Temporal Lobe Epilepsy

Temporal lobe epilepsy is a syndrome that results from recurrent epileptic seizures that can be traced back to the temporal lobe. In general, epilepsy is a brain disorder in which clusters of nerve cells, or neurons, in the brain sometimes signal abnormally. Neurons normally generate electrochemical impulses that act on other neurons, glands, and muscles to produce human thoughts, feelings and actions (NINDS, 2006). In temporal lobe epilepsy the normal pattern of neuronal activity becomes disturbed, causing strange sensations, changes in behaviour or emotions, muscle spasms, or convulsions and even partial seizures which originate from medial or lateral temporal lobe. During a seizure, neurons may fire as many as 500 times a second, much faster than the normal rate of about 80 times a second (NINDS, 2006). Anything that disturbs the normal pattern of neuron activity can cause epilepsy and the most common pathologies or causes of Temporal Lobe Epilepsy are: mesial sclerosis, hippocampal sclerosis, tumours, malformations, neoplasms and inflammatory scars from infection (Armstong D, 1993). Although this debilitating syndrome has caused vast human suffering, it has also given us a glimpse into the functions in which these areas of the brain subserve.

Most damage, including lesions, ongoing epileptic activity and undesired treatment effects associated to Temporal Lobe Epilepsy (TLE) is localised to the medial temporal lobe (Chelune, 1995). This area consists of the hippocampal region (CA fields, dentrate gyrus and subiculum) and the adjacent perirhinal, entorhinal and parahippocampal cortices. This system of anatomically related structures has been found to be essential for declarative memory (Squire & Clark, 2004). Declarative memory is one of the most essential human cognitive functions; it provides individuals basic biography, identity and is involved in cognitive behaviour development. One can see that the impairment of such memory functions would cause devastating implications to ones life and therefore has been a major focus of research relating to TLE.

Although there has been much debate surrounding whether or not TLE affects all declarative memory the same, most researchers at least agree that the memories associated with the acquisition of time and context are significantly hindered. These memories are known as episodic and are the only memories that make personally experienced past accessible through autonoetic awareness (Viskontas et al., 2000). Research indicates that patients suffering from damage to the medial temporal lobes caused by TLE have impaired personal episodic memory, but their personal semantic memory can be intact. For example, patients have been found to be unable to recall what they did for their last birthday, although they knew their date of birth and their age. These cases of retrograde amnesia for personal episodic memories but not for semantic, highlights how damage to medial temporal lobes pertained from TLE could most likely be effecting retrieval rather than consolidation (Viskontas et al., 2000). According to the Multiple Trace Theory (MTT) this is indeed the case. MTT states that the hippocampal complex rapidly binds novel information and experience into a coherent memory trace composed of hippocampal elements active at the time of encoding (Moscovitch et al., 2005). Each time an old memory is retrieved, a new hippocampally mediated trace is created so that older memories retrieved often become stronger. Therefore MTT suggests that episodic memories are more fragile due to their strong connection with the hippocampus. This connection ensures that as damage occurs from TLE to the hippocampus, memory traces between novel information and experience can no longer be activated and therefore episodic memories can not be retrieved (Moscovitch et al., 2005). While personal semantic memories seem to be more resistant to hippocampal damage because their function seems to at least be partially independent to the hippocampus.

Although most patients with TLE exhibit damage bilaterally to their medial temporal lobes, some patients show greater deficits in one hemisphere. This is usually due to the origins of their seizures starting on one side of the brain and therefore causing more damage to that side (Viskontas et al., 2000). As we know, the left and right hemispheres specialise in different functions, and therefore one would predict that greater damage to one side would cause greater deficits in certain types of behaviour. This has been proven to be the case, as Dupont and Moortele (2000), showed that memory impairment in lateralised TLE tends to be material-specific, with damage to the left side of the medial temporal lobe impairing verbal memory, while damage to the right impairing visual memory. RTLE patients have been shown to perform well below average on recognition and discrimination memory tasks, while LTLE patients have shown large deficits in word list learning, prose recall, and supraspan digit learning (Weintrob et al., 2002). This highlights that the right medial temporal lobe seems to be heavily involved in visuo-spatial aspects of memory such as recognition and discrimination, while the left medial temporal lobe and specifically the hippocampal region play an important role in verbal memory (Dupont & Moortele, 2000).

However, some research has found that not only is lateralisation material specific but different hemispheres are involved in the differing lengths of processing. In a test conducted by Glosser and Cole (2002), a dysfunction was found in patients suffering from RTLE in long-term memory processing for non-verbal, visuo-spatial information. In contrast those with LTLE did not have a deficit in long-term memory processing of verbal information. This long-term memory deficit was only observed in patients suffering from RTLE, and was inferred from the fact that their relative recall impairment increased from the initial learning trial. This tapped both immediate and long-term memory processes, to subsequent recall and recognition trials which were more heavily dependent on long-term memory operations (Glosser et al., 2002). One explanation for this could surround that semantic and therefore verbal memory seems to be more resistant to damage