Abstract
It has been known for ages that some form of spontaneous recovery usually follows a disabling injury. In the past, this was generally attributed to ‘the healing power of nature’ (Hippocrates’ vis naturae medicatrix) or to supernatural forces [1]. Scientific inquires have revealed the nature of many of these recovery processes, and we have learned, to some extent at least, to understand and influence the course of injury and disease. In the case of a fractured bone, for example, physical and physiological processes have been elucidated quite accurately, and several treatments have been developed that facilitate healing of the fracture and recovery of a person’s functionality. But clearly, in many other cases, in particular when there is damage to the brain, restoration of function is often incomplete or insufficient, and we are failing to grasp all the relevant factors that are involved in the process [2, 3]. This chapter reviews neural plasticity from a clinical point of view and specifically focuses on the brain’s potential to reorganize the neural circuitry for language functions at the macroscopical level (i.e. in terms of brain areas and white matter pathways).
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Notes
- 1.
Quote taken from The brain that changes itself by Norman Doidge (2007) [29]
- 2.
Quotation taken from Aphasia and Kindred Disorders of Speech by Head (1926) [10]
- 3.
See for other pioneers Tesak and Code’s Milestones in the History of Aphasia [24].
- 4.
Konorski published similar ideas on synaptic plasticity to Donald Hebb, who is usually credited for his rules on learning and the concept of distributed memory [50]. Konorski’s research was suppressed for political reasons, and the impact of his work in the West was therefore probably less than it should have been. According to Markram (2011), his proposals were nevertheless appreciated at an early stage by well-known researchers such as Hebb, Adrian and Eccles [51]. ‘Some researchers prefer to speak of Hebb–Konorski plasticity (…), although the concept of Hebbian plasticity is clearly in wider use’ [51].
- 5.
- 6.
Possibilities and pitfalls of functional neuroimaging techniques are extensively discussed in Chap. 8. In short, there are two main issues that put limitations on the use of fMRI: (1) averaging individual results improves statistical power, but will decrease spatial resolution of the group results to 1–2 cm. (2) Functional imaging techniques cannot differentiate between critical and involved language areas. When an area shows up on a brain map, this does not necessarily mean that it is crucially important for language nor that it is even involved in language functions per se. Consequently, the presence of right hemisphere activation does not automatically imply that there is atypical or ‘abnormal’ language organization. This is simply demonstrated by the fact that fMRI maps of healthy subjects invariably show bilateral language-related activation, obviously challenging the clinical dogma that most people have a language-dominant left hemisphere [70, 71].
- 7.
- 8.
The explanation frequently given is that a lesion—via the transcallosal pathways—causes disinhibition of homologue areas in the other hemisphere. This assumes that under normal circumstances, the language-dominant left hemisphere inhibits right hemisphere homologue areas via the transcallosal pathways. Due to a lesion, this inhibition is lost, and there is a reactive increase in the activation of the contralesional homologue area. There is some experimental evidence for this phenomenon (see Fig. 9.4) [80].
- 9.
The abnormal blood vessels of AVMs may disturb the local haemodynamic response and reduce fMRI signals. There is some concern in the literature that this may significantly affect the clinical interpretation of fMRI maps, although studies are not conclusive at this point [88, 114]. In the series of Deng, these local disturbances may have falsely exaggerated right-sided lateralization (pseudo-dominance), but obviously cannot explain the increased fMRI activity in the contralesional hemisphere.
- 10.
Low-grade gliomas are typically present for more than a decade before they become clinically manifest and in the majority of cases debut with a seizure [115]. High-grade gliomas grow much faster, presumably in the order of months, and frequently cause neurological and cognitive deficits.
- 11.
The works of Goldberg, Luria and many others emphasized that there is more to functional recovery than changes in neural architecture and spatiotemporal reorganization of functions. Brain-damaged organisms also retrieve their goals ‘through the employment of novel tactics or unusual behaviors’ [1, 120]. Social support, motivation and a positive rehabilitation environment play an important role.
- 12.
Speech-language therapy is defined as a formal intervention that aims to improve language and communication abilities, activity and participation [125]. Studies have predominantly been conducted with stroke patients.
- 13.
- 14.
See the book of Schwartz and Begley, The Mind and the Brain (2002) [131].
- 15.
Fast ForWord is a commercially available program; see http://www.scilearnglobal.com/.
- 16.
- 17.
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Rutten, GJ. (2017). Recovery from Brain Damage. In: The Broca-Wernicke Doctrine. Springer, Cham. https://doi.org/10.1007/978-3-319-54633-9_9
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