Journal of the History of the Neurosciences Basic and Clinical Perspectives
ISSN: 0964-704X (Print) 1744-5213 (Online) Journal homepage: http://www.tandfonline.com/loi/njhn20
A Patient With Word Blindness in the Seventeenth Century Jan van Gijn To cite this article: Jan van Gijn (2015) A Patient With Word Blindness in the Seventeenth Century, Journal of the History of the Neurosciences, 24:4, 352-360, DOI: 10.1080/0964704X.2014.1001697 To link to this article: http://dx.doi.org/10.1080/0964704X.2014.1001697
Published online: 16 Mar 2015.
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Date: 12 November 2015, At: 02:00
Journal of the History of the Neurosciences, 24:352–360, 2015 Copyright © Taylor & Francis Group, LLC ISSN: 0964-704X print / 1744-5213 online DOI: 10.1080/0964704X.2014.1001697
A Patient With Word Blindness in the Seventeenth Century JAN VAN GIJN
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Utrecht University, Utrecht, The Netherlands Johann Jakob Wepfer (1620–1695), city physician in Schaffhausen, Switzerland, published two books on “apoplexy.” He proposed new ideas about the events in the brain during such attacks, based on Harvey’s theory of the circulation of the blood. Wepfer postulated extravasation of whole blood or serum in the brain, in opposition to the Galenic notion of blocked ventricles. His case histories are remarkably precise and untainted by interpretation. This allows the recognition of a patient with word blindness, who was also unable to read words written by himself. Unlike patients with pure “alexia without agraphia,” he could not write complete sentences because of additional language defects, especially speech comprehension. Jules Dejerine (1849–1917) would, in 1892, not only describe a patient with the pure form of this syndrome (cécité verbale avec intégrité de l’écriture spontanée et sous dictée) but also provide an explanation of its anatomical basis. Keywords alexia without agraphia, word blindness, apoplexy, Johann Jakob Wepfer, Jules Dejerine
Introduction While in the process of translating Johann Jakob Wepfer’s first book on apoplexy (Wepfer, 1658), I came across a case report that was remarkable for reasons other than the point Wepfer was making in that section. What struck me was that he had recorded the clinical features, and especially the cognitive defects, in sufficient detail to allow us to reach several conclusions that would not have been possible in his day, even though no postmortem had been performed. The report was not included in an earlier account of patients with language disorders in Wepfer’s work (Luzzatti & Whitaker, 1995) because the collection of observations on which this publication was based (Wepfer, 1727) contained only material that had not been published during Wepfer’s lifetime.
The Author and His Work Johann Jakob Wepfer (see Fig. 1) was born in 1620, in Schaffhausen, Switzerland, as the eldest child of the judge Georg Michael Wepfer; his mother’s maiden name was Stokar (Eichenberger, 1969). In his native town, he received a sound education, including an excellent command of Latin; he then went on to study medicine in Strasbourg and Basle, where he graduated in 1644. Wepfer spent the next three years in Italy. For two years, he studied in Padua, where his tutors included the German Johannes Wesling (1598–1649) and Address correspondence to Jan van Gijn, Maliesingel 4, 3581 BA Utrecht, The Netherlands. E-mail: [email protected]
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Word Blindness in the Seventeenth Century
Figure 1. Johann Jakob Wepfer (1620–1695).
the Dane Thomas Bartholinus (1616–1680). The University of Padua was internationally orientated and liberal, owing to the patronage of Venice, then a powerful republic in contact with many other cultures overseas (Gallo, 2001). Wepfer followed in the footsteps of two giants in the history of medicine: Andreas Vesalius (1514–1564) had taught anatomy there, and William Harvey (1578–1657) had come to Padua to graduate a few decades before in 1602 (Ongaro, 2001).
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On his return, Wepfer obtained his doctorate at the University of Basle in 1647 with a thesis on palpitations of the heart (Eichenberger, 1969). Soon afterwards, he was appointed physician to the city of Schaffhausen. This office, probably shared with one or two others, involved providing care for the citizens, at home or in the local hospital, as well as for the inhabitants of the convents in a larger area. Other tasks included advising the court of justice on medical matters, examining candidate surgeons, overseeing pharmacists and, importantly, performing autopsies. In 1650, he married Barbara Rink; they had eight children, of whom five survived to adulthood. As Wepfer’s reputation increased, he was consulted by the aristocracy of independent counties in southwestern Germany. During his long life (in 1695, aged 75), Wepfer accurately and succinctly recorded his case histories, but he also wrote systematic treatises on a wide variety of medical subjects and animal experiments. Including correspondence with family members and colleagues, he left almost 12,000 handwritten pages. These were bought in 1774 by the University of Leiden for its library and still reside there (Eichenberger, 1969). Wepfer is especially well known by neurologists on account of his books on apoplexy. The first appeared in 1658, when he was 38 years of age (Wepfer, 1658), and the second, with new observations and further views, appeared almost 20 years later (Wepfer, 1675). The only other book he published, apart from a disputation and dissertation as part of his studies, was on the use and abuse of hemlock (Wepfer, 1679). Posthumously, a publisher in Amsterdam republished the two books on apoplexy with additions by other physicians (Wepfer, 1724); several further compilations followed, some with many new case histories (Wepfer, 1727). In his views on the pathophysiology of apoplexy, Wepfer made some advances in the “right” direction, that is, in agreement with twenty-first-century views. On the other hand, he was still a child of his time, deeply rooted in ancient models of body function (Karenberg, 1998). Indeed, he provided an accurate description — in words — of intracerebral hemorrhages (at least in three of his four postmortem studies in 1658) and of the arterial circle at the base of the brain eight years before Willis. On the other hand, his definition of apoplexy was still based on symptoms: sudden cessation of motion and sensation, while respiration was preserved, though labored, and the pulse continued to beat. Because of these broad criteria, several of his case histories would no longer be classified as cerebrovascular disease today. And indeed, he fully supported Harvey’s theory about the circulation of the blood (Harvey, 1628), which was still highly controversial at the time, but, on the other hand, he still accepted Galen’s theory of different forms of pneuma (spiritus in Latin translation). These were thought to be an invisible source of energy carried along with the blood and to be synthesized in the liver (natural spirits); they were then “upgraded,” at first in the heart, with air (to vital spirits), then in the brain, to their highest form (animal spirits). Finally — to conclude this brief and unavoidably incomplete summary of Wepfer’s views on “apoplexy” — he argued that the synthesis of “nervous energy” (animal spirits in his terms) took place in the cerebral substance and not in the ventricular system as Galen had believed. As a consequence, Wepfer attributed apoplexy to extravasation of whole blood or of blood serum alone, leading to congestion and compression of the brain substance and so to blockage of the nerve pores (which were supposed to be hollow). In that theory, he built on the work of Charles le Pois (Carolus Piso, 1563–1633) (Piso, 1618; van Gijn, 2010). It is the recurrent form of the “serous” variety of “apoplexy” that Wepfer wished to illustrate with the following case history (Wepfer, 1658).
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The Case History An outstanding example, better than many others, of apoplexy by serum invading the deepest parts of the vulnerable brain and cerebellum was provided by a certain Nobleman, from a leading family in our community. Having a very obese physique, with a dark red face, black hair and hands almost cold to the touch, he took hardly any exercise except a gentle walk. His main occupation consisted in unravelling Latin and German history. In the way of food he was utterly modest. For the last few years he had avoided banquets, because he felt that even a small quantity of wine would harm and inebriate him. In his youth he had occasionally been struck by epileptic seizures, from which he was completely relieved by the utmost diligence of the late Mr. Alexander Harder, at the time a highly esteemed physician in our town, so that for the rest of his life he experienced nothing more of this kind. At about 45 years of age he began to notice prodromal symptoms of apoplexy, which he carefully kept a secret from his excellent wife. Yet he did not spurn counter-measures, terrified as he was by the examples of his mother and sister. His mother had a series of apoplectic attacks initially and then suddenly died from a severe apoplexy. His unmarried sister of about 20 years also died suddenly. Three years before the fatal day he was seized by dizziness on a few occasions, mostly provoked by outbursts of temper, but these rapidly disappeared through appropriate measures. On one occasion, having risen from his bed because of some disturbance of mind he could not himself explain, he could not get back to bed, though it was illuminated by moonlight. More than once, because of humid weather, a troubled mind or bad food, he felt a certain weakness in his feet and could not get over the threshold of the heating system under the floor with his usual ease but got stuck against his will. He therefore often predicted that his mother’s fate was threatening him. On the 13th of August 1651, aged 49, he was suddenly seized by an unusual urge to sleep, an hour before lunch time. I was called upon and found him in deep sleep; with great difficulty he could be aroused from his stupor; he uttered nonsense, felt warm all over his body, his pulse was rapid, large and soft and his breathing frequent. The urine was too yellow in colour, and micturition made him instantly restless; often he moved a hand to the back of his head and his temples, as if he had much pain in that area. I already mentioned that he was lethargic. After removal of stools from his bowels by means of an enema I immediately performed venesection and applied oxyrrhodinum, with dissolvents added. His deep stupor remained. On August 14th I recommended a more powerful enema, small cuppings with scarification and poultices, yet the urge to sleep persisted. On August 15th I applied a rather powerful dehydrating purgative, thanks to which he had several evacuations and subsequently he could be aroused with less difficulty from his sleep; but once awake he could not recognise anybody. On August 16th I continued with emetics and I added topical dissolvents. During the whole period of four days he did not ask for food or drink, yet he did not spit out what was offered. He passed urine and stools at the same time. On August 17th I administered a stronger purgative, by which his bowels were more completely relieved. Subsequently his abnormal stupor was completely overcome and he began to speak and act with proper reason, completely ignorant of what had happened to him in the previous few days and of the way his illness had come about. On August 19th, the seventh day of his illness, he seemed completely recovered in his own eyes and in those of his household. Yet I noticed a certain weakness of memory and judgement, but in the course of time this problem was addressed by drugs for evacuation of serum, general as well as specific ones, so that one could not observe even the slightest inaccuracy. Thus restored to health, he laudably resumed his usual tasks. He had a habit of going out for a few hours before dinner, barely covering his head, taking a walk with neighbours
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in his street and talking about a variety of things; he observed this custom also during a wet period in November of this same year, often until dark. On November 27th he had a large portion of pork at dinner. On November 28th he went to the Court of Justice, of which he was a councillor, to judge someone’s case; after he had performed this duty for some time he felt that something untoward came over him, hastened home, took to his bed and immediately fell asleep. Soon afterwards I am called and I find him overwhelmed by deep sleep; I attempt everything to wake him up. While the enema is prepared, he develops paralysis of the entire right side and loses every motion and sensation; as a result he did not even feel painful pinching on that side. The urine was blood-stained and copious; the pulse clearly not febrile. With great force he could barely be aroused from his stupor. With a variety of measures I took pains to drive the serum from the brain and to enhance the numbed animal functions. In the afternoon of the next day his entire right side was shaken by a convulsive movement; after the jerking of the limbs had stopped, motion and sensation returned, but the stupor persisted for six days. During this entire period he forcefully turned away food and drink as well as any drug, so that during the first two days he did not accept a grain or drop of these; what was brought to him he rejected with abusive language. Around the seventh day his appetite returned. Therefore I surreptitiously added to his food drugs that evacuate and absorb serum and invigorate the head. On the ninth day the abnormal stupor abated and after this he was awake during the day, like healthy people. I then observed that his memory had been completely obliterated. Not only did he fail to recall what had happened before but also he could not accurately retain what he had heard, seen or done a moment ago, nor could he coherently render what he actually had retained, even concerning things that mattered to him. This poor state of his memory lasted a few weeks; he did not recognise his brothers or servants, let alone call them by their proper names. Though well versed in Latin, he had completely forgotten this language, so that he could not read a single word, despite good eyesight. In the course of time he started to recognise his wife and daughters, thanks to daily exercise or the multiple use of medicines. Without hesitation he recited the entire Lord’s Prayer, which he had also forgotten earlier; he sang some so-called melodies of psalms with the correct tune and clear voice, but he was completely lost with regard to the text. He could read some short Latin words, earlier than German, but was never able to read a longer word or a whole line, or to pronounce these. If I prompted him to read, he assured me that formerly this had been only too familiar to him, but that now, in whatever way the loss of reading had come about, he now knew nothing. Several times he wrote entire lines, even paragraphs, in Latin or German, in elegant handwriting but without meaning and afterwards he could not read this himself. With regard to servants, whenever he was in need of them, even if they were within his sight, he would call their attention with gestures or words, but not one of them could he address by name. At the beginning of his illness he had no interest at all in domestic affairs, but later he signified in various ways that he was concerned about them and repeatedly admonished his wife, with a stream of mostly inappropriate words, that the matter should be attended to. Frequently he started a monologue that promised a full command of memory and reason, but halfway through the discourse he got stuck and could not tie the story together because of defective imagination or confusion. In the end he often deplored his forgetfulness of these matters as well as in legal subjects and he anxiously expressed his hope to regain this in full at some time in the future. In other actions of any kind, no defect worth mentioning could be detected. No matter what treatments he underwent from me or others to restore his memory, everything was in vain.
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On March 18th 1652 he was seized by a heavy apoplexy and on March 22 he died, despite a great many therapeutic measures.
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Discussion Before taking a closer look at some unusual details in this case history, I propose to take a step back and to point out an important characteristic of Wepfer’s style of recording — that is, his accurate presentation of the patient’s symptoms, unadulterated by interpretation, translation into medical jargon, or both. Of course, readers may be distracted by Wepfer’s speculations about the “excess of serum” in the patient’s brain, as well as by the corresponding and unfamiliar therapeutic measures he applied. But apart from these digressions into pathophysiology and pharmacology, the patient himself and his deficits emerge almost as clearly as in a twenty-first-century report. A striking exception is the description of impaired consciousness, but it was not until 1974 that the medical community solved this thorny problem by adopting the Glasgow Coma Scale (Teasdale & Jennett, 1974). The aristocratic status of the patient may have contributed to the exactness of the description, but Wepfer is equally meticulous in the four case reports (with autopsy) in the initial section of the book; the only difference being that common citizens are identified by their full name. In Wepfer’s time, it was not at all common for physicians to observe and describe patients with “apoplexy” in such detail: Several contemporary and even later writers, up to the early-nineteenth century, mentioned little other than ‘sudden loss of sensation and motion, with difficult respiration,’ and an extensive description of the pulse. Word Blindness With Preservation of Handwriting, Together With Fluent Aphasia One of the striking features in Wepfer’s report is the complex of neuropsychological deficits the patient showed in the last phase of the second episode. After he had regained consciousness to the extent that he could again interact with his environment, though mostly with gestures, his speech was fluent but largely incoherent. Word finding was severely impaired, including the names of relatives and servants. Wepfer does not explicitly mention whether he could understand spoken language, but the inability to correct his own utterances suggests that verbal comprehension was severely defective and that it was mainly from the accompanying gestures of others that he gathered their intentions. With regard to written language, the patient was able to write — though incoherently, in keeping with the deficit of spoken language. Since the text mentions he could write in two different languages, it is probable that at least some words made sense, but apparently the sentences did not. Yet, surprisingly, he was unable to read his own handwriting. A similar combination of symptoms would be reported 15 years later by Johann Schmidt (1614–1680) from Danzig (Benton & Joynt, 1960). In Schmidt’s patient, Nicholas Cambier’s, 65 years of age, language comprehension recovered to the extent that he could write to dictation, but he still could not recognize what he had written. It was this very dissociation that led Schmidt to contribute the case history to the annual collection of “curious cases” published by the German “Academia Leopoldina” (Schmidt, 1673/1688). The language deficits imply that the lesion must have involved at least the area of the brain responsible for decoding verbal information, spoken as well written. The explanation of the additional “word blindness,” or “alexia without agraphia,” as it came to be called also, we owe to Jules Dejerine (1849–1917), some 240 years later (Dejerine, 1892). In this article, he distinguished two categories of word blindness (cécité verbale). In some patients, the inability to read coexisted with an inability to write and sometimes also with “word
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deafness” (surdité verbale), as in a patient whose case history and autopsy Dejerine had reported a year before (Dejerine, 1891). There had been other reports of patients with word blindness in whom handwriting was preserved, but the anatomical explanation was still unknown. Dejerine saw Mr. C, a 68-year-old retired and highly cultured merchant, after he had been referred by the ophthalmologist Landolt. The patient had suddenly become unable to read a single word, in print or in writing, and could not read letters or musical scores. Other than in Wepfer’s nobleman, his spoken and written language was perfectly normal, as was his comprehension of spoken language. Dejerine followed and tested him at length over a period of more than four years. Then a second episode also affected Mr. C’s speech and handwriting, and he died soon after. Dejerine obtained permission to perform a postmortem examination, with meticulous study of the brain. He found the right hemisphere completely intact. In the left hemisphere, the angular gyrus (pli courbe) showed only recent softening, whereas a more posterior and much older (ischemic) lesion involved the left visual cortex as well as part of the underlying white matter (see Fig. 2). Dejerine concluded that in the period between the first and second disease episode the angular gyrus, regarded by him as the area where visual symbols are decoded in terms of language (letters and words), had been disconnected from the visual cortex of both sides. This was obvious enough for the left side of the brain, where the occipital cortex as well as the optic radiation had been destroyed. Although the right occipital lobe was intact, in keeping with the preservation of the left visual field during the patient’s life, its connection with the left hemisphere, through the splenium (bourrelet) of the corpus callosum, was interrupted where it entered the infarcted tissue (see Fig. 2). Dejerine’s explanation is still valid today (Geschwind, 2007). Some argue that “letter blindness” might have been a more appropriate term for Mr. C’s condition, since, unlike some other patients with alexia (including Wepfer’s patient), he was unable to recognize letters or at least to name them (Hanley & Kay, 2003). Epilogue I am not a supporter of retrograde diagnostics in general, but at least the impairment of consciousness that was associated with each of the three major disease episodes in Wepfer’s patient suggests intracerebral hemorrhage. Furthermore, the neuropsychological defects are more compatible with a superficial location than with a lesion deep in the basal ganglia, where most “hypertensive” hemorrhages occur. Finally, the recurrences and the familial occurrence are reminiscent of some form of familial amyloid angiopathy (Revesz et al., 2003), but that may be already too speculative. Wepfer had no reason to be surprised about the dissociation between reading and writing in his patient, because the heyday of localization would not begin until some 200 years later (Pearce, 2009). His view on the pathogenesis of “apoplexy” was that lifestyle and climatic factors caused either whole blood or only serum to “boil over” into the arterial system of the brain. It would then pass through minute openings in the vessel walls, enter the equally invisible pathways in the hollow nerves of the white matter and so block the passage of “animal spirits” and abolish nervous activity. A theory based on invisible pores and channels may sound a little bizarre to twenty-first-century ears. Yet, a similar hypothesis was a key element in William Harvey’s theory on the circulation of blood, which was stoutly defended by Wepfer. It supposed the existence of equally invisible capillaries, which would form the transition between arteries and veins. That view was eventually vindicated by the studies using the microscope (Malpighi, 1685). The analogy helps to remind us that hindsight is often an obstacle in our understanding of the past.
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Figure 2. Dejerine’s schematic illustration of the ischaemic lesions in Mr. C. (Dejerine, 1892). Old lesion in the left occipital lobe, of the cortex and part of the underlying white matter. The left angular gyrus (Pc) showed signs of much more recent softening. The white bar (X) indicates the most “economical” lesion that might disconnect the angular gyrus not only from the left visual cortex but also from that in the right hemisphere, through a lesion of the splenium of the corpus callosum (CC) where it joins the left hemisphere.
Acknowledgement Dr. Ian R. Williams (Glackour, Loch Broom, Garve, Scotland) generously and graciously commented on earlier versions of this article.
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References Benton AL, Joynt RJ (1960): Early descriptions of aphasia. Archives of Neurology 3: 205–222. Dejerine J (1891): Sur un cas de cécité verbale avec agraphie, suivi d’autopsie. Comptes rendus hebdomadaires des séances et mémoires de la Société de Biologie 3: 197–201. Dejerine J (1892): Contributions à l’étude anatomo-pathologique et clinique de différentes variétés de cécité verbale. Comptes rendus hebdomadaires des séances et mémoires de la Société de Biologie 4: 61–90. Eichenberger P (1969): Johann Jakob Wepfer (1620–1695) als klinischer Praktiker. Basel/Stuttgart, Schwabe & Co. Gallo D (2001): L’età medioevale. In: Del Negro P, ed., L’Università di Padova - otto Secoli di Storia. Padova, Signum Padova, pp. 15–33. Geschwind N (2007): Disconnexion syndromes in animals and man — Part 1. Brain 88: 237–294. Hanley JR, Kay J (2003): Monsieur C: Dejerine’s case of alexia without agraphia. In: Code C, Wallesch C-W, Joanette Y, Roch Lecours A, eds., Classic Cases in Neuropsychology. Hove and New York, Psychology Press, Volume II, pp. 57–74. Harvey W (1628): Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus. Frankfurt, G. Fitzer. Karenberg A (1998): Johann Jakob Wepfers Buch über die Apoplexie (1658): Kritische Anmerkungen zu einem Klassiker der Neurologie. Nervenarzt 69: 93–98. Luzzatti C, Whitaker H (1995): Johannes Schenck and Johannes Jakob Wepfer: Clinical and anatomical observations in the prehistory of neurolinguistics and neuropsychology. Neurolinguistics 9: 157–163. Malpighi M (1685): Opera omnia, Figuris Elegantissimis in Aes Incisis Illustrata, Tomis duobus Comprehensa. Londini, apud Robertum Scott. Ongaro G (2001): Medicina. In: Del Negro P, ed., L’Università di Padova - otto Secoli di Storia. Padova, Signum Padova, pp. 153–193. Pearce JMS (2009): Broca’s aphasiacs. European Neurology 61: 183–189. Piso CCP (1618): Selectiorum Observationum et Consiliorum de Praetervisis hactenus Morbis Affectibusque praeter Naturam ab Aquâ seu Serosâ Colluvie & Diluvie Ortis. Ponte ad Monticulum (Ponte-à-Mousson, Lorraine), apud Carolum Mercatorem. Revesz T, Ghiso J, Lashley T, Plant G, Rostagno A, Frangione B, Holton JL (2003): Cerebral amyloid angiopathies: A pathologic, biochemical, and genetic view. Journal of Neuropathology and Experimental Neurology 62: 885–898. Schmidt J (1673/1688): De oblivione lectione ex Apoplexia salva scriptione. In: Miscellanea Curiosa Medicophysica Academicae Naturae Curiosorum sive Ephemeridum Medico-Physicarum Germanicarum Annus Quartus et Quintus, Anni MDCLXXIII & MDCLXXXIV. Francoforti et Lipsiae, pp. 186–188. Teasdale G, Jennett B (1974): Assessment of coma and impaired consciousness — A practical scale. Lancet ii: 81–84. van Gijn J (2010): Facts versus theories: An everlasting struggle. Cerebrovascular Diseases 30: 330–339. Wepfer JJ (1658): Observationes Anatomicae, ex Cadaveribus eorum, quos Sustulit Apoplexia, cum Exercitatione de ejus Loco Affecto. Schaffhausen, J. C. Suteri [also included in the 1675 edition, pp. 264–269]. Wepfer JJ (1675): Observationes Anatomicae, ex Cadaverum eorum, quos Sustulit Apoplexia. Cum Exercitatione de eius Loco Affecto. Schaffhausen, Onophrius, Novae ed. Wepfer JJ (1679): Cicutae Aquaticae Historia et Noxae. Basileae, J. R. Konig. Wepfer JJ (1724): Historiae Apoplecticorum, Observationibus & Scholiis Anatomicis & Medicis Complurimis Elaboratae & Illustratae. Amstelaedami, Janssonio-Waesbergios. Wepfer JJ (1727): Observationes Medico-practicae de Affectibus Capitis Internis & Externis. Schaffhausen, J. A. Ziegler.
ISSN: 0964-704X (Print) 1744-5213 (Online) Journal homepage: http://www.tandfonline.com/loi/njhn20
A Patient With Word Blindness in the Seventeenth Century Jan van Gijn To cite this article: Jan van Gijn (2015) A Patient With Word Blindness in the Seventeenth Century, Journal of the History of the Neurosciences, 24:4, 352-360, DOI: 10.1080/0964704X.2014.1001697 To link to this article: http://dx.doi.org/10.1080/0964704X.2014.1001697
Published online: 16 Mar 2015.
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Date: 12 November 2015, At: 02:00
Journal of the History of the Neurosciences, 24:352–360, 2015 Copyright © Taylor & Francis Group, LLC ISSN: 0964-704X print / 1744-5213 online DOI: 10.1080/0964704X.2014.1001697
A Patient With Word Blindness in the Seventeenth Century JAN VAN GIJN
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Utrecht University, Utrecht, The Netherlands Johann Jakob Wepfer (1620–1695), city physician in Schaffhausen, Switzerland, published two books on “apoplexy.” He proposed new ideas about the events in the brain during such attacks, based on Harvey’s theory of the circulation of the blood. Wepfer postulated extravasation of whole blood or serum in the brain, in opposition to the Galenic notion of blocked ventricles. His case histories are remarkably precise and untainted by interpretation. This allows the recognition of a patient with word blindness, who was also unable to read words written by himself. Unlike patients with pure “alexia without agraphia,” he could not write complete sentences because of additional language defects, especially speech comprehension. Jules Dejerine (1849–1917) would, in 1892, not only describe a patient with the pure form of this syndrome (cécité verbale avec intégrité de l’écriture spontanée et sous dictée) but also provide an explanation of its anatomical basis. Keywords alexia without agraphia, word blindness, apoplexy, Johann Jakob Wepfer, Jules Dejerine
Introduction While in the process of translating Johann Jakob Wepfer’s first book on apoplexy (Wepfer, 1658), I came across a case report that was remarkable for reasons other than the point Wepfer was making in that section. What struck me was that he had recorded the clinical features, and especially the cognitive defects, in sufficient detail to allow us to reach several conclusions that would not have been possible in his day, even though no postmortem had been performed. The report was not included in an earlier account of patients with language disorders in Wepfer’s work (Luzzatti & Whitaker, 1995) because the collection of observations on which this publication was based (Wepfer, 1727) contained only material that had not been published during Wepfer’s lifetime.
The Author and His Work Johann Jakob Wepfer (see Fig. 1) was born in 1620, in Schaffhausen, Switzerland, as the eldest child of the judge Georg Michael Wepfer; his mother’s maiden name was Stokar (Eichenberger, 1969). In his native town, he received a sound education, including an excellent command of Latin; he then went on to study medicine in Strasbourg and Basle, where he graduated in 1644. Wepfer spent the next three years in Italy. For two years, he studied in Padua, where his tutors included the German Johannes Wesling (1598–1649) and Address correspondence to Jan van Gijn, Maliesingel 4, 3581 BA Utrecht, The Netherlands. E-mail: [email protected]
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Figure 1. Johann Jakob Wepfer (1620–1695).
the Dane Thomas Bartholinus (1616–1680). The University of Padua was internationally orientated and liberal, owing to the patronage of Venice, then a powerful republic in contact with many other cultures overseas (Gallo, 2001). Wepfer followed in the footsteps of two giants in the history of medicine: Andreas Vesalius (1514–1564) had taught anatomy there, and William Harvey (1578–1657) had come to Padua to graduate a few decades before in 1602 (Ongaro, 2001).
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On his return, Wepfer obtained his doctorate at the University of Basle in 1647 with a thesis on palpitations of the heart (Eichenberger, 1969). Soon afterwards, he was appointed physician to the city of Schaffhausen. This office, probably shared with one or two others, involved providing care for the citizens, at home or in the local hospital, as well as for the inhabitants of the convents in a larger area. Other tasks included advising the court of justice on medical matters, examining candidate surgeons, overseeing pharmacists and, importantly, performing autopsies. In 1650, he married Barbara Rink; they had eight children, of whom five survived to adulthood. As Wepfer’s reputation increased, he was consulted by the aristocracy of independent counties in southwestern Germany. During his long life (in 1695, aged 75), Wepfer accurately and succinctly recorded his case histories, but he also wrote systematic treatises on a wide variety of medical subjects and animal experiments. Including correspondence with family members and colleagues, he left almost 12,000 handwritten pages. These were bought in 1774 by the University of Leiden for its library and still reside there (Eichenberger, 1969). Wepfer is especially well known by neurologists on account of his books on apoplexy. The first appeared in 1658, when he was 38 years of age (Wepfer, 1658), and the second, with new observations and further views, appeared almost 20 years later (Wepfer, 1675). The only other book he published, apart from a disputation and dissertation as part of his studies, was on the use and abuse of hemlock (Wepfer, 1679). Posthumously, a publisher in Amsterdam republished the two books on apoplexy with additions by other physicians (Wepfer, 1724); several further compilations followed, some with many new case histories (Wepfer, 1727). In his views on the pathophysiology of apoplexy, Wepfer made some advances in the “right” direction, that is, in agreement with twenty-first-century views. On the other hand, he was still a child of his time, deeply rooted in ancient models of body function (Karenberg, 1998). Indeed, he provided an accurate description — in words — of intracerebral hemorrhages (at least in three of his four postmortem studies in 1658) and of the arterial circle at the base of the brain eight years before Willis. On the other hand, his definition of apoplexy was still based on symptoms: sudden cessation of motion and sensation, while respiration was preserved, though labored, and the pulse continued to beat. Because of these broad criteria, several of his case histories would no longer be classified as cerebrovascular disease today. And indeed, he fully supported Harvey’s theory about the circulation of the blood (Harvey, 1628), which was still highly controversial at the time, but, on the other hand, he still accepted Galen’s theory of different forms of pneuma (spiritus in Latin translation). These were thought to be an invisible source of energy carried along with the blood and to be synthesized in the liver (natural spirits); they were then “upgraded,” at first in the heart, with air (to vital spirits), then in the brain, to their highest form (animal spirits). Finally — to conclude this brief and unavoidably incomplete summary of Wepfer’s views on “apoplexy” — he argued that the synthesis of “nervous energy” (animal spirits in his terms) took place in the cerebral substance and not in the ventricular system as Galen had believed. As a consequence, Wepfer attributed apoplexy to extravasation of whole blood or of blood serum alone, leading to congestion and compression of the brain substance and so to blockage of the nerve pores (which were supposed to be hollow). In that theory, he built on the work of Charles le Pois (Carolus Piso, 1563–1633) (Piso, 1618; van Gijn, 2010). It is the recurrent form of the “serous” variety of “apoplexy” that Wepfer wished to illustrate with the following case history (Wepfer, 1658).
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The Case History An outstanding example, better than many others, of apoplexy by serum invading the deepest parts of the vulnerable brain and cerebellum was provided by a certain Nobleman, from a leading family in our community. Having a very obese physique, with a dark red face, black hair and hands almost cold to the touch, he took hardly any exercise except a gentle walk. His main occupation consisted in unravelling Latin and German history. In the way of food he was utterly modest. For the last few years he had avoided banquets, because he felt that even a small quantity of wine would harm and inebriate him. In his youth he had occasionally been struck by epileptic seizures, from which he was completely relieved by the utmost diligence of the late Mr. Alexander Harder, at the time a highly esteemed physician in our town, so that for the rest of his life he experienced nothing more of this kind. At about 45 years of age he began to notice prodromal symptoms of apoplexy, which he carefully kept a secret from his excellent wife. Yet he did not spurn counter-measures, terrified as he was by the examples of his mother and sister. His mother had a series of apoplectic attacks initially and then suddenly died from a severe apoplexy. His unmarried sister of about 20 years also died suddenly. Three years before the fatal day he was seized by dizziness on a few occasions, mostly provoked by outbursts of temper, but these rapidly disappeared through appropriate measures. On one occasion, having risen from his bed because of some disturbance of mind he could not himself explain, he could not get back to bed, though it was illuminated by moonlight. More than once, because of humid weather, a troubled mind or bad food, he felt a certain weakness in his feet and could not get over the threshold of the heating system under the floor with his usual ease but got stuck against his will. He therefore often predicted that his mother’s fate was threatening him. On the 13th of August 1651, aged 49, he was suddenly seized by an unusual urge to sleep, an hour before lunch time. I was called upon and found him in deep sleep; with great difficulty he could be aroused from his stupor; he uttered nonsense, felt warm all over his body, his pulse was rapid, large and soft and his breathing frequent. The urine was too yellow in colour, and micturition made him instantly restless; often he moved a hand to the back of his head and his temples, as if he had much pain in that area. I already mentioned that he was lethargic. After removal of stools from his bowels by means of an enema I immediately performed venesection and applied oxyrrhodinum, with dissolvents added. His deep stupor remained. On August 14th I recommended a more powerful enema, small cuppings with scarification and poultices, yet the urge to sleep persisted. On August 15th I applied a rather powerful dehydrating purgative, thanks to which he had several evacuations and subsequently he could be aroused with less difficulty from his sleep; but once awake he could not recognise anybody. On August 16th I continued with emetics and I added topical dissolvents. During the whole period of four days he did not ask for food or drink, yet he did not spit out what was offered. He passed urine and stools at the same time. On August 17th I administered a stronger purgative, by which his bowels were more completely relieved. Subsequently his abnormal stupor was completely overcome and he began to speak and act with proper reason, completely ignorant of what had happened to him in the previous few days and of the way his illness had come about. On August 19th, the seventh day of his illness, he seemed completely recovered in his own eyes and in those of his household. Yet I noticed a certain weakness of memory and judgement, but in the course of time this problem was addressed by drugs for evacuation of serum, general as well as specific ones, so that one could not observe even the slightest inaccuracy. Thus restored to health, he laudably resumed his usual tasks. He had a habit of going out for a few hours before dinner, barely covering his head, taking a walk with neighbours
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in his street and talking about a variety of things; he observed this custom also during a wet period in November of this same year, often until dark. On November 27th he had a large portion of pork at dinner. On November 28th he went to the Court of Justice, of which he was a councillor, to judge someone’s case; after he had performed this duty for some time he felt that something untoward came over him, hastened home, took to his bed and immediately fell asleep. Soon afterwards I am called and I find him overwhelmed by deep sleep; I attempt everything to wake him up. While the enema is prepared, he develops paralysis of the entire right side and loses every motion and sensation; as a result he did not even feel painful pinching on that side. The urine was blood-stained and copious; the pulse clearly not febrile. With great force he could barely be aroused from his stupor. With a variety of measures I took pains to drive the serum from the brain and to enhance the numbed animal functions. In the afternoon of the next day his entire right side was shaken by a convulsive movement; after the jerking of the limbs had stopped, motion and sensation returned, but the stupor persisted for six days. During this entire period he forcefully turned away food and drink as well as any drug, so that during the first two days he did not accept a grain or drop of these; what was brought to him he rejected with abusive language. Around the seventh day his appetite returned. Therefore I surreptitiously added to his food drugs that evacuate and absorb serum and invigorate the head. On the ninth day the abnormal stupor abated and after this he was awake during the day, like healthy people. I then observed that his memory had been completely obliterated. Not only did he fail to recall what had happened before but also he could not accurately retain what he had heard, seen or done a moment ago, nor could he coherently render what he actually had retained, even concerning things that mattered to him. This poor state of his memory lasted a few weeks; he did not recognise his brothers or servants, let alone call them by their proper names. Though well versed in Latin, he had completely forgotten this language, so that he could not read a single word, despite good eyesight. In the course of time he started to recognise his wife and daughters, thanks to daily exercise or the multiple use of medicines. Without hesitation he recited the entire Lord’s Prayer, which he had also forgotten earlier; he sang some so-called melodies of psalms with the correct tune and clear voice, but he was completely lost with regard to the text. He could read some short Latin words, earlier than German, but was never able to read a longer word or a whole line, or to pronounce these. If I prompted him to read, he assured me that formerly this had been only too familiar to him, but that now, in whatever way the loss of reading had come about, he now knew nothing. Several times he wrote entire lines, even paragraphs, in Latin or German, in elegant handwriting but without meaning and afterwards he could not read this himself. With regard to servants, whenever he was in need of them, even if they were within his sight, he would call their attention with gestures or words, but not one of them could he address by name. At the beginning of his illness he had no interest at all in domestic affairs, but later he signified in various ways that he was concerned about them and repeatedly admonished his wife, with a stream of mostly inappropriate words, that the matter should be attended to. Frequently he started a monologue that promised a full command of memory and reason, but halfway through the discourse he got stuck and could not tie the story together because of defective imagination or confusion. In the end he often deplored his forgetfulness of these matters as well as in legal subjects and he anxiously expressed his hope to regain this in full at some time in the future. In other actions of any kind, no defect worth mentioning could be detected. No matter what treatments he underwent from me or others to restore his memory, everything was in vain.
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On March 18th 1652 he was seized by a heavy apoplexy and on March 22 he died, despite a great many therapeutic measures.
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Discussion Before taking a closer look at some unusual details in this case history, I propose to take a step back and to point out an important characteristic of Wepfer’s style of recording — that is, his accurate presentation of the patient’s symptoms, unadulterated by interpretation, translation into medical jargon, or both. Of course, readers may be distracted by Wepfer’s speculations about the “excess of serum” in the patient’s brain, as well as by the corresponding and unfamiliar therapeutic measures he applied. But apart from these digressions into pathophysiology and pharmacology, the patient himself and his deficits emerge almost as clearly as in a twenty-first-century report. A striking exception is the description of impaired consciousness, but it was not until 1974 that the medical community solved this thorny problem by adopting the Glasgow Coma Scale (Teasdale & Jennett, 1974). The aristocratic status of the patient may have contributed to the exactness of the description, but Wepfer is equally meticulous in the four case reports (with autopsy) in the initial section of the book; the only difference being that common citizens are identified by their full name. In Wepfer’s time, it was not at all common for physicians to observe and describe patients with “apoplexy” in such detail: Several contemporary and even later writers, up to the early-nineteenth century, mentioned little other than ‘sudden loss of sensation and motion, with difficult respiration,’ and an extensive description of the pulse. Word Blindness With Preservation of Handwriting, Together With Fluent Aphasia One of the striking features in Wepfer’s report is the complex of neuropsychological deficits the patient showed in the last phase of the second episode. After he had regained consciousness to the extent that he could again interact with his environment, though mostly with gestures, his speech was fluent but largely incoherent. Word finding was severely impaired, including the names of relatives and servants. Wepfer does not explicitly mention whether he could understand spoken language, but the inability to correct his own utterances suggests that verbal comprehension was severely defective and that it was mainly from the accompanying gestures of others that he gathered their intentions. With regard to written language, the patient was able to write — though incoherently, in keeping with the deficit of spoken language. Since the text mentions he could write in two different languages, it is probable that at least some words made sense, but apparently the sentences did not. Yet, surprisingly, he was unable to read his own handwriting. A similar combination of symptoms would be reported 15 years later by Johann Schmidt (1614–1680) from Danzig (Benton & Joynt, 1960). In Schmidt’s patient, Nicholas Cambier’s, 65 years of age, language comprehension recovered to the extent that he could write to dictation, but he still could not recognize what he had written. It was this very dissociation that led Schmidt to contribute the case history to the annual collection of “curious cases” published by the German “Academia Leopoldina” (Schmidt, 1673/1688). The language deficits imply that the lesion must have involved at least the area of the brain responsible for decoding verbal information, spoken as well written. The explanation of the additional “word blindness,” or “alexia without agraphia,” as it came to be called also, we owe to Jules Dejerine (1849–1917), some 240 years later (Dejerine, 1892). In this article, he distinguished two categories of word blindness (cécité verbale). In some patients, the inability to read coexisted with an inability to write and sometimes also with “word
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deafness” (surdité verbale), as in a patient whose case history and autopsy Dejerine had reported a year before (Dejerine, 1891). There had been other reports of patients with word blindness in whom handwriting was preserved, but the anatomical explanation was still unknown. Dejerine saw Mr. C, a 68-year-old retired and highly cultured merchant, after he had been referred by the ophthalmologist Landolt. The patient had suddenly become unable to read a single word, in print or in writing, and could not read letters or musical scores. Other than in Wepfer’s nobleman, his spoken and written language was perfectly normal, as was his comprehension of spoken language. Dejerine followed and tested him at length over a period of more than four years. Then a second episode also affected Mr. C’s speech and handwriting, and he died soon after. Dejerine obtained permission to perform a postmortem examination, with meticulous study of the brain. He found the right hemisphere completely intact. In the left hemisphere, the angular gyrus (pli courbe) showed only recent softening, whereas a more posterior and much older (ischemic) lesion involved the left visual cortex as well as part of the underlying white matter (see Fig. 2). Dejerine concluded that in the period between the first and second disease episode the angular gyrus, regarded by him as the area where visual symbols are decoded in terms of language (letters and words), had been disconnected from the visual cortex of both sides. This was obvious enough for the left side of the brain, where the occipital cortex as well as the optic radiation had been destroyed. Although the right occipital lobe was intact, in keeping with the preservation of the left visual field during the patient’s life, its connection with the left hemisphere, through the splenium (bourrelet) of the corpus callosum, was interrupted where it entered the infarcted tissue (see Fig. 2). Dejerine’s explanation is still valid today (Geschwind, 2007). Some argue that “letter blindness” might have been a more appropriate term for Mr. C’s condition, since, unlike some other patients with alexia (including Wepfer’s patient), he was unable to recognize letters or at least to name them (Hanley & Kay, 2003). Epilogue I am not a supporter of retrograde diagnostics in general, but at least the impairment of consciousness that was associated with each of the three major disease episodes in Wepfer’s patient suggests intracerebral hemorrhage. Furthermore, the neuropsychological defects are more compatible with a superficial location than with a lesion deep in the basal ganglia, where most “hypertensive” hemorrhages occur. Finally, the recurrences and the familial occurrence are reminiscent of some form of familial amyloid angiopathy (Revesz et al., 2003), but that may be already too speculative. Wepfer had no reason to be surprised about the dissociation between reading and writing in his patient, because the heyday of localization would not begin until some 200 years later (Pearce, 2009). His view on the pathogenesis of “apoplexy” was that lifestyle and climatic factors caused either whole blood or only serum to “boil over” into the arterial system of the brain. It would then pass through minute openings in the vessel walls, enter the equally invisible pathways in the hollow nerves of the white matter and so block the passage of “animal spirits” and abolish nervous activity. A theory based on invisible pores and channels may sound a little bizarre to twenty-first-century ears. Yet, a similar hypothesis was a key element in William Harvey’s theory on the circulation of blood, which was stoutly defended by Wepfer. It supposed the existence of equally invisible capillaries, which would form the transition between arteries and veins. That view was eventually vindicated by the studies using the microscope (Malpighi, 1685). The analogy helps to remind us that hindsight is often an obstacle in our understanding of the past.
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Figure 2. Dejerine’s schematic illustration of the ischaemic lesions in Mr. C. (Dejerine, 1892). Old lesion in the left occipital lobe, of the cortex and part of the underlying white matter. The left angular gyrus (Pc) showed signs of much more recent softening. The white bar (X) indicates the most “economical” lesion that might disconnect the angular gyrus not only from the left visual cortex but also from that in the right hemisphere, through a lesion of the splenium of the corpus callosum (CC) where it joins the left hemisphere.
Acknowledgement Dr. Ian R. Williams (Glackour, Loch Broom, Garve, Scotland) generously and graciously commented on earlier versions of this article.
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References Benton AL, Joynt RJ (1960): Early descriptions of aphasia. Archives of Neurology 3: 205–222. Dejerine J (1891): Sur un cas de cécité verbale avec agraphie, suivi d’autopsie. Comptes rendus hebdomadaires des séances et mémoires de la Société de Biologie 3: 197–201. Dejerine J (1892): Contributions à l’étude anatomo-pathologique et clinique de différentes variétés de cécité verbale. Comptes rendus hebdomadaires des séances et mémoires de la Société de Biologie 4: 61–90. Eichenberger P (1969): Johann Jakob Wepfer (1620–1695) als klinischer Praktiker. Basel/Stuttgart, Schwabe & Co. Gallo D (2001): L’età medioevale. In: Del Negro P, ed., L’Università di Padova - otto Secoli di Storia. Padova, Signum Padova, pp. 15–33. Geschwind N (2007): Disconnexion syndromes in animals and man — Part 1. Brain 88: 237–294. Hanley JR, Kay J (2003): Monsieur C: Dejerine’s case of alexia without agraphia. In: Code C, Wallesch C-W, Joanette Y, Roch Lecours A, eds., Classic Cases in Neuropsychology. Hove and New York, Psychology Press, Volume II, pp. 57–74. Harvey W (1628): Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus. Frankfurt, G. Fitzer. Karenberg A (1998): Johann Jakob Wepfers Buch über die Apoplexie (1658): Kritische Anmerkungen zu einem Klassiker der Neurologie. Nervenarzt 69: 93–98. Luzzatti C, Whitaker H (1995): Johannes Schenck and Johannes Jakob Wepfer: Clinical and anatomical observations in the prehistory of neurolinguistics and neuropsychology. Neurolinguistics 9: 157–163. Malpighi M (1685): Opera omnia, Figuris Elegantissimis in Aes Incisis Illustrata, Tomis duobus Comprehensa. Londini, apud Robertum Scott. Ongaro G (2001): Medicina. In: Del Negro P, ed., L’Università di Padova - otto Secoli di Storia. Padova, Signum Padova, pp. 153–193. Pearce JMS (2009): Broca’s aphasiacs. European Neurology 61: 183–189. Piso CCP (1618): Selectiorum Observationum et Consiliorum de Praetervisis hactenus Morbis Affectibusque praeter Naturam ab Aquâ seu Serosâ Colluvie & Diluvie Ortis. Ponte ad Monticulum (Ponte-à-Mousson, Lorraine), apud Carolum Mercatorem. Revesz T, Ghiso J, Lashley T, Plant G, Rostagno A, Frangione B, Holton JL (2003): Cerebral amyloid angiopathies: A pathologic, biochemical, and genetic view. Journal of Neuropathology and Experimental Neurology 62: 885–898. Schmidt J (1673/1688): De oblivione lectione ex Apoplexia salva scriptione. In: Miscellanea Curiosa Medicophysica Academicae Naturae Curiosorum sive Ephemeridum Medico-Physicarum Germanicarum Annus Quartus et Quintus, Anni MDCLXXIII & MDCLXXXIV. Francoforti et Lipsiae, pp. 186–188. Teasdale G, Jennett B (1974): Assessment of coma and impaired consciousness — A practical scale. Lancet ii: 81–84. van Gijn J (2010): Facts versus theories: An everlasting struggle. Cerebrovascular Diseases 30: 330–339. Wepfer JJ (1658): Observationes Anatomicae, ex Cadaveribus eorum, quos Sustulit Apoplexia, cum Exercitatione de ejus Loco Affecto. Schaffhausen, J. C. Suteri [also included in the 1675 edition, pp. 264–269]. Wepfer JJ (1675): Observationes Anatomicae, ex Cadaverum eorum, quos Sustulit Apoplexia. Cum Exercitatione de eius Loco Affecto. Schaffhausen, Onophrius, Novae ed. Wepfer JJ (1679): Cicutae Aquaticae Historia et Noxae. Basileae, J. R. Konig. Wepfer JJ (1724): Historiae Apoplecticorum, Observationibus & Scholiis Anatomicis & Medicis Complurimis Elaboratae & Illustratae. Amstelaedami, Janssonio-Waesbergios. Wepfer JJ (1727): Observationes Medico-practicae de Affectibus Capitis Internis & Externis. Schaffhausen, J. A. Ziegler.
