Lathyrism India Cause, Symptoms and Treatment Jacoby 1947

7/29/2019 Lathyrism India Cause, Symptoms and Treatment Jacoby 1947

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FEB . , 1947] CAUSE , SYMPTOMS AND TRE ATM E NT OF LATHYRISM : JACOBY 53V- quiet, no wound of entry seen. Cornea clear,pupil dilated and regular, lens clear. Thevitreous was full of blood and no fundus detailscould be seen. The left eye was normal.X-my localization.One foreign body about2 mm. in diameter was seen to be 13 mm. to thenasal side, 13 mm. posterior and 1 mm. belowthe horizontal. The foreign body was thuslocalized to be on the sciera under the internal

rectus muscle just behind the equator.Operation was performed and the foreign bodywas found on the sciera under the muscle.The case demonstrated that this method oflocalization can be accurate to 1 mm.Another case is as follows :W. D., male, aged 27, was injured by aJapanese grenade about 70 days before beingseen by us.Examina tion : Right eye.Vision 5/60.Cornea clear. No wound of entry seen. E yequiet. Pupil dilated, lens clear. A yellow masswas seen on the retina at the equator in the4 o'clock meridian. Left eye normal.L-ray localization with the ring.The foreignbody (about 2 mm. in diameter) was measuredto be 14 mm. posterior, 6 mm. nasal and 12 mm.below.This corresponds with the mass of scar tissueseen ophthalmo scopically. No operation was per-formed in this case as the ophthalmoscopic andradiological evidence showed that the foreignbody was in the scierai wall well sealed off infibrous tissue and hence siderosis bulbi was notlikely to supervene.Comment. X-ray of a 12 mm. silver ring sewnon the limbus is a very simple, yet very accurate,method of localizing intra-ocular and orbitalforeign bodies. No complicated apparatus orelaborate calculations are necessary and theaccuracy of the centering at the time of x-ray isapparent from the resulting pictures.

SummaryA description of the method of the localiza-tion of intra-ocular and orbital foreign bodies bymeans of the limbal ring is given and its accuracyshown by illustrative cases.REFERENCESRos s (1945) . . . . Brit. J. OphthalmoL, 29, 545.STALLARD, H. B. (1942). Brit. Med. J., ii, 629.

CAUSE, SYMPTOMS AND TREATMENTOF LATHYRISMAl SPECIFIC NUTRITIONAL NEUROPATHY

B y H . JACOB Y, M J> .Chief Physician, Prince of Wales Hospital, Bhopal,Bhopal SlateIntroduction.There is considerable differencein th e description^ of sym ptoms in lat hyr ism bydifferent authors. ? : - : -Shah (1939) and Minchin (1940). report,besides spastic paralysis of the legs, also involve-ment of the arms and sensory impairment as

well. Minchin also noted affection of thebladd er. Ruge and his co-workers (1925) andRa njan (1944) described incontinence of urineand fa?ces as well as sexual impa irmen t. I t hasbeen postulated that the disease is never pro-gressive after a few days or weeks beyond theinitial paralysis (Bicknell and Prescott, 1942).Ranja n (1944), however, notes rapid progressof the disease. The published accounts ofthe reflexes in lathyrism are equally puzzling.Minchin (1940) observed normal cremastericand abdominal reflexes along with spastic legsand extensor plantar responses. Trabaud andMouharram (1932) found completely normalreflexes, including the plantar responses, thoughthere was spasticity and clonus of the legs. Acommon symptom associated with lathyrism isnight-blindness according to McCombie Young(1928), and Ranjan (1944) reports markeddimness of vision.

Even the diseases which can experimentally beproduced in animals by feeding them on certain specieaof legumes of the genus Lathyrus have also been calledlathyrism, although they do not show the characteristicsymp toms of the human lathyrism. Geiger et al. (1033)fed rats "with a diet consisting of Lathyrus odoratus,the flowering sweet pea (at levels of 80, 50 and 25 percent of the diet). Characteristic symptom s were lame -ness, paralysis and contracture of the spine and sternum.In other experiments on white rate also fed with aLathyrus odoratus diet, carried out by Lewis and Esterer(1943), these authors produced a disease which they calllathyrism showing the following symptom s : Incon-tinence, lameness, paralysis of limbs, spinal curvatureof the thoracic region. Another nutritional disease byfeeding sheep with a certain speciea of legumes, viz,cull beans, has experimentally been produced by"Willman and his co-workers. They call the resultingdisease ' Th e Stiff L am b Disease ', which shows thefollowing sy mp tom s : The anim al concerned ha s diffi-culty in walking and rising. It gets tired very soonafter walking and tries to lie down whenever permittedto do so. On standing and walking there is disturbanceof keeping the balance; later on, inability to rise at all,not even with help .

Since the author is working in an area wherelathyrisrn patients are a common sight and sinceall of them show a uniform symptomatology, itappears advisable to establish first of all arecord of the symptoms of this disease, whichwe regard in this area of Central India as indis-pensable for the diagnosis of lathyrism.Symptoms.The following trail of symptomsis in our experience found in every lathyrismpatient :1. Spastic and painful rigidity in the musclesof the lower extremity, including loin muscles.From this results a typical spastic-ataxic gait,frequently associated with a so-called scissor-gait. . m .2. E xagg erated deep reflexes in the legs,generally clonus.3. The complete absence of disease-symptomsin other parts of the body, especially in theupper extremity and th head. ' :1. The" flexor and - frequently" also:-. theadductor muscles of calf and thigh, particularly,the M. gastrocnemius, feel hard and are tender-;on squeezing. All these muscles are invariably


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54 THE INDIAN MEDICAL GAZETTE [FEB. , 1947well developed and never flabby or atrophie.The patients complain of permanent pain inthese muscles which is increased on standingand walking. In more advanced cases even theleep is disturbed due to the pains. Theexamination of passive movements shows per-manent muscle resistance to flexion and extensionat the knee- and hip-joints. The degree of thisresistance runs parallel to the advancement ofthe disease. In very far advanced cases theresistance is such that it is not possible at allto achieve these passive movements by force.In this late stage all such movements are possibleonly by the patients themselves actively, veryslowly and with the help of their own hands.Most characteristic is the gait of the patients.The onlooker gets the impression as though thesepatients walk against the obstacle of their ownmuscles. The}' generally walk with a slight,apparently voluntary flexion at the knee-joints,which is associated or caused bj r a foot-drop,in an involuntary attempt to compensate forthe latter, resembling the so-called Striimpellphenomenon. Or another way of involuntarycompensation is achieved by swinging the leg ina convex arch instead of lifting the foot (circum-duction). The patients seem to walk on theirtoes only. Another group of patients who do notshow the above flexion at the knees will dragthe feet on the ground, as though their soles arepasted to it. These patie nts describe their gaitthemselves as ' scratching the ground '. Allthese S3rmptoms which appear on walking are' associated movem ents, as they are known tooccur in pyramidal lesions, but are not en-countered in extra-pyramidal motor lesions norin the normal individual. These modes of walk-ing rather belong to the advanced stages of thedisease. In the initial stages only the slight

muscle resistance and the slightly bent knees onwalking preva il. In man y cases of all stages,in whom the spasm of the adductor muscles ofthe thigh dominates, the so-called scissor-gaitresults. The p atients w alk' with crossed legs,resembling the somewhat opened blades ofscissors. Th e movements of the arms, normallyaccompanying the gait of healthy persons, arealways unimpaired in lathyrism. Walking andin more advanced stages standing of thesepatients is complicated by a peculiar kind ofswaying (ata xia) . This goes frequently alongwith fibrillary twitchings of the muscles of thelower extremity, which in combination with thecontractures result in inco-ordinated movements.This disturbance of inco-ordination of differentmuscle, groups is certainly the cause of thisparticular kind of ataxia of lathyrism patient.It is not due to cerebellar lesions, because thefollowing tests exclude this type of ataxia :(a ) There is no ' decomp osition; in thesequence of complicated single movements.(b ) The test of moving the leg and big toeaway from and back to the examiner's finger asa- target, with - eyes shut, does not show a*

deviation in any direction ( B arany 's PointingTest).(c) If the patient is made to walk forward.'and backwards with his eyes shut, he will notpresent the peculiar deviation of the so-callec'compass gait' (Krohn, 1938).2. The following reflex reactions are also.significant of py ram ida l lesion. Withou t excep-tion a greatly exaggerated knee-jerk is elicited,the ankle-jerks often being diminished or absent,In some cases, however, also the ankle-jerks areexaggerated. Almost always ankle-clonus ispresent and frequently also ' dancing of thepatella '. F ar advanced cases showon suddenbrisk passive dorsiflexion of the foot to elicitankle-clonusan involuntary complex reflexmovement consisting of flexion at the hip-jointand flexion at the knee-joint. F requently this* flexion reflex ' occurs already by a gentlestimulus, like deep pressure or pinching of thekin of the distal pa rt of the lower limb. E itherreflex, i.e. the flexion reflex as well as theincreased deep reflexes, is indicative of Iryper-irritability of pyram idal origin. So is theflexion reflex a p romin ent feature of theusual flexor contractu re (the tendon reflexesbeing frequently decreased) and exaggerateddeep reflexes are an equally characteristicfeature of extensor contracture. The latter formis indicative of a less severe lesion than theflexor contracture (B abinski). B abinski's signby stroking the sole along the lateral borderrather than the median border is as a ruleextensor and signifies a less severe pyramidalaffection than does an extensor response elicitedfrom the median border as well as from the lateralborder of the sole (Krohn , 1938). There is elec-trically no reaction of degeneration. The sensesof position and of movement are always anddefinitely unimpaired as well as the temperatureand touch senses. Th e Romberg sign, if positive,is of little significance on account of the abovedescribed inco-ordinatipn of muscle movements.The superficial reflexes va ry : All or some of theabdominal reflexes as well as the cremastericreflexes are in less advanced stages normallyelicitable, but are missing in far advanced cases.This pathological abdominal reflex is generallyassociated with the ' flexion reflex ' and theextensor pla ntar response all belonging to theorder of 'reflexes of spinal automatism ' and aresigns of pyramidal involvement. Anyhow, re-appearance of the previously absent superficialreflexes and of a normal plantar response andthe disappearance of the ' flexion reflex ' areamong the signs denoting improvement undersuccessful treatment.-3. There are definitely no abnormal nervoussigns whatsoever in a ny other p art of the .body. Never was any disturbance of sesa-tion encountered, no r. of the functions of t h ebladder, of the bowels, of the sex and of theme ntality . _ ./-. - ; ' : f < "Examination of the cerebrospinal fluid-s torpressure, cell count, albumin content and Kahn;


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EB:, 1047] CAUSE, SYMPTOMS AND TREATMENT OF LATHYIUSM : JACOBYtest' shows no abnorma lities. There arc also impathological finding s in urine and blood. B loodpressure is norm al. Radiologically, lungs andshape of the heart are always found normal.Differential diagnosis and (etiology. By the- well-defined signs, as described above, lathyrismcan be diagnosed with full certain ty. There isonly one other disease, the signs of which arcidentical with lathyrism,, tha t is. spastic spinalsclerosis of E rb (B eaum ont, 1942) or the purespastic type of amyotrophic lateral sclerosis ofother authors (Price, 1941). B oth diseases arer-auscd by lesions in the upper motor neurone ofthe pyramidal tract. The lesion of ' spasticspinal" sclerosis ' is confirmed by post-m ortemexaminations. Records of post-mortem examina-tions of the spinal cord and the cerebrum ofJathyrism patients appear not to be in theliterature.B ut the difference between these two nervousdiseases does not lie in a divergence of theirsigns. Their only difference is the ivtiology.Whereas we are not aware of the cause of spasticspinal sclerosis, the cause of lathyrism is wellknown, viz, consumption of certain species oflegumes of the genus Lathyrus for a period ofusually not less than ab out a month. This con-sumption is, therefore, to be regarded as indis-pensable for the diagnosis of lathyrism. We inthis area of Central India found invariably thatit was only Lathyrus sativus (teora or khesaridal) that was consumed by our patients. Tothe same conclusion comes also Shourie (1945)in his comprehensive review of lathyrism inCen tral India . This experience does, however,not exclude the possibility that other species ofLathyrus may also cause nutritional diseaseswhich may more or less resemble the diseasewhich is our subject.

Ruge and his co-workers state that besides Lathyrussativus, Lathyrus ccera an d Lathyrus clymenum alsocan. cause lathyrisin. B ut they associate with thedisease disturbance of sensation, urine incontinence andimpotency. Epidemics in France in 1770 and inEngland in 1785 were thought 1o be caused by eatingvetches of the species Lathyrus ciccra. This or Lathy-rus clymenum. was held responsible for an outbreak inSyria (Trabaud and Mouharram, 1932), but Shah (1939),investigating an outbreak in a Punjab village in 1939,found that seeds of Vicia sativa and not of Lathyrushad been eaten mixed with corn. McCombie Young(1928), however, reporta th at h is cases had eate nLathyrus but little or no Vicia sativa and Minchin(1940) describes ' lathyrism without Lathyrus' . Thelatter'a diagnosis appea rs rather doubtful in the lightof our above stated experience. In connection withMcCombie .You ng's rep ort on Vicia sativa being thecause of. lathyrism,- examinations of Lathyrus salivus-stocks, as" consumed by lathyrism patients , i n x th eImperial Agricultural Research Institute, Xew Delhi,failed to reveal the presence of Vicia sativa seeds(quoted by Shourie, 1945). The above quoted experi-ments on animals also show that legumes other thanLathyrus sativus are apt to caus nutritional diseasessomewhat similar to lathyrism. (Geiger et al, 1933;Lewis and Esterer, 1943)-Course' of lathyrism.W ith regard to theonset of the disease we entirely depend on thepatients5- own reports . About 30 per cent of

them state that before the occurrence of thefirst symptoms there was fever with shivering,resembling malaria. F requently, this statementwas confirmed by miliaria relapses taking placein our presence in the hospital. A min ority ofall lathyrism patientsloss than 20 per centremember to have had diarrhoea previous to theirfalling sick from lathyrism . Ac tually, we foundoccasionally amceba in their stools. Tt is, there-fore, quite possible that the latter diseases actedin these cases as a conditioning cause for thedeterioration of a latent background disease, viz.vitamin B deficiency state, on which the toxicinfluence of La thyr us was grafted. On the otherhand, the majority of our patients did not giveany history of a previous disease. All ourpatients are, however, unanimous in their state-ment that the disease, generally during or afterthe rainy season, started slowly, at first onlywith heaviness in their legs, followed bygradually increasing pains in the loin, thigh andcalf muscles. These s}rmptoms deteriorate tothe cripple stage, unless consumption of teora isdiscontinued. Even if it is continued in amixture with wheat, containing about 50 per centof teora, the condition goes on deteriorating.B ut if consumption of teora is completelystopped, the condition remains steady, showingneither improvement nor further deterioration.The latter statement of the patients could beconfirmed by our own observation in thehospital; there was in a batch of eight patientsneither improvement nor deterioration for aperiod of a month, in which no treatment wasgiven. We mu st, however, mention in this con-nection that during this time of observation thehospital diet itself was deficient, consistingmainly of chapattis about 8 oz. and of dalabout 2 oz. and occasionally of ghee 1 oz. andof milk 6 oz. per day.

Nutritional background.B esides the con-sumption of a special variety of Lathyrus, veryimportant for the type of symptoms appearingin different parts in the world, is in our view thenutrition al background of lathyrism. Althoughwe have not had the facility to prove thisexperimentally, by giving the same amount ofteora to one volunteer with normal nutritionalbackground - and to another volunteer withdeficient nutritional background, clinical experi-ence shows that outbreaks of lathyrism occurat all.times and in all countries only among thepoor and ill-fed classes of people.Special observations ori the particular ingredient defi-

cient in the diet are reported by McCombie Young(1928). He stresses a vitam in A deficiency amo ng hislathyrism patients . He not only found night-blindnesscommon in a village suffering from lathyrism, but alsonoticed that the disease did not occur in neighbouringvillages, where the diet contained as much Lathyrus butmore vitamin A, fish and meat; while Shah (1939) hasreported great improvement in patients , when vitaminsA and D were given. Apart from night-blindness noapparent deficiency diseases have been1 reported asoccurring;' with outbreaks of; lathyrism. ' A /l a te n tvitam in B /deficie ncy, how ever is suspected as a "result.of the "investigations on serum phosphatase of lathyriam


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55 THE INDIAN MEDICAL GAZETTE [ F E B . , 1947

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patients by Rudra and Bhattacharya (1946) in Fa taa .They found a high serum phosphatase and a consequentpossible cocarboxyJase deficiency in lathj'rism andrelated these findings to the tiology of the disease.They consider it, however, also possible that the highserum phosphata.se is the effect and not the cause oflathy rism . B ut, of course, Jack of ofher substances inthe diet., apart from vitamins, may be important, assuggested by Ba.?u ct al. (1937), who found that'theseeds of Lathyrus sativus, which often form the staplefood in famine villages, are a very poor source ofprotein, being especially deficient in tryptophane.The author (Jacoby, 1946) has found in thisarea here that the nutritional background of avast proportion of the population is a vitamin Bcomplex deficicnc}'. Although symptoms of thisdeficiency are visible in only about 14 per centof our lathyrism patients, the result of thetherapeutic test (see under treatment) suggeststh at a late nt vitamin B complex deficiency existsin a far greater proportion. It is a hitherto un-explained fact that in lathyrism villages thedisease attacks generally only one or twomembers of a family, but leaves the others un-touched who eat the same food and live underthe same conditions. Children arc affectedroughly in the same proportion and manner asadults, but the female sex to a much smallerproportion as compared with the male sex. InShourie's (1945) statistics only about 13 per centwere females.Treatment.This present description of thecurative influence of prostigmin in lathyrismis based on the analysis of 50 patients treatedwith prostigmin.There has been no effective treatment oflathyrism until now. Jacoby (1946a), how-ever, discovered that lathyrism responds wellto prostigmin treatm ent. . This response differsin degree in the different stages of the disease.The first stage in our classification comprisesall those patients who can walk with slightlybent knees and only some active and passiveresistance in their muscles as well as with thejust noticeable scissor-gait and slight musclepain . Th eir deep reflexes are, of course, greatlyexaggerated, the superficial reflexes as a rulebeing normal and plantar response extensor,elicrtablc from the lateral border of the sole.No ' flexion reflex ' is present. In this stagean apparently complete clinical cure is achievedthrough and during the treatment with pros-tigmin injection; in the beginning about 10intramuscular injections of 2 c.c. are givendaily, after which a course of another ten dailyinjections with 1 c.c. only follows. Afterwards,injections on alternate days may be sufficient to

keep the achieved condition unaltered. If thetreatment is discontinued, we invariably founda re-occurrence of the former symptom s. It wasnot possible to substitute, either for the short-term or the long-term treatment, the injectionsby tablets of prostigmin. The tablets haveproved to be ineffective in lathyrism.The required duration of the treatment oflathyrism with prostigmin is thus the same asin. Myasthema gravis. Disco ntinuance of.* the

treatment causes re-occurrence of S3'mptoms ineither disease.The second stage in our classification oflathyrism comprises the more advanced caseswith marked painful muscle spasm and a clearlyvisible spastic ataxic scissor-gait. Muscu larfibrillations are present. These patients arestill in a position to walk, although with con-siderable difficulty and discomfort, either justwithout or preferably with one or two sticks,according to the advancement of the case.The treatment of this stage with prostigmininjections does not achieve the same result asin the first stage. The symptoms are only con-siderably relieved, but it is generally onlypossible to reach an improvement whichresembles the earlier first stage in our classifica-tion. Those who were previously able to walkwith the described obstacles, but without a stick,can under the influence of the prostigmin treat-ment walk like untreated first-stage patients,and those who required the stick are enabledto walk without it.The third-stage patients are those who arepermanently confined to bed. The musclespasm and contractures are so extreme tha tthey prevent practically any movement withthe legs. Th e pains in the muscles of the lowerextremity, of the calves, thighs and loins arepermanent and severe. These patients have thusbecome cripples. A t the same time all otherfunctions of the body are unimpaired, the vegeta-tive as well as the mental functions. Thereflexes are such as we have described under' symptoms ; for the far advanced stages. Theprostigmin-injection treatment in this thirdstage achieves little with regard to the crippledstate of these patients, but succeeds in so faras the pains almost disappear and the musclerigidity becomes less. Th is results sometimes inan ability of these patients to leave their bed,slowly crawling on the floor for short distances.These third-stage patients are, of course, not ina position to work. Th e patien ts, however, whobelong to the first and second stage, are by thetreatment with prostigmin enabled to do almostevery kind of work.The achievements under prostigmin treatmentcan in every case and stage be accuratelychecked and even measured in the followingway : The exaggeration of the knee- and ankle-jerks becomes less and in early cases practicallynormal so that also the clonus may disappear;the extensor B abinsk i response in the early caseswill equally approach the normal. If in the

more advanced stages the superficial reflexeswere not to be elicited before, they will reappearin the course of the treatment and the 'flexorreflex ' disappear. The most accurate evidenceof improvement is the gait, which can bemeasured as follows : Th e patient is asked towalk in his usua l manner with wetted feet on ',the dry floor. The heel-to-heel distance ismeasured with a tape.. This distance showsunder prostigmin treatment a marked diminution


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1947] CAUSE, SYMPTOMS AND TRE ATM E NT OF LATHYtt lSM : JACOB Y 57^about 3 to 6 inches. Vice versa, if the !S e c ti o n s are .discontinued, the length of stepsSlowly increases again till after about a montht h e original length is regained. The symptomIKvhich shows improvem ent last is the ataxia . It'takes about 20 daily injections before thepatients can for instance stand quietly on oneleg or are able to stop walking immediately on

sudden order. B efore the treatme nt they werenot able to do so but had to proceed one or twosteps further in order to keep their balance.The improvement of ataxia can generally not beachieved in late stages. We tried to enhancethe effect of the prostigmin treatment byadministering at the same time massage, lightor electric treatment to the lower extremities oflathyrism pa tients. We did not, however, findany response to these methods.Vitamins.Several authors report improve-ment of the disease by the administration ofcertain vitamins. Ranjan advises plenty ofvitamin A besides all other vitamins and Ahmad(1944) reports relief of pains and regainedability to walk about freely after parenteral andoral administration of vitamin B . Mellanby(1934) classes lathyrism among the deficiencydiseases, since protective foods containingvitamin A and carotene, green vegetables, milkand eggs can prevent the detrimental effects ofthe toxic agent in the Lathyrus peas.Strongly against the argument of vitamindeficiency causing the disease is the factthat in our experience the administration ofvitamins in large doses does not improve thecondition to any significant degree. We havetried in different batches these vitamins A and Din the form of cod-liver oil for a period of twomonths. - We administered the vitamins B x , B 2complex with crude liver and the vitamin Cdaily by oral and parenteral route for a periodof one month. B ut no response was everappa rent. On the other hand, we do not knowof any vitam in deficiency sta te which does no trespond at least to some extent to the therapeuticapplication of the deficient vitamin alone or incombination with the other common vitamins.Another clinical evidence against the view ofvitamin deficiency being the cause of lathyrism,is the feature that no visible sign of any suchdeficiency occurs in the bulk of our lathyrismpatients. Only about 14 per cent showedsymptoms of v itamin B complex deficiency inthe form of a characteristic glossitis, showingalso the so-called inkspots. T ha t is a very smallpercentage in view of the high incidence ofvitam in B deficiency states , which the au thor(Jacoby , 1946) found in this area: These factsshow that the cause of lathyrism is surely nota deficiency of the above-quoted vitamins astried by us therapeutically. This statement,however, is in no contradiction of the likelihoodof, the presence qi".a latent vitamin deficiency,forming the clinical background upon which the.Lathyrus grain may exercise its toxic effect onthe nervous ^system, . ' -.' V

Two important factors have induced us tobelieve in the existence of such a background :firstly, the nature of food which the lathyrismpatien ts commonly consume. They live prac ti-cally on teora and dal only. Few of themcan very rarely afford some milk and greenvegetable also. As a rule they do not eat fish,meat, eggs and fruits. This diet resembles inqu ant ity and quality (except for teora) the dietof those people among whom a great percentagein this area suffers from the different stageslatent an d visibleof vitam in B complex defici-ency (Jaco by, 1946 ). There is therefore muchlikelihood to presume that the majority oflathyrism patients here also live in a permanent,although invisible, i.e. latent, state of vitaminB complex deficiency.Secondly, our practical observation at thebedside of lathyrism patients has taught usthat the response to prostigmin is moreimm ediate and more marked if vitamin B com-plex treatment precedes the prostigmin treat-ment. In a few cases this vitamin treatm entseemed even indispensable to the usual prostigmineffect.On the strength of these two clinical experi-ences of ours we have made it a rule to give toour lathyrism patients first a course of about12 vitam in B complex, fortified with 1 c.c. ofcrude liver extract, injections before starting onprostigmin treatment.Prevention.It is the duty of public healthauthorities in all countries to prevent diseasesrather tha n to cure them. The tackling of thedisease ' lathyrism ' represents such a publichealth problem to be undertaken by men ofscience in unison with the state's administrations.It seems to be a tough task, because of its mani-fold implication s. In a ny case, science has giventhe lead in this field also by dispersing anymysticism as to the cause of this disease. Toput the verd ict of science in a nutshell : Nolathyrism without consumption of Lathyrus.The first task resulting from this scientificknowledge is enlightenment of the public. . Thewriter has found that the villagers in lathyrism-affected places are alive to the fearful conse-quences of La thyr us consumption. They havebeen taught this lesson being confronted dailywith the sight of their crippled brethren whohave consumed teora. The next task of theauthorities concerned with the promotion ofpublic health is a statistical one; a study of theincidence of lathyrism in former years and now.. On the initiative of the former Revenue Ministerof Bhopal State, Sir C. C. . Garbett, such astudy was undertaken by a nutrition expert(Shourie, 1945) for the year 1944-45. Itestimated the occurrence in this district as ' atleas t 1,200 cases'.'.. Since then no further s tat ist i-cal data" have been available. and, the writerdepended, therefore, on observations of individ-uals. < The writer has attempted.to gather suchobservations as originate from police officials in


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THE INDIAN MEDICAL GAZETTE [ F E B . , 1947charge of the villages concerned. Th ey point toan increase in the incidence of lathyrism thereduring the year 1946.Whatever significance might be given to suchreports in view of the absence of official data,the writer has actually come across and treatedpatie nts wiio.se disease represents new outbreaksin 1946. If this fact of new outbreaks in 1946or of an increase in the incidence of lathyrismin general is recognized and appreciated by theiiuthorities, the third task should be a legislativeone. This should not prove too difficult, sincethis district (Bhopal) is a grain surplus area.The aAvareness of the villagers to the fearfulconsequences of teora consumption had appar-ently not the effect of inducing them to leaveteora voluntarily to cattle only instead of usingit for their consumption. They should, there-fore, be prevented by law from consuming teorathemselves. This ought to be a humanitarianduty and should not be governed by any otherconsideration. Such a step was in fact takenin November 1945 by the Department Com-missioner of Jubbulpore, banning the sale ofteora in the Sihora tehsil.Along with the legal prohibition of teora con-sumption should go the scientific research with aview to investigating a mixture of teora mixedwith other grains, i.e. mainly of wheat, in whichthe proportion of teora is too small to exerciseits toxic effect on men. Such research, whichthe writer had no facilities to carry out, wouldbe of greatest importance in view of the present-world food scarcity, because it would assist inovercoming this scarcity by stretching the avail-able food resources with the help of teora, whichgrows abundantly even on rocky soil in spiteof hailstorm, blight, excess of rain, etc.

SummaryLathyrism is a specific disease of thepyramidal tract, due to the consumption of teora,a species of the genus Lathyrus, in this area ofCentral India. A full account of its manifesta-tions and a description of the treatment withprostigmin injections is given. The rle, whichvitamins, if deficient in the diet, play inthe causation and treatment of the disease inmenand experimental animals, is discussed. Sugges-tions for the prevention of the disease are made.AcknowledgmentThe author desires to express his thanks to Sir Colin

C. Garbett , former Revenue Minister , Bhopal State, forhis keen interest and kind encouragement throughoutthe work. Thanks are also due to Messrs. Hoffmann-LaRoche, Switzerland, Branch Bombay, for the liberalsupply of prostigmin.R E F E R E N C E SAHMAD, S. K. (1944) . . Antiseptic, 41, 514.B A S U , X. P., N A T H , Indian J. Med. Res., 24, 1027.

M. C, G H A N I , M. O.,and M U K H E H J E E , R.(1937).BABU, K. P., NATH, /fcirf, 24, .1001.M. C, and MCKHER-JEB, R. (1937). /

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POST-MORTEM EXAMINATIONS IN THEPUNJAB : AN ANALYTICAL STUDY OF669 EXAMINATIONS FROM 1923 TO 1944

B y T. R. T E W A R an dAM AR NAT H GOYL E(From the Department of Pathology, K. E. MedicalColleje, Lahore)A STATISTICAL generalization of disease inci-dence based on post-mortem findings has itsdrawbacks as well as its advantages. In Indiawhere autopsies among the not-too-poor class ofpatients in the hospitals and the private patientsoutside are ' t aboo' , where the subjects aremostly unclaimed bodies of beggars, vagrantsand inmates of jails and asylums an adequatecross-section of the population cannot be said tocome on the post-mortem table. A considerablewastage of valuable post-mortem material couldbe avoided and more comprehensive populationgroups could be studied if the pathologists wereassociated or worked in co-operation with thepolice surgeon, a practice which obtains at onlya few places in India . The statistical advantageof post-mortem findings lies in the fact that thebasic pathology is discovered which ultimatelyled to death by a terminal disease of minorimport which however is more likely to beentered as the cause of death in the clinicalrecords.With the appreciation of the above facts ananalysis of the available autopsy records of the

Lathyrism India Cause, Symptoms and Treatment Jacoby 1947

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