- Email: [email protected]
NERVE-GAS POISONING
574
Annotations OSTEITIS IN THE NEWBORN THE fall in neonatal mortality has concentrated attention on -infection as the most important single Particular cause of death after the first week of life. concern has been expressed about hsematogenous osteitis, for although the mortality of this condition is now low, the results of inadequate treatment can be crippling. Dennison1 pointed out that it is hard to compare the results achieved in different series : nevertheless it is encouraging to note the improvement on previously published results recorded in the paper by Professor Boyes and his colleagues on p. 544. Tlxeir frank discussion of failures is particularly informative. Most instances of osteitis in the newborn are caused by the obtrusive staphylococcus ; and the invasion of the antibiotic-resistant organism has been nowhere more threatening than in the care of newborn infants, particularly those born in hospital. The osteitis is a local manifestation of a generalised infection and its clinical course varies considerably. It can be quite mild, and has usually been so described in the past, or it can be rapidly fatal. Any bone may be affected, and the region of the hip is a common site and one where the effects can be serious. Bones developed in membrane are often among those attacked, and many infections involve the maxilla ; in these flat bones where the resistance is low the infection is specially virulent. It seems that the severe form is a new and violent manifestation of an old disease, and, since it is an eminently treatable condition, its early diagnosis is of prime importance. Any swelling of the soft tissues, any signs of irritability in a child that is being moved or washed, any suggestion of immobility, or any generalised infection associated with an apparently superficial lesion, must raise the suspicion of this severe underlying condition. Tenderness over bone is the sign to look for. One important lesson is that soft-tissue infections are not at all common in the newborn and all suspicious lesions should be treated as arisingin bone until the contrary is proved. As in the now rare osteomyelitis of older children, the radiographs are slow to i-eflect the bone changes and they never give the full picture of the havoc, since much non-opaque cartilage may be
destroyed. The first line of treatment is
vigorous, uninterrupted, Penicillin and long-continued chemotherapy. streptomycin are given at once, and the sensitivities of the organism determined if possible. Once the infection is well under control, treatment by injection can give One of the way to an appropriate drug by mouth. that is that has treatment important points emerged must be continued for a long time. The average length of treatment in the series described by Professor Boyes and his colleagues was five to six weeks, and experience and
has tended to rather than shorten the course. Pus should be aspirated, and here again it is necessary to needle repeatedly and at the slightest provocation. Even the keenest supporters of bone-drilling for infection could hardly say that it wa,s the treatment of cvhoice in patients of this age. Sequestra should be removed and it is important to think of loose teeth as sequestra. Even with the sustained care and interest which Professor Boyes and his associates devoted to their treatment, a quarter of the children were left with a crippling deformity of one or more joints. The analysis of these failures discloses some valuable facts. Apart from late diagnosis, the two big causes of failure were inadequate length of treatment and failure to aspirate pus. Where the infection was in the neighbonrhood of
lengthen
1.
Dennison, W. D. Lancet, 1955, ii, 474.
the hip, the results were really bad : in spite of longcontinued chemotherapy and orthopaedic treatment, the destruction was severe, except in one case diagnosed early. How can this damage he prevented ?° Doctors and midwives should always he on the lookout for " minor sepsis," and be ready to seek a second opinion if they have any doubts whether it is truly minor. And they should urge mothers not to hesitate to seek advice for such conditions. When it (’0I1H’8 to antibiotic treatment, it must be assumed that the organism is hardy if not immune ; and large doses must he given for a long time. But all rests on early diagnosis, and early diagnosis depends on suspecting osteitis when the bony changes are still slight. NERVE-GAS POISONING
THE nerve gases are organic phosphorus compounds which powerfully and irreversibly inhibit cholinesterase. They were first synthesised in Germany in the 1930s by Schrader, who was searching for new insecticides. Except for their greater potency, they have the same pharmaco. logical and toxicological action as the rapidly expanding group of organic phosphorus insecticides.1 The nerve gases can enter the body through the lungs, the intact skin, or the eye. In the conscious animal a lethal dose causes muscular fasciculation, followed bv
incoordination, convulsions, prostration, gasping respiri. tions, " air hunger," engorgement of veins, and often micturition and defecation. The animal falls unconscious and stops breathing, the heart slows, cardiac output and blood-pressure fall, and the pupils may contract (miosis is an early sign if the eyes are directly exposed). Finally, the skin capillaries collapse and the heart stops beating. In all species so far studied the general post-mortem appearance is that of asphyxia, Respiration can fail because of paralysis of the respiratory
precipitate
centre
(the
most
important factor), bronchoconstriction,
of the muscles of respiration by neuromuscular block. The degree of bronchospasm and iiiuscular paralysis depend on the compound used and the species poisoned. Breathing is made even harder by the profuse secretion of mucus from the bronchial glands, and the abolition of the cough reflex. or
paralysis
Normally, acetylcholine is hydrolysed almost as soon it is released ; but when cholinesterase is destroyed, acetylcholine accumulates where it is produced. The symptoms of poisoning are the result of excessive parasympathetic stimulation (muscarine action), neuromuscular block (nicotine action), and paralysis of the vital centre5 in the brain-stem (central action). The parasympathetic and central effects of acetylcholine are prevented and reversed by atropine, which is the most effective antidote to poisoning by organic phosphorus compounds. Iarge doses must be given early and must be continued, more atropine being given as indicated by bradycardia or miosis. Cullumbine2 emphasises that there should he no hesitation in giving more doses if the patient’a condition demands it, since acetylcholine is continually being released. But atropine does nothing to combat the nicotine action, so that peripheral neuromuscular paralysis persists. Since death is due to caused central failure respiratory by paralysis, broncho. constriction, or neuromuscular block, the efficacy of atropine in different species depends on the relative importance of these three mechanisms. In man and the monkey, respiratory failure is central in origin and the Certain oximes and response to atropine is good. hydroxamic acids can reactivate inhibited cholinesterase and hasten the destruction of absorbed nerve gas. They promise to be useful adjuncts to atropine, but the compounds of this type so far investigated are too toxic for general use, and the search for better ones continues. as
1. See annotation, Lancet, Feb. 2, 1957, p. 260. 2. Cullumbine, H. J. R. Army med. Cps, 1957,
103,
21.
575 and it has been recommended the individual Serviceman should be responsible for his own treatment. But the first signs and symptoms of poisoning are vague, and it is hard to know when atropine is really needed. The dose to be self-administered must therefore be a compromise between one of therapeutic value in nerve-gas poisoning and one which can be given safely to a normal person. Trials under different conditions have shown that 2 mg. (gr.l/30’) of atropine sulphate intramuscularly is a reasonable dose. In severe poisoning, positive-pressure artificial respiration will support the action of atropine by improving oxygenation of the tissues (in asphyxia atropine is a less effective stimulant of the respiratory centre). Positive pressure is needed to overcome the resistance due to bronchospasm, but ordinary manual methods of artificial respiration should form part of first-aid, preferably by the Holger-Nielson (arm-lift/back-pressure) method. A manually operated positive-pressure respirator, such as a bellows resuscitator or a mask-to-mask device, is being considered for field use.
Early treatment is vital,
that, in
war,
TETANUS AFTER OPERATION THE power of tetanus to strike a hospital with sudden ferocity is again evident in recent events at the North Staffordshire Royal Infirmary, Stoke-on-Trent. Tetanus attacked 5 patients lately operated on in the main surgical block at the infirmary : 2 have died and the latest information about the others is that they are unchanged and still very ill." All operations at the infirmary have been suspended for the time being and work is being transferred to other hospitals in the group. The source of the infection has not yet been identified. Those concerned will have in mind particularly previous disasters in which tetanus has been attributed to dust entering the operating-theatre,l to infected hair used in repairing plaster walls,2 to infected talc powder,2 to catgut,3 and to the use of other imperfectly sterilised materials.45
EPIDEMIC VERTIGO IN the
study of the
more
benign
diseases of short
duration, the general practitioner has advantages
over
in hospital ; and this is well illustrated by what has been written about epidemic vertigo. In 1949 Walford6 described a case of vertigo during an epidemic of influenza. In the following year Meulengracht7 pointed out that what was thought to be an example of drug toxicity was in all probability a disease known in Denmark
his
colleagues
"
" vertigo epidemica," or neurolabyrinthitis epidemica." Subsequently Rogers8 described 3 further patients, and Stewart 9 suggested that the cause might be a virus labyrinthitis. Since then rather more than 50 cases have been reported from general practice in different parts of the country. Further attention has lately been drawn to this condition by Charters, 10 who, in a paper from Kenya, discusses 13 cases that he has seen in the eight years as
between 1947 and 1955. The clinical picture of
epidemic vertigo seems to be reasonably clear. The patient has a sudden attack of severe vertigo accompanied by nausea and vomiting. The vertigo may last from one day to two weeks and then gradually ease (being brought on at this stage by movements of the head) until it subsides entirely. There is, however, considerable variation in the recorded duration of vertigo, Worster-Drought 1i stating that it gradually 1. See Lancet, 1956, ii, 29. 2. Sevitt, S. Ibid, 1949, ii, 1075. 3. Dalrymple-Champneys, W. Proc. R. Soc. Med. see Lancet, 1937, ii, 589. 4. Pulvertaft, R. J. V. Brit. med. J. 1937, i, 441. 5. Cane, L. H. Lancet, 1938, ii, 1059. 6. Walford, P. A. Brit. med. J. 1949, i, 821. 7. Meulengracht, E. Ibid, 1950, ii, 1493. 8. Rogers, S. C. Ibid, 1951, i, 1391. 9. Stewart, M. Ibid. 10. Charters, A. D. East Afr. med. J. 1957, 34, 7. 11. Worster-Drought, C. Lancet, 1952, i, 371.
1936, 29, 35 ;
improves in six to nine weeks, rarely lasting a,s long as twelve months. The vertigo is accompanied by nystagmus, and sometimes by headache, generalised pains, and slight fever for a day or two at the onset. Tinnitus and deafness, though not the rule, do affect a small proportion of patients. Leishman 12 mentions that 3 of his patients had diplopia, and this symptom was present in 2 of Dalsgaard-Neilsen’s series 13 of 21 ca,ses in Copenhagen and in 2 of Charters’s patients. The disease may affect either sex and the patient may be of any age, the youngest described being three years old ; but it is generally mild in children and is more common as well as more severe in those over twenty. There has been much discussion about the setiological agent, its infectivity, and the site of damage, but many more facts are needed. Cases have occurred during epidemics of influenza, but vertigo as a direct result of influenza is usually accompanied by deafness. Moreover, epidemic vertigo may appear at any time of year, and often it is unassociated with pyrexia. It is tempting, therefore, to consider this disease as an infection by a distinctive virus, though Alcock 14 takes the view that there are several different causes. In Charters’s series of 13 cases, 10 appeared between May, 1954, and August, 1955. There was no special predilection for any particular month, and the cases were widely scattered throughout Kenya. He supports Burrowes’s view 15 that the disease may be spread by carriers. This point might be settled by wider study of the condition in general practice and a comparison with other diseases prevalent at the time. In most infections the labyrinth and cochlea are often involved together. Since tinnitus and deafness are relatively uncommon in epidemic vertigo, it seems unlikely that the end-organ itself is affected (virus infections very rarely attack this structure). The electro-encephalogram showed a " mild abnormality " in 6 of Dalsgaard-Neilsen’s 13 cases, but it was .normal in the remaining 7. Moreover, the cerebrospinal fluid has been normal almost every time it has been examined. It also seems unlikely that a brain-stem encephalitis would confine itself to the labyrinthine nuclei, with occasional involvement of the cochlear nucleus and even more rare damage to one oculomotor nucleus ; what is more, it would have to do so without causing any general upset in most patients (DalsgaardNeilsen mentions slight changes in reflexes or sensibility). On the other hand, it is hard to explain in any other way the involvement of the oculomotor nerves if this condition is to be attributed to one cause. Embryologically and phylogenetically, the vestibular nerve and ganglion develop before the cochlea, and this may be a factor in the localisation of the damage. If so, then epidemic vertigo would be one variety of vestibular neuronitis. The disease does, in fact, show many points of resemblance to vestibular neuronitis as described by Dix and Hallpike,16 in particular the age-distribution, the onset associated with a febrile illness, and the localisation to the vestibular apparatus. It differs from vestibular neuronitis in its short course and in the possible involvement of the auditory apparatus. These differences, however, may well be differences of pathology rather than of anatomy. Charters suggests that the condition is a ganglionitis and that spread might be occasionally expected from Scarpa’s ganglion to the cochlear nerve. This is an interesting postulate, and, while the analogy he draws with herpes zoster cannot be pushed very far, it is not an unreasonable hypothesis. Aschan and Stahle 17 have lately described 10 cases of vestibular neuritis (neuronitis) some of which might well 12. 13. 14. 15. 16.
Leishman, A. W. D. Ibid, 1955, i, 228. Dalsgaard-Neilsen, T. Acta. psychiat., Kbh. 1953, 28, 263. Alcock, N. S. Lancet, 1952, i, 467. Burrowes W. L. Ibid, 1955, i, 408. Dix, M. R., Hallpike, C. S. Proc. R. Soc. Med. 1952, 45, 341. 17. Aschan, G., Stahle, J. J. Laryngol. 1956, 70, 497.
Annotations OSTEITIS IN THE NEWBORN THE fall in neonatal mortality has concentrated attention on -infection as the most important single Particular cause of death after the first week of life. concern has been expressed about hsematogenous osteitis, for although the mortality of this condition is now low, the results of inadequate treatment can be crippling. Dennison1 pointed out that it is hard to compare the results achieved in different series : nevertheless it is encouraging to note the improvement on previously published results recorded in the paper by Professor Boyes and his colleagues on p. 544. Tlxeir frank discussion of failures is particularly informative. Most instances of osteitis in the newborn are caused by the obtrusive staphylococcus ; and the invasion of the antibiotic-resistant organism has been nowhere more threatening than in the care of newborn infants, particularly those born in hospital. The osteitis is a local manifestation of a generalised infection and its clinical course varies considerably. It can be quite mild, and has usually been so described in the past, or it can be rapidly fatal. Any bone may be affected, and the region of the hip is a common site and one where the effects can be serious. Bones developed in membrane are often among those attacked, and many infections involve the maxilla ; in these flat bones where the resistance is low the infection is specially virulent. It seems that the severe form is a new and violent manifestation of an old disease, and, since it is an eminently treatable condition, its early diagnosis is of prime importance. Any swelling of the soft tissues, any signs of irritability in a child that is being moved or washed, any suggestion of immobility, or any generalised infection associated with an apparently superficial lesion, must raise the suspicion of this severe underlying condition. Tenderness over bone is the sign to look for. One important lesson is that soft-tissue infections are not at all common in the newborn and all suspicious lesions should be treated as arisingin bone until the contrary is proved. As in the now rare osteomyelitis of older children, the radiographs are slow to i-eflect the bone changes and they never give the full picture of the havoc, since much non-opaque cartilage may be
destroyed. The first line of treatment is
vigorous, uninterrupted, Penicillin and long-continued chemotherapy. streptomycin are given at once, and the sensitivities of the organism determined if possible. Once the infection is well under control, treatment by injection can give One of the way to an appropriate drug by mouth. that is that has treatment important points emerged must be continued for a long time. The average length of treatment in the series described by Professor Boyes and his colleagues was five to six weeks, and experience and
has tended to rather than shorten the course. Pus should be aspirated, and here again it is necessary to needle repeatedly and at the slightest provocation. Even the keenest supporters of bone-drilling for infection could hardly say that it wa,s the treatment of cvhoice in patients of this age. Sequestra should be removed and it is important to think of loose teeth as sequestra. Even with the sustained care and interest which Professor Boyes and his associates devoted to their treatment, a quarter of the children were left with a crippling deformity of one or more joints. The analysis of these failures discloses some valuable facts. Apart from late diagnosis, the two big causes of failure were inadequate length of treatment and failure to aspirate pus. Where the infection was in the neighbonrhood of
lengthen
1.
Dennison, W. D. Lancet, 1955, ii, 474.
the hip, the results were really bad : in spite of longcontinued chemotherapy and orthopaedic treatment, the destruction was severe, except in one case diagnosed early. How can this damage he prevented ?° Doctors and midwives should always he on the lookout for " minor sepsis," and be ready to seek a second opinion if they have any doubts whether it is truly minor. And they should urge mothers not to hesitate to seek advice for such conditions. When it (’0I1H’8 to antibiotic treatment, it must be assumed that the organism is hardy if not immune ; and large doses must he given for a long time. But all rests on early diagnosis, and early diagnosis depends on suspecting osteitis when the bony changes are still slight. NERVE-GAS POISONING
THE nerve gases are organic phosphorus compounds which powerfully and irreversibly inhibit cholinesterase. They were first synthesised in Germany in the 1930s by Schrader, who was searching for new insecticides. Except for their greater potency, they have the same pharmaco. logical and toxicological action as the rapidly expanding group of organic phosphorus insecticides.1 The nerve gases can enter the body through the lungs, the intact skin, or the eye. In the conscious animal a lethal dose causes muscular fasciculation, followed bv
incoordination, convulsions, prostration, gasping respiri. tions, " air hunger," engorgement of veins, and often micturition and defecation. The animal falls unconscious and stops breathing, the heart slows, cardiac output and blood-pressure fall, and the pupils may contract (miosis is an early sign if the eyes are directly exposed). Finally, the skin capillaries collapse and the heart stops beating. In all species so far studied the general post-mortem appearance is that of asphyxia, Respiration can fail because of paralysis of the respiratory
precipitate
centre
(the
most
important factor), bronchoconstriction,
of the muscles of respiration by neuromuscular block. The degree of bronchospasm and iiiuscular paralysis depend on the compound used and the species poisoned. Breathing is made even harder by the profuse secretion of mucus from the bronchial glands, and the abolition of the cough reflex. or
paralysis
Normally, acetylcholine is hydrolysed almost as soon it is released ; but when cholinesterase is destroyed, acetylcholine accumulates where it is produced. The symptoms of poisoning are the result of excessive parasympathetic stimulation (muscarine action), neuromuscular block (nicotine action), and paralysis of the vital centre5 in the brain-stem (central action). The parasympathetic and central effects of acetylcholine are prevented and reversed by atropine, which is the most effective antidote to poisoning by organic phosphorus compounds. Iarge doses must be given early and must be continued, more atropine being given as indicated by bradycardia or miosis. Cullumbine2 emphasises that there should he no hesitation in giving more doses if the patient’a condition demands it, since acetylcholine is continually being released. But atropine does nothing to combat the nicotine action, so that peripheral neuromuscular paralysis persists. Since death is due to caused central failure respiratory by paralysis, broncho. constriction, or neuromuscular block, the efficacy of atropine in different species depends on the relative importance of these three mechanisms. In man and the monkey, respiratory failure is central in origin and the Certain oximes and response to atropine is good. hydroxamic acids can reactivate inhibited cholinesterase and hasten the destruction of absorbed nerve gas. They promise to be useful adjuncts to atropine, but the compounds of this type so far investigated are too toxic for general use, and the search for better ones continues. as
1. See annotation, Lancet, Feb. 2, 1957, p. 260. 2. Cullumbine, H. J. R. Army med. Cps, 1957,
103,
21.
575 and it has been recommended the individual Serviceman should be responsible for his own treatment. But the first signs and symptoms of poisoning are vague, and it is hard to know when atropine is really needed. The dose to be self-administered must therefore be a compromise between one of therapeutic value in nerve-gas poisoning and one which can be given safely to a normal person. Trials under different conditions have shown that 2 mg. (gr.l/30’) of atropine sulphate intramuscularly is a reasonable dose. In severe poisoning, positive-pressure artificial respiration will support the action of atropine by improving oxygenation of the tissues (in asphyxia atropine is a less effective stimulant of the respiratory centre). Positive pressure is needed to overcome the resistance due to bronchospasm, but ordinary manual methods of artificial respiration should form part of first-aid, preferably by the Holger-Nielson (arm-lift/back-pressure) method. A manually operated positive-pressure respirator, such as a bellows resuscitator or a mask-to-mask device, is being considered for field use.
Early treatment is vital,
that, in
war,
TETANUS AFTER OPERATION THE power of tetanus to strike a hospital with sudden ferocity is again evident in recent events at the North Staffordshire Royal Infirmary, Stoke-on-Trent. Tetanus attacked 5 patients lately operated on in the main surgical block at the infirmary : 2 have died and the latest information about the others is that they are unchanged and still very ill." All operations at the infirmary have been suspended for the time being and work is being transferred to other hospitals in the group. The source of the infection has not yet been identified. Those concerned will have in mind particularly previous disasters in which tetanus has been attributed to dust entering the operating-theatre,l to infected hair used in repairing plaster walls,2 to infected talc powder,2 to catgut,3 and to the use of other imperfectly sterilised materials.45
EPIDEMIC VERTIGO IN the
study of the
more
benign
diseases of short
duration, the general practitioner has advantages
over
in hospital ; and this is well illustrated by what has been written about epidemic vertigo. In 1949 Walford6 described a case of vertigo during an epidemic of influenza. In the following year Meulengracht7 pointed out that what was thought to be an example of drug toxicity was in all probability a disease known in Denmark
his
colleagues
"
" vertigo epidemica," or neurolabyrinthitis epidemica." Subsequently Rogers8 described 3 further patients, and Stewart 9 suggested that the cause might be a virus labyrinthitis. Since then rather more than 50 cases have been reported from general practice in different parts of the country. Further attention has lately been drawn to this condition by Charters, 10 who, in a paper from Kenya, discusses 13 cases that he has seen in the eight years as
between 1947 and 1955. The clinical picture of
epidemic vertigo seems to be reasonably clear. The patient has a sudden attack of severe vertigo accompanied by nausea and vomiting. The vertigo may last from one day to two weeks and then gradually ease (being brought on at this stage by movements of the head) until it subsides entirely. There is, however, considerable variation in the recorded duration of vertigo, Worster-Drought 1i stating that it gradually 1. See Lancet, 1956, ii, 29. 2. Sevitt, S. Ibid, 1949, ii, 1075. 3. Dalrymple-Champneys, W. Proc. R. Soc. Med. see Lancet, 1937, ii, 589. 4. Pulvertaft, R. J. V. Brit. med. J. 1937, i, 441. 5. Cane, L. H. Lancet, 1938, ii, 1059. 6. Walford, P. A. Brit. med. J. 1949, i, 821. 7. Meulengracht, E. Ibid, 1950, ii, 1493. 8. Rogers, S. C. Ibid, 1951, i, 1391. 9. Stewart, M. Ibid. 10. Charters, A. D. East Afr. med. J. 1957, 34, 7. 11. Worster-Drought, C. Lancet, 1952, i, 371.
1936, 29, 35 ;
improves in six to nine weeks, rarely lasting a,s long as twelve months. The vertigo is accompanied by nystagmus, and sometimes by headache, generalised pains, and slight fever for a day or two at the onset. Tinnitus and deafness, though not the rule, do affect a small proportion of patients. Leishman 12 mentions that 3 of his patients had diplopia, and this symptom was present in 2 of Dalsgaard-Neilsen’s series 13 of 21 ca,ses in Copenhagen and in 2 of Charters’s patients. The disease may affect either sex and the patient may be of any age, the youngest described being three years old ; but it is generally mild in children and is more common as well as more severe in those over twenty. There has been much discussion about the setiological agent, its infectivity, and the site of damage, but many more facts are needed. Cases have occurred during epidemics of influenza, but vertigo as a direct result of influenza is usually accompanied by deafness. Moreover, epidemic vertigo may appear at any time of year, and often it is unassociated with pyrexia. It is tempting, therefore, to consider this disease as an infection by a distinctive virus, though Alcock 14 takes the view that there are several different causes. In Charters’s series of 13 cases, 10 appeared between May, 1954, and August, 1955. There was no special predilection for any particular month, and the cases were widely scattered throughout Kenya. He supports Burrowes’s view 15 that the disease may be spread by carriers. This point might be settled by wider study of the condition in general practice and a comparison with other diseases prevalent at the time. In most infections the labyrinth and cochlea are often involved together. Since tinnitus and deafness are relatively uncommon in epidemic vertigo, it seems unlikely that the end-organ itself is affected (virus infections very rarely attack this structure). The electro-encephalogram showed a " mild abnormality " in 6 of Dalsgaard-Neilsen’s 13 cases, but it was .normal in the remaining 7. Moreover, the cerebrospinal fluid has been normal almost every time it has been examined. It also seems unlikely that a brain-stem encephalitis would confine itself to the labyrinthine nuclei, with occasional involvement of the cochlear nucleus and even more rare damage to one oculomotor nucleus ; what is more, it would have to do so without causing any general upset in most patients (DalsgaardNeilsen mentions slight changes in reflexes or sensibility). On the other hand, it is hard to explain in any other way the involvement of the oculomotor nerves if this condition is to be attributed to one cause. Embryologically and phylogenetically, the vestibular nerve and ganglion develop before the cochlea, and this may be a factor in the localisation of the damage. If so, then epidemic vertigo would be one variety of vestibular neuronitis. The disease does, in fact, show many points of resemblance to vestibular neuronitis as described by Dix and Hallpike,16 in particular the age-distribution, the onset associated with a febrile illness, and the localisation to the vestibular apparatus. It differs from vestibular neuronitis in its short course and in the possible involvement of the auditory apparatus. These differences, however, may well be differences of pathology rather than of anatomy. Charters suggests that the condition is a ganglionitis and that spread might be occasionally expected from Scarpa’s ganglion to the cochlear nerve. This is an interesting postulate, and, while the analogy he draws with herpes zoster cannot be pushed very far, it is not an unreasonable hypothesis. Aschan and Stahle 17 have lately described 10 cases of vestibular neuritis (neuronitis) some of which might well 12. 13. 14. 15. 16.
Leishman, A. W. D. Ibid, 1955, i, 228. Dalsgaard-Neilsen, T. Acta. psychiat., Kbh. 1953, 28, 263. Alcock, N. S. Lancet, 1952, i, 467. Burrowes W. L. Ibid, 1955, i, 408. Dix, M. R., Hallpike, C. S. Proc. R. Soc. Med. 1952, 45, 341. 17. Aschan, G., Stahle, J. J. Laryngol. 1956, 70, 497.