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These observations serve to remind us that we stillknow too little about the basic mechanisms of

immunity of mucous membranes. Such mechanismsmust be studied both in mice and man if there is to be

any hope of producing vaccines which are as

successful as those against systemic infections such aspoliomyelitis or yellow fever.

THIRD-NERVE HEADACHE

IN Beijing, China, 5% of women and 2% of mencomplain of occasional severe or disabling headache,compared with 10-50% of the British population and overhalf the entire population of Finland. 1-3 Headache is thirteentimes as frequent in women traders as in housewives in theChinese capital, with differences between the urban andrural populations not seen in other countries. Despite thedifferences in frequency and headache pattern, the basiccauses of serious headache are likely to be similar world-wide. Although migraine is the chief culprit, disease of thesecond and third, if not the other cervical vertebrae, canundoubtedly sometimes cause head pain.

Atlas, condemned by Zeus for his part in the war of theTitans to uphold the heavens on his shoulders from his loftyabode in Africa, may not have suffered headache. The dorsalramus of the first cervical nerve has no cutaneous branch,4 4and headache has never been ascribed to arthritis of the

atlanto-occipital joint. Surprisingly, stimulation of the Clnerve root at operation causes frontal, not occipital pain.5 Asearly as 1813, Lazzaretto recorded the history of a seamanwhose atlas was dislocated by a blow from a falling sailyard.6The dislocation was reduced, and the man made a completerecovery without subsequent neck pain. As with the atlas,disease of the lower cervical vertebrae probably does notcause headache unless associated with muscle spasm. In

contrast, disease of the lateral atlanto-axial joint, and morecommonly the axial-vertebral C2-3 zygapophyseal joint(zygon, a yoke), can cause headache.7-10

Rotation of the head occurs mainly at the Cl-2 levelwhereas flexion and extension occur at the lower cervicallevels. Movement takes place at interpedicular synovialjoints formed by the articulation of adjacent superior andinferior facets of the vertebral pedicles. These joints formthe posterior and lateral borders of the intervertebralforamina, and, although small, they play a major part in thetransmission of weight and in resistance to compression andshearing forces in the neck. 11 The C2-3 zygapophyseal jointstake much of this strain, and may be especially vulnerable toosteoarthritis. If osteophytes encroach on the intervertebralforamen, the C3 nerve root itself is in jeopardy. This root,

1. Cheng X-M, Ziegler DR, Shi-Chuo LI, Qin-shun D, Chandra V, Schoenberg BS. Aprevalence survey of incapacitating headache in the People’s Republic of China.Neurology 1986; 36: 831-34.

2. Green JE. A survey of migraine in England 1975-1976. Headache 1977; 17: 67-68.3. Nikiforow R. Features of migraine—comparison of a questionnaire study and a

neurologist-examined random sample. Cephalgia 1981; 1: 157-66.4. Romanes GJ, ed. Cunningham’s textbook of anatomy. 12th ed. Oxford: Oxford

University Press, 1981: 768.5. Kerr FWL. A mechanism to account for frontal headache in cases of posterior fossa

tumours. J Neurosurg 1961; 18: 605-09.6. Lazzaretto E. A remarkable case of dislocation of the atlas Edinburgh Med Surg J 1813;

9: 165.7. Ehni G, Benner B. Occipital neuralgia and the C1-2 arthrosis syndrome. J Neurosurg

1964; 61: 961-658. Trevor-Jones R. Osteoarthritis of the paravertebral joints of the second and third

cervical vertebrae as a cause of occipital headache. S Afr Med J 1964; 38: 392-94.9. Maigne R. Signes cliniques des céphalées cervicales: Leur traitement. Med Hyg 1981;

39: 1174-85.10 Bogduk N, Marsland A. On the concept of third occipital headache. J Neurol

Neurosurg Psychiatry 1986; 49: 775-80.

together with C2, supplies large areas of the neck and back ofthe head.The idea of third-nerve headache-headache due to

irritation of the third cervical root-is not new. In 1964,Trevor-Jones reported three patients in whom he found thethird occipital nerve to be entrapped by osteophytes from anarthritic C2-3 joint; surgical relief of the entrapment relievedtheir headache.8 Maigne in France reported ninety-eightpatients whose headache he successfully treated with localanaesthetic injection and manipulation of the C2-3 joints.9Bogduk and Marsland have lately reported considerablesuccess with third occipital nerve blocks which relieved theheadache of seven out of ten unselected consecutive patientsreferred to a pain clinic with occipital or suboccipitalheadache Most of these patients were tender over theC2-C3 zygapophyseal joints and also had restricted neckmovements, but neck radiographs gave no evidence of localarthropathy. None of this amounts to proof, but there is

. increasing evidence that upper cervical nerve irritation cancause headache. This is perhaps most convincinglydemonstrated by groups of patients described by Cyriax andby Lance and Anthony with neck-tongue pain, in whomsudden neck turning caused severe ipsilateral tongue as wellas occipital pain, ascribed to irritation of the second cervicaldorsal root which carries proprioceptive fibres from thetongue via the hypoglossal nerve and its communicationswith the second nerve.12-13

Upper cervical nerve blocks are technically fairly simpleand have few complications, although they may causeshort-lived lightheadedness, dizziness, or slight ataxia. Thismay be due to interference by the local anaesthetic withproprioceptive afferents from the joint capsule and uppercervical muscles involved in the tonic neck reflex.14 Patients

may need to rely on visual clues for balance, and concentrateon the horizontal whilst walking. However, third occipitalnerve blocks may relieve occipital headache as long as theanaesthetic lasts, and, if the procedure is successful,prolonged relief can be achieved by subsequent radio-frequency coagulation. At present, in patients with cervicalspondylosis and no other obvious cause for occipitalheadache, a trial C3 nerve block may be justified. Lowerblocks may relieve neck ache, but rarely pain in the head.

ADVICE TO THE ASPIRING PHYSICIAN

QUALIFICATION is only the beginning of a lifelongcommitment to training and learning in medicine. Advice onfuture prospects is available to young doctors from variousmore-or-less informal sources, including colleagues andcompetitors, clinical tutors, postgraduate deans, regionaladvisers, the British Medical Association, the MedicalWomen’s Federation, and publications such as thehandbook of the Joint Committees on Higher Training andHealth Trends (retrospective). However, giving advice ishazardous and possibly irrelevant when good timing may bethe most appropriate requirement in the rapidly changingscene of medical employment.

11. Bowden RE, Abdullah S, Gooding MR. Anatomy of the cervical spine, membranes,spinal cord, nerve roots and brachial plexus. In: Brain R, Wilkinson M, edsCervical spondylosis and other disorders of the cervical spine. London:

Heinemann, 1967: 10-97.12. Cyriax J. Textbook of orthopaedic medicine. 4th ed. Vol 1. London: Cassell, 1962

158.

13. Lance JW, Anthony M. Neck-tongue syndrome on sudden turning of the head.J Neurol Neurosurg Psychiatry 1980; 43: 97-101.

14. Bogduk N. Local anaesthetic blocks of the second cervical ganglion. A technique withapplication m occipital headache. Cephalgia 1981; 1: 41-50.

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A report by the Standing Committee of Members (SCM)of the Royal College of Physicians of London’ is unusualand makes a welcome contrast. It covers the formal

requirements of general professional and higher medicaltraining (full and part time), the importance of highstandards in medicine, career choice, and keeping abreast ofknowledge, and even includes a whiff of comment aboutmanagement. Like all good things, it is divided into threeparts: (a) contributions from authoritative sources on therequirements for basic training and the general need toprepare for a future consultant appointment; (b) datacollected by the SCM in a survey of MRCP diploma holdersencompassing aspects of study, research, overseas

experience, career planning and achievement; and (c)accounts of individual medical specialties which containmany personal views on the present position with respect toopportunities and difficulties facing aspirants.The first section underlines the College’s real concern in

postgraduate education-the maintenance of high standardsin medicine and the relation between the Colleges and theJoint Committee on Higher Medical training. Both thebenefits and the limitations imposed by part-time trainingare recognised; it is important that these training posts are ofequal standard to full-time appointments. Results are

presented of a study by the SCM on training for physiciansafter the MRCP. Three separate surveys of between 500 and900 doctors who obtained the MRCP were carried outduring the years 1968-83 (keeping up to date in medicine);in selected years between 1972 and 1981 (research experience);and between 1966 and 1975 (achievement in career posts).Factors (not identical) which appeared to be related to careerachievement and exam achievement are discussed. Thereview of individual specialties provides many personalopinions, but much contained in it would be echoed by themanpower advisory panels in medicine; the views of

specialty representatives and the College specialist advisorycommittees (SACs) are collated. In such a changing world itis understandable, but slightly surprising, that there is littlemention of the precise figures given in the reviews of theSAC or specialty societies. Continuing uncertainty is a

recurring thread. This alone emphasises how important it isfor young doctors to be constantly aware of "market forces";whilst the profession must be flexible in its staffmgrequirements at and to consultant level, there is a pressingneed to increase the consultant to senior registrar ratio.The report gives much factual, much subtle, and some

direct advice to aspiring physicians. It is especially appositeat a time when the profession is faced with consultant

training post imbalances in medicine, a balance that shiftsmore rapidly than the educational pattern can reflect. It is aspecial credit to the SCM and their continuing tradition of aserious contribution and corrective balance to College life (ifone were needed) from younger members of the profession.

CYCLOPHOSPHAMIDE FOR PARAQUATPOISONING?

ONE of the more controversial contributions to theSecond European Symposium on Paraquat Poisoning heldin London earlier this year1 was that by Addo from Trinidadwho described his experiences with cyclophosphamide. Thesymposium proceedings are due to be published in full laterthis year in Human Toxicology, but Lancet readers have had

1 Training to be a Physician. A report compiled by the Standing Committee of Membersof the Royal College of Physicians of London. J R Coll Phys Lond. 1986; 20: 75-115.(Copies of the report may be obtained from the College, price £3).

an earlier opportunity to see2 and comment3 on this study.Addo and Poon-King’s treatment was complex, and insummary consisted of gastric lavage; oral administration offuller’s earth, activated charcoal, and magnesium sulphatepurges together with forced diuresis; and vitamins B and C,dexamethasone, and cyclophosphamide intravenously for 2weeks. With this regimen the mortality from severe

paraquat poisoning, defined as the ingestion of 5 ml or moreof either the 20% or 24% concentrate, declined dramaticallyfrom 68% to 28%. Although these results are encouraging itis unwise at this time to recommend such potentially toxictreatment as routine. People who take overdoses of paraquator other chemicals often miscalculate the amount ingested,therefore it is important to determine plasma concentrationswhen assessing the efficacy of any treatment. Unfortunately,such measurements were done in only 25 of Addo andPoon-King’s 72 patients; in 6 of these no paraquat wasdetected, indicating that insignificant amounts had beeningested. Of the 19 remaining patients, 12 with very highconcentrations died. We are left with the question: wouldthe 7 who survived have done so if they had been treatedwithout the intensive regimen? There is a reasonably goodrelation between time of ingestion, plasma paraquatconcentration, and outcome;4 Hart and colleaguess haverefined this to produce centile survival curves. Transposingthe data from Addo and Poon-King’s study to the survivalcurves of Hart et al reveals that the chance of survival in the 7who lived was only 30% or less. Thus 1 or 2 of them mighthave been expected to live but not all 7. Since plasmaparaquat concentrations fall very quickly after an overdosean error of an hour or two in the estimate of time of ingestioncan move a patient from the 30°. to the 70% survival curve.Again, practical experience suggests that such inaccuraciesare not that uncommon. Most physicians would thereforefeel that more detailed research is required before

cyclophosphamide treatment can be recommended.For the moment, therefore, the treatment of paraquat

poisoning should remain unchanged. Oral sorbents such asfuller’s earth, bentonite, or activated charcoal should begiven and fluid losses replaced. Plasma paraquat concentra-tion should be measured as a matter of urgency. Most

patients will fall into two groups. The first group consists ofthose with low concentrations who will recover; these

patients and their families need to be reassured. The secondgroup are those who have taken massive overdoses and who,as in Addo and Poon-King’s study, will die no matter whattreatment is given; for them the emphasis should be onappropriate terminal care and support for their families andfor the nursing staff who have to treat them. For patientswhose plasma concentrations fall on or near the 5000survival curve the more active treatments discussed at the

paraquat symposium, such as haemodialysis or haemoper-fusion, Addo and Poon-King’s cyclophosphamide regimen,or even radiotherapy, may eventually be shown to save somepatients who would otherwise have died. Readers will beable to judge for themselves when the full proceedings arepublished, and it is also intended that the leading authoritiesin this field will give more definitive advice on how tomanage paraquat poisoning. Perhaps these same experts can

1. Crome P. Paraquat poisoning 1986. Lancet 1986; i: 333-34.2 Addo E, Poon-King T. Leucocyte suppression m treatment of 72 patients with

paraquat poisoning. Lancet 1986; i: 1117-20.3. Vale JA, Meredith TJ, Buckley BM. Paraquat poisoning. Lancet 1986; i: 1439.4. Proudfoot AT, Stewart MS, Levitt T, Widdop B. Paraquat poisoning. Significance of

plasma-paraquat concentrations Lancet 1979; ii 330-32.

5. Hart TB, Nevitt A, Whitehead A. A new statistical approach to the prognosticsignificance of plasma paraquat concentrations. Lancet 1984; ii: 1222-23.