| Aphasia |
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Contents BioModResearch- Lang-Acqu- Cortical Ling. - AphasiaMembers- G. Kochend.- D. Veit- Kochend. - 1997 - 1998 - 1998(2) - 1999 - 2000- Veit - 2002CommentsLinks |
Current aphasiological research presents a mixture of phenomena, hypotheses, assumptions and speculations, all of which do hardly focus on causalities in the sense of biologically plausible explanations of the defect that ends in an aphasic phenomenon. Therefore the huge amount of assumptions concerning the therapy of these deficits are highly speculative and show little sensitivity concerning the biological properties of the apparatus that shall be "healed". The aim of this project is to explain the cause of aphasic phenomena by biologically precise models and to apply these insights to therapeutical concepts. This close binding of the linguistic phenomena to the neurobiological deficits shall make it possible to make detailed and realistic assumptions to both, eplanations of phenomena and therapy. The project is currently limited to post-ischemic deficits. However, a general exclusion of other causes of aphasic language deficits is not intended. |
Basic thesis |
| Die Grundthese ist, dass die beobachtbaren Stoerungen (...) nicht nur damit erklaert werden koennen, dass man entsprechende Gewebeteile als abgestorben, also funktionslos annimt, sondern auch damit, dass Nervenzellen nur in ihrer Funktion beeintraechtigt sind. (Veit 1999: Neuronale Simulationen aphasischer Sprachproduktion. In: Kleiber, Kochendoerfer, Riegel & Schecker (Hrsg.): Kognitive Linguistik und Neurowissenschaften. Tuebingen: Narr: S. 191 |
The basic idea is that single cells can be functionally impaired after hypoxia, e.g. Berg-Johnson, et al. (1995): Changes in amino acid release and membrane potential during cerebral hypoxia and glucose deprivation. In: Neurological Research 17: 201-208:
"As the neuron was depolarized during hypoxia, the input resistance was reduced and evoked activity was suppressed. Following 10 min hypoxia current injection reestablished the membrane potential and the input resistance of the neuron (dV/dl). The cell could then be activated, but a stronger stimulus (1.1 nA - Note: 0.6 nA bevore Hypoxia) was required to evoke an action potential with approximately the same latency as in control, indicating an elevated firing threshold. (Berg-Johnson, et al., 1995: 204)"
The aspect of the "elevated firing threshold" could be an interesting point concerning a biologically adequate modelling of aphasic phenomena with probably even therapeutical consequences.
Greener, Enderby & Whurr wrote about the benefit of language therapy of aphasic symptoms after stroke in: Speech and language therapy for aphasia following stroke (Cochrane Review):
"The main conclusion of this review is that speech and language therapy treatment for people with aphasia after a stroke has not been shown either to be clearly effective or clearly ineffective within a RCT. Decisions about the management of patients must therefore be based on other forms of evidence. Further research is required to find out if effectiveness of speech and language therapy for aphasic patients is effective. If researchers choose to do a trial, this must be large enough to have adequate statistical power, and be clearly reported." (http://www.update-software.com/abstracts/ab000425.htm)
Therefore we cannot claim any objective benefit of language therapy to aphasics (post-ischemic aphasia) except the social or psychotherapeutical one.
Another concept could then be based on the idea that some cells are not totally damaged (post-stroke) but only functionally impaired (see above and Berg-Johnson, et al., 1995). There might be a possibility to reactivate these functionally impaired cells. One of the most interesting aspects might then be based on pharmacological/medical treatments.
Since it is not possible to locally substitute medicals in the brain, concrete and valid hypotheses have to be proposed so that a medical treatment of aphasic patients shall be justified.
A first result of this project is that, despite the post-ischemic functional impairment of all cells in a specific area, a specific type of cells causes the breakdown of (language-) processing. The goal is then to determine the transmitter system that synapses to these cells belong to and to formulate concrete hypotheses on the effect a medical must take to reach a positive effect to the network and therefore to the patient without taking intolerable effects to different, "healthy" ares of the network.
At any questions or comments please contact: Dominic Veit
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[BioMod]
[Research]
[- Lang-Acqu]
[- Cortical Ling.]
[- Aphasia]
[Members]
[- G. Kochend.]
[- D. Veit]
[- Kochend.]
[ - 1997]
[ - 1998]
[ - 1998(2)]
[ - 1999]
[ - 2000]
[- Veit]
[ - 2002]
[Comments]
[Links]
| Aphasia |
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