Brain damage can impair and enhance functions of the brain in many ways

Brain damage can impair and enhance functions of the brain in many ways, but how does this effect behaviour? This study will include Paul Broca’s (1861) study of Victor Leborgne, referred to as “Tan” in literature. As well as the account of Milner’s (1966) study of patient Henry Gustav Molaison. Using the evidence collected and methods used at the time, I will compare and contrast the different effects and approaches to explore how the damaged brain has provided evidence for the relationship between brain and behaviour.
Our first study, the case of Victor Leborgne, a nineteenth century patient whose case helped to aproximate “Broca’s Area” (Broddmann areas 44 & 45) as key players in language production and processing.
From a young age Leborgne suffered fits of epileptic seizures, which he continued to battle against while living an otherwise normal life as a show craftsman. At the age of 30, Leborgne suffered a sudden loss of speech, replaced with the vocal production of just one syllable “Tan”, often muttered twice in a row. Leborgne was immediately hospitalized due to the nature of his symptoms. It remains unclear whether this sudden loss of speech had occurred as a result of one of his seizures or a progressive issue. At the time it could have been presumed that Leborgne was only suffering from a temporary loss of speech since he was admitted as a fully capable person/patient.
Sadly, this changed for Leborgne as ten years later, he began to show signs of paralysis on the right side of his body relating to damage to the left side brain, specifically his arm and leg on the right-side. Losing function keeping Leborgne bed ridden for six to seven years. Over these years those in close relation to him noticed a vast decline in general intelligence of Leborgne.
12th of April, 1861 Leborgne was transported for surgery at the Bicetre hospital to combat a gangrenous infection of his right side, starting at his elbow and extending down to his buttock, which was caused by the paralysis in his limbs and hypoxia due to paralysis.
This is the first time Broca (1861) would see Leborgne, Leborgne showed freedom of his left arm and leg as well as his face and his tongue despite the paralysis present on the right side. Leborgne died age 51 in 1861, The death of Leborgne allowed an autopsy of his brain by Broca, noting a lesion on his left temporal lobe, which had led to tissue softening in the left hemisphere and a large cavity capable of housing an egg, formed due to the breakdown of cerebral substance, resulting in the area to be filled with serous fluid. It is likely that the softened tissue around the brain accounted for Leborgne’s speech impediments in the years prior to his paralysis.
Now digging into Milner (1966) H.M. knocked down by a bicycle at age 7, although in some reports H.M’s age was listed as 9 (See Corkin, 1984; Journal of neuroscience 15/05/1997). By the age of 27 H.M had become incapacitated by his seizures, putting a stop to his normal life and work on an assembly line. H.M had already been prescribed a high dose of anticonvulsants to combat the seizures but to no avail.
H.M was later approached and offered an experimental procedure, later described in Scoville (1954). This consisted of a bilateral resection of H.Ms hippocampus approximately 8 – 9cm extending to the tips of the temporal lobes. After the operation H.M presented a severe case of anterograde amnesia which left him unable to retain new information and complete basic tasks. Past memories were still present to H.M, surprisingly though H.M remained unable to remember his age, often underestimating it.
Posing the question, was his underestimation of his age linked to the memories before his seizures and operation or was his perception of age changed as a result of a decrease in intelligence? The extent of the damage was shown through Milners (1966) account of meeting with H.M, describing him as someone who forgot daily events just as fast as they occurred, unable to even remember someone’s name after just being introduced to them. H.M was then continuously studied for five decades by Milner and Corkin until and after his death on December 2, 2008 aged 82.
Contrasting to Scoville’s initial report of H. M’s procedure, we have Corkin et al (1997)’s MRI of H.M. Which allowed for the discovery of the true extent of damage caused to H. M’s brain during Scoville’s procedure, as well as the early accident at the age of 7 and injuries caused by his seizures. Through the MRI and the technique of measuring fields of distortion Corkin et al established that H.M’s lesions originally described as 8 – 9cm, only extended 5cm to the temporal lobe. Corkin’s MRI examination also showed damage to the parahippocampus gyrus, previously thought to have only experienced the removal of the hippocampus during surgery mentioned earlier to combat seizures. We can tell from this that the damage to this region affected H.M’s memory impairment further than damage which would have been limited to the hippocampus region. The timing of this study was fortunate to have MRI technology as opposed to the previously discussed study, which was examined by autopsy allowing for human error and limited observation.
Looking at both cases you can see a severe decline in health over the course of their brain injuries as impaired verbal behaviour and as a result interaction, H.M. unable to intake new information changed from an intelligent young man into someone who was no longer able to behave like a normal human as his brain prohibited him from conducting and having normal interactions with objects and people, thus severely limiting his social capacities and basic task executions.
Leborgne on the other hand who was unable to speak more than one syllable helped identify Broca’s area as an important part of speech production. It is seen in patients who experience damage to Broca’s area have a hard time producing full sentences and often produce only staccato phrases, completely impairing their verbal behaviour as seen in Leborgne.
In conclusion, we can identify a clear link between physical damage in a specific area of the brain (Brodmann’s areas 44 & 45) and speech production & processing. Lesions to these areas severely limited the speech capacities of the patients which had further implications such as physical and social deficiencies in both our case studies (although not inherently linked to Broca’s area). As such we can safely establish a connection between physical brain damage and its impact on speech behaviour.

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