Lathyrism India Acton 1922

download Lathyrism India Acton 1922

of 10

Transcript of Lathyrism India Acton 1922

  • 7/29/2019 Lathyrism India Acton 1922

    1/10

    J U L Y . 1922. j C A U S A T I O N C) ~ F L A T H Y R I S M X M A N : A CT O X .

    Original Articles.AX INVESTICATION INTO THECA U S A T I O N O F L A T H Y RI S M I N M A X .

    B y M A. H U G H \ V . A C T O X . I . M . S . ,Professor of I'atlwlotjy and Bacteriology , School ofTropical Medicine and Hygiene. C alcutta.

    IN August 1921, Major H. W. Pierpoint ,I . M . S . . invited me up to Sutna to investigate thedisease lathyrism , a type of spastic paraple gia,common amongst the inhabitants of XorthRewah.The paralysis is regarded by the people as due-to eating an exclusive diet of kesari dl(Lathyrus sat ivus ').M ajo r Pierpoint assured me that the diseasewas ven- prevalent in this part of the State andduring the few days 1 had at my disposal, 1 oughtto have no difficulty in exam ining at least acouple . of hundred cases. He w anted lo knowwhat mea sures to take to prevent this terribleaffliction which .crippled for life so many of thesubjects of this State.I was anxious to collaborate, hut Major Pier-point requested me to conduct my own investiga-tions on this disease, for he was onlv too glad tohave given me the lead. I am therefore indebtedto him. not only for having instigated this re-search, but also for his help during the clinicalexamination of these cases, and furtherm ore forobtaining the necessary information from thevario us St ate officials abo ut the harvvar systemand other factors that play so large a part in thecausation of this disease.

    Th ree species of lathyru? are regarded ascausing epidemic and endemic poisoning in mjanand animals . They are:( 1 ) Lath y rus satiz'us.Generally known inIndia as kesari dl. tcora, or bitttorah ka dl.The peas are of two sizes, the larger known aslakh is grown on dry wheat land, and the smallerlakhari is cultivated on wet rice fields.In Re wa h, the larger .grain lakh which isimported from Bhagalpur, is regarded as morepoisonous than the smaller indigenous vetch. 3^T h e kesari dl is taken in various ways by thecommon people. It may be ground into flour,and eaten raw ; the raw flour is moistened withwater; salt and chillies added, and the mash isknown as sutto; or the flour may be ma de upinto hand-bread or chappatics, and baked on aniron plate.The vetch is also boiled in water with salt andonione, the thick pea soup is known as dl, andeaten with the hand-bread ; or the boiled vetchniay be made up into small thick cakes, fried inclarified butter (ghee), ior oil and called pun's.The vetch is used both as a food for cattle, aswell as for man, and owing to its cheap price,it is eaten all the year round by these people.

    In tinier of plenty it is eaten as a dl, withwheat hand-brea d, or rice, or as pun's, but intimes of famine owing to the high price

  • 7/29/2019 Lathyrism India Acton 1922

    2/10

    242 THE INDIAN MEDICAL GAZETTE. [J uyr, 1922.walking on the road side. We saw 94 individualsof whom 8 were suffering from lathyrism, twtoof these cases were returning home after we hadexamined them 'at the h ospital.' This wouldcorrespond to Irving's 6 per cent., and w ouldmean that there were about 60 ,00 0 lathvrismcases in North Rewah. \^sI carefully examined 204 individuals, whowere chosen at random, in order to ascertain thevarious factors that played a part in the causa-tion of this disease. Some of the cases werecollected by Major P ierpoint, but the maj oritywere seen at the Sutna lime works and I amindebted to Mr. Holden the Manager for all thehelp he gave me in getting together these indivi-duals.In the lime works, two or three hundred ofthese men and women are employed in breakingup the lime stone, before it is burnt in the kiln.Th e large boulders of lime stone are placedbefore them in heaps, arid they smash them intosmiall pieces, the crushed stone is1 taken away insmall baskets by the able bodied men andwomen.Each individual was examined separately, inorder to prevent any errors in their answ ers.These ignorant people are apt to be very suspici-ous of any examination, and to save themselvesfrom thinking or to possibly avoid trouble later,would merely repeat the answer they had heardgiven by the person in front of them.For this reason, they were collected in a court-yard and examined one at a time, and then allow-ed to go away, so that there was no communica-tion between the persons examined and thosewaiting their turn.

    Age.The age interval is given in 5 yearlyintervals for the first thirty years of life, be-cause these people when young usuallv estimatetheir age in 5 year intervals. After 30 years ofage, the age is generally reckoned in ten yearintervals. The following table gives the age ofonset of lathyrism according to their statement.A ge andOnset.N o . ofOases

    110

    o111

    11

    34

    T A B L E

    12

    622

    52

    1.38

    tc9

    45

    256

    2

    T O T A L .

    201Th e earliest age at which the disease wasstated to have occurred was three years of age,and fifty-eig ht the oldest age. The maj ority ofcases, i.e., 170 out of 204 occurred between the15th and 30th year, when the individual is mostactive, and after marriage has to leave hisparents in order to earn a living wage for him-self and family in a poor country.Sex. Am ongst the 204- cases exam ined, 181were men, and 23 women. This difference is notdue to any difficulty in getting the women tocame for examination, as they were all of the

    lowest Sudra class, an d both men and women {work in the quarries as stone ' breakers. An 'explanation that, was given to me by the moreintelligent men employed as overseers, was that'during famine years, the women eat less in orderto save the food for their husbands and children,and consequently many die from starvation.The women that survive by eating less kesari dalge t less of the poison.Occupation.All these cases, with the excep-tion of two poor Brahmin beggars, were of thelowest Sudra class, Teli, Kachi, Koals, etc., and

  • 7/29/2019 Lathyrism India Acton 1922

    3/10

    J U L Y , 1922.] C AU S ATIO N O F L A TH Y R ISM IN M AN : A CTO N ,

    fy

    Der

    No. of yearsNo. of eases

    CM

    11

    1

    216

    19181

    3

    10

    >

    47

    1916-1

    51

    16t

    176

    1913-1

    82

    19121

    91

    11161

    1032

    1910-

    11

    TABLE

    1-6061

    1226

    1

    132

    2.*cO N

    145

    1IS39

    a16

    3

    117

    118

    7

    119

    1901-C

    2025

    *OON

    218

    9

    11

    221

    19

    2319

    24

    *

    19

    258

    19

    2619

    271

    TTL

    20 4Th e asterisk denotes th e famine years as reported by the state officials.

    especially in the month of (Asar), Ju ly ,distrib ution was as follows :See table 3.T A B U 3 .

    The

    Month ofOnset uu."* '5

    es510

    une

    j

    19uly1

    "5122

    S

    21

    jjam10

    'ctober1

    12ov.

    5

    T O T A L .

    201 cases.The tehsildar informed me that in mostyears the local crops in Rewah are exhaustedby Mardi or April , and kesari dl is importedfrom Bha galp ur as the food supply becomesscarce by J uly . The common people have there-fore to subsist on the cheapest article of diet,viz., kesari dl, if the monsoon fails in J un e,then all the fresh food supplies, e.g., vegetables,etc., are unobtainable except at very high prices,and the people have to subsist on an entirelyvetch diet.When the local crops1 of rice and wheat havefailed owing1 to a bad monsoon, kesari dl isplanted and ripens in October. The absence ofcases during the months of December to Marchis very suggestive of one of two factors.(1 ) Th e indigenous small grained kesari dlis nof poisonous, or (2) the diet is sufficientlyvaried with other articles, e.g., local grasses, etc. ,so that the amount lof kesari dl is kept belowpoisonous limits.Both factors play a part in preventing lathy-rism dur ing these months, as I will show later.With the advent of April the first few casesare seen, whilst in July over 50 per cent, of thecases occur during the mon th. The evidencethis table shows is :(1 ) Th at the disease , is associated withi eating imported d l (Bhagalpur dl) as the inci-dence coincides with the importation of thisi.vetch in M arch and April and is maintainedOctob er and Novem ber when the local'tesari dl is gathered for consumption.i- (2 ) Th e high incidence of the disease inFuly is probably associated with the production of~^isonous amines during germination. TheBhagalpur vetch germinates more readilyin the bca l small grain .w hich sprouts withA cu ity . . ^V"ft

  • 7/29/2019 Lathyrism India Acton 1922

    4/10

    244 THE INDIAN MEDTCAL GAZETT1 [ J U L Y , 1 922.men state that they were working in the field,ploughing, cutting grass or wood, mending theroofs of their houses, and even whilst at stool.A few state that the onset came on gradu ally,they got ill with fever, and when they got upand tried to walk, they found that they wereparalysed in the lower limbs.As far as I am aware the actual onset of thedisease has never been observed by any com-petent investigator. The following is a typicalaccount by an intelligent loyerseer." Du ring the famine year of 1 90 8-09, whilstploughing, I suddenly noticed that my legs wereweak, there was no pain, but I had difficulty insi t ting down and gett ing up from a squatt ingposition. I did not know I was paraly sed, u ntilmjy friends told me that I had lathy rism . Onthat day 1520 men of my village also becameparalysed . I realised that I was suffering fromlathyrism because I fell down when I tried torun ; a few days later I felt pain in the calfmuscles ."Th e gait is very typical and depen ds on thedegree of involvement of spinal tracts, a singleattack leaves the patient paralysed as is depictedin Plate I , figs. 1 or 2, the worst cases, figs.3 or 4, have usually suffered from two or moreattacks.For descriptive purposes I have described thegait as seen in this disease, in fou r stages :se c Pla te I. figs. 1 to 4. In the eai liest stage(Plate I . fig. 1.) the patient can walk withoutany aid, or only requires a short walking stick.The knees are flexed ; with each step the shoulderis thrown forward; as he rises from the groundon his toes, the movement ends with a peculiarspring owing to the spastic condition of thegastrocnemius. The feet are kept apart , and asthe spasm; of th is muscle still pe rsi sts , th e heelis well raised off the ground, so that when thefoot is advanced for the next step, the toes justclear or drag across the ground. Th ere is nostamping as is seen in locomotor ataxia, nor isthe fioot swung round as in the flaccid paralysisof a hemiplegia.The characteristic point about the gait is itspeculiar hesitating springy character as thepatient walks on tip toes. Prog ression is very badwhen the patient star ts walking, but improvessomewhat after he has gone a little distance.In the second stage (fig. 2 ) , a long stick hasto be used as a supp ort. Th e body and theshoulder on the same side are thrown forwardwith each step. Th e knees are mo re flexed, andthey walk more on their toes; the foot is slightlyturned in, and owing to the. addu ctor spasm , onefoot is broug ht in front of the oth er. Th e gaitbecomes much more hesirating owing to the mark-ed spasm of the gastrocnemius and post-peronealgroup of 'muscles.In the third stage (fig. 3 ) , two long stickshave to be used to enable them) to walk at all .The body is thrown well forward, and the musclesof the arm and chest are well developed as theyhave to sup port the weight of (the body . Th e

    knees are acutely flexed, and owing to the markecadductor spasm the knees are drawn one in frontof the other (scissors pro gres sion ) . At thisstage these patients usually walk with the footwell inverted, caused by the spasm of the pos-terior-peroneal group, so that the outer toes andthe extre me end of the outer pa rt of the soleonly touch the gro un d. Occasion ally t:he footmay be everted instead of inverted.In the last stage (fig. 4), the knees are flexedalmost on to back of the thighs, so that progres-sion is only possible by crawling on the handsand knees, or by using wooden shoes for thehands.There is never any loss of consciousness, noris there any involvement of the bladder or rec-tum . On exam ination of the legs, there are nosensory disturbances present, on pressing themuscles of the calf and thigh no tenderness iselicited although the patients complain of muscularpain.On closing their eyes with the feet together inthe erect po sture , no a:axia is seen. The knee.:jerks are increased, ankle clonus is well marked,and when the skin of the soles of the feet is nottoo thick and horny, an extensor response of thegreat toe is given on stroking the sole.Major Pierpoint pointed out to me that on tap-ping the adductor muscles of the thigh a markedreflex contrac tion occurs. I found this addu ctorreflex present in every case I examined, and con-sider it a characteristic sign in this disease.There is no paraly sis, but a spastic conditioninvolves the following muscle groups, quadricepsextenso r, add ucto rs, gastrocnemii and posteriorperoneals . Th e trun k and upper l imbs are un-affected, and the chest and arm muscles areusually well developed owing to the extra workthat is thrown on them.Pathological Anatomy.T hese cases rarely dieduring the acute stages, and post mortem exami-nations are iimpossible to obtain owing to religi-ous preju dices. Th e nat ure of the lesion hastherefore largely to be surmjised from the signsand symptoms.As the knee jerks are increased, ankle clonusand Babinski 's sign are present, the lesion is anupper neuron lesion.The posterior columns of Goll and Bardack,and the posterior root ganglia are not involvedas is shown by the absence of hyperaesthesia,girdle pain, stamping gait , e tc .There is no ataxia so the cerebellar tracts areintact.The absence of any bladder or rectal trouble,either at the onset or in the advanced stages ofthe disease shows that the lesion is outside orbelow these centres. The involvement of thequadriceps extensor, adductor, gastrocnemius and* post-peroneal gro up indicates that the lesion is*below the second lumbar root. There is no loss :of consciousness during any stage of the disease, 'confirming the lopinion that the site of the lesionis not in the craniu m. ! J

  • 7/29/2019 Lathyrism India Acton 1922

    5/10

    P L A T E IThe character of the gait in the different stages of Lathvrism.

    1st Stage. 2nd Stage.

    Final Stage.

  • 7/29/2019 Lathyrism India Acton 1922

    6/10

    m

    (a) Microscopical draw ing of a section of the cord of a rabbit , to show the a r rangem ent ofthe blood vessels and finer capillaries .

    fasciculus cuTieatuafasciculus fraciZs

    II.

    I 'fasciculus tmptorn.CLroiytM.lisI / r *

    C K - C U L S epinoCccCalt- s - '/

    (b ) Diagrammatic section of the spinal cord showing the arrangement of the different tracts.

  • 7/29/2019 Lathyrism India Acton 1922

    7/10

    J U L Y , 1922.] CA U SA TIO N O F LA TH Y RISM IN M A N : A CTO N . 245vSo far we have deduced that the lesion is anupper neuron lesion situated below the secondlumbar root, involving the motor tracts as is evi-denced by the increase in the reflex arc andBabinki 's s ign.Now the upper neuron mo'.or path .cionsists ofmain conducts (see Plate 2, fig. b) .( 1 ) . The cortico spinal motor system.Con-sisting of the crossed and direct pyramidal tracts,lesions cf which are associated with flaccid para-lysis followed by tonic rigidity, and increasedreflexes.( 2 ) . The strio-spinal m otor system.Con-sis ting of Monakow's bundle, the tecto-spinal andvestibule-spinal bundles, lesions of which areassociated with no loss of movement, rigidity ofvoluntary muscles, no alteration in reflexes.Th e increased reflexes show that the. pyram idaltracts are 'damaged, but the absence of paralysisindicates that the lesion is, only partial, and notcom plete. Th is is furth er exemplified by thepatient , who after walking a short dis tance beginsto im pro ve in his gait. Th e rigidity of the volun -tary muscles indicates tha t the strio-spinal m oto rsystem; is also involved. In the early stages ofthe disease the rigidity of these muscles is onlyobserved during voluntary movement and hencethe dam age is only partial. In the advan cedstage of the disease (P lat e 1, fig. 4) the rigidityis con stantly presen t showing that the wholestrio-spinal motor system has been destroyed asthe result of disease. We have therefore deducedfrom clinical signs, that the lesion of the cortico-spinal system is always partial, and never co m-plete, but that the strio-spinal motor system maybe completely destroyed in advanced cases of the

    disease, and that the lesion is below the secondlumbar root.The nature of the lesion.W e have alreadyseen that the disease comes on suddenly, oftenwhils t at work.The sudflen onset suggests that the cause maybe due to one of the ; following : embolism,haemorrhage or thrombosis .i A Embolism can be dismissed at once, owing to-p the invariable selection of such a minute vessel as^ !a spinal vessel, and there is nothing in the heart$ sounds to suggest valvular disease.On an analogy with ergot poisoning, one would[at first expect that haemorrhage would be a very^likely cause of this lesiqn,;i>ut the patients give' no history of bleeding from an y other vessels,[and it is difficult to conceive why the fine branchesI'Jii the anterior-spinal vessels should be selecteda site of rupture rather than vessels in otherf parts of the body.Thrombosis is finally left for consideration andI will show that thereris^a good ideal of evi-ice in sup por t tof this view. W e know th at^ bilateral spastic paraplegia can occ ur in this"ituation of the cord in ; certain grave forms oflemia, and toxic conditio^ j : Th e lesions are>nsidered to be due to thf^bosis caused by end-ir terit is , or a ve ry low s tat# pf-the blood pressure,ms ider that the an at o j ^a l ar rangement of

    the blood supply in this region is a predisposingcause of lathyrism. Th e anterior-spinal arterybelow the lower thoracic region becomes extreme-ly fine and attenu ated , and is only preserved inits dow nw ard course by fine reinforcem entsfrom the dorsal and lum bar arteries. Plate 2, fig.a shows a section of the spinal cord of a rabbitwith the capillaries injected with a gelatine-carmine mass . One sees that the grey matter ofthe cord, vis., the anterior and posterior hornsare richly supplied with num erou s capillaries.The white matter consisting of the various motorand sensory tracts is not so well supplied asthe grey matte r . Of the various columns of thecord the poste rior columns are mo re richly sup-plied with blood than the lateral colum ns, andthe poo rest supply is given to the anterio rcolumns. (See Plate 2 , f ig . a) .Thrombosis if it occurs in this region of thecord is imore likely to select the avascular re-gions rather than those more richly supplied withblood, vis., the antero and antero-lateral tracts .In thes e two areas of the cord are found thetwo motor systemsthe cortico-spinal and s tr io-spinal systems. The direct pyramidal tract atthe second lumbar root has practically disappearedas a tract . Th e lesion is probably due to athrom bosis .cutting off the blood supply of theantero and antero-lateral tracts and causing dege-nerative changes which only partially affect thecrossed pyramidal tract, and partially or whollythe s tr io-spinal system. From experimentalevidence on anim als, Stoc km an and myself didnot find any microscopic lesions such as embolismor haemorrhages. Th e thrombo sis is probablydue to an arteria l spasm of these vessels as theparalysis in animals comes on suddenly, and ifthe diet is changed, it disappears within a fewdays , leaving no permanent damage of the cord.Clinically in man , we have the evidence thatthese persons only suffer from (the disease intimes of famine, i.e., semi-starva tion with lowblood pressure, and that wet or chill precipitatesthe disease by inducing arterial spa&m, whichis directly caused by. the. toxin in kesari dl.Evidence that kesari dl is the cause of thedisease : -(A). C linically.The first thing that one hadto exclude in this investigation was the possibilityof any other food causing the disease. The fol-lowing grasses and pulses are eaten by thesepeople fnom the end-of A ugu st , when the im-ported kesari dl gets scarce, until the ripeningof their crops in October .( 1 ) . Samai (See Plate 3 , f ig . 1) a wild grasswhich ripens at th e end of A ugu st I D the begin-ning of Septe mb er, and lasts .for about afortnight 's food supply.( 2 ) . Samah (See Plate 3 , f ig . 2) is generallysown and r ipens about the end of August or Sep-j tember , and gives about two months ' food supply.( 3 ) . L uptowah or Narw al (See P la te 3 , f ig . 3 )a small grass seed which ripens in September; thewom en collect it by brushin g the seeds . intobaskets, this lasts for about three weeks or so.

  • 7/29/2019 Lathyrism India Acton 1922

    8/10

    246 THE INDIAN MEDICAL GAZETTE. [ J U L Y . 1922.These grass seeds are ground into flour andare used to make hand -bread. The differenceis ma rked between the yield of the cultivatedand w ild heads of these grasses as is seen inPlate 3 .(4 ) Puchchoar (See Plate 3, f ig. 4) a wildpulse which grows all over the place, and ripensin Septembe r. The seeds are generally spokenof as jungly mungh. It is used as a dl, an dlasts for about three weeks.Besides these articles of diet, in famine-strick-,en years, the mozvah fruit various root s,etc. , are eaten by the people. J uly is themonth that has. the greatest incidence of lathyr-ism!, a nd these food stuffs are not available unti lthe end of August or September. They there -fore cannot play any part in the production ofthis paralysis.The question of adulterants had next to beconsidered. Thre e other seeds are sometimespresent. ( 1 ) The ordinary dried pea. (Pisumsativus. etc.,) a n d (2 ) g r a m o r chunnar, (Circer,Arietinum) both of which we know to be non-poisonous. A third (3) , a small black grain calledAkri (Withania coagulons) which grows wildand ripens in October, is a slight adulterant, but if

    seen, is always removed during the cleaning andfanning of the dl. So we can exclude thepossibility of an adulterant of kesari dl causinglathyr ism.The possibility that this vetch m:ay be attackedby a fungus at once suggests itself to the mindowing to the analogy with ergot. The follow-ing evidence may be quoted against thisview :(1) Stockman found that all the samples ofkesari dl he tested contained the poison, but invarying amounts .(2 ) On e specimen of the large grainedkesari (lakh) contained a large quantity of thispoison compared with the other samples tested.H e does not mention having noticed anyobvious signs of disease in any of his samplesof this vetch.(B) Experimental Evidence.Stockman hasconclusively shown that if susceptible anim als,e.g., monkeys are fed on an exclusive diet ofkesari dl, they develop paralysis at varying in-tervals depending on the toxicity of the grain onwhich they are fed. On my return from Sutn aI placed nine ducks on a diet of kesari dl.(1 ) First group of three ducks were giventhe crush ed grai n soaked for 24 hours in asufficient quan tity of water to mak e it soft,otherwise the ducks could not masticate it .On the 18th day the first duck showed signsof paralysis; which increased in intensity ; onthe 22nd day it could not rise from the ground.It was killed and there were no signs ofhaemorrhage in the cord. The second duck showedsymptoms on the 20th day and the third duck onthe 22nd day. Neith er of these ducks were sobadly affected as the first one.(2) Th e second group of three ducks werefed on an exclusive diet of kesari dl, but the

    grain was washed in three changes of water dur-fing the 24 hours. None of these ducks showedithe slightest symptoms of paralysis.(3 ) The third group of three ducks were fedlon washed grain as in group (2) but they weregiven some chopped vegetables in addi tion. Theywere quite well up to the 60th day of the experi-ment, and I considered the experiment practi- 'cally finished. On the 80 th day one duck showedsymptoims of paralysis which may have been dueto the fact that I was not then supervising thewashing of the grain.This experimen t shows that the poison iswater soluble, and the paralysis is not due to anydeficiency in vitam ines caused by living onan exclusive vetch diet, because all the duckst ingrou p 2 remained perfectly well duri ng theexper iment .Stoc km an considered the poison o be analkaloid in nature, as it gave all the chemical testsand the crude alkaloid produced paralysis inanima ls. The following points may be advancedagainst this view :(1 ) Most alkaloids are not very soluble inwater .(2 ) in a plant the alkaloid is fairly evenlydistributed in the leaves, etc. W e know that theleaves are not poisonous to cattle.(3 ) Few alkaloids have a cum ulative effectin the system. To explain the high incidenceduring the month of J uly we would have to as-sum e a cum ulative effect. I am in favour ofthe to xin being an amine for the follow ing'reasons :(1 ) Am ines give all or most of the alkaloidaltests .(2)(3) They are all water soluble. ^The amount of amines in the seed is 'increased, during germination, e.g., Hordenine in ibarley.(4 ) The high incidence of lathyrism in July-;;would correspond to the conditions necessary forjgermination, viz.. temperature and humidity.(5 ) The tox ici ty of the la rge g ra in jd l (lakh) could be explained similarly, as the]large grain germinates in 24 48 hours inpresence of m oisture at 37 degrees C. The small!grain even at the end of four days shows njsigns of sprouting. | |(6 ) Man y lof these amines cause a marked!contraction of involuntary muscle and bkvessels.Dr. Sudhamoy Ghose is working atchemistry of this poison. For several monthsfollowed Stockman's technique and practicall|got no yield from large quantities of this vetFrom grain that was not germinating hefair amoun t of a non-toxic amine in astate . Th irty mgrm s. of this am ine had no effeon the guinea-pig. W e are now attemptingisolate the toxic amine from germinating seed/well as commencing feeding experiments on dueDifferential Diagnosis.Most medical men'Calcutta have been taught that the diseaseprimary lateral sclerosis of unknow n oi

  • 7/29/2019 Lathyrism India Acton 1922

    9/10

    P L A T E H i .Grasses.

    Fig. 1. ( a )b)Samai.Panicum Crus-galli L- var. frumentaceum(6) Panicum colonum L.

    Fig. 2.Saman-Panicum ramo sum Lm n t

    Fig. 3.L,i}ptowah or Narwal,tria glauca Beauv.

  • 7/29/2019 Lathyrism India Acton 1922

    10/10

    JULY.. 1922. J C A U S A T IO N O F L A T H Y R I S M IN M A N : A C T O N . 247"possibly syphilitic in nature. The peculiar hesitat-ing springy gait, the throwing forward of the bodywith each step, the increase in the reflex arc anda marked adductor reflex, are however character-istic and peculiar to this type of paralysis.Prognosis.The degree of paralysis that isproduced by the original attack remains perma-nent for the rest of their lives. In a very sm allpercentage of cases some improvement occurs in4i gait af.ter-a few months r year s, but thepeople are very definite in their statement thatcomplete recovery is> impossible. The first attackprodu ces the degre e of pa ralysis show n inthe gait by Plate 1, figs. 1 and 2. Tw o or mo reattacks cause an extension of .the injury, to thecord and pnoduce the gait shown in Plate 1, figs.3 and APrevention of the disease.In 1907 the la'eMaharajah of Rewah attempted to prevent thisdisease in his1 State. H e issued an orde r datedthe 29th N ovem ber, 190 7, in Hindi and it wasread out to me by the Hom e Member. Th e gistof the order was as follows :The paralysischiefly affected the labouring classes, more parti-cularly those of s-mjall caste and especially thosewho were given their wages in food (h ar w ar s) .It was due to the eating of kesari dl itherespoken of as butturah, which was cheap in faminetimes. H e forba de the cultiva tion :of this vetch ,. and placed import and export duties on thegra in. As the vetch w as the staple food of thepopulation, it was impossible to prevent its culti-vation in out-lying villages. In a year or sio theorder was forgotten, and now the d l is cultivatedwithout any restraint. The preventive mea suresshould consist in.(1 ) The abolition of the har w ar system,because in times of fam ine the bondm en a re cc.m-pelled to subsist on a diet composed entirely ofkesari dl.(2 ) To (decrease the amo unt of kesari dlconsumed by the population by institutingfamine reliefs during the years of a bad mionscon,as well as controlling the price of wheat, rice, anddl, so that the poor can afford to buy thesearticles of food.(3 ) To increase the popu lar knowledge re-gardin g the toxicity of this grain, (a ) Th epoison is water soluble so that soaking 'the grainfor twenty-four hours1 in three, changes of wa 'erremoves the poison, and the grain can be usedfor making d l or puris. (b). The small grain-ed kesari is less toxic than the large grainedBhagalpur dal, so that every effort should bemade to grow a sufficient quantity of the indigen-ous grain to meet local requirements. (c )During the hot damp months of July and August ,the grain should be stored in a dry place toprevent germination.(4) By improvemen ts in the agriculturalmethods now employed. The system of cultivationdiffers considerably in North and South Rewah.In the No rth, the inhabitants largely relv onthe bund system, i.e.. an embankment 45 feethigh is thrown up to enclose a square area in

    order to catch the nuonsoon rain. W hen w ateri.v required for the fields, the embankment is .cutand the water allowed to run into the field. Ifthe monsoon fails , no water is available and thecrops fail. The people are then compelled tolive ion kesari dl and hence lathyris m is very-common in North R ewa h. In "the South, theGonds do all their cultivation by forest clearing,and irrigation from streams, with the result thatlathyrism is rare in this portion of the State, asthe crops 10f rice, wheat, etc. , rarely fail. TheState is rich in mineral wealth, if this source ofrevenue was allowed to be opened up, it wouldafford an oc cupation which is inde pen dent ofrainfall, and so largely prevent lathyrism in NorthRewah .This research has been a mos t fasc inat ingone from every point of view . An invest iga-t ion car r ied out am ong s t a poor i l l i te ra tepopula t ion is imposs ib le wi t hou t a good com-mand of the i r l anguag e . The backw ardnes sof this state w as well exemp lified by theant ique h igh sprung- baro uch e wi th i t s twohorses , accom panied by a bev y of four red-coated , b rass bel ted a t t en da nt s who droveme back to the statio n. Th e statisticalenquiry made clear the relationship duringtimes of famine betwee n an exclus ive kesarid l diet and the har w ar system : whilsti t dem ande d an exp lan atio n for the highincidence of the disease du rin g the mon th ofJ u ly , the suddenness of the onset , and thepecul iar d is t r ibu t ion of the cord les ions . Thewater soluble natu re of the toxin is a mostsatis fact ory result from t he point of view ofthe prevention of the disease. The surmou nt-ing of difficulties in any prob lem makes thesolu t ion more precious than those that areeasily won. Fo r mon ths D r. SudhamoyGhose, M.sc, laboriously worked to obtaina sufficient quan tity of the alkaloid tha tStockman considered to be the toxin in kesaridl. Wh ilst working on the natu re of Shigtoxin . MLJ or Boyd wa s ab le to iso la te anam ine for me similar to hista mi ne in its effecton isolated guinea-pig's u terus. Since thenDr. Chatterji has been able to isolate a similaramine from a broth culture of the cholera vibrio.This amjine also causes a very marked contrac-tion of uterine muscle. The production of an amine(Hordenine) during the germination of barley,at once suggested itself as a possibility in itfcecase of kesari dl and lathyrism , and I havegiven the evidences in favour of this view. Th eisolation of the toxic amine from the other ntoii-toxic amines in the grain still requires a gooddeal of labour before the problem can be solved.In India one publishes results and waits patientlyfor years to see them carried out into practice.U ltimately there will be the satisfaction of know-ing tha t the w ork ha& been the me ans 10f savingmany of these poor oppressed people from a life-long paralysis. Even if only the harw ar systemcan be abolished, it alone will do great dealtowards the prevention of this paralysis.

    I