years: Dominant activity is at 7 • 5 - 8 c/sec. Large deflections in channels F P 2 - F P 4 and F P 1 - F 3 are due to eye-movements. Fig. 4. E E G in Unilateral Blindness: Case 6: Girl, 9 years old, almost blind right eye (Table 3): focal sharp waves in the left parietal area (channels C 3 - P 3 and P3-O1). Tydskrif van die Suid-Afrikaanse Logopediese Vereniging, Vol. 13, Nr. : Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G. Κ. Nelson Λ, P4-OZ FP! - f=3 R ERG L ena ^ y y W W «>2 - £4 C4-OZ a - 01 Photic Stimulation *T 4 -1 L k k ί i I I I I 1 ' • > » I ι » l· © / Fig. 5. E E G in Epilepsy with Visual Defect: Case 9: Boy, 7 years (Table 3): focus of slow waves and spikes in the right frontal area (channels F P 2 - C 4 and C4-O2), suggestive of a localized epileptogenic abnormality. Fig. 6. E E G and E R G in Unilateral Visual Defect: Case 15 (see Table 3 and text): Boy aged 14 years. Record shows approximately equal ampli- tude of cortical response to photic stimulation at 9 flashes per second, but marked reduction of E R G on right side. Irregular trace above photic stimulation registration is automatic frequency analyzer write-out, show- ing dominant activity at 4 c/sec. in R E R G . Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders 27 4-34 c \ V C4· - PA- RI - OZ FP! - Fi FZ-CS I IOC Λ» P3- Ol Fig. 7. E E G in Delayed Speech: Case 22: Girl, 7 J years (Table 4). Ex- cessive slow activity with occasional high-voltage 4-5 c/sec. bursts. Fig. 8. E E G in Aphasia: Case 39 (see text): Focus of delta activity i n ' left occipital region, spreading to right side. Tydskrif van die Suid-Afrikaanse Logopediese Vereniging, Vol. 3, Nr. 1: Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G. Κ. Nelson FP! - C3 PHOTIC 57 mULt)7tON NE 78 c. ( J V A A A A A / ' ^ ' — — . 1 stc . I too 1 < · " 1 / / " < CO*. © . Λ 1.1 — 1233 FP2 - 7 4 T4--02 C+-T4· FP / - 73 οι V Fig. 9. E E G in Aphasia: Case 42 (see text). Photic stimulation at 9 flashes per second evokes high-voltage theta and delta burst with spikes. Fig. 10. E E G in Aphasia: Case 43 (see text): Clear left temporal delta and theta focus. Automatic frequency analyzer shows that dominant activity in channel T3-.O1 is at 1 · 5 - 6 c/sec. Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders 29 4-os Ffi - C4 C4--OZ C4-T4- FPt - C3 C3-T3 Τ loo 1 Μ" , t i*£t ^ COM. FPZ-F+ . .. 1806 c. φ F* - C.4- C+ - P4- FPt-Fi eyes ΛΑ'· I ioo , ' Fig. I I . E E G in Dyslexia: Case 47 (see text): Alpha rhythms more prominent anteriorly than posteriorly (anterior rhythms underlined). Fig. 12. E E G in Dyslexia: Case 49 (see text): Focal 3-4 c/sec. wave-and- spike activity in the right parietal area on eye-opening. Tydskrif van die Suid-Afrikaanse Logopediese Vereniging, Vol. 13, Nr. 1: Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G. Κ. Nelson 2749 Tt - 02 T3- TS 60M. n/to iECONH QfTLR sr**T or HV/V /v Λ/νΛ/ν I SEC I 5» -«Mr— Fi£. 13. E E G in Stuttering: Case 52 (see text): Upper sample: right post-temporal delta and theta focus in resting record; lower sample: severe slowing with hyperventilation. Journal of the South African Logopedic Society, Vol. 13, No. 1: May 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) Cerebral Electrical Activity and Communication Disorders 31 IIS3 C4-OZ 5-6 V>rv 12. ιΛΛί^Αν, · 1 sec © Fig. 14. E E G in Stuttering: Case 54 (see text): Eyes open: burst of 12 c/sec. alpha activity at start of a block during reading. F r e - quency analyzer trace shows wide range of E E G frequencies (channels C 4 - O 2 analyzed). Tydskrif van die Suid-Afrikaanse Logopediese Vereniging, Vol. 13, Nr. 1: Mei 1966 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2) G . Κ . N elson — χ: 73 . ' υ ~ Ν rt ί ε Α ω ω 3 οο Ο Λ 0> — . •δ 2 8-8 ω '' ω 3 οο 73 .i ω ~ Ν Λ ~ ε •J Ο ί C ηΧ Ι Α 0J — . •δ 2 8 a 3 οο α C Ο . ω „ ω tC ο — ι a ^ Ή ο ϊ o a ^ υ a cfl > "B Ο 512 S g>-Si « oo a ™ u u X ! u* 3 I •3 rt to w o> a £5. ε u .» o - <" U ι >-. c*3 ι ι (H S a S ° (ji h Ul C -s ·« β υ c 's-g-g-s «I S " --R 8 a .δ .a .5:2 ο S fi.SfS - " « ι" a s 5 ΐ ω SP - S -a tj S ω ο c b ω 3 y C/3 U I I 2 .g ts n f- Ο Q . I I v-1 « Ο ΰ ο a •/l 3 t-1 .... •3X 1 « Λ & H S_ 3 „ > e l » S ο " a Τ » I 0> > Μ « ^ s <υ ο Β O -'S) •Μ η μ > <*> rt '<*> ,. υ «β .y ,> υ > '< λ ΰ αϊ υ <υ ο υ Χ τΐ « C Λ Λ Ο — < » - _ <Λ ο Λ <υ α υ ν ο " χ I Λ υ ^ ι ο G f ο Π Χ ! 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Κ . N elson Ο til 2 u Cfl 4-1 rt « m ο Ι-» Q , rr* ™ a a (U u — . β . • - a js > O .SP 4-» 4-» 'J ^ Ο η S 3 £ ώ ° S Ε ^ α 9 & > <υ Ο Ά Ο » 1?? Ζ c.£ Ρ « ω β 5 ο. 1* ο ' Ε υ g Ί Ο ^ 2 '«•g a 's'S ε J" ° Β ° S β , a s sf sp.s, > 4-» > Ο ι •Γ* I 'Γ* 4-1 ι ω - ω 3 00 I 2 | 4-1 ^ «1 α « S « ί 2JS ο ω " ω— S bo t-ι 3 3 Ρ 00 00 υ ο υ <υ 3 Ifl f t Μ U Μ U bO κη ω 3 00 3 00 00 ο υ ο a a ε ο a ε » i g •"1 ΕΛ C Μ a 3 υ ,ο ο a a « * ω § 2 •α c « Ά Λ Γ-- υ . Ο Μ ) S C/J CO e j « « u ? β <υ ^ υ Λ 41 Ο 3 2 ο 9 -Η β ·5 ό δ g χ 3 « ί « C ο Cfl 8 υ ο •α c « 4-1 ra rtl t-l Ο a •a ε -a ο a ε ο a ε Ji 2 β υ __ c a S Ό <υ ε ε "β β "3 β "β 2 Ρ υ fi υ C = ^ — 1 h h μ h Ο rt ο β β c Λ J3 Λ < < < X 'C u β a 3 § •2 1 ο •» ε « « . . ι ε M i; ε s i s z < ζ 1 8 · " « .5 £ •a -a ε g ^ ω .. α .. ω .. < ·° "β « "3 1 ,3 'β "2 ε s ε ·2 ε β Ε λ Ε S Β =3 « ο « ο β ο 2 β β β 3 Λ J3 J3 S < < < ω 3 Μ 3 Ch S 'ω "α ε ο a .ο « u u β 3 c S « g S τ ε ω ,ο Ή "g "β β H > Τ3 ο ε - . & λ S ε a-2 « • •Η «1 .3 Λ ϋ « Τ3 — 3 « ω α oi Τ3 α 3 σ· « a 00 •α « 3 σ· υ « a 00 a « ε ο a i· 2 =3 -α 3 G • κ Ο „ 2 > S S3 H β υ ς/5 C υ υ Τ3 •S ό C . ω IS O 's ηη υ S c S • -Η yj « T3 u •α S u 3 Ο _ 3 J3 3 ε •s i Η 2 η b • c β Ο In 00 υ u bO bfi c3 a ε ε eg cti T3 T3 3 a m 05 bj) ο ^ si Λ >> O 2^ •IS r- ®!h®'H SO SO υ-t Journ al of the South A frican L ogopedic Society, V ol. 13, N o. : M ay 1966 Reproduced by Sabinet Gateway under licence granted by the Publisher (dated 2012) C erebral E lectrical A ctivity and C om m u n ication D isord ers 35 rt ε Ο C J3 a C3 Β Ό ΙΗ υ Ο ο C ο Χ) u C3 Ο a υ Β '5 <υ υ 4-1 I bO Ο Ο 4-1 4-1 a Ο υ C3 a a υ α. * - > < ο C J3 u -ti •S a h ^ ΓΛ 4-» 4-< (Λ « « ω 6 6 ^ g g ω υ 'Λ 8 2 · o -c j (2 ο υ ο ο ο υ υ υ a ι Ο +-Ι C ο 00 < 2 Ο α J3 rt υ β rt Ο β Ο ο § a ε ε ε D --Η ά 8 Ο υ = λ ϊ « ο - til ο a Π ΊΠ •a ε Τ3 C •α C a * 3-S 4-1 W .5 δ § 2 •S « C 00 (U <υ ' ω C c t" 1 2 ε χ rt ε .S a 2 °··2 rt J > Κ ο. 2? Eh w u C ν u Η υ „ » ι g rt .. Ο .. ^ * - * .a Μ Η Μ h 6 ·"· 6 g E a Ε a ο a ο c c J3 J3 < < "α ε ο •α rt ° «ί C Q J ί-ι * Λ tn a S 'fi ω ·α c rt •s 3 55 cr 4J Crt c/j rt o a ChC/3 S ο α c Β I υ ω ti <υ « υ a Ο rt ι " a - σ· ω υ . •5 ω a rt.2 a u « 4-1 V) - ' a οο 3 σ· • b rt Λ SS IE g D S 05 bp α O 2^ •c -Io. T ydskrif van die Suid-A frikaan se L ogopediese V eren igin g, V ol. 13, N r. 1: M ei 1966 Reproduced by Sabinet Gateway under licence granted by the Publisher (dated 2012)