The Case of Louis Victor Leborgne (“Tan”)
Louis Victor Leborgne, born on July 21, 1809, was one of six children in a middle-class family. Leborgne suffered from epileptic attacks beginning about age 24, but he was able to work. He was employed as a formier, an individual who creates wooden molds for hat or shoe manufacture. He began having terrible headaches in his thirties and eventually became unable to work.
By this time, he had begun to lose his expressive language ability, although whether the loss was sudden or gradual, is not known, His family declined to support him so the Prefect of Police arranged for Leborgne’s residence at Bicêtre Hospital in Paris in 1834. Ten years after his admission to Bicêtre, he gradually developed complete paralysis of his right arm followed by paralysis of his right leg.
On April 11, 1861, Louis Victor was transferred to the surgical ward of the hospital because he had developed gangrene of his right leg; the physician Pierre Paul Broca was called to see him.
Broca made note of the 50 years old patient’s history, including that he had been a long-term patient at Bicêtre and that he had been admitted because he had “lost the ability to speak.” On admission, it had been noted that Leborgne “differed from a sane man only in the loss of articulated speech.” According to Broca, Leborgne “understood almost everything that was said to him,” “but regardless of the question addressed to him, he always responded: ‘tan, tan.’” This verbal stereotype was “accompanied by a gesture of his left hand.” At the hospital, apparently the patient was commonly called Tan.
Leborgne was bedridden during the last 7 years of his life, finally succumbing to gangrenous bed sores. Broca reasoned from the evolution of Leborgne’s symptoms that “[the] probable diagnosis was therefore: original lesion in the left anterior lobe, propagated to the striate body of the same side.” Broca deduced that Leborgne’s expanding hemiparesis had been an extension of the original lesion that had produced his expressive language deficit. From what was known at the time about motor control, Broca reasoned that the seat of expressive language had to be in the left hemisphere.
Leborgne died 6 days after Broca first saw him in 1861. When Broca had the opportunity to examine Leborgne’s brain at autopsy, he observed “a loss of substance of the cerebral mass” in the left anterior frontal lobe to which he attributed the loss of expressive language. A “softening extended well beyond the limits of the cavity” and these, presumably newer lesions, extended to the parietal lobe, the “temporal-sphenoidal” lobe, the insula and extra ventricular nucleus of the striate body, the last of which caused paralysis of Leborgne’s right limbs.
One hundred and forty-six years after Broca’s report, an MRI of Leborgne’s preserved brain revealed that the left hemisphere lesion extended more medially than had been appreciated by Broca. The cause of Leborgne’s malady remains uncertain, although an inflammatory vascular etiology, possibly meningovascular syphilis, could explain the late progression of deficits in the same vascular territory as the initial deficits.
Importance of this case:
Broca’s presentation of Leborgne and, later that same year, another patient named Lelong, supported the concept of cerebral lateralization of language.
On April 4, 1861, just one week before Broca first examined Leborgne, he had attended a meeting of the Anthropological Society of Paris and had heard Bouillaud’s son-in-law, Ernest Auburtin, argue for the frontal localization of language. Auburtin described his examination of a Mr. Coulerier whose failed suicide-by-gunshot had exposed the left frontal region of the patient’s brain. When Auburtin compressed Mr. Coulerier’s left frontal lobe with a spatula, he observed a speech arrest; release of the spatula allowed the return of language.
When Broca presented Tan, he did not initially argue for the lateralization of language but rather for consideration of the cerebral convolutions in groups or functional regions. Broca’s main achievement was that he published a total of seven additional cases of aphasia after that of Leborgne, with careful autopsy correlation that ultimately provided evidence for the left inferior frontal gyrus as the seat of language.
Broca’s work opened the door to exploration of the complex neurological basis of language. However, while Broca’s aphasia is named for the expressive aphasia and associated left hemisphere lesion that Broca identified in Leborgne’s brain at autopsy, modern imaging has demonstrated that Leborgne’s left hemisphere had more extensive damage than is now known to be sufficient to produce “Broca’s” aphasia.
Excerpted from: “Six Landmark Case Reports Essential for Neuropsychiatric Literacy”
Authors: Sheldon Benjamin, M.D., Lindsey MacGillivray, M.D., Ph.D., Barbara Schildkrout, M.D., Alexis Cohen-Oram, M.D., Margo D. Lauterbach, M.D., Leonard L. Levin, M.S. L.I.S., M.A.