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Page 1: Nervous shock and disease of the nervous system as a cause ... · Nervons Shock and Disease of the Nervous System as a Cause ofPernicious Anemia. Read intheSection onPractice o£

Nervons Shock and Disease of the NervousSystem as a Cause of Pernicious Anemia.

Read in the Section on Practice o£ Medicine at the Forty-seventhAnnual Meeting of the American Medical Association held at

Atlanta, Ga., May 5-8, 1896.

JAMES B. HERRICK, M.D,CHICAGO, ILL.

REPRINTED FROM

THE JOURNAL OF THE AMERICAN MEDICAL ASSOCIATIONJUNE 20, 1896.

CHICAGO;American Medical Association Press.

1896.

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NERVOUS SHOCK AND DISEASE OF THENERVOUS SYSTEM AS A CAUSE OF

PERNICIOUS ANEMIA.

JAMES B. HERRICK, M.D.

It is the object of this paper to direct attention tonervous shock or disease of the nervous system as apossible, or probable, exciting cause of grave or per-nicious anemia. My attention was called to the rela-tions between these conditions by the following case:

The patient, Mrs. M., white, 68 years of age, claimedto have been in good health up to November, 1893. Shehad rosy cheeks, was plump, weighed 137 pounds, ledan active, busy life as a quasi-practitioner of medi-cine. She scarcely knew what it was to be confinedto bed save when her children were born, five ofwhom she had brought into the world alive andhealthy. She had never miscarried and there was noother evidence leading to the suspicion of syphilis.Her father had lived to the age of 87, to die an acci-dental death. Her mother succumbed to pleurisy at63. One brother had died from some cardiac troubleand one sister from asthma. Two brothers and onesister were living.

In November, 1893, she fell on the sidewalk, hurt-ing her back and left side. To use her own words:“ The hurt extended from the back of the neck downthe left side and left leg.” She walked home, butfrom the time of this injury she found herself weaker,both physically and mentally. She was obliged tolie down the greater part of the day, and thought shewas becoming paralyzed. Soon the legs began tobloat; and she would, upon sitting up for a short time,

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feel dizzy and perhaps faint. The patient becameunable to walk for any great distance; had difficultyin picking up small objects such as a pin. The skinbecame paler; the appetite, notwithstanding, remainedgood; the bowels were constipated. She was oftenquite thirsty.

On admission to the Presbyterian Hospital June 30,1894, her complaint of somewhat vague pain, of weak-ness of the arms and legs, and mental deterioration,for all which she assigned the injury as the efficientcause, coupled with the fact that there could be dis-covered no evidence of organic lesion to account forsuch phenomena, and also that she referred often to a$2,000 accident insurance claim that she had placedin the hands of a lawyer for collection, all this arouseda suspicion of exaggeration of symptoms as in railwayspine, if not of malingering.

The increasing pallor of the skin led later to aninvestigation of the blood and a more thorough exam-ination of the patient. I condense the results ofseveral examinations.

Physical Examination Nov. 8, 1894.—Skin andmucous membranes of a lemon-yellowish white. Con-junctive show light yellowish tinge. Skin is dry,wrinkled, panniculus adiposus scanty. Patient talksrather slowly, as if taking a long time for framinganswer and separate words. Speech reminds one ofscanning speech of insular sclerosis. She moveshands and legs slowly and somewhat uncertainly;appears weak and unable to walk or stand unsup-ported; complains of great dizziness on being put inerect posture. Hair is gray, thin and falling outfast; ears and nose negative; tongue pale, flabby,not tremulous, protruded in median line; fetorex ore\ frequent spasmodic contraction of lowerportion of orbicularis palpebrarum. Right eyebeginning cataract; numerous retinal hemorrhages;left eye, retinal field practically the same; in righteye six hemorrhagic areas counted, in left twelve.The existence of retinal hemorrhages was confirmed

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by Dr. Alfred Hinde, whokindly examined the eyesfor me. External jugular pulsates sychronously withapex-beat as does a vein (probably a perforatingbranch of the internal mammary) running just to theright of the sternum and parallel with it for its upperone-quarter. The chest is slightly flattened, of mod-erate length, intercostal spaces rather wide; respira-tory movements regular, fairly deep, eighteen to theminute. Apex-beat faintly seen and felt in the fifthinterspace just inside the left mamillary line; palpa-tion otherwise negative. Percussion reveals no in-creased area of cardiac dulness. Pulmonary resonanceon the right side in the mamillary line on expirationas low as to the sixth rib, on inspiration over seventhrib. Respiratory sounds are normal save an occasionalmoist rale; (in the last two days has “taken cold”).Systolic blowing is heard over entire precordia, bestat apex; systolic humalso over vessels of neck. Abdo-men is flabby, marked with linese albicantes; occa-sional peristaltic movements in region of umbilicusand to right of same. Edge of liver is felt very indis-tinctly about one inch below costal arch; inguinalglands are palpable but not perceptibly enlarged. Notumor mass or point of tenderness is found on palpa-tion. Liver dulness is heard in median line, one-halfway between ensiform cartilage and umbilicus; areaof splenic dulness increased in posterior axillary linereaching as high as to the eighth rib; Stomach reso-nance apparently increased in area. Stomach reachesbelow umbilicus (gastroptosis); it appears moder-ately enlarged. Lesser curvature apparently made outbetween ensiform and umbilicus. After test breakfast(Ewald) no free HCI, no mucus, no remains of pre-vious meal are present; pepsin uncertain; no lacticacid by Uffelmann’s test. Lower extremities aremoderately edematous; rectum negative, no parasitesin stools; pelvic organs negative; bones negative, notenderness. No evidence of organic or local nervouslesions can be made out. Sensation seems to be per-fect, the reflexes normal. There is no paralysis. The

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bowels are inclined to constipation. There is no greatfrequency of urination, no difficulty in urinating, orirritation from urine. Movements of muscles areslow and feeble, not coordinated with certainty.Raises dynamometer to 10 with either hand. Urine is1012, 30 to 50 ounces; no albumin, no sugar; solids,660 grains; no formed elements. Blood is pale; markedpoikilocytosis, microcytes and macrocytes; few nucle-ated red; megaloblasts, i.e., the large nucleated reds,few; leucocytes increased relatively; many lympho-cytes; number of red globules to cubic millimeter666,666; hemoglobin (Fleischl) 25 per cent.; no para-sites. I desire to acknowledge the kindly aid of thelate Dr. D. D. Bishop. Several of the numerous bloodexaminations were made by him.

I present temperature chart showing continuousirregular fever.

The patient remained in the hospital, though notunder my immediate observation, until the middle ofthe summer of 1895. On increasing doses of arsenicthere was a perceptible improvement, both as regardsthe subjective and objective symptoms. There wasless dizziness, more certain movements of the handsand legs, clearer mind, greater strength. The bloodcount gradually changed so that on March 22, 1895,the hemoglobin was 80 per cent, and the red corpus-cles 2,575,000, with no increase in the white. Asevere attack of bronchitis or influenza seemed aboutto carry off the patient, but she rallied from this andfinally left the hospital at her own request. I amunable to state facts concerning her subsequenthistory.

The case was seen by several physicians and allfailed to locate any organic cord or brain lesion or anymalignant growth.

The intense pallor of the skin, the subjective sensa-tions of dizziness and palpitation, the great mentaland bodily weakness, the retinal hemorrhages, theanemic murmurs, the enormous reduction in thenumber of red corpuscles with such marked varia-

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tions in their form and size, the presence, though insmall numbers, of nucleated corpuscles, the increasedglobular richness in hemoglobin, the corpuscles beingreduced to 18 per cent., while the hemoglobin wasreduced to but 25 per cent., the continued irregularfever, the temperature ranging from 97 to 102 F., gavean almost typical symptom-complex of the so-calledprogressive pernicious anemia of Biermer, or the pri-mary essential anemia of Addison. Enlargement ofspleen and liver have been often noted in these casesas well as venous pulsation.

But many oases clinically perfect as progressiveand pernicious in character and apparently due tosome primary disease of the blood or of the blood-making organs, have been found postmortem to havesome organic lesion overlooked during life that shouldbe regarded as primary. Thus a hidden carcinoma,an intestinal blood-consuming or toxin-producingparasite, as the anchylostomum duodenale or thebothriocephalus latus, an atrophy of the gastric andintestinal glandular structure may explain an appar-ently primary anemia. Some authors incline to putthese cases in the category of the essential anemiasbecause of the predominance of blood changes andblood symptoms. Thus Eichhorst says that onlythose deuteropathio or secondary anemim are to beregarded as progressive pernicious anemise wherethere is a great disproportion between cause andeffect. (Bd. iv, S. 22.) A case, therefore, of atrophyof the stomach or of anchylostomum disease, wherethe symptoms of the anemia completely overshadowedthose of the primary trouble he might class as pro-gressive pernicious anemia. It seems better, how-ever, with most writers to regard only the cases asprogressive pernicious anemia in which the affectionis a primary blood disease, in which so far as our presentknowledge of the etiology and pathology goes, nochange is found during life or after death save in theblood or the hematopoietic organs. That this isusually fatal is wellknown. Recoveries, however, are

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occasionally recorded. The term progressive pernicioushad better be discarded, and the term employed firstby Addison, primary essential anemia, substituted.

Looking upon this case as one of primary essentialanemia, there remains to be noted the interesting con-nection between the injury with its nervous shockand the anemia. The patient and her friends assertthat from a condition of apparent health, she almostimmediately following the injury became an invalid,weak, dizzy, easily fainting, with swollen limbs, paleskin, in a word, anemic. Just how nervous shockproduces anemia I will not attempt to say. Yet, ifthrough a shock to the nervous systern the secretionof the sweat glands, of the gastric glands, or of thekidneys can be checked or increased, if the heart’saction can become rapid and irregular, or perhaps ceasealtogether, if a chorea or an exophthalmic goitre canbe roused to activity, it can be assumed thatthe func-tion of the blood-producing organs may become per-verted, and this suddenly, through the influence ofa deranged nervous system. I recall a case of cerebralhemorrhage with aphasia and hemiplegia in whichthere was fatal anemia; also a fatal case of anemiafollowing upon a sunstroke.

I am inclined to rule out atrophy of the glandulartissue of the stomach, largely from the absence ofany symptom indicating a previous catarrhal inflam-mation, though the emaciation different from the well-preserved condition of pernicious anemia, the absenceof mucus and of free hydrochloric acid and the enlarge-ment of the stomach might seem to point in thatdirection.1 There was certainly not present the smallcontracted stomach with exuberantdevelopment ofcon-nective tissue—cirrhosis ventriculi. The dilatation,more apparent than real, because of dislocation of theorgan, was probably, as not infrequently occurs, due torelaxation of the atonic stomach walls. I believe

i Some, for example Striimpell, regard the changes in the glands ofthe stomach as secondary to the condition of anemia. Likewise thechanges in the cord and other nervous structures.

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there was no hidden carcinoma as the cause of theanemia because of the comparatively sudden onset; theabsence of subjective or objective local symptoms;the unusually severe oligocythemia, reduction oferythrocytes to 1,000,000 per cubic millimeter beingunusual in the terminal anemia of carcinoma; themarked improvement under arsenic, the improvementlasting for at least six months, and being scarcelyreconcilable with a carcinomatous anemia after it hadreached a stage indicated by a blood count of only666,666; the retinal hemorrhage and the absence ofcachexia.

Whether or not an organic disease of the brain orcord or of the sympathetic or peripheral nerves waspresent no one who saw the case would say. Theinteresting researches of Minnich in this connectionare recalled by some of the symptoms.

While nervous shock or disease of the nervous sys-tem is not recognized in many of our text-books as animportant etiologic factor in pernicious anemia, anumber of cases are reported in which this is theassigned cause.

Under this head are not included those cases ofnervous diseases as complications or sequelse of per-nicious anemia, such as degenerations of the posteriorcolumns or the other parts of the cord, etc., and whichMinnich has recently gone into so fully. (Of. alsoLichtheim, Trechsel, Burr, etc.)

Eichhorst quotes the case of an author who, after amost severe mental strain, succumbed to a fatalanemia.

Curtin, in 1885, under the title “Nervous Shockas a Cause of Pernicious Anemia,” reports the case ofa woman, 88 years of age, who was unexpectedlybrought face to face with the body of her suicidedbrother with his throat cut. From that time healthbegan to fail, and in four years and two months shewas dead of a grave anemia. No blood examination;no autopsy.

2. A young lady was suddenly and brutally informed

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of her brother’s death. Nervous prostration followedfor many months, then pernicious anemia anddeath.

3. Practice of Dr. Musser: A woman, aged 42, afteran attempt at her own murder by her husband, be-came nervous, excitable, almost insane; gradual fail-ure of health, pronounced anemia; death in threeyears.

Curtin quotes also the case of a woman becomingprofoundly anemic following fright at the house catch-ing on fire. He also quotes from Mackenzie, whocites the case of Sir H. Marsh, where the young lady,who accidentally poisoned her father, was over-whelmed by grief, took to bed and died of anemia.Also the case of a young man who saw a child runover in the street, was greatly shocked, began to growanemic; no organic lesion postmortem.

Under Sir William Gull, a young man died inGuy’s Hospital of extreme anemia that had devel-oped after he had been attacked by a sheep in a field.

Musser in 1885 gave a resume of thirty-nine casesof pernicious anemia up to that time reported inAmerica, and quotes cases of Curtin, Osier, Pepperand himself, where anemia seemed to be due to nerv-ous shock.

Hutchinson cites cases in which nervous influenceseemed to him to be the exciting cause. 1. A case ofhis own where mental worry over the death of a wifewas the cause. 2. Case in consultation where a man-ufacturer who had worried about business had be-come anemic, apparently from no other cause thanbusiness worry. 8. Four daughters died in one weekof smallpox. The father, apparently from the shockand the excessive grief, developed pernicious anemia.

Dr. Brower cites a case of pernicious anemia devel-oping in a previously healthy young woman followinga railway accident. Death in six months. He alsocalls attention to mental worry as an exciting causeof the milder grades of anemia and of chlorosis, andis authority for the statement that in a student wor-

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rying and apprehensive about the approaching finalexamination, the hemoglobin became reduced totwenty per cent.

Schiile, in three cases of pernicious anemia in theinsane, seemed to see some genetic relation betweenthe incurable cerebro-spinal lesions and the progres-sive anemia. He quotes the experiments of Goltz,Heubel and Von Tarchanoff as tending to prove theinfluence of the nervous system on blood formation,apart from the trophic influence of the spinal cord.

Macphail also describes pernicious anemia as itdeveloped in two insane patients.

Holst believes that through neurasthenia thesecretory nerves and the trophic nerves are influ-enced in such a way that blood deterioration results.He regards the anemia therefore, in many cases, as aresult and not the cause of the neurasthenia.

Hale White refers to a patient who fell on the ice.For fourteen days no symptoms, then weakness, numb-ness in legs and progressive severe anemia; apparentrecovery.

Among those who assign to the nervous system,chiefly through what we must, for want of a moreaccurate term, call nervous shock, a certain role inthe production of anemia may be mentioned Heiberg,Fabre, Germain See, Trousseau.

A number of observers believe there is some causalconnection between lesions of the nervous system andpernicious anemia. Thus Saaski believes the gastro-intestinal form depends on nerve atrophy in Meiss-ner’s and Auerbach’s plexuses. These changes he isinclined to look upon as primary and not as second-ary to the anemia, though others reverse the order ofpathologic change. . He examined two oases andforty-eight control cases.

Brigidi examined the body of a woman, aged 53,dead after two years of anemia. The only weightypostmortem finding was an inflammatory and fattydegenerative change in the celiac ganglia. Hethinks the influence on the circulation of the diges-

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tive tract might explain the poor digestion andconsequent anemia.

Pokrowski, autopsy on a case of pernicious anemia,found changes in cerebellum, fourth ventricle andmedulla, and was led to conclude that the finding inthe central nervous system must have had an influ-ence, if not the sole influence, in producing theanemia.

Banti refers to a group of anemias—anemia gangli-onare—in which he believes the primary change is inthe sympathetic nervous system.

Little also regards many cases as due to an irrita-tion of the vaso-motor system.

I feel warranted from my study of this case and aperusal of the literature bearing upon this subject, indrawing the conclusion that in some cases of pernic-ious anemia there is a causal connection betweenshock or injury to the nervous system and the result-ing anemia. Whether such shock acts by interfer-ence with the nervous mechanism of the digestiveorgans, the stomach, intestines, liver, pancreas, theultimate result being a severe anemia, or whetherthrough altered nervous influence, there is abnormalperformance of function on the part of the hemato-poietic organs, it is impossible to say. In assigningto nervous shock an influence in the production ofanemia it is not necessary to regard it as the solecause or even the prime cause. Just as in the caseof pneumonia we look upon the pneumococcus as themain cause of the disease, but yet regard exposure tocold as an exciting cause that favors the localizationor pathogenic action of the specific organism, so inthe case of pernicious anemia, the nervous shock mayin some way merely favor the action of some other-wise inert microorganism or toxin, that under thesealtered circumstances produces a profound or evenfatal anemia.

REFERENCES IN THE TEXT.

Eichhorst: Specielle Pathologie und Therapie. Bd. IV.Minnich: Zeltschr. fiir Klin. Med. Bd. XXI-XXII.

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Curtin: Nervous Shock as a Cause of Pernicious Anemia. Phila.Med. Times, April 4, 1885.

Mackenzie: Lancet, Dec. 7 and 14,1878.Musser; Three Cases of Pernicious Anemia, etc. Med. and Surg.

Reporter, 1885.Hutchinson: Medical News and Library, 1879.Bell and Osier; Trans. Canada Med. Asso., 1879.Gardner and Osier: Canada Med. and Surg. Jour., 1877.Pepper: Amer. Jour. Med. Science, 1875.Brower: Trans. Chicago Pathological Society, Vol. 1,1895, p. 50.Schiile: Aligem. Zeitsch. f. Psych., Bd. 22, s. 1,1875.Macphail: Edinburgh Med. Jour., June, 1885.Holst: Dorpater med. Ver.. VI, s. 15 (Ref. in Virchow and Hirsch,

1875, 11, 85).Hale White: Guy’s Hosp. Reports, 1890.Saaski; Virchow’s Archiv, Vol. 96, p. 287.Brigldi; La Sperimentale, Aprile, 1885 (Ref. in Virchow and Hirsch).Pokrowski: Petersh. Med. Wochenschr.. No. 47,1885.Banti: La Sperimentale, 1881 (Ref. in Virchow and Hirsch).Little; N. Y. Med. Rec., March 20, 1880.

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