'The (rnrnburn Jll hbical fJ5so datt rn

NOVEMBER 15, 1958 * VOL. 79, NO. 10

COXSACKIE B5 VIRUS INASSOCIATION WITH PERICARDITISAND PLEURODYNIA

D. M. McLEAN, M.D.,*SELMA J. WALKER, B.Sc.* and

H. W. BAIN, M.D.,t Toronto

ALTHOUGH COXSACKIE B VIRUSES have been describedin association with epidemics of pleurodynia since19491-3 and of aseptic meningitis,4" there are fewreports of Coxsackie B viruses as possible etiologi-cal factors in pericarditis occurring in adults andnone regarding pericarditis of children. Movittet al.7 reported the isolation of Coxsackie BS virusfrom the faeces of a 22-year-old man who developedserosanguineous pericarditis; a 30-fold increase inthe level of neutralizing antibody against thisvirus in sera obtained 12 and 33 days after onsetstrongly suggested that Coxsackie B3 virus couldhave caused the patient's illness. On the basis ofa fall in complement fixing antibody from a titreof 512 in serum taken seven weeks after onset ofpericarditis in a 25-year-old man to a titre of 16in serum obtained six months after onset,Weinstein8 considered that Coxsackie B5 virusmight have caused pericarditis in this instance.Fletcher and Brennan9 reported an elevated com-plement fixation titre against Coxsackie B4 antigenin serum obtained 15 days after onset of acutepericarditis in a 28-year-old woman, whichsuggested a possible etiological role of CoxsackieB4 virus in this patient. Infection of the newbornchild with Coxsackie B viruses has been followedfrequently by severe or fatal myocarditis,'0'3whilst in an older child non-fatal myocarditis hasbeen reported following infection with CoxsackieB virus.14The present paper reports the cases of four

children who developed pericarditis during thesummer of 1958 in Southern Ontario, at a timewhen many patients suffered from pleurodynia oraseptic meningitis after infection with CoxsackieB5 virus. In all children with pericarditis, Cox-sackie B5 virus was isolated from the feces

*Virology Department, Research Institute, The Hospital forSick Children, Toronto.tAssistant Physician, The Hospital for Sick Children,Toronto.

789

collected between 6 and 16 days after onset ofillness, and elevated titres of neutralizing antibodyagainst Coxsackie B5 virus confirmed that thisvirus caused an active infection at the time ofillness.

CLINICALBetween the last week of July and the first

week of September 1958, four patients withacute benign pericarditis and four patients withsevere pleurodynia were admitted to the Hospitalfor Sick Children. Stool and blood samples wereobtained from these patients immediately afteradmission, and further blood samples were obtainedone to six weeks later. Fecal and blood sampleswere also received from four patients withpleurodynia who were under the care of their owndoctors. The first patient became ill on July 17,and the last patient of this series became ill onSeptember 2. In addition to patients admitted tohospital, medical staff members were seeing a largenumber of cases of similar though less severeillness outside. These patients were treated athome. A number of adults developed conditionssimilar to those described for children.

In all instances the onset was sudden, withfever, malaise and weakness. Several patients hadsore throats which were unaffected by chemo-therapy. Those with pleurodynia complained ofa severe sharp pain in the chest anteriorly orposteriorly, which was aggravated by deep breath-ing or coughing. In three patients the pleuriticpain was accompanied by severe abdominal pain,usually in the epigastrium. Despite the severity ofthe symptoms which persisted for one to threeweeks and the intensity of the pleural or peri-cardial friction rubs found on examination, allpatients looked reasonably well throughout thecourse of illness.The clinical features of all four cases of peri-

;carditis studied in this series are as follows:

CASE 1.-P.K., a four-year-old girl, was admitted tothe Hospital for Sick Children on July 27. Ten dayspreviously she developed a sore throat and tempera-ture of 102° F. which did not subside after six days'chemotherapy. On the sixth day of illness a peri-cardial friction rub was first heard. Four days laterthe rub was again heard over the lower sternal area,

790 McLEAN AND OTHERS: COXSACKIE INFECTION

at which time fluoroscopy revealed a somewhatstencilled outline with loss of chamber contour to theheart and only a mild degree of cardiac enlargement(cardiothoracic ratio 10.6/19.0). An electrocardiogramshowed some flattening of T waves over the leftchest leads. No pericardial friction rub was heardafter three more days in hospital.

Coxsackie B5 virus was isolated from a sample offieces obtained 13 days after onset of illness. Serumsamples obtained 13 and 26 days after onset bothshowed high titres of neutralizing antibody againstCoxsackie B5 virus.

CASE 2.-A.S., a seven-year-old girl, developed feverand a severe sore throat which persisted, despitechemotherapy, for one week before admission tohospital on August 3. No pain or swelling of thejoints occurred at any time preceding admission. Aloud pericardial friction rub was heard all over theprecordium, but there was no evidence of cardiac en-largement on clinical and radiological examination.There was no evidence of venous congestion. The elec-trocardiogram was normal. The pericardial rub whichwas first heard one day before admission was stillaudible at diminished intensity when the patient wasdischarged after spending eight days in hospital.

Coxsackie B5 virus was present in a fecal sampleobtained six days after onset of illness. High titres ofCoxsackie B5 neutralizing antibody were detected insera obtained five and 44 days after onset.

CASE 3.-J.T., an 11-year-old boy, was admitted tothis hospital on August 30 with a two-week historyof sudden onset of severe chest pain, mainly in theprecordium on deep inspiration, which had not re-mitted during continuous bed rest at home. The chestpain was accompanied by dyspncea on moderateexertion, and orthopncea. On admission a loud peri-cardial friction rub was heard over the left borderof the sternum, extending down to the apex. A systolicmurmur was heard at the apex. An enlarged tenderliver extended two fingers' breadths below the costalarch, but the neck veins were not distended. One dayafter admission a pleural friction rub was heard overthe left base of the chest. X-ray showed no cardiacenlargement and no pericardial effusion. The lungswere clear radiologically and no pleural effusion wasdemonstrated. An electrocardiogram showed non-specific flattening and inversion of the T waves fromV1 to V6. The temperature became normal five daysafter admission. The pericardial friction rub persistedfor one week but it was not heard on the 12thhospital day. The pleural friction rub increased tomaximum intensity between seven and 12 days afteradmission. The patient was discharged on September14.

Coxsackie B5 virus was recovered from freces ob-tained 16 days after onset of chest pain. High titresof neutralizing antibody against Coxsackie B5 viruswere detected in sera taken on the 16th and 23rddays of illness.

CASE 4.-J.G., a 10-year-old girl, was admitted tohospital on September 6 with a four-day history ofsudden onset of sharp pain in the right lower chestanteriorly. The pain was aggravated by deep breath-ing. This pain persisted, but also on the day of ad-mission she developed pain in the left lower chest.

Canad. M. A. J.Nov. 15, 1958, vol. 79

The temperature was 105' F., and a loud pericardialfriction rub was heard over the base of the heart inthe second and third left interspaces. A radiographshowed slight cardiac enlargement, with cardiothoracicratio 11.5/20.8. The lungs were clear radiologically.Abnormal features of electrocardiograms taken on ad-mission and two days later were inversion of T wavesin leads V3 and V4 and a biphasic T wave in lead V5.On the fifth hospital day the pericardial rub was

audible only in the pulmonary area, and a split pul-monary second sound was heard. The pericardial rubwas not heard four days later, when the patient wasclinically well.

Coxsackie B5 virus was isolated from a faecalsample obtained seven days after onset. Elevatedlevels of antibody against Coxsackie B5 virus weredetected in sera obtained both at six and 12 days afteronset.

The range of symptoms and signs in thosepatients who presented with pleurodynia areexemplified by the following two histories:

CASE 5.-J.V., a 13-year-old girl, presented onAugust 16 with cough followed by bilateral pain inthe lower chest aggravated by deep breathing orcoughing. The pain had persisted for 14 days. Shehad been febrile one week previously. On examination,the temperature was 990 F., and- a loud pleural frictionrub was heard all over the bases of both lungs. Achest radiograph showed some blunting of the rightcostophrenic angle and slight thickening of the pleura.The left costophrenic angle and both diaphragmdomes appeared clear.

Coxsackie B5 virus was isolated from a stool ob-tained on the 15th day after onset, and high titres ofneutralizing antibody against Coxsackie B5 virus werefound in sera obtained on the 15th and 34th daysafter onset.

CASE 6.-W.H., an 11-year-old boy, complained offever and pleuritic pain in the lower chest anteriorlyfor three days before hospitalization on September 17.The chest was normal both clinically and radiologicallyand no pleural rub was heard. Temperature was 1010F. on admission. Despite penicillin therapy, it rose to102.80 F. three days later but returned to normalafter a further 24 hours.

Coxsackie B5 virus was isolated from a frecal sampletaken five days after onset of illness. Neutralizing anti-body to Coxsackie B5 virus rose from titre 20 in serumobtained five days after onset to a titre of more than250 on the 22nd day after onset.

The clinical features of one patient who. sufferedboth from pleurodynia and aseptic meningitis areexemplified in the following:

CASE 7.-P.B., a nine-year-old boy, was admitted tohospital on August 22, with intermittent pain in theleft side of the chest, aggravated by deep breathing,during the previous 10 days. In addition he had boutsof fever and he complained of pain in the left hypo-chondrium and severe pain in the upper parts of boththighs. On the day of admission he developed painin the neck and back. On examination he showed con-

Canad. M. A. J.Nov. 15, 1958, vol. 79 MCLEAN AND onEIERs: COXSAaKIE INFECTION 791

siderable neck stiffness and he sat up stiffly in bedwith the arms extended behind the body (the tripodsign). Pains in the back and legs and neck stiffnesspersisted for four days. Cerebrospinal fluid on ad-mission contained 750 cells per c.mm., over 90% ofwhich were lymphocytes.

Coxsackie B5 virus was isolated both from cerebro-spinal fluid obtained on the 10th day after onset andfrom fteces obtained 12 days after onset. Elevatedtitres of Coxsackie B5 neutralizing antibody weredetected in sera taken both on the 12th and 23rddays after onset.

METHODS AND MATERIALSRoller tubes containing monolayers of monkey kidney

epithelial cells were prepared from trypsinized cellsuspensions of rhesus monkey kidneys, kindly providedby the Connaught Medical Research Laboratories. Themaintenance medium used during virus titrations was0.5% lactalbumin hydrolysate and 0.1% yeast extractin Earle's balanced salt solution containing penicillin500 units per ml. and streptomycin 250 microgramsper ml. (ELY medium). After 5 to 8 days' outgrowthin a lactalbumin-horse serum medium, the monkeykidney cell sheets remained intact for a further 7days' incubation in ELY medium.

Fxeces were shaken with 20 ml. of Hanks' balancedsalt solution to give a 10% suspension. This was centri-fuged at 2500 r.p.m. for 30 minutes in a horizontalcentrifuge. Ten ml. of supernatant was centrifugedfor 1 hour at 40,000 r.p.m. in a Spinco model L centri-fuge, the supermatant was removed and the pellet wasresuspended in 2.5 ml. of ELY medium. Both the re-maining supernatant after low speed centrifugationand the resuspended ultracentrifuged deposit werestored in screw-capped vials at -20° C. -until tested.To examine f2ecal extracts for virus content, 0.1 ml.

of supernatant after low speed centrifugation wasinoculated into each of 4 monkey kidney culture tubescontaining 1 ml. of ELY medium, and 0.1 ml. of re-suspended ultracentrifuged deposit was inoculated intoa further 4 monkey kidney culture tubes. After 1hour's incubation at 370 C., the fluid in the culturetubes was removed and replaced by fresh ELYmedium. Incubation was continued for periods up to7 days. If virus were present, the characteristic cyto-pathogenic effect of rounding, granularity and necrosisof cells eventually involving the entire cell sheet wasfirst observed frequently on the third day of incuba-tion. The cytopathogenic effect was indistinguishablefrom that caused by poliomyelitis virus. When mostof the cell sheet was necrotic the tubes were frozen,after which their contents were thawed and pooled.These pools of virus-containing first passage culturefluids were titrated in monkey kidney cultures. Dilu-tions of newly isolated viruses, calculated to contain100 TCD50, were mixed with sera prepared againsteach of the following viruses: Coxsackie A9, Bi, B2,B3, B4, B5, ECHO 2, ECHO 6, ECHO 9, ECHO 13,and a pool of sera prepared against poliomyelitis types1, 2 and 3. Each serum was diluted to contain between5 and 20 antibody units. Serum-virus mixtures wereheld at room temperature for 1 hour, after which 0.8ml. aliquots of each were inoculated into groups of 4drained monkey kidney culture tubes. Incubation for4 to 7 days resulted in production of cytopathogeniceffects in all cultures except those inoculated with

virus plus serum of one particular type. The virus typecorresponded to the serum by which it was neutralized.

Neutralization tests on sera from patients wereperformed similarly to a virus-typing test. Patient'ssera were heated at 56° C. for 30 minutes beforetesting. Sera were diluted 1:10, 1:50 and 1:250 inELY medium. An equal quantity of Coxsackie B5virus, Faulkner strain, diluted in ELY medium to con-tain between 100 and 300 TCD50, was mixed witheach serum dilution. After standing for 1 hour at roomtemperature, 0.8 ml. aliquots were inoculated intopreviously drained monkey kidney tubes in groups oftwo. The result was read after 4 days' incubation,when the control tubes regularly showed the presenceof 100 to 300 TCD50 of virus.

RESULTS

Coxsackie B5 virus was isolated from thefreces of all four patients with pericarditis and allnine patients with pleurodynia. Antibody tests onpaired sera from four patients with pericarditisrevealed high titres of antibody against CoxsackieB5 virus in early and late sera of all. Out of thepaired sera from eight patients with pleurodynia,a tenfold or greater increase in titre was observedin four patients, whilst the others had a high anti-body titre in the early serum samples and noincrease was detected in the late sample. The re-sults shown in Table I demonstrate clearly thepresence of infection with Coxsackie B5 virus atthe time the patient was ill.

Results from this laboratory (to be publishedelsewhere) show that during the month of August,of 18 children admitted to the1 infectious wardsof this hospital with the aseptic meningitis syn-drome from Southern Ontario, 13 excreted Cox-sackie B5 virus in the faeces' and in seven ofthese, virus was detected in the cerebrospinalfluid also. Elevated or rising titres of antibodyagainst Coxsackie B5 virus have been demon-strated in seven children out of nine from whompaired blood samples were taken. However, of 11children with aseptic meningitis in July, nine yieldedno virus in the fieces or cerebrospinal fluid, onegave Coxsackie A9 and one excreted Coxsackie B5virus. The first patient with aseptic meningitis dueto Coxsackie B5 virus and the first patient withpericarditis in this -series both became ill duringthe third week of July, both excreted CoxsackieB5 virus in the faeces, and both had high levels ofantibody against this virus in early and late serumsamples. On the contrary, during this same period,no virus was recovered from children with otherclinical conditions such as pyrexia of uncertainorigin, gastroenteritis, and various neurologicaldisturbances. This showed that Coxsackie B5 viruswas disseminated widely through Southern Ontarioduring late summer 1958, but the only clinicalmanifestations of infection with this virus werepericarditis, pleurodynia or aseptic meningitisoccurring either singly or in combination.

792 .MCLEAN AND OTHERS: COXSACKIE INFECrION Canad. M. A. J.Nov. 15,1958, vol. 79

TABLE I.-COXSACKIE B5 VIRUS IN FRECES AND SERUM ANTIBODY LEVELS IN PATIENTS WITH PERICARDITIS AND PLEURODYNIA

Age Date of Days after Virus in Days after AntibodyPatient Syndrome (years) onset onset feces onset titre

Pericarditis .............................. 4

Pericarditis .............................. 7

Pleurodynia ............................. 13

D.B. Pleurodynia

Pleurodynia.

12

8

Pleurodynia 8

Pleurodynia, aseptic meningitis. 9

Pleurodynia ............................. 11

Pleurodynia 9

Pericarditis, pleurodynia .................. 11

D.C. Pleurodynia, abdominal pain. 10

D.W. Pleurodynia, abdominal pain ............... 10

J.G. Pericarditis .............................. 10

17-7-58 13 + 1326

28-7-58 6 + 544

1-8-58 15 + 1534

7-8-58 4 + n.t.26

8-8-58 3 + 112

8-8-58 3 + 114

12-8-58 12* + 1023

14-8-58 5 + 522

15-8-58 7 + 726

16-8-58 16 + 1623

27-8-58 7 + 817

1-9-58 - 2 + 218

2-9-58 7 + 612

*Coxsackie B5 virus isolated from C.S.F. obtained from this patient 10 days after onset.n.t.-Not tested.

DISCUSSION

During late summer 1958, an unusually largenumber of children were admitted to hospital withpericarditis or pleurodynia. Increase in the seasonalincidence of aseptic meningitis, which has beenobserved repeatedly during 11 summers, was

again observed in 1958. An occasional patient pre-

sented with features of pericarditis and pleuro-dynia, or of pleurodynia and aseptic meningitis.All patients studied either with pericarditis orwith pleurodynia gave evidence of concurrentinfection with Coxsackie B5 virus, as shown byexcretion of this virus in the fleces at the time ofillness and elevated or rising titres of antibody tothis virus in sera obtained during acute and con-

valescent phases of illness. The unique and regularassociation of Coxsackie B5 virus only with. chil-dren exhibiting the syndromes of pericarditis,pleurodynia or aseptic meningitis, but not withthose children suffering from other febrile con-

ditions at the same time, provides further evidencein favour of an etiological relationship betweenthis virus and pericarditis or pleurodynia, as wellas aseptic meningitis.Although the cerebrospinal fluid was not ex-

amined in patients with pericarditis or those whohad pleurodynia alone, fluid was obtained frompatient P.B. (Case 7), who showed features bothof pleurodynia and aseptic meningitis. Pleocytosisin the cerebrospinal fluid and isolation of Cox-sackie B5 virus from it confirmed that this patientwas infected with this virus.The clinical features shown by the present four

children with Coxsackie B5 pericarditis are con-sistent with those described in former years as

acute non-specific pericarditis of uncertain etiology.The general wellbeing of these patients through-

out their illness, the suddenness of onset, thepericardial rub persisting for a week or more, andthe complete recovery after illness were featureswhich clearly distinguished this condition frompericarditis observed in rheumatic fever, osteomy-elitis or tuberculosis.

Although the clinical features of patients whoexhibited pleurodynia differed in no way fromthose described following infection with the Conn.-5 strain of Coxsackie Bl virus,1 2 all the presentseries of pleurodynia patients were infected withCoxsackie B5 virus. Infection with Coxsackie B5virus has caused symptoms both of pleurodyniaand aseptic meningitis in one patient, producinga picture resembling that caused by accidentalinfection of a laboratory worker with the Ohio-lstrain of Coxsackie B2 virus.15

Patients responded to infection with CoxsackieB5 virus by production of high titres of neutraliz-ing antibody, which was detected even during thefirst week of illness. This was also observed inMinnesota following epidemic spread of CoxsackieB5 virus in 1956.4 In many instances the firstsample of serum was not obtained from the patientuntil the second week of illness, by which time theantibody titre was already high, and a further risein titre was not demonstrated in a subsequentserum sample. However, four patients with pleuro-dynia showed more than a five-fold increase intitre of neutralizing antibody, which confirmedconcurrent infection with Coxsackie B5 virus.

Hitherto, Coxsackie B5 virus has been describedas the etiological agent in two large outbreaks ofaseptic meningitis which occurred in Minnesota4and Iowa16 during summer 1956. In Toronto during1958 it has spread in epidemic fashion, producingpericarditis and pleurisy in addition to asepticmeningitis.

P.K.

A.S.

J.V.

W.C.

L.C.

P.B.

W.H.

M.L.

J.T.

250+250+250+250+250250+n.t.250+20250+20250+250+250+20250+250+250+250+250+250+250+

0250+250250+

NOV. 15, 1958, VOl. 79 PENNER AND COLDWELL: DRIVING AND ALCOHOL 793

SUMMARY

During July, August and early September 1958,four children with acute benign pericarditis and ninechildren with epidemic pleurodynia excreted Cox-sackie B5 virus in the faeces at the time of illness.Elevated antibody titres against Coxsackie B5 viruswhich were found in paired sera obtained from allfour pericarditis patients and three out of seven pleu-rodynia patients, and rising titres against this viruswhich were found in paired sera of another fourpatients with pleurodynia, provided good evidencethat infection with Coxsackie B5 virus produced thesesyndromes.

REFERENCES

1. CURNEN, E. C., SHAW, E. W. AND MELNICK, J. L.: J. A.M. A., 141: 894, 1949.

2. WELLER, T. H. et al.: J. Immunol., 65: 337, 1950.3. HUEBNER, R. J. et al.: New England J. Med., 248: 267,

1953.4. SYVERTON, J. T. et al.: J. A. M. A., 164: 2015, 1957.5. RHODES, A. J. AND BEALE, A. J.: Ann. New York Acad.

SC., 67: 212, 1957.

6. JOHNSSON, T.: Arch. ges. Virusforsch., 6: 250, 1955.7. MovITT, E. R. et al.: New England J. Med., 258: 1082,

1958.8. WEINSTEIN, S. B.: Ibid., 257: 265, 1957.9. FLETCHER, E. AND bRENNAN, C. F.: Lancet, 1: 913, 1957.

10. JAVETT, S. N. et al.: J. Pediat., 48: 1, 1956.11. KIBRICK, S. AND BENIRSCHKE, K.: New England J. Med.,

255: 883, 1956.12. DELANEY, T. B. AND FUKUNAGA, F. H.: Ibid., 259: 234,

1958.13. HoSIER, D. M. AND NEWTON, W. A. JR.: A.M.A. Am. J.

Dis. Child., 96: 251, 1958.14. MCLEAN, D. M. et al.: Ohio M. J., 53: 907, 1957.15. SHAW, E. W., MELNICK, J. L. AND CURNEN, E. C.:

Ann. Int. Med., 33: 32, 1950.16. CHIN, T. D. Y. et al.: Am. J. Hyg., 67: 321, 1958.

-RiSUME,Pendant les mois de juillet et aofut 1958 ainsi qu'au

debut de septembre, quatre enfants atteints de p6ricarditeaigue mais benigne et neuf autres souffrant de pleurodynie6pidemique passerent du virus Coxsackie B5 dans leursselles au cours de leur maladie. On trouva un taux elev6d'anticorps specifiques a ce virus dans des echantillonsconjugues de serum des quatre cas de pericardite et aussichez trois des sept cas de pleurodynie. Les quatre autrescas de pleurodynie montrerent une augmentation du titrede ces memes anticorps. On voit la la preuve que l'infectiona virus Coxsackie B5 a cause ces syndromes.

CAR DRIVING AND ALCOHOLCONSUMPTION: MEDICALOBSERVATIONS ON ANEXPERIMENT

D. W. PENNER, M.D.,* Winnipeg,and B. B. COLDWELL, Ph.D.,t Ottawa

INCREASINGLY, doctors are called on to assesswhether or not an individual is intoxicated and toestimate the degree of intoxication. Often this typeof opinion is required when there has been a trafficaccident. Subsequently, the physician may be re-quired to give evidence in court either on a speci-fic case or as an expert witness concerning alcoholconsumption and the ability to drive safely. Theproblem relating to drinking and driving is con-sidered by many to be very complex. Medical opin-ion, the results of medical examinations, and con-clusions drawn from them, all show such greatvariation that the evidence is sometimes consideredof little value. Most doctors are quite competent todo a physical examination, but few have receivedtraining in this special field and virtually nothingis taught in medical school about this complexmatter. To variation in experience and training maybe added the examiner's personal prejudices con-cerning alcohol because of his own social habits.Another difficulty is the relationship between alco-holic initoxication as seen in the doctor's office andimpairment of ability to drive a car. For example,one cannot assume normal ability to drive a car

*Pathologist, Winnipeg General Hospital: Assistant Professorof Pathology, University of Manitoba; Medico-legal Consul-tant to the Attorney General's Department, Manitoba Govern-ment.tChemist in Charge, Scientific Research Section, Crime Detec-tion Laboratory, Royal Canadian Mounted Police, Ottawa.

because no evidence of intoxication is found duringthe medical examination.Recognizing the numerous problems relating to

alcohol and traffic, Commissioner L. H. Nicholsonof the Royal Canadian Mounted Police authorizedtheir Crime Detection Laboratories in 1955 to setup an experiment to study various aspects of alco-hol consumption and car driving.*

This pappr is concerned primarily with the med-ical portion of the experiment which was designedto evaluate:

(a) The accuracy of the medical examination asa means of determining alcoholic impairment com-pared with actual driving performance.

(b) Comparison of the two independent sets ofmedical examinations.

(c) The relationship between medical observa-tions, volume of alcohol consumed and blood alco-hol levels.

(d) The sensitivity and validity of the scoringsystem used to assess car-driving ability in the ex-periments.

EXPERIMENTAL METHODSA driving course was set up on a 65 x 130 ft. paved

surface with four areas outlined by metal stanchionssimulating (1) a garage to back into and drive out of,(2) a narrow alley to back in and drive out of, (3)a "curb" parking area, and (4) a roadway test wherethe car had to be turned around in an area 26 ft. wideand 30 ft. long. The experimental subject was requiredto drive through the various test areas in sequencegiven above, using a 1955 Chevrolet with standardgear-shift transmission. The time required to make acomplete run was noted as well as the time to complete

*For the complete report on impaired driving tests see:Report on Impaired Driving Tests. Ed. by B. B. Coldwell,Queen's Printer and Controller of Stationery, Ottawa, 1957.