Hans Förstl


G. Anton

Herderkrankungen des Gehirnes, welche vom Patienten selbst nicht wahrgenommen werden.

Wiener klinische Wochenschrift 1898;11:227-229.

On Focal Diseases of the Brain which are not Perceived by the Patient. 

(this paper is after a talk presented to the Society of Physicians of Styria on December 20, 1897 by Prof. Dr. G. Anton).

It is a well-known clinical fact that patients do not become aware of various brain diseases. In particular, generalized mental disturbance often prohibits insight into such diseases and the perception of illness. 

However, there are also focal brain disorders that cause remarkable symptoms, but are nevertheless not felt, not observed, and not noted by the patient. I must pronounce that there are also focal brain disorders that cannot be demonstrated by medical examination. They are called latent focal disease. In contrast to such diseases, the diseases mentioned above do not remain unnoticed by the physician or observer, but they remain latent or at least almost unobserved and are soon forgotten by the patient. The unilateral loss of proprioception (Muskel-Empfindungen), with or without paralysis, is one type of these disorders. Such patients pay little attention to the loss of sensation or of motor functions. They try to walk in spite of their paresis, and they fall, only to repeat the same attempt after a short time. Patients with such brain lesions often also show a unilateral blindness or deafness. In these cases it appears psychologically understandable that the side of the body from which no signal and no stimulus reaches the center, consequently becomes indifferent, and it is ignored by the patient himself. Mental combinations are simply not triggered by the affected side. These disturbances of perception (Gefühlsstörungen) show a great similarity to other forms that develop in the course of hysteria. In those cases, not only the perception (Empfindungen) related to one side of the body or to one extremity, but also the corresponding concepts (or ideas; Vorstellungen) are lost. I have presented a patient in an earlier talk3 in order to demonstrate that she was unaware of her total blindness, although her visual perception (optische Wahrnehmung) ofthe external world was completely abolished. In this patient, the defect did not cause any further thoughts or conclusions nor any concern or unhappiness. In a sense, the patient was mentally blind to her blindness (seelenblind für ihre Blindheit). At postmortem, the patient showed bilateral wedge-shaped areas of softening at the convexities of the occipital brain. These areas affected the central visual pathways. The region of the calcarine fissure, which is regarded as the visual center, was intact on both sides. But it was conceivable, that the strata of the central visual pathways were involved in a secondary degeneration. It can be demonstrated that the perception of disease (Krankheitswahrnehmungen) can be similarly deficient in central disturbances of the acoustic system. In the frequent diseases of the first left temporal gyrus it is striking that the individual does not understand spoken words and that he chooses the wrong words when speaking. The patient is not aware of his confused language. He is not capable of correcting his errors, and he lacks the right insight into how [he is impaired] and how severely he is impaired. We can observe patients with sensory aphasia who do not have any idea of the severe loss of their comprehension. They do not reason or draw any conclusions, and their affects are in no way involved. Many patients do not take any notice that they do not receive answers to their questions or addresses. They neither expect nor miss such acoustic replies or continuations of their thoughts. There are aphasias that are neither felt nor considered correctly by the patient. I would now like to discuss a patient who is unaware of his deafness.

A 64-year-old man suffered a severe head injury roughly 10 years ago. He has been a changed person ever since. He does not react to the loudest noises. His complete deafness was confirmed by an ear specialist. The outer appearance of the ear is completely normal. He suffers from vivid auditory hallucinations. He only hears his hallucinations, as is often reported in deaf people. But the patient is not aware of not hearing external auditory stimuli. He sees other people speaking, and it does not strike him that this is not connected to sound and noises. He does not pay any attention to questions, and he does not expect any answers himself. He reacts in quite a lively way to gestures. The patient can read primitive sentences. Confronted with the sentence "Mr. Fuchs is deaf," he protested in a lively manner and insisted that he could hear quite well. "He could hear comrade St. quite well," particularly in his right ear. He disregards all hearing tests completely, although he is otherwise fully oriented as to his personal situation and the situation of the external world. His expressive language is somehow primitive, but he chooses the right words for his thoughts and for his delusional ideas. He names objects correctly. The syntax of his spoken language, however, is deficient; in particular, he uses infinitives almost exclusively. Sometimes he reads and writes completely meaningless words. In this case, the normal findings at the external ear in conjunction with the complete deafness and his behavioral change lead to the assumption that the former head injury consisted of a bilateral temporal lesion. His lack of insight into this deficient function (Funktionsdefizit), and the fact that he draws no conclusions nor consequences, distinguish this patient from other deaf people. This case differs in another respect from the bilateral lesions of the temporal lobe that have been reported so far. In all the previously published cases, the lesion of the left temporal lobe is followed by the symptoms of word deafness and word confusion (Wortverwechslung) typical of sensory aphasia. One has to consider that such language disturbances do not represent a stationary condition, but that they may be followed by a remarkable improvement. The present brain lesion also dates back to more than 10 years. It is therefore legitimate to assume that this patient is an aphasic with a partial recovery. 

A second case of unperceived (unbewusster) deafness after a central cerebral lesion appears worth reporting, because the diagnosis was confirmed by a post-mortem (I am obliged to Direktor Böck in Troppau for this case and to the generosity of Direktor Dr. Sterz in Feldhof).

A 69-year-old farmhand, J.H., from the Styria, was admitted for psychiatric treatment because of severe confusion and excitation. Soon after her arrival it was established that she could not understand spoken words. She did not react by turning her head or answering loud shouting or strong noises near both her ears. Even bone conduction could not elicit any acoustic sensation. The patient watched these tests without understanding or interest. At the same time her spontaneous speech was, and remained, remarkably disturbed. She chose the wrong words to express her thoughts and she partly deformed words she had started to say correctly. The grammatically incorrect connection of words (Wortfügung) was also striking. Her reading ability was rather well preserved. She read letter by letter and then frequently found the correct word. She showed a tendency to use a word once found all over again. The patient recognized the persons around her and she soon behaved as was adequate to her situation. She usually named objects correctly and she found the right words for her touch and body sensations. Auditory tests were performed under a large variety of conditions. A reaction to acoustic stimuli could never be observed. She never complained about her deficits and she always remained completely indifferent to this defect. Even during conversations she never became aware that she did not hear and understand the questions. Her responses were nothing but a continuation of her present thoughts (Gedankengang). Affective language was relatively better preserved. The patient died of bronchitis. Briefly, the neuropathology yielded these results: In both hemispheres the first and partly the second temporal gyri were destroyed by a widespread softening, which continued to the most occipital part of these gyri and to the lower occipital gyrus. In certain areas the lower temporal lobulus was affected by this softening. Both these lesions were almost symmetrical on the left and on the right sides. Cuts through the whole brain, which were stained after Weigert and Pal with osmium and projected onto a wall with an electric microscope, gave a clear picture of the destruction. With very few exceptions, the pathways to the first and second temporal gyrus were almost completely interrupted. The central auditory pathways from the temporal lobe to the crura cerebri were almost completely degenerated. Even the pathways leading from this brain area to the optic thalamus could be recognized as pale degenerated zones. The fasciculus longitudinalis inferior, the large connecting system between the temporal and occipital lobes, was in some places diminished and affected by these areas of softening. Also the commissural fibers that line the temporal horns of the lateral ventricles were partly degenerated. The corpus geniculatum internum was atrophied on both sides. The focus in the lower temporal lobe destroyed different categories of pathways. I would like to emphasize one area of degeneration that extended into the body of the corpus callosum and made it appear brighter in its lower part.

(a) First, this softened area has interrupted the pathway that connects the temporallobe with the nucleus ofthe auditory nerve and it has thereby disconnected the cerebral cortex from the auditory organ.

(b) Moreover, the connection of both temporal lobes was naturally abolished.

(c) Finally, those fibers associating the temporal lobes with other parts of the cortex were largely destroyed.

Remnants of the association pathways left other parts of the temporal lobe connected to other neighboring brain areas.

 According to our present knowledge based on animal experiments and on clinical observation, the deafness of J.H., after a central brain lesion, is explained by these findings. It is also in agreement with our earlier finding of the patient becoming aphasic and showing an impairment of her generative language (innere Wortbildung). In this last case and in the first case we are particularly interested in the curious phenomenon that the patients did not become aware of their deafness, but that they remained completely indifferent and did not draw any conclusions or consequences from this defect. The corresponding thoughts were eliminated. In a way, everything relating to acoustics was extinct from their minds-not only the raw material of acoustic perception, but also the connected ideas (Vorstellungen) and mental combinations (seelische Combinationen). We have found this symptom together with different diseases of various sensory modalities (verschiedene Sinnescentren), this nonrecognition (or nonvaluing; Nichtbewertung) of the defect by the patient himself was observed in hysterical pareses and anesthesia, and in certain pareses with a loss of proprioception, but also in bilateral lesions of the occipital and temporal lobes. Such patients are, in the absence of a sufficient degree of dementia (Blödsinn), not aware of being paralyzed nor of being blind or deaf; they are mentally blind (seelenblind) for these defects. I abstain from any attempts to explain this phenomenon according to our present physiological knowledge. It is a fact that the subjective understanding of the mental state of such patients presents great difficulties. As the patient has lost the awareness and consciousness of this severe deficit of function, it would be justified, if physicians paid more attention to this challenging problem.

 COMMENTARY: Gabriel Anton's paper of 1898, presented in the Wiener Klinische Wochenschrift (Viennese Clinical Weekly) and translated here, provides a brief description oftwo patients who, although pronounced completely deaf seemed to be unaware of and in the latter case denied an impairment of hearing ability. Both cases were presented against a complex background of accompanying neuropsychological deficits. In addition to auditory hallucinations, the first patient was described as having numerous disturbances of language, including both sensory and expressive aphasia, dyslexia, and dysgraphia. The description of the second patient also includes symptoms of aphasia, dyslexia, and perseveration. Anton claims in the final paragraph that these occur "in the absence of a sufficient degree of dementia" (Anton's emphasis). Since these early observations, anosognosia and the eponymous syndrome have been described many times, although these descriptions rarely include "pure" cases with complete lack of awareness of an isolated deficit, for example, in the absence of significant generalized cognitive decline. Most frequently, the anosognosic phenomena described were accompanied by disorientation, confusion, andjor generalized intellectual impairment. In 1908, Redlich and Bonvicini (1) published details of three patients with Anton's symptom (see Table 1). All three cases showed severe mental confusion, disorientation, and some evidence for intellectual deterioration. A fourth patient, described in a subsequent paper (2), was badly orientated in space and showed a "slight impairment of intelligence." Similarly, in 1945, Redlich and Dorsey (3) presented a further six patients with unawareness for cortical blindness (see Table 1). All six patients showed a moderate degree of intellectual deterioration, were sometimes disoriented, tended to confabulate, and in three cases, there was significant memory loss. AIthough the authors emphasize that intellectual deterioration alone does not satisfactorily account for the anosognosia for blindness, in more recent publications, anosognosia for blindness has almost always been described in the presence of such impairments of intellect (5-7). A slightly different case reported with "imperception of peripheral blindness" by Stengel and Steele (4) showed impairments in the recollection of memories, aIthough there was no gross deficit in intellectual function (see Table 1). In this particular patient, the symptoms of unawareness may not have been specific to his almost complete blindness, since, when questioned, the patient also trivialized an ulcerated limb. Many cases of "lack of awareness for a deficit" have appeared in the literature in the years since Anton's original observations (for an extensive review, see ref. 8), although in almost every case, the patients have been presented with myriad clinical symptoms, including disorientation, confusion, and intellectual decline. The inclusion of such patients, who clearly do not fit Anton's, and later Albrecht's (9), original definition of the syndrome, has had two main consequences:

(a) no consensus has yet been reached concerning the key neuropsychological mechanisms underlying anosognosic phenomena, although motivational factors, with particular reference to coping mechanisms (10), self-monitoring deficits (11), and deranged body schemes (12) have all been implicated; and

(b) no consistent correlation has been found between the neuropsychological symptoms characteristic of anosognosic phenomena and any neuropathological findings. We have argued that, according to Anton's original description, for anosognosic deficits to unquestionably represent a pure "lack of awareness" they should occur without generalized intellectual impairment. We would also like to suggest, then, that we readopt these criteria such that patients described with "lack of awareness" are also unquestionably shown to be "in the absence of a sufficient degree of dementia." This will clearly identify those cases of "pure" lack of awareness from those in which lack of awareness forms only part of a far less specific clinical picture. This would, for example, limit the symptom to those cases in whom unawareness occurred in the absence of confusional states and would certainly exclude cases where unawareness accompanied generalized neuropsychological deterioration, that is, in cases of severe Alzheimer's disease. In short, clarification of this issue requires a more precise and consistent delineation of Anton's symptom.

(translated by Hans Förstl, Adrian Owen and Anthony David and published with comments in “Neuropsychiatry, Neuropsychology and Behavioral Neurology” 1993:)


1. Redlich E, Bonvicini G. Über das Fehlen der Wahrnehmung der eigenen Blindheit bei Hirnkrankheiten. Jahrb Psychiatr 1908;29:1-134.

2. Redlich E, Bonvicini G. Weitere klinisiche und anatomische Mitteilungen Ÿber das Fehlen der Wahrnehmung der eigenen Blindheit bei Hirnkrankheiten. Neurol Centralbl1911 ;30:227, 301.

3. Redlich FC, Dorsey JE Denial of blindness by patients with cerebral disease. Arch Neurol Psychiatry 1945;53:407-17.

4. Stengel E, Steele GDF. Unawareness ofphysical disability (anosognosia). I Ment Sei 1946;92:379-88. 
5. Sandifer P. Anosognosia and disorders of body schema. Brain 1946;69:122-37.

6. Bergmann CS. Cerebral blindness. Arch Neurol Psychiatry 1954;78:568-84.

7. Morley JB, Cox FN. Cortical blindness and anosognosia subsequent simultaneous agnosia and persistent gross recent memory defect. Proc Austral NeuroI1874;11:41-47.

8. Prigatano GP, Schacter DL, eds. Awareness of deficit after brain injury: clinical and theoretical issues. Oxford: Oxford U niversity Press, 1991.

9. Albrecht O. Drei Fälle mit Antons Symptom. Arch Psychiatry 1918;59:883-941.

10. Goldstein K. After-effects of brain injuries in war. Orlando, FL: Grune & Stratton, 1942.

11. Stuss DT, Benson DF. The frontal lobes. New York: Raven Press, 1986.

12. Roth M. Disorders of the body image caused by lesions of the right parietal lobe. Brain 1949;72:89-111.

Gabriel Anton (1858-1933) wrote extensively about frontal lobe disease, agenesis of the corpus callosum, and numerous other neuropsychiatric disorders. Anton described hepatolenticular degeneration 4 years before Wilson, but he has become best known for his reports on patients who were unaware of severe neurological impairment caused by focal brain disease. After a brief biographical note, we review the early history of"Anton's symptom," a term first used in 1918. The c1inical and neuropathological findings of Anton's cases published in 1893, 1896, 1898, and 1899 (3, 17-19,27) are summarized. His paper "On focal diseases ofthe brain which are not perceived by the patient" (1898) gives a concise presentation ofhis evidence and thought.

Biography: Gabriel Anton was born on July 28, 1858 in Saatz, Bohemia. He studied medicine at the German University in Prague, where he received his medical doctorate in 1882. After a short prologue in internal medicine, he began his psychiatric career in the government hospitals at Dobrzan and later in Prague. From 1887 he worked at Meynert's department of neuropsychiatry at the University of Vienna. Two years after his Habilitation in 1889, he became honorary professor and director of the neuropsychiatric hospital in Innsbruck. From 1894 until 1905 he held the chair of neuropsychiatry in Graz. After Wernicke's early death, Anton was awarded the chair of neuropsychiatry in Halle. He held this position unti11926. Anton died on January 3, 1933 in Halle (1, 2). Anton's papers and books cover a wide variety of neurological, psychiatric, and neuropsychological subjects, including "The Agenesis of the Corpus Callosum" (3), "The Anatomy, Physiology and Pathology of the Frontal Lobes" (4), "Dementia Choreoasthenica with Nodular Hyperplasia of the Liver" (probably the first description ofWilson's disease) (5, 6), and "The Treatment of Hydrocephalus, Tumours and Epilepsy with Transcallosal Puncture" ("Anton's Procedure") (7). Among his best known pupils or collaborators, who continued his research on "Anton's symptom," were M. Probst (8), H. Zingerle (9), and P. Schilder (10).
 The Early History of "Anton's Symptom". Findings relating to the eponymous symptom had been described before Anton. Several cases showing a lack of insight into or awareness of various neurological deficits had been published before Anton even started his academic career. Wernicke, Anton's predecessor in Halle, had already described aphasics who were unaware of their correct or incorrect usage of language (11). Westphal studied a patient with leftsided hemianopsia and right-sided hemiparesis, who had lost the proprioception his paretic extremities and the corresponding "concepts of movement" (Bewegungsvorstellungen) (12). As pointed out by Gerstmann (13), it was von Monakow (14) who had first reported the nonrealization of cortical blindness. Similar observations on patients with cortical blindness were soon published by Friedrich Müller (15) and by Dejerine and Vialet (16). 
In 1893 Anton published his observations on four patients with focal cerebral lesions and pareses who showed an impaired perception, mostly of their proprioceptive deficits (Table 1). He described his first case of cortical blindness in a Styrian nonspecialist journal (17) and again, together with two cases of cortical deafness, in 1899 (18). His first five patients (Table 1) developed a left sensorimotor paresis. Four of them showed an impaired perception of passive movements. All of these first patients had a uni- or bilateral hemianopsia, only one was unaware of her blindness. None of them had a global cognitive impairment severe enough to account for the lacking perception of their deficit. Postmortems were available in five of the seven cases. They showed widespread uni- or bilateral lesions, primarily of the subcortical white matter in the parietal, occipital or temporal lobes. Anton's brief presentation of two patients with cortical deafness from the Wiener Klinische Wochenschrift (Viennese Clinical Weekly) (19), which is translated below, presents his first concise attempt to develop a theory regarding the patients' striking lack of insight. Anton's observations were soon quoted (20). Studies on cortical blindness were carried further by numerous researchers, some of them Anton's former collaborators (8,21-24). The term "Anton's symptom" was first proposed by Albrecht (25). Albrecht's paper includes a list of other reports on "Anton's symptom" that had been published up to 1918. By that time, Babinski (26) had suggested the term "anosognosia" for a lack of insight into a neurological deficit. The usage of Babinski's "anosognosia" has frequently been limited to the unawareness of paresis, whereas the term "Anton's symptom" or "Anton's syndrome" has been reserved for unawareness of cortical blindness. Both authors, however, intended to describe a deficiency of awareness independent of the sensory modality. Anton himself did not keep or suggest a strict terminology for the phenomenon he had been working on, and it is not our intention to unravel the difficult terminology of "Anton's symptom," "Anton's syndrome," "anosognosia," "anosodiaphoria," "neglect," and "alien hand" as inadequate or lacking insight, unawareness, denial, nonrecognition, nonrealization, or ignorance of a neurological deficit. It may be the right of elderly neuropsychiatrists to insist on a terminology of their own. Anton had not reached that stage when he wrote his articles. Albrecht justified the eponym "Anton's symptom" as follows (25, p. 883): Anton understood the benefit of studying a specific psychopathological symptom in cases of organic brain disease which permit considerations about their pathogenesis: the lack their selfperception ("das Fehlen der Selbstwahrnehmung") of a deficit caused by afocal disease. This symptom had been recognized by other authors in single cases (v. Monakow, F. Müller, etc.), but his achievements are the intensive description of the psychology of this focal disease and the attempt to develop a fundamental pathogenetic theory based on neuropathological examination.