Year : 1982 | Volume
: 30 | Issue : 3 | Page : 135--138
Electroencephalography in retinitis pigmentosa
DK Gahlot, GK Ahuja
Dr. Rajendra Prasad Centre for Ophthalmic Sciences and Department of Neurology, All India Institute of Medical Sciences, New Delhi, India
D K Gahlot
Dr. Rajendra Prasad Centre for Ophthalmic Sciences, A.I.I.M.S. New Delhi-110029
|How to cite this article:|
Gahlot D K, Ahuja G K. Electroencephalography in retinitis pigmentosa.Indian J Ophthalmol 1982;30:135-138
|How to cite this URL:|
Gahlot D K, Ahuja G K. Electroencephalography in retinitis pigmentosa. Indian J Ophthalmol [serial online] 1982 [cited 2020 Oct 30 ];30:135-138
Available from: https://www.ijo.in/text.asp?1982/30/3/135/28192
Retinitis Pigmentosa (RP) is a disease syndrome which can manifest clinically in a variety of forms involving neurologic and endocrinologic systems. A well known association of retinitis pigmentosa with epilepsy, spastic quadriplegia, familial paraplegia, pituitary disturbances and cerebral atrophies,, is known. Electroencephalographic studies have, therefore, been conducted by several workers to ascertain if the EEG could be of help in the diagnosis of the disease. However, widely different findings have been reported,. The present study concerns the electroencephalographic recordings of our cases of retinitis pigmentosa.
MATERIALS AND METHODS
51 cases of retinitis pigmentosa in the age group of 4-55 years, (30 males and 21 females) were selected from the neuroophthalmology clinic of the centre on the basis of history of night blindness and characteristic fundus picture. The diagnosis was confirmed by electroretinography and electrooculography. Patients with a history of acute or chronic systemic infection, preceding the ocular symptoms were excluded. The duration of illness ranged from 3 years to 45 years. 10 patients had family history of RP.
There was no evidence of chronic infection like syphilis or tuberculosis or any clinical neurological deficit. None of the patients had a history of epilepsy or viral infection.
Electroencephalography was performed on a Grass 8 or 16 channel electroencephalograph using the international 10-20 system of electrode placement. The gain was 50 uv per 7 mm per deflection and time constant 0.3 sec. Hyperventilation and photic stimulation was done in all cases. In 5 cases spontaneous sleep records were also taken.
The records were studied for the presence of alpha rhythm. Its voltage, frequency, symmetry and response to visual attention were recorded. Presence or absence of slow or fast activity in the background and it present its distribution were noted. The records were also studied for occurrence of any paroxysmal discharge including spikes or sharp waves. Changes produced by hyper ventilation & photic stimulation were noted.
The EEG was classified normal, abnormal, or borderline. Amplitude of less than 20 uv was classified as low voltage activity and cases with only low voltage activity without any other abnormality were considered as normal. Age of the patient and state of consciousness were considered while deciphering the records.
Out of 51 cases 36 had normal, 14 abnormal and 1 borderline records.
The normal cases (36) had alpha rhythm ranging between 8-12, the average being 10 per second. Attenuation of alpha activity on opening the eyes was seen in 27 out of 36 cases. [Figure 1] The voltage range was 20-60 uv, the average being 30 uv. In 8 patients the amplitude was less than 20 uv. Two female patients aged 12 and 10 also showed occasional slow waves (3-4 Hz). One 22 year old female showed low voltage fast background activity. On hyperventilation 4 male patients (28, 34, 18 & 51 years) showed interruption of alpha waves and one 10 year old male had slight slowing. The remaining 31 patients showed no change.
Out of abnormal records alpha activity was absent in 9 patients. The remaining 5, all adults had alpha at 9-10HZ and 20-60 uv. On hyperventilation all these cases showed bursts of slow wave activity ranging between 4-7 HZ [Figure 2] while 4 showed occasional fast activity in addition. Photic stimulation initiated no change. One patient 3 2 year old female had 8.9 HZ focal activity confined to left frontal region associated with a generalised low voltage record. This abnormality was not altered either on hyperventilation or photic stimulation
One patient had a borderline record. The dominant feature was low voltage, indeterminate activity of less than 20 uv amplitude with only occasional alpha waves. [Figure 3]. The activity showed no change on photic stimulation.
Sleep record in 5 cases showed no abnormality. None of the patients had sharp waves or spikes.
Retinitis pigmentosa is a genetically determined primary degenerative disorder of the retina. This is often associated with various types of neurologic, endocrinal and psychological disturbances our series of 51 cases, 36 had normal records (70.2%), 14 abnormal (27.3%) and 1 record was considered borderline. Sleep records in 5 cases did not induce any abnormality. Alpha attenuation on visual attention was observed in 27 patients but no correlation between visual acuity and alpha blocking was seen. The commonest abnormality was absence of definite alpha rythm in 9 patients showed burst of symmetrical and synchronous slow wave activity on hyperventilation. Thus, the abnormalities seen in our cases neither showed any characteristic pattern nor could be correlated with age of the patient, duration of illness or clinical picture. They also did not form part of any neurological syndrome. Therefore, according to this study electroencephalogram does not appear to be useful in the differential diagnosis of retinitis pigmentosa.
51 cases of typical retinitis pigmentosa without any neurological abnormality were studied by electroencephalograph ic examination. Only 27.3% showed abnormal record. The abnormality consisted of absence of alpha activity and bursts of slow wave activity on hyperventilation. These changes were nonspecific. The findings suggest that EEG is neither useful in detection nor in the differential diagnosis of retinitis pigmentosa.
|1||Wortis, S.B. and Shaskan, D., 1939, Tr. Amer. Neurol. 65 : 118.|
|2||Kjerrumgaard, E., 1978. Acta ophthalmol. 26 ; 55.|
|3||Alfano, J.E. and Berger, J.P., 1957, Amer. J. Ophthalmol. 43 : 237.|
|4||Francois J., stefans, R. and DeRouck, A. L., 1954, Ann ocul, 187 : 908.|
|5||Krill, A.E. Stamps F.W., 1960, Amer J. Ophthalmol. 49 : 762.|
|6||Guiner, L and Bruger, M., 1947, Arch, Ophthalmol. 37 :261.|
|7||Riecher, T., 1933, Klin Monat. F. Augen. 91 163,|
|8||Hagen, P.B., Noad, K.B. and Latham, O., 1951, Med. Journ. Australia 1 : 217.|
|9||Streifler, M. and Landau, J., 1955, Ophthalmologica 130 : 1 i6.|
|10||Cordier, J. Dureux J.B. and Barbier, J.L, 1956, Rev. Oto-Neuro-Ophthalmol. 28 : 193.|
|11||Francois, J., 1958, AMA. Arch. Ophthalmol. 59: 88.|