- Email: [email protected]
CORTICAL BLINDNESS
1108 not been done immediately. However, in a boxerI with transitory blindness and papillary pallor, there was retinal artery constriction, pupillary dilatation, and photomotor abolition. Sedan and Alliesl cite Worms and Bailliart, who established a link between post-traumatic retinal hypotension, low cerebrospinal fluid pressure, and labyrinthine hypo-excitability. In fact, the retinal pressure seemed to be generated by the labyrinth (vestibuloretinal reflex). The labyrinth is involved in many diverse reflexes and decreased or increased excitability can lead to bizarre sensory, perceptual, or motor disorders including visual hallucinations, epilepsy, and blindness-darkening of the visual field was regularly noted in cases of labyrinthine fistula.2 Hence I postulate that transient blindness is due to acute labyrinthine dysfunction and not to any primary disorder of the visual system- Certainly a rupture of oval or round windows or pneumolabyrinth is a far more plausible result of minor head injury than are bilateral cortical lesions. This would also explain the conspicuous absence of neurological signs, the disorientation, the vertigo, the vomiting, the unsteady gait, the electroencephalogram abnormalities, and the full recoveries.
had
CORTICAL BLINDNESS
StR,—Iwas very interested in Mr Eldridge and Mr Punt’s description (April 9, p 815) of transient traumatic cortical blindness in childhood. Although previously unaware of this condition, I am sure I experienced it as a child. At the age of 12 or 13, when playing football, I was struck forcefully on the occiput. I did not lose consciousness, but felt lightheaded and dizzy for half an hour or so; I was able to continue playing. However, the sense of wellbeing that had accompanied the light-headedness was replaced by nausea, together with an occipital headache which increased in severity until it was difficult to tolerate. This heralded a gradual diminution in my field of vision which contracted symmetrically from its periphery to leave a tunnel of vision from 15° to 30° or so. Within this narrow field, objects were blurred and partly obscured by rapidly changing coloured bands of light. I was allowed to lie down and, at the height of the symptoms, bright lights and changes in posture produced agonising exacerbations of pain. Symptoms receded over two to three hours, and there were no residual effects, apart from a spectacular bruise. I do not suffer from migraine or from epilepsy; nor do any members of my family. These symptoms are similar to those described by migraine sufferers, and until reading that account in The Lancet I had thought that I had experienced an isolated attack of migraine induced by trauma. Indeed this episode and those described by Eldridge and Punt are all compatible with such an interpretation. Perhaps some individuals are prone to migraine-like symptoms when banged on the head--or there may be something special about the location or force of the blow. Any test of such hypotheses is welcome to proceed
32 Love Walk, London SE5 SAD
J, Allies P. Contrôle de la pression artérielle rétinienne au cours même d’un knock-out. Revue d’oto-neuro-ophtalmologie 1951; 23: 374-77. 2. Schilder P. The vestibular apparatus in neurosis and psychosis. J Nerv Ment Dis 1933; 1. Sédan
78: 1-23, 137-64.
RUBELLA INFECTION AND REINFECTION DISTINGUISHED BY AVIDITY OF IgG
without me. Department of Pathology, University of Manchester, Manchester M13 9PT
E. W. BENBOW
SIR,-Mr Eldridge and Mr Punt’s discussion of the pathophysiology of transient attacks of cortical blindness induced in children by mild head trauma suffers from a "category mistake"I that obscures what has been learned about these attacks. The mistake is to consider the clinical entity "migraine" as though it belonged in the logical category of physiological abnormalities, such as spreading depression and vasospasm. This mixing of categories leads to illogical questions, such as whether the attacks are more likely to be due to vasospasm or to migraine, when neither of these conditions excludes the other. The traumatic attacks cannot be due to migraine, for migraine is not a pathophysiological process, but they can be by having the same underlying pathophysiological processes as migraine, whatever these may be. By keeping the categories separate, one can more clearly appreciate the considerable clinical evidence indicating that the traumatic attacks of blindness and the related traumatic attacks, such as hemiparesis, are classical or complicated migraines.2
migraines
Department of Neurology, State University of New York Health Science Center at Syracuse, Syracuse, New York 13210, USA
DAVID C. HAAS
1. Ryle G. The concept of mind. New York: Barnes and Noble, 1949: 16-18. 2. Haas DC. Trauma-triggered migraine: an explanation for common neurological
attacks after mild head injury. Review of the 181-88.
A. G. GORDON
literature. J Neurosurg 1988;
68:
SIR,-Mr Eldridge and Mr Punt state that little is known of the pathophysiology of transient traumatic blindness. However, a study’ of a 20-year-old rugby player blinded by a severe kick on the neck clearly implicated retinal angiospasm, and directs attention to the vestibular labyrinth. Findings 20 min after the blow included mydriasis, reduced pupillary reflexes, low retinal artery pressures but increased arterial pressure, arterial narrowing but increased venous calibre, and slightly oedematous fundi. Within 15 min there was recovery of retinal pressure, arterial diameter, and acuity. He had vertigo but not neurological signs. In two other cases’ of transient blindness ophthalmoscopic examinations were normal but
rubella reinfection may pose little risk to the tests that can distinguish between rubella reinfection and subclinical primary rubella are needed,2 especially with the proposed introduction of measles, mumps, and rubella vaccine.3 One solution for the identification of primary infections could be the measurement of the antigen-binding avidity of specific IgG. The avidity, or affinity, of IgG is initially low after primary antigenic challenge and matures slowly over weeks and months.4,5 We have developed a novel technique for the serodiagnosis of primary rubella by the measurement of the avidity of rubellaspecific IgG. Urea is added to washing fluid during one step of an indirect ELISA to dissociate low avidity IgG from immobilised antigen, in conditions where high avidity IgG remains mostly antigen bound. The test distinguishes primary rubellas from pre-existing rubella immunity.6 Briefly, purified rubella antigen from the Therien strain is immobilised on microtitre trays. Patients’ sera are allowed to react for 2 h at 37°C. Plates are washed three times in phosphate-buffered-saline/’Tween’ with or without 8 mol/1 urea. Bound IgG is detected with antihuman IgG conjugated to alkaline phosphatase, the final step involving addition of p-nitrophenyl phosphate. The optical densities (OD) are measured automatically and an "avidity index" is calculated by (OD with urea — OD without urea) x 100. To assess this assay, sera from 64 patients were sent under code from Luton Public Health Laboratory to Helsinki. 6-18 months earlier these sera had been tested by a standard radial haemolysis test7 and by an M antibody capture test for rubella specific IgM.8 The figure shows the results of the avidity-ELISA test and the original conclusions (definite rubella or rubella likely [34 patients], rubella reinfection [4], parvovirus B19 infection [6], and rubella unlikely if the patient was a contact and deemed to be immune [20]). Correlation was high between the sera with low avidity indices (below 30%) and cases of recent primary rubella, and between sera with high avidity indices (above 50%) and conclusions of past immunity or other virus infections. Of particular interest, however, was the finding of high IgG avidity in all 4 rubella reinfections. We based our original conclusions about the 4 reinfections on low or borderline levels of IgG, measured within weeks before contact, combined with a significant rise in IgG and low-level rubellaspecificIgM in a post-contact sample. The 4 cases of rubella reinfection had serum samples drawn 14, 15, 38, and 60 days,
SIR,-Although
fetus,
laboratory
had
CORTICAL BLINDNESS
StR,—Iwas very interested in Mr Eldridge and Mr Punt’s description (April 9, p 815) of transient traumatic cortical blindness in childhood. Although previously unaware of this condition, I am sure I experienced it as a child. At the age of 12 or 13, when playing football, I was struck forcefully on the occiput. I did not lose consciousness, but felt lightheaded and dizzy for half an hour or so; I was able to continue playing. However, the sense of wellbeing that had accompanied the light-headedness was replaced by nausea, together with an occipital headache which increased in severity until it was difficult to tolerate. This heralded a gradual diminution in my field of vision which contracted symmetrically from its periphery to leave a tunnel of vision from 15° to 30° or so. Within this narrow field, objects were blurred and partly obscured by rapidly changing coloured bands of light. I was allowed to lie down and, at the height of the symptoms, bright lights and changes in posture produced agonising exacerbations of pain. Symptoms receded over two to three hours, and there were no residual effects, apart from a spectacular bruise. I do not suffer from migraine or from epilepsy; nor do any members of my family. These symptoms are similar to those described by migraine sufferers, and until reading that account in The Lancet I had thought that I had experienced an isolated attack of migraine induced by trauma. Indeed this episode and those described by Eldridge and Punt are all compatible with such an interpretation. Perhaps some individuals are prone to migraine-like symptoms when banged on the head--or there may be something special about the location or force of the blow. Any test of such hypotheses is welcome to proceed
32 Love Walk, London SE5 SAD
J, Allies P. Contrôle de la pression artérielle rétinienne au cours même d’un knock-out. Revue d’oto-neuro-ophtalmologie 1951; 23: 374-77. 2. Schilder P. The vestibular apparatus in neurosis and psychosis. J Nerv Ment Dis 1933; 1. Sédan
78: 1-23, 137-64.
RUBELLA INFECTION AND REINFECTION DISTINGUISHED BY AVIDITY OF IgG
without me. Department of Pathology, University of Manchester, Manchester M13 9PT
E. W. BENBOW
SIR,-Mr Eldridge and Mr Punt’s discussion of the pathophysiology of transient attacks of cortical blindness induced in children by mild head trauma suffers from a "category mistake"I that obscures what has been learned about these attacks. The mistake is to consider the clinical entity "migraine" as though it belonged in the logical category of physiological abnormalities, such as spreading depression and vasospasm. This mixing of categories leads to illogical questions, such as whether the attacks are more likely to be due to vasospasm or to migraine, when neither of these conditions excludes the other. The traumatic attacks cannot be due to migraine, for migraine is not a pathophysiological process, but they can be by having the same underlying pathophysiological processes as migraine, whatever these may be. By keeping the categories separate, one can more clearly appreciate the considerable clinical evidence indicating that the traumatic attacks of blindness and the related traumatic attacks, such as hemiparesis, are classical or complicated migraines.2
migraines
Department of Neurology, State University of New York Health Science Center at Syracuse, Syracuse, New York 13210, USA
DAVID C. HAAS
1. Ryle G. The concept of mind. New York: Barnes and Noble, 1949: 16-18. 2. Haas DC. Trauma-triggered migraine: an explanation for common neurological
attacks after mild head injury. Review of the 181-88.
A. G. GORDON
literature. J Neurosurg 1988;
68:
SIR,-Mr Eldridge and Mr Punt state that little is known of the pathophysiology of transient traumatic blindness. However, a study’ of a 20-year-old rugby player blinded by a severe kick on the neck clearly implicated retinal angiospasm, and directs attention to the vestibular labyrinth. Findings 20 min after the blow included mydriasis, reduced pupillary reflexes, low retinal artery pressures but increased arterial pressure, arterial narrowing but increased venous calibre, and slightly oedematous fundi. Within 15 min there was recovery of retinal pressure, arterial diameter, and acuity. He had vertigo but not neurological signs. In two other cases’ of transient blindness ophthalmoscopic examinations were normal but
rubella reinfection may pose little risk to the tests that can distinguish between rubella reinfection and subclinical primary rubella are needed,2 especially with the proposed introduction of measles, mumps, and rubella vaccine.3 One solution for the identification of primary infections could be the measurement of the antigen-binding avidity of specific IgG. The avidity, or affinity, of IgG is initially low after primary antigenic challenge and matures slowly over weeks and months.4,5 We have developed a novel technique for the serodiagnosis of primary rubella by the measurement of the avidity of rubellaspecific IgG. Urea is added to washing fluid during one step of an indirect ELISA to dissociate low avidity IgG from immobilised antigen, in conditions where high avidity IgG remains mostly antigen bound. The test distinguishes primary rubellas from pre-existing rubella immunity.6 Briefly, purified rubella antigen from the Therien strain is immobilised on microtitre trays. Patients’ sera are allowed to react for 2 h at 37°C. Plates are washed three times in phosphate-buffered-saline/’Tween’ with or without 8 mol/1 urea. Bound IgG is detected with antihuman IgG conjugated to alkaline phosphatase, the final step involving addition of p-nitrophenyl phosphate. The optical densities (OD) are measured automatically and an "avidity index" is calculated by (OD with urea — OD without urea) x 100. To assess this assay, sera from 64 patients were sent under code from Luton Public Health Laboratory to Helsinki. 6-18 months earlier these sera had been tested by a standard radial haemolysis test7 and by an M antibody capture test for rubella specific IgM.8 The figure shows the results of the avidity-ELISA test and the original conclusions (definite rubella or rubella likely [34 patients], rubella reinfection [4], parvovirus B19 infection [6], and rubella unlikely if the patient was a contact and deemed to be immune [20]). Correlation was high between the sera with low avidity indices (below 30%) and cases of recent primary rubella, and between sera with high avidity indices (above 50%) and conclusions of past immunity or other virus infections. Of particular interest, however, was the finding of high IgG avidity in all 4 rubella reinfections. We based our original conclusions about the 4 reinfections on low or borderline levels of IgG, measured within weeks before contact, combined with a significant rise in IgG and low-level rubellaspecificIgM in a post-contact sample. The 4 cases of rubella reinfection had serum samples drawn 14, 15, 38, and 60 days,
SIR,-Although
fetus,
laboratory