German neuroanatomist, pathologist, and psychiatrist who made fundamental discoveries about brain function.
Carl Wernicke was an influential member of the nineteenth-century German school of neuropsychiatry, which viewed all mental illnesses as resulting from defects in brain physiology. A practicing clinical neuropsychiatrist, Wernicke also made major discoveries in brain anatomy and pathology. He believed that abnormalities could be localized to specific regions of the cerebral cortex and thus could be used to determine the functions of these regions. Wernicke was one of the first to conceive of brain function as dependent on neural pathways that connected different regions of the brain, with each region contributing a relatively simple sensory-motor activity. At the time, most scientists conceived of the brain as functioning as a single organ. Wernicke also helped demonstrate dominance by either the right or left hemispheres of the cerebrum.
Wernicke was born in 1848 in the German town of Tarnowitz in Upper Silesia, in what is now Tarnowskie Gory, Poland. He earned his medical degree at the University of Breslau in 1870 and stayed on to work with Heinrich Neumann. Wernicke also spent six months studying with Theodor Meynert in Vienna. He earned his psychiatry qualification in 1875 and moved to Berlin, where he spent three years at the Charité Hospital as assistant to Karl Westphal, before starting a private practice in Berlin. With his mentors, Meynert and Westphal, Wernicke continued the neuropsychiatric tradition begun by Wilhelm Griesinger.
Describes Wernicke's aphasia
In 1873, Wernicke studied a patient who had suffered a stroke. Although the man was able to speak and his hearing was unimpaired, he could barely understand what was said to him. Nor could he understand written words. After he died, Wernicke found a lesion in the rear parietal/temporal region of the patient's left brain hemisphere. Wernicke concluded that this region, which is close to the auditory region of the brain, was involved in speech comprehension. Wernicke named the syndrome sensory aphasia, although now it is usually called Wernicke's aphasia. The affected region of the brain is known as Wernicke's area. The syndrome is sometimes called fluent aphasia since the victim is capable of speech; however words may be misused and the speech may be disordered or even without content. For this reason, scientists now believe that Wernicke's area may be involved in semantic processing, and it is sometimes called the receptive language area.
Wernicke published The Aphasic Symptom Complex in 1874 when he was 26. In this work, he developed many of his ideas about brain localization, and he related different types of aphasia to specific damaged regions of the brain. In contrast to Wernicke's aphasia, motor aphasia involves damage to the part of the brain known as Broca's area. With this syndrome, a patient understands speech, but cannot speak himself. Wernicke postulated that Broca's area and Wernicke's area were connected, and he predicted that damage to this connection would cause conduction aphasia, a syndrome wherein a patient could both speak and understand language, but would misuse words and could not repeat words. Wernicke's prediction turned out to be correct. Two of Wernicke's early aphasia papers were published in English in 1994.
Describes Wernicke's encephalopathy
The three volumes of Wernicke's comprehensive work, Textbook of Brain Disorders, appeared between 1881 and 1883. In this work, based on careful case studies, Wernicke attempted to relate all known neurological diseases to specific regions of the brain. The volumes included many of Wernicke's original observations on brain anatomy, pathology, and clinical manifestations. Based on his observations, he predicted the symptoms that would result from blockage of the posterior inferior cerebellar artery. Again, his hypothesis was later confirmed. In the second volume, Wernicke described for the first time a syndrome resulting from the ingestion of sulfuric acid, which caused specific mental and motor abnormalities and paralysis of muscles in the eyes. He called this syndrome acute hemorrhagic superior polioencephalitis. It now is called Wernicke's encephalopathy and is known to be caused by a nutritional thiamine deficiency.
In 1885, Wernicke became an associate professor of neurology and psychiatry at the University of Breslau. Five years later, he was awarded the department chair. Wernicke's clinical studies were published as Grundriss der Psychiatrie in klinischen Vorlesungen in 1894, with a second edition in 1906, and as Krankenvorstellungen aus der psychiatrischen Klinik in Breslau, in the years 1899-1900. Between 1897 and 1903, Wernicke published the three-part Atlas des Gehirns on neuroanatomy and pathology. His last work on aphasia appeared in 1903 and was translated into English in 1908.
Wernicke moved to the University of Halle in 1904 as a full professor. The following year, he died in Dörrberg im Geratal, Germany, of injuries suffered in a bicycling accident. Wernicke's research laid the foundation for the Wernicke-Geschwind model of language, which predicted the neural pathways involved in simple language tasks, such as reading a word aloud.
Bynum, William F. "Wernicke, Carl." In Dictionary of Scientific Biography, edited by Charles Coulston Gillispie. Vol.14. New York: Charles Scribner's Sons, 1970.
Lanczik, M., and G. Keil. "Carl Wernicke's Localization Theory and its Significance for the Development of Scientific Psychiatry." History of Psychiatry 2 (1991): 171-180.
We report the results of a cognitive investigation of the language deficits of a single Wernicke's aphasic patient. The patient, R.D., showed poor speech comprehension but good reading comprehension. His spontaneous speech and his attempts at reading aloud contained many neologisms and some verbal paraphasias. Following Butterworth (1979) we interpret the neologisms as due to problems with retrieval of the phonological specifications of words from a speech output lexicon, and we present evidence showing that success in lexical retrieval was affected by word frequency and not by any syntactic distinction between content (open-class) and function (closed-class) words. R.D.'s spelling was better preserved than his spoken naming and he could spell many words he was unable to say correctly. His spelling errors appeared to be attempts at a target word based on retrieval of partial orthographic information (just as his neologisms seem to be based on partial retrieval of phonological information). We argue that normal subjects may make similar speech and writing errors under certain circumstances.
Garrett's (1982) model of speech production is presented and we discuss how neologistic jargonaphasia and other forms of Wernicke's aphasia may be explained in terms of it. We also argue that when R.D.'s deficits are analyzed and compared with those of other patients in the literature a number of implications emerge for theories of normal language processing. These include 1) that the comprehension and production of familiar written words do not involve obligatoruy phonological mediation, 2) that there are distinct phonological and orthographic lexicons, 3) that morphemes are seperately represented in the phonological lexicon, 4) that ease and speed of retrieval of items from the phonological lexicon is affected by frequency of usage, and 5) that retrieval from both lexicons is not all-or-nothing.