The biggest issue when treating amnesia is that there is no remediation of lost memories; the memories lost, and those not fully formed, due to an amnesic disorder are often permanently lost (Squire, 2006). In some instances, the forgetting of amnesia is a result of loss of access/failures in retrieval of information (Macleod & Macrae, 2001). When the issue lies within access and retrieval, ‘reconsolidation’ and ‘reconciliation’ may lead to patients fully recovering memories that were once unobtainable (Power, Berlau, McGaugh, & Steward, 2006). Thus, treatment in these cases must be centred around addressing the disorder causing persistent amnesia; as oppose to trying to recover memories lost due to the disorder and providing patients with ongoing support.
The challenge with WKS is to prevent the patient developing the syndrome but if this fails, to manage WKS to improve brain function and to aid the patient in adapting to their cognitive impairment, suggesting that the cognitive deficits are irreversible in cases that have progressed too far; how far is too far remains unclear.
The straightforward treatment for WE and WKS is to simply supplement the diet with thiamine; administered orally. However, as previously mentioned it is often the case that oral treatment is inadequate in cases of WKS (Thomson, Guerrini, & Marshall, 2012). This could be for several reasons such as insufficient quantities; ingested nutrients are often lost to vomiting or diarrhoea caused by poor diet as well as the fact that metabolism of alcohol increases the body’s requirements of thiamine. Another reason could be impaired absorption, alcohol-related liver damage impairs the phosphorylation of thiamine (see Figure 1) which is vital for the active transport in the absorption of thiamine for cell metabolism (Thomson & Marshall, The Treatment of Patients at Risk of Wernicke Encephalopathy in the Community., 2006). Finally, this could be due to thiamine transport issues, prolonged damage by the above causes could affect transport, meaning thiamine concentrations high enough to traverse the blood-brain barrier cannot be produced (Thomson, Guerrini, & Marshall, Wernicke’s Encephalopathy: Role of Thiamine, 2009). These factors mean that effective thiamine supplementation must be administered via parenteral routes; not via the digestive tract i.e. intravenously.
Beyond the supplementation of thiamine, it is believed that treatment packages should be designed to maintain abstinence of alcohol in a supported housing/rehabilitation environment. Ongoing follow-ups are key to monitoring cognitive status as well as psychiatric and functional wellbeing (Leenane, 1986). A cognitive behavioural approach has shown to be useful in develop coping strategies for day to day routines, things such as writing down information, keeping a diary and breaking tasks down into smaller steps (distributive practice).
As stated, TGA tends to leave no lasting effects meaning that direct treatment of the neuropsychological effects would be largely unnecessary. Though it is advised that individuals document the events leading up to the episode, so they may address any underlying issues or take preventative measures. However, that’s not to say that no treatment takes place. The sudden nature of an episode can be quite distressing for the individual, especially as the cause/trigger may not be totally obvious at first glance, so some level of counselling and understanding may need to take place for the individual to fully recover.
Neuropsychology 