J. Neurol. Neurosurg. Psychiat., 1965, 28, 282

Neuropsychiatric manifestations of chronicmanganese poisoning

S. ABD EL NABY AND M. HASSANEIN

From the Departments of Neurology and of Industrial Medicine, Faculty of Medicine, Cairo University

Clinical manifestations appearing in labourersworking with manganese in various industrial fieldswere discovered about 125 years ago. Couperin 1837 was the first to report the appearance of apeculiar neurological picture similar to Parkinson'sshaking palsy in five men grinding manganesedioxide in France. Forty-two years later, Schlockow(1879) reported another 42 cases. In addition vonJaksch from 1901 to 1907 reported another 15 cases.Though he was the first to describe the peculiar'cock walk' gait, yet he diagnosed them as having adisease similar to disseminated sclerosis. It was notuntil 1919 that the definite relation between theepidemiological, clinical, and pathological or toxiceffects ofmanganese poisoning on the central nervoussystem was established by Edsall, Wilbur, andDrinker (1919). Their review drew attention to theserious effects on the central nervous system of thisoccupational disease. Subsequently a large numberof cases have been reported from many countries.The first few cases in Egypt were described byBaader in 1932, and a few years later, in 1936, 26cases were reported by Nazif and 11 cases by Scanderand Sallam. Abd El Naby and Hassanein (1963),surveying chronic manganese intoxication from theindustrial and hygienic points of view, commentedon 32 cases with neuropsychiatric manifestationssecondary to exposure to manganese ore in the mines.In this paper, another survey was done in which 13further cases were added to the previous group,with the aim of studying and analysing the variousclinical neuropsychiatric presentations of chronicmanganese poisoning among Egyptians.

MATERIAL AND METHOD

This study was made on 45 male patients, ages rangingat the time of onset from 21 to 54 years with a median of34 years (Fig. 1). Three of them were brothers and alsocousins of a fourth patient. Another three cases werecousins.

All the patients are inhabitants of El Khattara villageand the surrounding district, Kous and Keft, near Luxorin upper Egypt. This area provides the main source of

labourers for the manganese mines in the Sinai Desertat Abozeinema and Ombogma. They consist of twogroups: the first began work in the mines at variousintervals from 1925 to 1952, the second were workingthere after 1952 until 1963, i.e., after the introduction ofwet drilling as a preventive measure and they were em-ployed in various jobs there. It has to be stressed that thework in the mines was intermittent and each labourerused to work for only five months each year; they leftwork after the appearance of the signs and symptoms oftoxicity.

Thirty-seven of them (82-20 ) worked as dry-rockdrillers, five (111-%) as wet drillers, and only three (6-7 %)as porters loading broken pieces of manganese ore. It isworth mentioning that even after using the wet drillingmethod in 1952, toxic manifestations appeared in fourwet drillers.

Certain routine investigations were carried out in allthe patients: e.g., urine and stools were analysed formanganese, and the blood picture, blood Wassermannreaction, and cerebrospinal fluid were examined, andradiographs were taken of the chest and long bones. Allthe results showed no abnormality. In addition 15 of them,who were severely incapacitated, were admitted to KasrEl Aini Hospital where they stayed for several months,and theirclinical manifestations werefollowedup. Furtherlaboratory investigations were carried out, includingliver function tests, liver biopsy, glucose tolerance

16

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20-29 30-39 40-49 50-59

DECADE 3 4 5 6

AGE GROUPS

FIG. 1. Age distributian1 at time of onset of manganiesepoisoning in 45 cases.

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Neuropsychiatric manifestations of chronic manganese poisoning

curves, and electrophoretic serum protein patterns, andthey were given the proper treatment.

RESULTS

DURATION OF EXPOSURE TO MANGANESE The periodof exposure before the appearance of the manifesta-tions of toxicity was not constant (Table I). Theshortest was five months and the longest was 25years with a median of nine years.

TABLE IDURATION OF EXPOSURE TO MANGANESE

Duration of Exposure in Years No. of Cases

>i-I-2-5-10-15-20-25

Total

428

11104645

of such a study, especially in view of the long periodwhich elapsed between the appearance of the initialsymptoms and the time of examination in 1963.

Symptoms

TABLE IIIINITIAL SYMPTOMS

No. of Cases Total

NeurologicalExhaustion syndromeWeakness of extremities

Inability to walk without supportBedridden

Subjective sensory disturbancesTremorsOculogyric crisisSleep disturbancesInsomniaHypersomniaLethargyInverted sleep rhythm

PsychologicalAcute psychosisMild psychotic disturbancesDisposition

Spontaneous laughterSpontaneous crying

31

26}3

30

3J

22

29

59

45

27

18

MODE OF ONSET The onset of clinical symptoms wasacute in 13 cases and insidious in the remaining32 (Table II). In those of acute onset, the initialsymptoms were neurological in seven cases and infive took the form of a psychotic disturbance. Inonly one case were there constitutional symptoms inthe form of fever and rigors. The symptoms of thoseof insidious onset were variable. Seventeen casespresented with neurological disturbances, 11 withneuropsychiatric signs and symptoms, and in theremaining four there were psychiatric symptoms inthe form of mental fatigue, retardation of thoughtprocess, and lack of concentration.

TABLE IIMODE OF ONSET IN 45 CASES OF

POISONING

Alode of Onset

A cuteNeurologicalPsychologicalConstitutional (fever and rigors)

InsidiousNeurologicalPsychologicalCombined

Total

CHRONIC MANGANESE

No. of Cases

7}15 ~-13

1

17)4 32

45

INITIAL SYMPTOMS Table III summarizes the dataof the initial symptoms of the whole group, and itmay be noticed that they were multiple and ofvarying combinations. Since the data in 41 cases areretrospective, it may be subject to the discrepancies

It is interesting to report that those cases of in-sidious onset gave the history of generalized weak-ness, langour, and of being easily fatigued onexertion, which is a picture simulating the exhaustionsyndrome of myasthenia gravis. These were some ofthe earliest symptoms and invariably preceded anyothers.

Twenty-five patients complained of weakness andmarked stiffness of the limbs, especially the calves ofthe legs with mild cramp-like pains on walking,and later they were unable to walk without support.In addition they showed propulsion, retropulsionand lateropulsion. In another three, these disabilitieswere sufficiently incapacitating for the patients tobecome bedridden.

In only eight patients was there an early complaintof a marked tremor of the extremities leading toclumsiness in the use of hands and legs. This wasassociated with involuntary nodding of the head andneck. In only one case, however, were there frequentattacks of oculogyric crises early in the onset of thedisease.

Nearly all of them gave a history of sleep dis-turbances; 30 reported insomnia, seven diurnalhypersomnia, and five lethargy. Only three showed adefinite history of inverted sleep rhythm.

In five patients, there were definite subjectivesensory disturbances. All had distressing paraes-thesiae in all four limbs; in one case the face wasinvolved and in two others severe, spontaneouscramp-like pains occurred in the calf muscles,especially at night.

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S. Abd El Naby and M. Hassanein

Among the acute psychotic disturbances, two ofthe patients became severely excited, agitated,hallucinated and deluded, necessitating admissionto the Abbassiah Mental Hospital as they becameunmanageable. However, their mental conditionimproved after a few weeks. The outstandinghistory from the other three cases was one ofemotional instability, irritability, various behaviourdisorders, insomnia, and occasional refusal of food.Mild psychotic disturbances of insidious onset werereported by 22 patients or by their relatives during theearly stage of the disease. They were irritable with aslight change in mood, conduct, and behaviour andin some, an occasional period of confusion. Spon-taneous, incongruous laughter was reported by 15of these patients, and spontaneous crying by three.The psychiatric symptoms invariably regressed whilethe neurological ones became either stationary orshowed gradual progress, culminating in the variousfull-blown clinical pictures which will be discussedlater.

PRESENTING SIGNS AND SYMPTOMS At the time ofexamination, the presenting signs and symptomswere a combination of neurological, neurovegetative,and psychiatric features (Tables IV, V, VI). For

TABLE IVPRESENTING SIGNS AND SYMPTOMS IN 45 CASES

Neurological Disturbance No. of Cases

Extrapyramidal 29Extrapyramidal and pyramidal 10Extrapyramidal, pyramidal, and cerebellar 6Total 45

TABLE VNEUROVEGETATIVE DISTURBANCES IN 45 CASES

Type of Disturbance No. of Cases

SialorrhoeaGreasy seborrhoeaSleep disturbancesInsomniaHypersomniaLethargyInverted sleep rhythm

Weakness of libido

Type

simplicity and clarity, our case material will be clas-sified in three main groups according to the clinicalfindings.Group I In this 29 cases (64 4%) presented with

extrapyramidal manifestations (Table IV); group II,10 cases (22-2 %), presented with combined extra-pyramidal and pyramidal manifestations; group III,six cases (13-4%), presenting with extrapyramidal,pyramidal, and cerebellar manifestations, i.e.,disseminated or systemic syndrome.

Group I Most of the patients in this groupexhibited a syndrome in which tremors, rigidity,facial immobility and loss of associated movementswere dominant. This group presented abnormalinvoluntary movements, either tremor or athetoidmovements being present in all the cases, but differingin distribution and sequence. The lips and tonguewere by far the most constant sites for static tremorswhich were fine and rhythmic but ceased during sleep.Less frequently affected were the extremities, neck,and lower jaw muscles. Tremors of the extremitieswere present in 21 cases and involved mainly thehands and fingers, especially when fully extended.Those of the neck muscles were characterized byalternating flexion and extension of the head whichappeared in three patients and by lateral rotation inanother one. In three cases the type of tremoraffected the lower jaw causing the mouth to openand close or to move laterally from one side to theother. In only one case did the tremor resemble the'pill rolling' movements of paralysis agitans, beingmore marked in the right hand than the left. Themetacarpo-phalangeal joints were flexed, but theinterphalangeal joints were extended. In anothercase, slight athetoid movements involving bothhands and wrists were present.

Dyskinetic features were minimal and localizedin this group but in four cases there were tonic

2323

307537

TABLE VIGAIT AND ATTITUDE DISTURBANCES IN 45 CASES

No. of Cases

Disturbance of gaitVon JakschFestinantShufflingWide-based

Disturbance of attitudeFlexionExtension

22l16 t456J FIG. 2. Classical Parkinsonian facies and attitude (a) and39} (b) risus sardonicus affecting the facial muscles and the3J42 platysma.

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Neuropsychiatric manifestations of chronic manganese poisoning

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[-1I. 3a.. Ici. 3h r[-I. 3c. iuic. 3d. iI(.i. 3c.FIG. 3. Attitude offlexing (a), attitude ofextension (b), unilateral (c) and bilateral (d) von Jaksch's gait, andpatient withquadriparesis (e).

spasms in the facial and neck muscles. One patient(Fig. 2) had grimacing movements amounting torisus sardonicus affecting the facial, platysma, andneck muscles. In two others the sternomastoidmuscles were mainly involved leading to mild,spasmodic torticollis. The fourth case had occasional,spasmodic, tonic flexion at the elbows and hands.In none of these cases were the trunk muscles affected.

All the patients in this group presented withslowness in initiating and maintaining movements,lack of spontaneity and marked reduction in fre-quency and range of both voluntary and involuntarymovements. The classical mask-like Parkinsonianfacies, with increased sebaceous secretion, wasevident in 23 cases.

Muscular rigidity, equally involving agonist andantagonist groups leading to cog-wheel rigidity, andespecially affecting the trunk and lower limbs, wasevident in all the cases. In 26 of these it gave rise to ageneral attitude of flexion (Fig. 3a) and in the re-maining three to an attitude of extension (Fig. 3b).The 'cock-walk' gait of von Jaksch with talipes

equinus or equinovarus and the characteristictendency to walk on the metatarso-phalyngealjoints was a striking feature in 17 cases. It wasbilateral in 11 (Fig. 3c) and unilateral in the remain-ing six cases (Fig. 3d).A festinant gait was seen in eight cases and the

patients appeared to be rooted to the ground onwalking. The phenomena ofpropulsion, retropulsion,and lateropulsion were present in all the patients ofthis group but propulsion was the commonest.

Other neurological findings were: the tendonjerks were normal in 21 cases, exaggerated in six,

and diminished in the remaining two. The hyper-reflexia differed in distribution in being generalizedin both upper and lower limbs in four cases; in threeof them there was evidence of both cervical andlumbar spondylosis and in the fourth a pellagrousrash was present on the face, extremities, andpressure points. The hyperreflexia was localizedin the lower limbs in another two patients; in one,both the knee and ankle jerks were exaggerated,and in the other, only the ankles.On the other hand, in the two patients showing a

hyporeflexia it was generalized in one, while in theother it was limited to the knees and ankles and thispatient had a history of laminectomy for prolapseddisc and the operation scar was apparent on hisback.As regards the superficial reflexes, the plantar

response was flexor in the whole group, and theabdominals were also intact.

All types of sense modalities, whether deep orsuperficial, were normal in 24 cases, while in theremaining five, there were sensory changes of differ-ent distributions. It was of the peripheral neuritictype in the pellagrous patient, of the radicular typein the case with laminectomy, and irregular in thespondylitic cases.Though sphincter disturbances were absent, seven

patients complained of weakness of libido. In onlytwo cases were there disturbances of lateral conju-gate movements and accommodation-convergencereflexes of the eyes. In the remaining cases all thecranial nerves were intact and the fundi were normal.

Group IH This group showed extrapyramidalmanifestations similar to those previously described

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in group I, but they were associated with definitesigns of pyramidal involvement in varying degreesand combinations. In all the patients of this group,the hyperkinetic signs were relatively minimal andnone of them showed any dyskinetic disturbance.In all the cases, weakness of the pyramidal distribu-tion could be demonstrated. It was more markeddistally than proximally, involving the extensormuscles of the upper limbs more than the flexors butthe reverse in the lower limbs. The weakness wasbilateral and symmetrical in all cases except one inwhich it was right sided and of a hemiplegic distribu-tion.

All the cases presented a mixture of hypertoniaand spasticity. The deep tendon jerks in both upperand lower limbs were exaggerated. Ankle clonuswas present bilaterally in two cases, and unilaterallyin two others. The abdominal reflexes were absentin six out of the 10 cases. The plantar response wasextensor bilaterally in six, unilaterally in one, andequivocal in the remaining three.

In contradistinction to the previous group,sphincteric disturbances in the form of precipitancyof micturition and constipation were present inseven cases. The gait was of the von Jaksch's type onboth sides in five patients and unilateral, with righttalipus equinovarus in another one, spastic andshuffling in another three. The remaining two patientswere bedridden, one being completely paraplegic andthe other quadriplegic (Fig. 3e). Sensation wasnormal in eight cases, and affected in the remainingtwo. The hemiplegic patient had right-sided hypo-aesthesiaandthepellagric one had glove and stockinghypoaesthesia.The cranial nerves were unaffected except in the

hemiplegic patient, who had right-sided upper motorneurone affection of the right seventh and twelfthnerve. The fundi were normal except in this lastpatient who had evidence of retinal and peripheralatheromatous vascular disease and had been hyper-tensive for a long period.Group III Clinical examination of this group

showed the presence of cerebellar deficit in additionto extrapyramidal and pyramidal signs in fivepatients while the remaining case showed a combina-tion of extrapyramidal and cerebellar dysfunctiononly.

In all these cases there were gross kinetic inten-tion-type tremors with dysmetria in the extremities,and dysdiadochokinesis was observed in the upperlimbs of three cases. Speech was staccato in three,monotonous in two, and slow in the remaining one.The deep tendon jerks were exaggerated in fivepatients. Ankle clonus was elicited in two patients.The plantar response was bilaterally extensor inone case, unilateral in another, equivocal in two, and

normal in the remainder. While the abdominalreflexes were diminished in two and present in theremaining four cases, the gait was wide based of thecerebellar type in all cases. None of them showednystagmus or any other cranial nerve affection. Allsense modalities whether superficial or deep wereintact in all the patients.

DISCUSSION

Our group of 45 labourers, showing the variousneuropsychiatric manifestations of chronic mangan-ese poisoning, is one of the largest that has beenreported. They were affected while working in thevarious processes of extraction of the black dioxideof manganese (pyrolusite), either during mining,grinding, sorting, packing, or loading the ore.According to the records of the Egyptian Ministry

of Public Health and Ministry of Labour, the totalnumber of workers in the mines of Abo-Zeinemaand Om-Bogma was only about 500 till 1952 andit increased to 1,850 in 1962. The total number ofthe reported cases of chronic manganism in theU.A.R., including our material, does not exceed 75persons. Even ifwe make allowance for those patientswho have been missed or wrongly diagnosed, itwould appear that this type of poisoning is still ararity in this country.However, its incidence appears to be relatively

high compared with that in other countries. Thiscan be easily explained if the method of extractionof the ore is considered. During the period between1925 and 1952, the process of extraction of themanganese ore was by dry rock drilling where noprophylactic hygenic measures were undertaken andduring this period 41 of our cases developed toxicmanifestatidns. After the use of wet rock drillingwith proper ventilation, only four workers becameaffected. Nevertheless the factors which may beresponsible for the appearance of the toxic manifes-tations are difficult to explain. However, at least twofactors may play a role in our material: first theremay be a special susceptibility or vulnerability of thecentral nervous system in certain persons. Secondly,the degree of concentration of the manganese dustin the atmosphere is likely to be important, since themain route of absorption is through the lungs ratherthan from the digestive tract. In favour of the firstfactor is the fact that 15-5% of our cases werebrothers or cousins, that only a very small percent-age of the labourers developed the toxic manifesta-tions though they were working under the sameconditions, and that the duration of exposure tomanganese is very variable, ranging from five monthsup to 25 years. It may be that the more vulnerable

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Neuropsychiatric manifestations of chronic manganese poisoning

persons developed the signs and symptoms after arelatively short period.The significance of the second factor can be shown

clearly from the incidence of manganism in thevarious jobs. While it is highest (80 2 %) in the drydrillers who worked in the dusty atmosphere of theunderground galleries, it is lowest in porters (6-7 %)loading and unloading the ore in the open air. Inaddition, the marked change in the incidence ofchronic manganism that occurred in our series isworth mentioning. Before 1952, about 14% of thelabourers developed the toxic manifestations, butwhen wet rock drilling under adequate ventilationwas used the percentage dropped to about 0-2.These findings are in accordance with those of

other authors (Flinn, Neal, Reinhart, Dallavalle,Fulton, and Dooley, 1940). In addition Freise(1932) and Bubarev (1931) could not find any neuro-logical manifestations in an extensive study ofmanganese loaders. Similarly, Baader (1932a and b)reported such manifestations in only one porteramong all porters unloading manganese ore in theharbour of Hamburg.

In order to throw some light on the pathogenesisand to explain the variability of the symptoms andclinical pictures of the neuropsychiatric manifesta-tions in chronic manganese poisoning, we mustsurvey the few pathological reports of other authorson necropsies (Ashizawa, 1927; Trendtel, 1936)and in experimental monkeys (Mella, 1924).The essential and characteristic lesion, common in

all the necropsies and experimental animals, isdestruction of the ganglion cells of the basal ganglia.Ashizawa found 'histopathological changes in thepons, the internal capsule and the cerebral peduncleTrendtel reported degeneration and gliosis in thecorpus striatum, in addition to a decreased numberof neurones in the putamen and globus pallidus.He likewise found the same kind of changes in otherparts of the brain.

Canavan, Cobb, and Drinker (1934) describedthe pathological changes in a manganese workerwho died after 14 years of disability from manganesepoisoning. There was atrophy of the cerebral cortex,especially in the frontal lobes and in the cerebellum,but the main changes were in the basal gangliawhich were shrunken and distorted. Histopatho-logical studies revealed gliosis and degeneration ofthe nerve cells, particularly in the optic thalamus,globus pallidus, lentiform nucleus, caudate nucleus,and the putamen.On the whole, the clinical and pathological picture

of manganese poisoning points to involvement of thebasal ganglia, sometimes of the globus pallidus andfrequently of other parts of the nervous system suchas the pyramidal system, cerebellum, and its connex-

ions. But they are not consistently affected to thesame extent, hence the variability from one group ofcases to another.The high incidence of acute onset in our cases

(28-9%) has never been reported before, since themost commonly reported mode of onset was insidi-ous (McCrae, 1925; von Jaksch, 1901).

In none of the previous reports were the clinicalmanifestations of cerebellar deficit so marked as inour third group, constituting 13-4 % of the cases.Although Loebe (1936) attributes the von Jaksch's

gait to cerebellar dysmetria, in none of our cases wasit associated with clinical evidence of cerebellaraffection. On the contrary this gait results frommarked rigidity in the lower limbs unequally affect-ing the agonists and antagonists and it is similar towhat occurs in decerebrate rigidity.

But on the whole, our results conform with thosepreviously reported (McNally, 1935).

SUMMARY AND CONCLUSIONS

Forty-five cases ofmanganese poisoning are reported.Neuropsychiatric symptoms had developed fromfive months to 25 years after the onset of exposure tomanganese.An insidious onset with fatigue and langour was

commonly observed, and this proceeded to weaknessand stiffness of the gait, and disturbances of balanceof the type observed in Parkinsonism.

In 50% of the cases von Jaksch type of gait ap-peared. The motor signs might be purely extra-pyramidal or pyramidal or cerebellar, or a mixtureof these. Marked emotional and neurovegetativedisturbances were observed.To conclude, chronic manganese poisoning is a

crippling disease with permanent disabilities, especi-ally in regard to the use of the lower limbs. None ofour cases showed any improvement after beingremoved from the mines; on the contrary, in all ofthem, the neurological disabilities progressed andonly the psychic changes regressed.

REFERENCES

Abd El Naby, S., and Hassanein, M. (1963). Clinical study ofchronic manganese poisoning in Egypt. Lecture delivered atthe International Congress of Industrial Medicine, London.

Ashizawa, R. (1927). Ueber einen Sektionsfall von chronischerManganvergiftung. Jap. J. med. Sci. Trans., sect. VIII. Intern.Med. Pediat. and Psychiat., 1, 173-191.

Baader, E. W. (1932a). Manganvergiftungen in Elementefabriken.Arch. Gewerbepath. Gewerbehyg., 4, 101-116.

(1932b). Manganismus eines Trimmers. Zbl. Gewerbehyg., 19,n.s. 9) 1-3.

Bubarev, A. (1931). On the poisoning associated with loading andunloading manganese on ships. (In Russian.) Gig. Bezopasn.Pat. Tr., 9, no. 6, pp. 85-87.

Canavan, M. M., Cobb, S., and Drinker, C. K. (1934). Chronicmanganese poisoning: report of a case, with autopsy. Arch.Neurol. Psychiat. (Chicago), 32, 501-412.

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Couper, J. (1837). On the effects of black oxide of manganese wheninhaled into the lungs. Brit. Ann. Med. Pharm., 1, 41-42.(Also published in French as: Note sur les effets du p6roxidede Mangan6se. J. de Chim. med. Pharmacie ToxicoL, ser. 2, 3,233/237.)

Edsall, D. L., Wilbur, F. P., and Drinker, C. K. (1919). The occurrence,course and prevention of chronic manganese poisoning. J.industr. Hyg., 1, 183-193.

Flinn, R. H., Neal, P. A., Reinhart, W. H., Dallavalle, J. M., Fulton,W. B., and Dooley, A. E. (1940). Chronic manganese poisoningin an ore-crushing mill. Publ. Hlth Bull. (Wash.), no. 247.

Freise, F. W. (1932). Berufskrankheiten von Manganerz-Bergleutenund Verladern. Beobachtungen aus brasilianischen Betrieben.Arch. Gewerbepath. Gewerbehyg., 6, 1-13.

Jaksch, R. von (1901). Ueber gehAufte diffuse Erkrankungen desGehirns und Ruckenmarks, an den Typus der multiplenSklerose mahnend, welche durch eine besondere Aetiologiegekennzeichnet sind. Wien. klin. Rdsch., 15, 729-733.

(1907). Ueber Mangantoxikosen und Manganophobie. Munch.med. Wschr., 54, 969-972.

Loebe, C. V. (1936). Ober Manganismus, insbesondere tiber den'Hahnentritt'. J. Psychol. Neurol. (Lpz.), 47, 220-221.

McCrae, T. (1925). In Modern Medicine: Its Theory and Practice,ed. W. Osler, 3rd ed., rev. by T. McCrae, Vol. 2, pp. 682-684.Lea and Febiger, Philadelphia.

McNally, W. D. (1935). Industrial manganese poisoning-with areview of the literature. Industr. Med., 4, 581-599.

Mella, H. (1924). The experimental production of basal ganglionsymptomatology in Macacus rhesus. Arch. Neurol. Psychiat.(Chicago), 11, 405-417.

Nazif, M. (1936). Manganese as an industrial poisoning. J. Egypt.Publ. Hlth Ass., 10, 1-20.

Scander, A., and Sallam, H. A. (1936). A Report on eleven casesof chronic manganese poisoning. J. Egypt med. Ass., 19,57-62.

Schlockow (1879). Ueber eine eigenartiges Ruckenmarksleiden derZinkhtitenarbeiter. Dtsch. med. Wschr., 5, 208-210, and 221-222.

Trendtel, F. (1936). Zur Frage des Manganismus. Mschr. Unfall-heilk., 43, 69-84.

The April 1965 IssueTHE APRIL 1965 ISSUE CONTAINS THE FOLLOWING PAPERS

Histochemistry of the neuroglia and myelin in experi-mental cerebral oedema M. Z. M. IBRAHIM, R. S. MORGAN,and c. w. M. ADAMS

Changes in the enzyme histochemistry of skeletal muscleduring experimental denervation and reinnervationBARBARA SMITH

Serum enzyme variations and histological abnormalitiesin the carrier state in Duchenne dystrophy JAMESSTEPHENS and EDWARD LEWIN

Electroencephalographic studies in hereditary myopathyDAVID D. BARWICK, J. W. OSSELTON, and JOHN N. WALTON

Relation of multiple cranial nerve dysfunction to theGuillain-Barr6 syndrome THEODORE L. MUNSAT andJAMES E. BARNES

Aberrant peripheral nerve fibres in the medulla oblongataof man WILLIAM DEMYER

Haemodynamics of the circle of Willis and the lepto-meningeal anastomoses: an electromagnetic flowmeterstudy of intracranial arterial occlusion in the monkeySUSUMU ISHIKAWA, JYOJI HANDA, JOHN S. MEYER, andPETER HUBER

The connexions of the amygdala W. M. COWAN, G.RAISMAN, and T. P. S. POWELL

An evaluation of surgical treatment for spinal cordcompression due to metastatic carcinoma RODERICKSMITH

A case of metastasizing meningionta A. GORDON andA. F. J. MALONEY

Familial meningiomas ROBERT J. JOYNT and GEORGE E.PERRET

Phenylketonuria presenting an intermittent progressivecourse M. BECHAR, B. BORNSTEIN, M. ELIAN, and u.SANDBANK

Incidence of hyperostosis frontalis intema in patients at ageneral hospital and at a mental hospital T. D. HAWKINSand LAURENCE MARTIN

Aneurysms of the middle meningeal artery N. 0. AMELI

Antibody response to central and peripheral nerveantigens in rat and guinea-pig E. A. CASPARY and E. J.FIELD

Proceedings of the Society of British NeurologicalSurgeons

Book reviews

Copies are still available and may be obtained from the PUBLISHING MANAGER,

BRITISH MEDICAL ASSOCIATION, TAVISTOCK SQUARE, W.C. I, price 18s. 6D.

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