Resultados del Pretest para el grupo control

Injury in the brain, following a stroke or other forms o f damage, produces both primary and secondary changes (Keefe, 1995). The immediate changes that occur following the lesion can be classified as primary (directly related to the trauma area) and secondary (indirectly, as a consequence o f the primary changes). (Powell, 1981; Keefe, 1995). The primary changes evolve from the first hours up to a number o f days and then become static. The secondary changes continue to evolve over time and are set in motion as a consequence o f the primary damage (Keefe, 1995). Importantly, because these processes develop over a longer time scale than the primary changes associated with the lesion, the organisation and function o f the brain a few days after the injury will be different from that a few weeks after the injury. Secondary changes are the processes that determine and contribute to the behavioural recovery and the residual deficits observed, and not the site o f lesion as traditionally thought (Powell, 1981; Keefe, 1995).

According to Powell (1981), the primary changes are immediate necrosis, signs o f inflammation in the cell, retrograde cell degeneration proximal to the lesion, and anterograde cell degeneration distal to the lesion within a week o f the trauma. Keefe (1995) reports that the indirect changes are: transneuronal degeneration, in which areas receiving neural input from or providing input to the infarcted area degenerate due to the loss o f connections, denervation supersensitivity, in which neurons that have lost most o f their input from the infarcted area become increasingly sensitive to any residual input received from that area, development o f diaschisis, in which injury to a certain area will temporarily inhibit connected non injured areas remote from the infracted tissue but yet functionally connected to, vascular disruption, which will result in ischemia, and

collateral sprouting, in which axons from nearby neurons grow new synaptic contacts on sites vacated by the lesioned cells.

As described above, these secondary changes have a longer time scale and contribute to behavioural recovery, which takes place in the adult brain. These changes take place via different physiological mechanisms, which can be summarised as:

Regenerative sprouting (Powell, 1981): This regeneration concerns changes in the severed neurons. The impaired axon regenerates fibres from other branches o f the lesioned axon that are capable o f forming a functional network. They form working synapses proximal to the area o f destruction, which will pass on an impulse to another neuron.

concerns growth in other non-lesioned cells. These cells grow new synaptic connections that are connected to the synaptic connections, which are not functioning after the lesion. These new terminals o f connection may enable the affected site to function “normally” again by providing them with their lost input.

Relatively ineffective synapses (Powell, 1981): This concept concerns the possibility that what appears to be the formation o f new connections, may in fact be the ‘waking up ’ o f pre-existing eonnections that were originally ineffeetive for this function and overshadowed by the main connections o f the cell.

Denervation sensitivity (Powell, 1981; Keefe, 1995): The cell following the injury shows a lower response threshold to any remaining afferent fibres. Subsequently, the remaining fibres who use the same neurotransmitters as the lesioned fibres will cause a larger effect in the recipient cell, so that although the number o f afferents might be reduced they have the same innervating effect.

Long term potentiation (LTP) (Keefe, 1995; Leonard, 1998): LTP is the neural explanation for learning and memory. It is a rapidly indueed and sustained increase in the efficiency o f neural transmission at a given synapse between the stimulating axon and its post-synaptic cell. So, the synapse that is highly active, secondary to increased stimulation o f input, will exhibit LPT and thus enhanced activity. This neural mechanism can cause long-term changes in the transmission o f a synapse, and subsequently in the funetional systems related to this synapse.

The exaet role o f the above physiological mechanisms in the recovery o f function in clinical terms, still need further explanation, as the interaetion between them and their

link to specific behavioural changes are not yet understood. At an interactive level, some mechanisms may contradict others, for example the inhibitory character o f the diaschisis may not facilitate collateral sprouting. However, as these mechanisms have been observed in experimental situations, the challenge is to find the correlations between neuronal and behavioural changes, which is the most difficult task. Great insight into this challenge is provided from the use o f pharmacological agents to facilitate and enhance recovery o f function. Adequate cognitive function requires a relatively high level o f neurochemical capacity (Blomert, 1998). Functional (metabolic) “lesions” may represent depressed levels o f neurotransmitters and thus form the basis o f many processing limitations. Luria et al (1969) used a combination o f pharmacological and behavioural treatment for seemingly permanent disorders and showed significant behavioural improvement by boosting the level o f the neurotransmitter acetylcholine. Also recently, Huber et al (1997) showed beneficial effects o f the drug piracetam, when it was used in a chronic aphasie patient in combination with systematic language training. Walker- Batson et al (1996) have shown that the administration o f amphetamine accelerates recovery from aphasia. These findings suggest that pharmacological and/or stimulation treatment preceding training may sufficiently alter neurochemical activity levels to make improvements and enhance the recovery process.