Pellagra among alcoholics: of cases

Journal of Neurology, Neurosurgery, and Psychiatry, 1981, 44, 209-215

Pellagra among chronic alcoholics: clinical andpathological study of 20 necropsy cases

NOBUYOSHI ISHII AND YASUO NISHIHARAFrom the Departments of Pathology and Neuropsychiatry, Kurate Kyoritsu Hospital, Miyatacho,Kurategun, Fukuokaken, Japan

S UMM A R Y Twenty cases of pellagra, diagnosed on neuropathological grounds, were foundamong 74 necropsy cases of chronic alcoholism. Although these patients had presented withvarious mental, neurological and gastrointestinal symptoms, the diagnosis of pellagra had notbeen established clinically because, in the majority, there were no skin lesions. It is emphasisedthat whenever chronic alcoholics exhibit certain mental, neurological or gastrointestinal symp-toms, one should strongly suspect pellagra even in the absence of skin lesions (pellagra sinepelle agra).

Pellagra is a disease caused primarily by niacindeficiency. It is characterised by the classical triadof dermatitis, diarrhoea and dementia. If un-treated, patients eventually die. Some people there-fore add "death" to the triad, thus making "4 D's".Nowadays, the disease has virtually disappeared indeveloped countries, except in association withchronic alcoholism. The conspicuous associationbetween severe alcoholism and pellagra has beencommented upon clinically by many previousworkers. 1-4We found 20 cases showing neuropathological

features of pellagra among 74 chronic alcoholicswho came to necropsy. The pellagra had not beensuspected clinically, because of the absence ofcharacteristic skin manifestations. The aim of thispaper is to show the clinical and pathological find-ings of these cases of niacin-deficiency encephalo-pathy and to call attention to "pellagra sine pelleagra" among chronic alcoholics.

Cases and methods

Between 1965 to 1979, 758 chronic alcoholics wereadmitted to our hospital. Of these, 81 died and 74underwent complete postmortem examination. Allorgans including the brain were kept in 10% formalin

Address for reprint requests: Dr N Ishii, Department of Pathology(Neuropathology), University of Occupational and EnvironmentalHealth, School of Medicine, Iseigaoka 1-1, Yahatanishiku, Kitakyu-shushi, 807, Japan.

Accepted 10 December 1980

for two weeks and sections were taken from eachorgan. Recently 14 to 20 additional sections were pre-pared from the brain in each case and stained withhaematoxylin and eosin, Nissl, periodic-acid-Schiff,luxol fast blue and Bodian stains. Sections examinedwere frontal lobe (areas 4, 6, 8, 11, 12, 24), parietallobe (areas 1-3, 7), temporal lobe (areas 20, 21, 38),occipital -lobe (areas 17, 18), insula, Ammon's horn,hippocampal gyrus, amygdala, caudate, putamen,thalamus, hypothalamus, midbrain, upper and lowermedulla, cerebellum (vermis, hemisphere, dentatenucleus) and upper cervical cord. In two cases thebrain was postfixed with 2 % osmium tetroxide, de-hydrated and embedded in Epon 812 and examinedwith an electron microscope. Clinical data were ob-tained from the charts. A representative case is des-cribed below.A 39 year-old man (case 12) was admitted because

of mental confusion. He was a severe alcoholic andhad been admitted eight times during the previous 10years. Ten days prior to admission, he was found tobe speaking incoherently. He had lost his appetite,and become unable to take even alcoholic beverages.He was emaciated, confused, disoriented and agitatedon account of hallucinations. He mumbled unintelli-gible words and did not answer questions. He wastremulous and markedly ataxic. After admission hisdelirium tremens persisted, and the level of conscious-ness fluctuated. Profuse sweating, insomnia, visual andauditory hallucinations persisted until his death. Onthe 14th hospital day he developed severe diarrhoea.This could not be controlled despite the administrationof vitamin B1, B07, B12, C, various antibiotics andantidiarrhoeal agents. He developed a spastic para-paresis and was confined to bed with incontinence of

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both urine and faeces. He expired of bronchopneu-

monia six weeks after admission.

Necropsy revealed bilateral aspiration broncho-

pneumonia and severe decubi-tus ulcers. There were

no other signific-ant findings in the viscera and no

liver d'iseases. The brain weighed 1280 grams. Grossly

the cerebrum showed no abnormalities. The superior

vermis was atrophic with narrow cerebellar folia and

widened sulci. Histologically, the most significant find-

ing was central chromatolysis of neurons occurring

in wide areas. The Betz cells and other relatively large

pyramidal cells of the cortex, as well as the neurons

of the pontine nuclei, dorsal vagal nuclei, gracile and

cuneate nuclei, vestibular nuclei and anterior horn

cells of the spinal cord showed severe chro,matolyticchanges (figs and 2). A section of the atrophic

cerebelliar vermis revealed complete disappearance of

Purkinje cells with Bergmann's astrogliosis and de-

population of the granular cell layer.

The clinical and pathological findings of the 20 cases

are summarised in the table.

Fig Central chromatolysis in neurons of pontine

nuclei. Nissl X200, case 12.

Fig 2 Central chromatolysis in Betz cells (a) and

anterior horn cells (b). Nissl X200, case 12.

Nobuyoshi Ishii and Yasuo Nishihara

Summary of the clinical findings All the patientswere male alcoholics. Their age ranged from 38 to89 years with a mean of 52 years. The average drink-ing history extended over 19 years. The mean durationof the terminal illness was 13,5 weeks. In 19 of the20 cases, the clinical diagnosis on admission had beendelirium tremens. Neuropsychiatric symptoms ob-served were confusion (20/20), hallucination (18/19),insomnia (16/17), tremor (14/17), gait disturbance(19/20), extrapyramidal rigidity of the limbs (16/17),inconitinence of urine and faeces (19/20), polyneuro-pathy (7/16) and seizures (3/20). Anxiety, depression,excitement and neuraesthenia were also observed infrom one-third to one-half of the cases. Deep tendonreflex was increased bilaterally in the majority ofcases, except for those patients who also had per-ipheral neuropathy. The disturbance of tone was morepronounced in the legs than in the arms in all 16 casesshowing rigidity. This was severe enough to causeparaparesis, confining the patients to bed, particularlyin the terminal stages of -their illness. In one case(case 19) the clinical diagnosis was Wernicke's ence-phalopathy and this was later confirmed by pathologi-cal examination.

Gastrointestinal symptoms observed in the patientswere anorexia (12/20), diarrhoea (9/20), vomiting(5/20) and constipation (3/20). Glossitis was noted in13 cases. Seven patients had relatively good appetiteduring hospitalisation. Diarrh-oea was seen at the be-ginning of the illness in some cases, but in others, itonly appeared in later stages. One patient (case 1)had severe di'arrhoea at the onset, but later becameconstipated. In most cases the diarrhoea did notrespond to various me-dications.

Skin lesions were only observed in six cases. Thelesions were described as vesicles or builae over theextremities, eczema-like lesion around the mouth andnose, desquamation and roughened skin over thehands, and reddish discoloration of the scrotum. Noneof these lesions was considered to be typical of pel-lagrous dermatitis. Pellagra was not suspected by thephysicians in charge.

Laboratory data indicated malnutrition in approxi-mately half the cases. Anaemia (red cell counts ofless than 3.5X1012/1 or a haemoglobin below 70%)was seen in nfine cases. There were 11I cases with hypo-proteinaemia (scrum proteins less than 6-0 g/1). In fivecases, liver function tests showed moder-ate elevationsof SGOT and SGPT. Jaundice was not noted in anyof the 20 cases.

Treatm-ent ccmprised intravenous administrationof glucose, electrolytes, vitamin B1, B, B12 andvarious antibiotics for associa-ted bronchopneumonia,decubitus ulcers and diarrhoea. Niacin was not pre-scribed in any of the cases.The clinical features and evolution of the disease in

18 cases (excluding cases 11I and 19) were surprisinglysimilar. The chronic alcoholics were hospitalisedbecause of delirium tremens. They subsequentlydeveloped neurological signs and symptoms, suchas extrapyramidal rigidity, gait disturbance, double


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Pellagra among chronic alcoholics: clinical and pathological study of 20 necropsy cases

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incontinence, polyneuropathy, seizures and gastro-intestinal symptoms. They deteriorated progressively,developing terminal bronchopneumorfia, and expiringwithin several weeks to a few months from the onsetof symptoms.Summary of the necropsy findings Malnutrition wasobvious in most cases. Body weights at necropsyranged from 33 kg to 72 kg, with an average of45 2 kg. The mean weight of the brain was 1279grams. This is less than the average brain weight ofJapanese males (1363 grams) of the same age. Onmacroscopic examination 11 cases showed slight tomoderate cerebral gyral atrophy and 12 cases showedventricular dilatatlion. The blood vessels at the base ofthe brain including the circle of Willis ghowed minimalatherosclerot'ic changes in most cases. Two cases (2and 19) had small infarcts in the basal ganglia and inthe white matfter of the frontal lobe. No other vascu-lar lesions were noted. There were no subduralhaematomas.

Histologically the most striking finding was centralchromatolysis of neurons. This chromatolytic changewas constantly observed in Betz cells and in theneurons of the pontine nuclei. The neurons wererounded, and showed peripheral displacement of thenuclei and Nissl substance. The same changes werenoted in the relatively large cortical neurons (18/20),dorsal vagal nuclei (19/20), gracile and cuneate nuclei(15/15), descending trigeminal nuclei (19/20), vesti-bular nuclei (19/20), parahypoglossal nuclei (nucleiof Rolller) (17/20), in the nuclei ambigui (10/20),arcuate nuclei (12/18), dentalte nuclei (10/14), oculo-motor nuclei (8/16), and anterior horn cells (3/4). Afew neurons in the basal ganglia, thalami and mam-milary bodies exhibited similar changes in some cases.The Purkinje cells, and the neurons of the substantianigra and Ammon's horn never showed chromatolysis.

Electron microscopy revealed that, in the chroma-tolytic neurons, RNA granules and lipofuscin pigmentdeposits were pushed to the periphery of the cyto-plasm. The central portion of the cytoplasm was oc-cupied by mitochondria, lysosomes and dilated vesicles.Neurofilaments were not increased in number (fig 3).The entire length of the spinal cord was available

for histological examfination in only two cases. Therewere no degenerative changes in the long tracts. Cases18 and 19 showed changes of Wernicke's encephalo-pathy. Cases 10, 12 and 18 exhibited pictures of alco-holic cerebellar degeneration. Case 19 also showeddemyellinating lesion in the pons, consistent with cen-tral pontine myelinolysis.

Histological examination of the tongue was carriedout in all 20 cases. In 13 there was histological evi-dence of glossitis, such as parakeratosis, acanthosis,elongation of the rete ridges and chron'ic inflammatorycell infilitration of the submucosa (fig 4). There wereno morphologically significant lesions in the gastro-intestlinal tract, except for chronic atrophic gastritisseen in 10 cases. The neurons of the Auerbach's plexusrevealed chromatolysis in five cases. The heart weighed150 to 310 grams, with an average of 240 grams. There


st,.."h| l | rIN,~~~~~~~~~~~~~~~~~~~~~~~~5

Fig 3 Electron micrograph of a chromatolyticpontine neuron, showing displaced nucleus (N),ribosomes (R) and lipofuscin granules (L) at theperiphery of the cytoplasm. X3000.

Fig 4 Severe glossitis showing parakeratosis,acanthosis, elongation of rete ridges and chronicinflammatory cell infiltrates. H and E X30, case 13.

were no right ventricular dilatation suggestive of beri-beri heart disease. Other associated findings includedcirrhosis of the liver in two cases, fatty liver in threecases, and hepatic fibrosis in three cases. Broncho-pneumonia was observed in 16 cases and was thoughtto be the most frequent cause of death. Other causesof death included oedema of the lungs in three casesand -asphyxia due to tracheal obstruction in one case.


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Discussion

None of these 20 patients exhibited the classicalcutaneous features of pellagra and none had thediagnosis confirmed by biochemical methods(excretion of N'-methylnicotinamide etc). How-ever, we believe these 20 cases had "pellagra" onneuropathological and clinical grounds. The mostconsistent neuropathological abnormality in pel-lagra is said to be central chromatolysis of theneurons in various areas: Betz cells, pontinenuclei, dorsal vagal nuclei, gracile and cuneatenuclei, nucleus ambiguus, descending trigeminalnuclei, arcuate nuclei and anterior horn cells.4-9The Purkinje cells, neurons in Ammon's horn andhypoglossal nuclei, although among the largestneurons, are not affected. The distribution ofchromatolytic neurons in our 20 cases mirroredthe distribution reported in pellagra by manyauthors. Myelopathy closely resembling subacutecombined degeneration of B12 deficiency has alsobeen reported. The spinal cords in the two casesexamined did not show these myelopathic lesions.They are infrequent and their absence cannot betaken to invalidate the diagnosis of pellagra.The presence of glossitis in 13 out of 20 cases is

also in favour of the diagnosis, although the histo-logical picture of pellagrous glossitis (as of pella-grous dermatitis) is non-specific. Only six patientsdeveloped skin lesions, usually in their terminalstages. One of the reasons for the rarity of thecutaneous manifestations of pellagra amongchronic alcoholics may be that pellagrous derma-titis develops in the exposed parts of the body,namely the face, neck, dorsum of hands, arms andfeet, whereas our alcoholics generally have littleoccasion to be exposed to the sun. They wereusually kept in darkened side rooms while theyhad severe mental symptoms.Although gastrointestinal symptoms such as

diarrhoea, constipation and vomiting were ob-served in 12 cases, much attention was not paidto these symptoms. The patients with severe diar-rhoea were treated with antibiotics and anti-diarrhoeal agents without obtaining any benefit.Gillmann and Gillmann'0 stated that pellagrinsexhibited no remarkable pathological findings inthe intestine. In our cases too, there were no sig-nificant changes in the gastrointestinal mucosa.However, careful examination revealed thatneurons of the dorsal vagal nuclei demonstratedmarked chromatolytic changes in almost all cases(fig 5). Similar changes were also noted in theAuerbach plexus of the intestinal wall. In con-trast, neurons of the dorsal vagal nuclei and the

Fig 5 Central chromatolysis in dorsal motornucleus of vagus. H and E X150, case 10.

gastrointestinal wall in 10 non-alcoholic controlcases showed no such chromatolytic changes. Theautonomic nervous system controls gastrointestinalperistalsis, and both nausea and vomiting may becaused by stimulation of the medullary tegmentumwhere the dorsal vagal nuclei are located. Webelieve that the gastrointestinal symptoms in pel-lagrins may be due to an abnormality of theautonomic nervous system, namely the centralchromatolysis of its neurons.The mental symptoms shown by our 20 cases

varied greatly. They included confusion, hallucina-tions, insomnia, delirium, anxiety, depression, ex-citement and neurasthenia. All of these symptomsmay occur in non-alcoholic, endemic pellagrins.11'14However, the mental symptoms in our cases wereconsidered to be those of delirium tremens, be-cause all the patients were severe alcoholics andbecause pellagra was not suspected clinically.Klauder and Winkelman' reported 100 patients

with cutaneous features of pellagra, the majorityof whom were chronic alcoholics. They dividedthe patients into three groups. Group 1 consistedof those cases in whom the dermatitis was a con-spicuous, apparently initial symptom. There was apaucity or entire absence of somatic symptoms,such as diarrhoea. The patients in group 2 pre-sented pellagrous dermatitis and frank somaticsymptoms, characteristic of pellagra (diarrhoea,mouth and tongue lesions, in addition, some hadmental or neurologic symptoms). In group 3, severecutaneous and somatic symptoms of pellagra de-veloped suddenly after a prolonged debauch. Inaddition, there was an acute delirium with in-creased psychomotor activity (necessitating re-straint), complete disorientation and auditory andvisual hallucinations. On admission, the diagnosis

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had been delirium tremens. They stated that it wasnot always possible to differentiate mental symp-

toms of pellagra from those of alcoholism.Spies et al"l also reported 60 cases of pellagra.

The mental symptoms were acute, consisting ofdisorientation, confusion, excitement, mania, de-pression, delirium etc. The authors gave a de-tailed description of a 55-year-old non-alcoholicpellagrin who had visual and auditory hallucina-tions. It seems impossible to differentiate pella-grous psychosis from alcoholic delirium tremenson the ground of the mental symptoms alone.There seem to be differences, however, in the

neurological symptoms. Jollife et all5 observed 150cases of what they called nicotinic acid deficiencyencephalopathy. About half their 150 patientshad clinical evidence of pellagra. Their symptomswere characterised by clouding of consciousness,cogwheel rigidity and uncontrollable grasping andsucking reflexes. Leigh5 collected 14 necropsycases of non-alcoholic pellagra, among whomspastic paraplegia was observed in three cases. Inalmost all of our 20 cases, extrapyramidal rigidityof the extremities with gait disturbance, incon-tinence and hyperreflexia were observed. In our

experience, these neurological symptoms are notseen in ordinary alcoholics with delirium tremens.Of 758 chronic alcoholics admitted to our insti-tution during the 14 year period, there were 158cases who were diagnosed as delirium tremens or

transient hallucinosis. In 138 patients (other thanour 20 cases of pellagra), the mental symptomssubsided within a few days to two weeks of ad-mission and the forementioned neurological symp-

toms and signs were not observed. Therefore,when an alcoholic shows neurological signs, par-

ticularly extrapyramidal rigidity, in addition tovarious mental and gastrointestinal symptoms, oneshould strongly suspect pellagra, a curable dis-order. The relevant treatment (niacin) should notbe delayed until the appearance of skinmanifestations.

Diarrhoea, vomiting and the elimination ofniacin-synthesising bacteria (by antibiotics) may

have played a part in the enhancement of thedeficiency state of our patients. However, we are

convinced that our 20 cases are not instances ofpellagra superimposed on the terminal stage ofother conditions. We believe that the mental symp-toms in our cases had been those of pellagrapsychosis from the onset. Case 11 provides goodevidence on this point. The patient was a 40 year

old man who expired rather suddenly of pulmonaryoedema. He had mental symptoms without any

neurological signs or progressive disability. Neuro-


pathologically typical pellagrous changes wereidentified in wide areas of the nervous system, asin the other cases.

Pellagrins are not only deficient in niacin butalso in other vitamins. Some of the clinicalfeatures seen in pellagrins (polyneuropathy forexample) are believed to be caused by associatedthiamine deficiency.'6 Seven of our 20 patientsdeveloped polyneuropathy with severe par-aesthesiae and burning pains of the extremities, lossof deep tendon reflexes and muscle weakness whenconfined to bed. Five of these seven patients hadbeen taking thiamine (50-75 mg/day) either bymouth or intravenously, when they developedpolyneuropathy. We are not certain whetherthiamine deficiency alone is responsible for pel-lagrous neuropathy or whether deficiency of niacinand other vitamins group B should be incriminated.

Pellagra is now believed to be a disappearingdisease. Figueroa et al17 found only two pellagrinsamong 451 newly admitted alcoholics in Chicago.They attributed this unexpectedly low incidenceof pellagra to the fortification of bread with niacin.More recently, however, Spivak and Jackson3 wereable to collect 18 pellagrins with characteristicskin lesions during a four year period. Fifteen ofthese were chronic alcoholics. Sporadic case re-ports of alcoholic pellagra with autopsy confirma-tion have been published in Japan.'8 19The clinical diagnosis of florid pellagra is easy.

It is rare, however, to see a typical pellagrin, pre-senting with the classical triad.20 It is importantto recognise the neurologic and mental manifesta-tions of the disease when it occurs without derma-titis or gastrointestinal symptoms. 12 It was un-fortunate that neither clinical nor pathologicaldiagnoses of pellagra were made in our 20 casesfor over a decade, because of the absence of skinlesions and, because the brains were not examinedby a neuropathologist. Recently four further alco-holics have come to us with severe mental, neuro-logical and gastrointestinal symptoms. Theyshowed a dramatic response to the administrationof niacin and other vitamins. Still9 mentioned that"pellagra sine pelle agra" still lies hidden andunsuspected in the mortality data of mentalhospitals. We whole-heartedly agree with thisstatement.

The authors thank Professor Siko Takeya whoexamined the neuropathological sections and Pro-fessor Tamaki Imai who critically read the manu-script and gave us valuable advice. This study wasundertaken with the collaboration of Miss ToyokoOkada and Miss Hiroko Noguchi.


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2 Spies TD, DeWolf HF. Observations on the etio-logical relationship of severe alcoholism to pel-lagra. Am J Med Sci 1933; 186:521-5.

3 Spivak JL, Jackson DJ. Pellagra: an analysis of18 patients and a review of the literature. JohnsHopkins Med J 1977; 140:295-309.

4 Zimmerman HM, Cohen LH, Gildea EF. Pellagrain association with chronic alcoholism. ArchNeurol Psychiatr (Chicago) 1934; 31:290-309.

5 Leigh D. Pellagra and the nutritional neuro-pathies, a neuropathological review. J Ment Sci1952; 98:130-42.

6 Hsu YK. Pathologic anatomy of human nervoussystem in avitaminosis. Arch Neurol Psychiatr1942; 48:271-319.

7 Langworthy OR. Lesions of the central nervoussystem characteristic of pellagra. Brain 1931; 54:291-302.

8 Greenfield JG, Holmes JM. A case of pellagra.The pathological changes in the spinal cord. BrMed J 1939; i:815-9.

9 Still CN. Nicotinic acid and nicotinamide de-ficiency: pellagra and related disorders of thenervous system. In: Vinken PJ, Bruyn GW eds,Handbook of Clinical Neurology vol 28, Amster-dam: North-Holland, 1975; 59-104.

10 Gillmann J, Gillmann T. Perspective in the humanmalnutrition: a contribution to the biology ofdisease from a clinical and pathological study ofchronic malnutrition and pellagra in the African.New York: Grune and Stratton, 1951.

11 Spies TD, Aring CD, Gelperin J, Bean WB. Themental symptoms of pellagra. Their relief withnicotinic acid. Am J Med Sci 1938; 196:461-75.

12 David CS. Pellagra. In: Beeson PB, McDermottW eds, Textbook of medicine. Philadelphia: WBSaunders, 1967:1153-6.

13 Shah DR, Singh SV, Jain IL. Neurological man-ifestations of pellagra. J Ass Phys India 1971;19:4434.

14 Shah DR, Pandy SK, Rathi R. Psychiatric man-ifestation in Pellagra. J Ass Phys India 1972; 20:575-8.

15 Jollife N, Bowman KM, Rosenblum LA, FeinHD. Nicotinic acid deficiency encephalopathy. JAm Med Ass 1940; 114:307-12.

16 Lewy FH, Spies TD, Aring CD. The incidence ofneuropathy in pellagra. The effect of cocarboxy-lase upon its neurologic signs. Am J Med Sci1940; 199:840-9.

17 Figueroa WE, Sargent F, Imperiale L, Morey GR,Paynter CR, Vorhaus LJ, Kark RM. Lack ofavitaminosis among alcoholics: its relation tofortification of cereal products and the generalnutritional status of the population. J Clin Nutr1953; 1:179-99.

18 Okeda R, Nakao T. An autopsied case of chronicalcoholism with alcoholic laminar cortical sclero-sis (Morel) and so-called pellagra encephalopathy.Adv Neurol Sci 1976; 20:385-99.

19 Suzuki H, Takahata N, Satomi R, Suzuki T. Twoautopsied cases of alcoholics, from view point ofpellagra psychosis. Seishin-lgaku 1975; 17:845-9.

20 Darby WJ. Nicotinic acid deficiency (Pellagra).In: Harrison TR ed, Principles of Internal Medi-cine, New York: McGraw-Hill, 1962; 542-5.

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Pellagra among alcoholics: of cases