Tag Archives: Author: Dr Shibley Rahman 2016

March 2016 research wrap: Identity and dementia

who am iThis month, Dr Rahman has written a really interesting research blog on identity, and we are extremely grateful to him for his expertise, his continued willingness to make time to do this for us at no charge.

This support of Dementia Alliance International and all people with dementia in general is greatly appreciated. Thank you Shibley.

What happens to identity when somebody is diagnosed or ‘undiagnosed’ with dementia?

A curious problem has arisen in English dementia service provision.

As a result of the perfect storm of the pressure on primary care to diagnose dementia, and the lack of sufficient resources to primary care, as well as the burgeoning pressures on the memory clinic service, there has been a significant number of people being ‘undiagnosed’ with dementia too.

But having any diagnosis of dementia forces you to make sense of your life as it is, against the background of how it was.

Recent research in dementia has thrown much light on self and identity, and, whilst interesting in itself, provides further clues about how best person-centred integrated care pathways might be best designed in future.

This article in my ‘research roundup’ series looks at recent advances in the research on self and identity in dementia, a hugely important area of research. 

  1. Inaccurate diagnoses of dementia in recent English dementia policy

Last year (20150, it was reported that researchers at the University of Sheffield had found that the number of ‘inaccurate’ referrals by GPs to memory clinics – centres to diagnose dementia – has doubled since the Government’s financial incentivising scheme had been introduced.

A study of 150 patients found that just over half – 52 per cent – who had been sent to memory clinics for scans since October were later found not to have dementia. This compared to rates of between 25 and 30 per cent before the scheme was introduced. Many had temporary memory problems brought on by depression or old age rather than dementia. Inevitably, every misdiagnosis of dementia has a back story too, although the opposite, of people languishing without a diagnosis, is frightful too.

On 26 February 2016, this policy issue had gathered momentum: in an article “Revealed: the dementia diagnosis drive that went too far” in Pulse magazine, Caroline Price (2016) wrote:

“Figures obtained from 11 NHS trusts showed 152% increase in the number of patients wrongly labelled as potentially having dementia under the diagnosis drive, causing them unnecessary anxiety and affecting the GP-patient relationship.

These data, obtained under a Freedom of Information request, reveal there were 10,019 GP referrals across 11 trusts in 2011/12, when the Prime Minister launched his ‘challenge’ on dementia, and that this more than doubled to 22,109 in 2014/15.”

  1. The impact of a diagnosis of dementia: the notion of ‘patienthood’

Being given a diagnosis of dementia has a huge impact on your sense of personal identity.

The diagnosis is bound to invest a lot of emotional energy – particularly if you then go onto advocate in a public arena on behalf of people living with dementia as someone living with dementia yourself.

But if your diagnosis changes – this could well be not because a physician ‘has made a mistake’, but because more information has come to light – e.g. a change in thinking, or a change in the appearance of a brain scan.

The disclosure of the diagnosis heralds, arguably, the beginning of an additional identity of ‘patienthood’, which undoubtedly requires particular sensitivity. Sabat and colleagues are particularly helpful here.

Another ‘fixed’ category would be the ‘patienthood’ of the person that is then combined with a particular diagnosis. Thus, a person’s diagnosis and status as a patient become the key features of identification in a narrative about the person, and the diagnostic label becomes an adjective that then describes the person and thereby restricts his or her social identity. As a result of such a limited identity that is, itself, based on a pathological attribute or set of pathological attributes, the person so labelled can easily become marginalized and essentially imprisoned in a web of negative stereotypes.” (Sabat et al., 2011)

The diagnosis itself can lead to a change of perceived identity with others around you, as Sabat, Napolitano and Fath (2004) note.

When healthy persons refrain from engaging in malignant positioning of the person with AD in the early stages of the disease, the degree to which the person with AD experiences a loss of control, humiliation, embarrassment, and other losses can be ameliorated. As a result, the person’s remaining intact cognitive abilities may be sustained for a longer period of time than might otherwise be the case.”

It is often emphasised how empowering a diagnosis of dementia could be, in that it provides an account of symptoms, and allows you and your closest to plan for the future.

But a complete account, in honesty, needs to embrace how the identity of patienthood can be potentially disempowering too. In a recent study, some participants struggled with their newly acquired label of behavioural variant of frontotemporal dementia, whilst for others “the threat came from their reduced abilities or from lifestyle restrictions imposed upon them due to their illness” (Griffin, Oyebode and Allen, 2015).

  1. The general importance of self and identity

The notion of what makes up “the self” is therefore relevant. From a research perspective, the self is very difficult to define, and researchers have based their studies on a wide variety of models and concepts (Caddell and Clare, 2010). However, empirical evidence regarding the impact of dementia on the self remains limited. (Clare et al., 2013)

Personal identity is defined as the state and feeling of being the same as a person described or claimed, and having unique identifying characteristics that remain stable over time.

Recently, there has been much debate in the literature regarding the extent to which identity remains intact in people with dementia (Caddell and Clare, 2011) – although this seems at odds, potentially, with rapidly disappearing fragments in “the orange” as depicted in the recent Alzheimer’s Research UK campaign for raising dementia awareness entitled “Share the orange”.

This chimes with the prevailing image of dementia as a loss of self and a change of identity leads to the situation that persons with dementia represent difference and otherness. Policies for an ageing society with a large number of persons living with dementia are influenced by this ‘shock doctrine’ of the fear of losing one’s identity and self (Naue and Kroll, 2008): though this may be altogether rather unfair.

Martin Conway (2005) in a challenging, and hugely interesting, article a decade ago threw back to the classical work of William James, emphasising that memory is an important feature of yourself. It would appear intuitively correct that your idea about yourself is based on your recollections of memories about yourself. But this can go wrong – and it is not impossible that this will go wrong in dementia.

Conway describes previous work on ‘coherence’, how the fact pattern about events say in the past are refashioned to emphasise information relevant to your current life. This link with your autobiographical past remains one of the most enduring enigmas of dementia ‘self’ research. Latterly, however, a distinction has been drawn between the continuous, coherent sense of identity that characterises normal human experience, the ‘ontological self’, and the types of self-knowledge that underpin and support it (reviewed in Clare et al., 2013).

But Conway also cites other work where this coherence can strikingly break down; for example a patient living with chronic schizophrenia who convinces himself he is a ‘grandmaster’ of chess despite a complete inability to play chess.

How you perceive changes in self and identity in diagnosis might relate to underlying cognitive processes, according to most recent research.

For example, from a cognitive point of view, patients in the early stages of semantic dementia with a complicated picture of loss of semantic knowledge, knowledge for types of things. This generally involves knowledge of objects, concepts, famous people, and public events, and engenders some particular language deficit.

According to Duval and colleagues (2011), a novel finding of theirs was that persons with semantic dementias had problems in recalling semantic personal events (though not episodic ones to do with events) related to their past selves, and also they seemed to have considerable difficulty imagining what they might become in the future.

This has implications for how people with dementias deal with their concepts of the future, and this field of ‘prospection’ is very interesting indeed.

  1. Looking for the ‘ME’ in dementia

Or an “ecological self” represents awareness of the self as perceived with respect to the physical environment, through the processing of visual, auditory, and somatosensory stimuli. The continuous flow of visual information means that the entity is constantly aware of its position, posture and movement with respect to the environment (Caddell and Clare, 2013).

But such a theory clearly is ill equipped to predict distortions of self and identity which could be hypothesised to take place in the context of people living with higher order visual processing disturbances, say in posterior cortical atrophy?

The trick will be – as it is for most other areas of dementia research and service provision – not to consider dementia as one homogenous mass, and fall back on the individuality of all people living with dementia. This is looking for the ‘ME’ in ‘dementia’.

This is of course the heart of personhood.



Borland, S. (2015) Patients wrongly told they may have dementia by GPs on a controversial £55 bonus scheme, researchers warn, 24 February 2015, http://www.dailymail.co.uk/health/article-2966163/Patients-wrongly-told-dementia-GPs-controversial-55-bonus-scheme-researchers-warn.html#ixzz43fTkhAbm (accessed 22 March 2016).

Caddell LS, Clare L. (2010) The impact of dementia on self and identity: a systematic review. Clin Psychol Rev. 2010 Feb;30(1):113-26.

Caddell LS, Clare L. (2013) Studying the self in people with dementia: how might we proceed? Dementia (London). Mar;12(2):192-209.

Caddell, LS, Clare, L. (2011) I’m still the same person: The impact of early-stage dementia on identity, Dementia, 10(3) 379–398.

Clare L, Whitaker CJ, Nelis SM, Martyr A, Markova IS, Roth I, Woods RT, Morris RG. (2013) Self-concept in early stage dementia: profile, course, correlates, predictors and implications for quality of life. Int J Geriatr Psychiatry. 2013 May;28(5):494-503.

Conway, M.A. (2005) Memory and the self. Journal of Memory and Language 53, 594–628.

Duval C, Desgranges B, de La Sayette V, Belliard S, Eustache F, Piolino P. (2012) What happens to personal identity when semantic knowledge degrades? A study of the self and autobiographical memory in semantic dementia. Neuropsychologia, Jan;50(2):254 65.

Griffin J, Oyebode JR, Allen J. (2015) Living with a diagnosis of behavioural-variant frontotemporal dementia: The person’s experience. Dementia (London). Feb 2.

Hulko, W. (2009) From ‘not a big deal’ to ‘hellish’: Experiences of older people with dementia. Journal of Aging Studies 23, 131–144.

Naue U, Kroll T. (2009) ‘The demented other’: identity and difference in dementia. Nurs Philos. Jan;10(1):26-33.

Price, C. (2016) Revealed: the dementia diagnosis drive that went too far, http://www.pulsetoday.co.uk/clinical/more-clinical-areas/neurology/revealed-the-dementia-diagnosis-drive-that-went-too-far/20031247.fullarticle (accessed 22 March 2016).

Sabat SR, Johnson A, Swarbrick C, Keady J. (2011) The ‘demented other’ or simply ‘a person’? Extending the philosophical discourse of Naue and Kroll through the situated self. Nurs Philos. Oct;12(4):282-92; discussion 293-6.

Sabat SR, Napolitano L, Fath H. (2004) Barriers to the construction of a valued social identity: a case study of Alzheimer’s disease. Am J Alzheimers Dis Other Demen. May Jun;19(3):177-85.

Author: Dr Shibley Rahman 2016

February Research Wrap: Logopenic Primary Progressive Aphasia

research 5This month, we have just made it to post our Research Wrap for February, but with a mega effort by Dr Shibley Rahman in writing this today, we have made it! Sincere thanks for this ongoing support for our members Shibley.

Many of our members have PPA or LPPA, and this particular article will be particularly enlightening.

Living beyond a diagnosis of logopenic PPA requires a multi-pronged approach

One of the most important questions for persons receiving a diagnosis is the issue of in what way the diagnosis benefits him or her.

It is said that one of the strongest attractions of receiving a correct diagnosis of diagnosis is that you can plan ahead. That is not to ‘pack up your bags’ and be encouraged to ‘give up’, but to look ahead to living beyond a diagnosis of dementia. See Kate Swaffer’s excellent book “What the hell happened to my brain?” (Swaffer, 2016), a testament to this, and worth more than a million charities or think tanks.

  1. What is PPA? What is LPPA?

There’s also the issue of how exactly knowing the type of dementia can possibly help. Common reasons include having a coherent explanation for symptoms, and having some help.

The very specific type of dementia known as “logopenic primary progressive aphasia” (“LPPA”) is a form of dementia whose hallmark is a progressive loss of function. It is due to the loss of function of parts of the brain involved in speech and language. It comes under the umbrella of dementias called the frontotemporal dementias, under the class of primary progressive aphasias (“PPA”), first described in the modern literature by Mesulam (reviewed by Henry and Gorno-Tempini, 2010, responsible themselves for putting LPPA ‘on the map’).

Concentrating on the language to the other needs of a person with LPPA is wrong, however. From the Mayo Clinic, Tarun Singh and colleagues (2015) reported that often appetite and mood changes accompanied early progressive primary aphasia.

The centrepiece of the cognitive problem in “logopenic PPA” (LPPA) is a problem with word finding. In small talk, speech is pretty fluent, but tends to break into mispronounciations and word-finding pauses when more difficult or more precise words are needed. The naming of objects can become impaired, and replaced in speech by phrases such as “you know what I mean”.

Logopenic PPA is rarer, in terms of the numbers of people involved, than other forms of dementia, but throws into focus crucial questions about how we view dementia. And research in this area in the last five or six years has been rapid. It also throws into question how we can best support people living beyond a diagnosis. 

  1. Is LPPA in fact a form of Alzheimer’s disease?

The pattern of pauses in speech can be helpful in working out the neural networks which go wrong in LPPA. We know this now from recent work by Mack and colleagues (2015). There’s been a question as to which parts of the brain are involved. Whilst there might have seemed to be a very focal start to the underlying disease from previous research, such as the left temporal and inferior parietal parts of the brain, very recent work published from Cristian Leyton, Anna Britton, John R. Hodges, Glenda M. Halliday, and Jillian J. Krill recently (2016) found all of their patients had quite extensive Alzheimer’s changes extending to ‘deep cortical areas’ of brain. This of course is truly fascinating.

Indeed, Stephanie Awad and Amer Awad (2011) had earlier mooted whether one of their patients had presented with LPPA but in fact as a “precursor to Alzheimer’s disease”. The patient is a 54-year-old left-handed Caucasian lady who had been referred to their centre for evaluation of speech difficulties. The patient noted a gradually progressing speech problem about two years prior to her presentation. Her main difficulties were related to word finding and inability to express herself very well with frequent pauses.

The authors correctly concluded, “The early symptoms are very subtle and require a high index of suspicion. Healthcare providers need to be aware of this entity and other entities that present with subtle cognitive abnormalities.” (Awad and Awad, 2011)

A series from Japan (Funayama et al., 2013) then notably suggested that some patients with LPPA develop an atypical type of dementia with apraxia and semantic memory deficits, suggesting that these cases should be classified as a type of early-onset Alzheimer’s disease.

Taken as a whole, a recent neuroimaging study by Matias-Guiu and colleagues (2015) supported the notion that PPA is a heterogeneous clinical syndrome, which may progress into various forms of diseases with time.

  1. Is a pharmacological treatment for LPPA possible?

This leads us to the interesting position that the cluster of cognitive symptoms clinically might lead to a particular diagnostic label, such as logopenic PPA, but ultimately might have a common underlying disease process. This is similar to the position Pharma was in on how antidepressant drugs were said to be effective, irrespective of the exact neurobiological causes of unipolar depression.

The rôle of abnormal levels of tau and amyloid in the brains of people living with dementia remains under scrutiny, and rightly so. What is becoming quite clear though is that they may not be specific to what clinicians view as Alzheimer’s disease. This of course offers a window of opportunity for Pharma medically to ‘cure dementias’, in the sense that the exact diagnostic label of the dementia may not be quite as important as first thought.

Indeed, in a short report which has only just been published (Pascual and Masdeu, 2016), high uptake of proteins binding to tau and amyloid (with variable areas of metabolism) have been reported for a 57-year old lady thought to have a 8 year history of LPPA.

Fang and colleagues (Fang et al., 2014) in a remarkable paper for Nature Communications had found that toxic amyloid oligomers could indeed build up in “frontotemporal lobar dementia-TDP” patients. Nonetheless, it is possible that some medications may be efficacious for symptomatic treatment for LPPA, even if not arresting the disease.

Tiffany Chow (Chow et al., 2011) in work from Toronto has been evaluating critically the possible beneficial effects of a medication called memantine. At roughly the same time, Nancy Johnson and colleagues (Johnson et al., 2010) reported on a trend to a significant effect of memantine in a double-blind placebo-controlled trial with 18 PPA subjects. Persons living with PPA will always be guided by their own responsible physicians as to what might possibly work best for them. Memantine is of course not “the only fruit”.

  1. Conclusion – but there’s clearly a need to look ‘beyond drugs’.

Any modern critique of dementia needs now to look ‘beyond drugs’ (Power, 2010).

Looking beyond drugs, as speech and language are such critical features of logopenic PPA, it makes sense for a speech and language specialist to carry out a detailed assessment of speech and language.

Approaches to intervene might include skills to enhance word-retrieval abilities, or alternative communication strategies. This approach is consistent with reablement for a disability, akin to a crutch for a broken leg.

But LPPA shows graphically it would be wrong to put all your eggs in the medical basket. Living beyond a diagnosis requires a multi-pronged approach.

[Disclaimer: This article is not to be used in any way, or construed as, medical advice. This of necessity is true for all posts and information on the Dementia Alliance International blog.] 


Awad SM, Awad AM. (2011) A middle-aged woman with logopenic progressive aphasia as a precursor of Alzheimer’s disease: case report and review of the literature. Case Rep Neurol Med. 450301. doi: 10.1155/2011/450301. Epub 2011 Sep 29.

Chow TW, Graff-Guerrero A, Verhoeff NP, Binns MA, Tang-Wai DF, Freedman M, Masellis M, Black SE, Wilson AA, Houle S, Pollock BG. (2011) Open-label study of the short-term effects of memantine on FDG-PET in frontotemporal dementia. Neuropsychiatr Dis Treat. 7:415-24. doi: 10.2147/NDT.S22635. Epub 2011 Jul 13.

Fang YS, Tsai KJ, Chang YJ, Kao P, Woods R, Kuo PH, Wu CC, Liao JY, Chou SC, Lin V, Jin LW, Yuan HS, Cheng IH, Tu PH, Chen YR. (2014) Full-length TDP-43 forms toxic amyloid oligomers that are present in frontotemporal lobar dementia-TDP patients. Nat Commun. Sep 12;5:4824. doi: 10.1038/ncomms5824.

Funayama M, Nakagawa Y, Yamaya Y, Yoshino F, Mimura M, Kato M. (2013) Progression of logopenic variant primary progressive aphasia to apraxia and semantic memory deficits. BMC Neurol. Nov 1;13:158. doi: 10.1186/1471-2377-13-158.

Henry ML, Gorno-Tempini ML. (2010) The logopenic variant of primary progressive aphasia. Curr Opin Neurol. Dec;23(6):633-7. doi: 10.1097/WCO.0b013e32833fb93e.

Johnson NA, Rademaker A, Weintraub S, Gitelman D, Wienecke C, Mesulam M. (2010) Pilot trial of memantine in primary progressive aphasia. Alzheimer Dis Assoc Disord. Jul-Sep;24(3):308. doi: 10.1097/WAD.0b013e3181cf468d.

Leyton CE, Britton AK, Hodges JR, Halliday GM, Kril JJ. (2016) Distinctive pathological mechanisms involved in primary progressive aphasias. Neurobiol Aging. Feb;38:82-92. doi: 10.1016/j.neurobiolaging.2015.10.017. Epub 2015 Oct 26.

Mack JE, Chandler SD, Meltzer-Asscher A, Rogalski E, Weintraub S, Mesulam MM, Thompson CK. (2015) What do pauses in narrative production reveal about the nature of word retrieval deficits in PPA? Neuropsychologia. Oct;77:211-22. doi: 10.1016/j.neuropsychologia.2015.08.019. Epub 2015 Aug 20.

Matias-Guiu JA, Cabrera-Martín MN, Moreno-Ramos T, García-Ramos R, Porta-Etessam J, Carreras JL, Matías-Guiu J. (2015) Clinical course of primary progressive aphasia: clinical and FDG-PET patterns. J Neurol. Mar;262(3):570-7. doi: 10.1007/s00415-014-7608-0. Epub 2014 Dec 10.

Pascual B, Masdeu JC. (2016) Tau, amyloid, and hypometabolism in the logopenic variant of primary progressive aphasia. Neurology. Feb 2;86(5):487-8. doi: 10.1212/WNL.0000000000002340.

Power, G.A. (2010) Dementia beyond drugs: changing the culture of care, Baltimore: Health Professions Press.

Singh TD, Duffy JR, Strand EA, Machulda MM, Whitwell JL, Josephs KA. (2015) Neuropsychiatric symptoms in primary progressive aphasia and apraxia of speech. Dement Geriatr Cogn Disord. 39(3-4):228-38. doi: 10.1159/000369062. Epub 2015 Jan 21.

Swaffer, K. (2016) What the hell happened to my brain? London: Jessica Kingsley Publishers.

Research roundup on memory and dementia

Slide7For our last blog post in January 2016, we are indeed lucky Dr Shibley Rahman has once again found time in his incredible schedule as an academic and author to write this research wrap for us.

Thank you Shibley, as without volunteers like yourself, and others, it would be difficult indeed to offer the kinds of services and information we are able to offer to our members, all people with dementia, and which are all provided at no charge to them.

Shibley writes:

In this ‘research roundup’ for Dementia Alliance International, I’d like to describe some of the latest developments in memory research.

I will explain how they relate to some classic historic research.

And also I explain why this is relevant to our current understanding of dementia.

Memory impairment is a prominent defining feature of Alzheimer’s disease, yet the degree to which the profile of memory impairment is uniform across patients is not fully resolved. Alzheimer’s disease is the most common form of dementia worldwide.

Recall or retrieval of memory refers to the subsequent re-accessing of events or information from the past, which have been previously encoded and stored in the brain.

Recognition is the association of an event or physical object with one previously experienced or encountered, and involves a process of comparison of information with memory, e.g. recognising a known face, true/false or multiple choice questions, etc.

That there’s a difference has been interesting to cognitive neurologists for ages.

And crucial when it comes to developing new tests in the clinic to develop and distinguish some types of dementia.

Intriguingly, some researchers – Craik and colleagues – recently described a person “VL” (published 2014).

VL was a female who exhibited frequent episodes of erroneous recollections triggered by everyday events.

Based on neuropsychological testing, VL was classified as living with dementia, and indeed was given a diagnosis of probable Alzheimer׳s disease.

Her memory functions were uniformly impaired but her verbal abilities were generally well preserved. A structural MRI brain scan showed extensive areas of gray matter atrophy particularly in frontal and medial-temporal (MTL) areas of the brain.

Results of experimental recognition tests showed that VL had very high false alarm rates on tests using visual pictures, faces and auditory stimuli, but lower false alarm rates on verbal tests.

This is interesting from the point of view that visual and verbal memory might be organised differently in the human brain.

On a different note, it has been unclear to what extent memory is affected in another type of dementia known as frontotemporal lobar degeneration.

Since persons living with this dementia usually have atrophy in regions implicated in memory function, the frontal and/or temporal lobes of the brain, one would expect some memory impairment (see for example and colleagues, 2008).

And this prediction has been generally borne out in clinical observations.

There’s a part of the brain which historically has been associated with aspects of memory – the hippocampus.

This is really classic work.

Scoville and Milner (1957) described the seminal case of H.M. who fell off his bicycle when he was 7 years old, injuring his head. H.M. began to have epileptic seizures when he was 10. By the age of 27 the epileptic attacks prevented him from living a normal life.

Scoville performed an experimental surgery on H.M.’s brain to stop the seizures.  Specifically he removed parts of HM’s temporal lobes (part of his hippocampus along with it). The seizures stopped but H.M. had amnesia for the rest of his life.

This case study of H.M. provides information on how particular brain areas and networks are involved in memory processing. This helped scientists to formulate new theories about memory functioning.

H.M. could no longer store new memories (anterograde amnesia). Most of his memories from before the operation remained intact (partial retrograde amnesia).

It’s from work like this that people have been drawn to believe that the hippocampus play a critical role in converting memories of experiences from short term memory to long term memory (“the permanent store”).

H.M. was able to retain some memories for events that happened long before his surgery. This indicates that the medial temporal region with the hippocampus is not the site of permanent storage in itself. It rather seems to play a role in how memories are organised and then stored elsewhere in the brain.

All of this is fascinating in relation to the very commonly held observation about the decline of memory in people living with Alzheimer’s disease: that memory for new events declines comes before the decline in old memories.

This is introduced, indeed, in the ‘bookcase analogy’ of the “Dementia Friends” information sessions which originated in England.

Bringing this all right up to date, Patai and colleagues have recently investigated further the role of the hippocampus part of the brain (2015).

The availability of a large cohort of patients who had sustained relatively selective hippocampal damage early in life enabled us to determine which type of mnemonic deficit showed a correlation with extent of hippocampal injury.

They assessed their patient cohort on a test that provides measures of recognition and recall that are equated for difficulty and found that the patients’ performance on the recall tests correlated significantly with their hippocampal volumes.

However, they also found that their performance on the equally difficult recognition tests did not and, indeed, was largely unaffected regardless of extent of hippocampal loss of volume.

The results provide new evidence in favour of the view that the hippocampus is essential for recall but not for recognition.

So, the story continues. This excellent research benefits our understanding of dementia, and how we can develop new ways of identifying and people living with memory problems “living beyond dementia” (Swaffer, 2015).


Craik FI, Barense MD, Rathbone CJ, Grusec JE, Stuss DT, Gao F, Scott CJ5 Black SE. VL: a further case of erroneous recollection. Neuropsychologia. 2014 Apr;56:367-80. doi: 10.1016/j.neuropsychologia.2014.02.007. Epub 2014 Feb 20.

Patai EZ, Gadian DG, Cooper JM, Dzieciol AM, Mishkin M, Vargha-Khadem F. Extent of hippocampal atrophy predicts degree of deficit in recall. Proc Natl Acad Sci U S A. 2015 Oct 13;112(41):12830-3. doi: 10.1073/pnas.1511904112. Epub 2015 Sep 28.

Scoville WB, Milner, B. Loss of recent memory after bilateral hippocampal lesions. J Neurol Neurosurg Psychiatry. 1957 Feb;20(1):11-21.

Söderlund H, Black SE, Miller BL, Freedman M, Levine B. Episodic memory and regional atrophy in frontotemporal lobar degeneration. Neuropsychologia. 2008 Jan 15;46(1):127-36. Epub 2007 Aug 9.

Swaffer, K. Living beyond dementia website https://livingbeyonddementia.wordpress.com (accessed 27 January 2016).