top of page

Don’t Forget About the Thalamus….

Laurie Miller, PhD, Clinical Neuropsychologist

Ever since the publication that described amnesia following HM’s bilateral mesial temporal lobe removal (Scoville & Milner, 1957), much of the focus with regard to memory function has been on the hippocampus.  However, as a neuropsychologist who has worked with a variety of neurological patients over the years, I have encountered a range of memory impairments associated with lesions involving the thalamus.  In some of these, detection of the underlying cause was delayed because this area had not been considered a possible lesion site initially.

Positioned at the top of the brain stem and surrounded by the cerebrum, the thalamus is the major relay nucleus of the brain, connecting peripheral sensory organs to the cortex and various regions of the cortex to one another.  Parts of the thalamus (e.g., anterior nuclei, mammillary bodies) also contribute to the Papez circuit, which is critical to memory. Here I describe five patients that I assessed (and in some cases studied for years) who developed different types of memory disorders as a result of damage to the thalamus.

A half-cut lateral view of the brain the brain with the Thalamus in the centre.

Korsakoff’s amnesia

One of the best-known memory disorders caused by thalamic damage is Korsakoff syndrome.  This most commonly develops in association with alcoholism and presents acutely after a period (e.g., several days) of excessive alcohol intake, but little food consumption. Patients can experience a sudden onset of ataxia, abnormal eye movements, confusion and amnesia (“Wernicke’s encephalopathy”).  If treated with Vitamin B1, proper nutrition and hydration, symptoms of the condition are usually reversible.  In some cases, however, or if left untreated, a severe amnesia affecting both anterograde and retrograde memory persists. In these cases, a careful look at an MRI can reveal shrinking in the mammillary bodies of the thalamus.

It is important to note, however, that a Korsakoff syndrome can also occur as a result of Vitamin B1 (thiamine) deficiency related to other conditions, such as extreme fasting or anorexia.  While working in Canada, I encountered a woman who had lost most memory abilities after undergoing bariatric surgery as a weight loss procedure.  Presumably, as a result, her body was not absorbing sufficient B1.  Her brain scan showed the characteristically shrunken mammillary bodies.  She spent some of her time in the years that I knew her presenting lectures entitled “My brain is a Teflon pan… nothing sticks!”  She had developed an impressive technique of using a notebook with lots of tabs to record and re-find things she had done and things she needed to remember.  She used this external memory store to do to replace her (former) biological anterograde and prospective memory.  Her thoroughly organised notebook took up a good deal of her time and effort, but was a good example of how an external aid can help to replace a normally fairly effortless biological process.

On another occasion, in Sydney, I assessed a very well-educated young woman (SL), who developed Korsakoff’s amnesia in association with alcoholism at the age of 43. She presented to hospital with all the classic symptoms and, after treatment, was left with an ongoing persistent memory disorder that rendered her unable to live independently.  She could remember very little from one day to the next and was accumulating piles of clothing at home, because she would forget what she had obtained previously in her volunteer job at a St Vincent de Paul store.  On testing, her amnesia was dense and global. In spite of interacting with SL on multiple occasions, she never showed any evidence of remembering previous encounters or recognising me (Tedder et al., 2016).

For a year or so after the onset, SL managed in Sydney with her boyfriend, but her mother eventually took her back to Europe to supervise her care.  For several more years, I received updates from her mother. SL was able to develop some routines to aid her daily functioning, but in spite of many attempted interventions, including her participation in the Making the most of your Memory program (Radford et al., 2010), few other improvements were evident.  As far as I know, SL continues to live in her mother’s care and perform volunteer duties in a highly supervised environment.

Amnesia in conjunction with temporal lobectomy

In 1994, while working in a surgical epilepsy unit in Canada, I met Patient EM.  She was a 13 year-old, right-handed girl, who developed a severe anterograde memory impairment after a left temporal lobectomy.  This operation had been carried out to remove the origin site of her intractable seizures, which she had experienced since age 5.  Typically, a left temporal lobectomy in a right-handed patient might be expected to result in a mild drop in verbal learning and memory, but for EM, the change in her memory skills was much more dramatic and pervasive. It was only with hindsight that the importance of a small right thalamic lesion was appreciated.   

Prior to surgery, EM’s cognitive testing yielded results consistent with the expected pattern caused by a focal left temporal lobe lesion; she showed more difficultly learning and retaining verbal material compared to visual.  In fact, pre-operatively, her retention of novel geometric drawings had been excellent. This is the pattern expected in a right hander with a history of left temporal, focal seizures.  EM’s striking memory decline after the unilateral surgery, particularly for non-verbal material was unexpected. 

 In the year following her operation, EM struggled at school.  In addition to classroom material, she had trouble learning the names of new students, new violin pieces, or the location/combination of her school locker.  Eight months after her surgery, her IQ score remained in the Superior range, but on standardised testing, she showed almost no memory for drawings she had copied, or stories/ word lists she had been told (and repeated) when retention was tested again after over a 30 min delay.

The pathology investigation of the removed temporal lobe tissue indicated significant abnormalities in the amygdala, but none in the hippocampus.  It was felt that this removal of part of a seemingly intact hippocampus would be enough to explain the drop in verbal, but not non-verbal memory abilities.  Even three years later (when I last tested her) EM was showing very significant memory difficulties on both verbal and visual material.  It was only at this point, with careful review, that the pre-operative MRI yielded evidence of a small right-sided lesion in the anteromedial thalamus (thought to be an old infarct or developmental venous anomaly).  In other words, the removal from the left mesial temporal region had added to the pre-existing lesion in the right hemisphere’s memory circuitry.  Bilateral lesions to the memory system have a much greater impact than unilateral ones.  EM’s rather tragic case illustrated the importance of considering the contralateral thalamus in addition to the contralateral mesial temporal structures in predicting the impact of a temporal lobectomy on memory (Miller & Harnadek, 1995).


A rare case of isolated retrograde amnesia

JG was probably the most fascinating case of memory deficit after thalamic lesion that I encountered (Miller et al., 2001, 2003).  Following a small, bilateral, posteromesial thalamic stroke, this 33 year-old man developed an isolated retrograde amnesia for the whole of his life with preservation of some memories from his most recent past.  His deficit was “isolated” in that it spared his anterograde memory; he could store new memories of events that took place after the stroke, but he had almost no memory of specific details from his previous life. For example, he could no longer remember his parents, growing up in England, moving to Australia, the previous year’s holiday in Thailand, music he had listened to, or movies he had seen.  His pattern of deficits led me to postulate a role for this area of the thalamus in the “search” mechanism necessary to locate cortically stored, longer-term episodic memories and memory for unique entities.  


Interestingly, a bit like EM, the cause of JG’s memory loss was not obvious initially.  A CT scan carried out upon his admission to the hospital failed to reveal any abnormalities.  At this point, his extremely rare memory profile was thought to be the consequence of some psychological trauma.  It was only a few days later (and after a thorough review by the psychiatry team turned up no significant stressors) that the thalamic lesion was detected with an MRI.

For the next few years, JG lived a fairly normal life in spite of a persistent inability to access retrograde memories from before the stroke.  On a day-to-day basis, his memory loss was associated with feelings of insecurity when socialising (fearing he would fail to remember people or events in conversation), which led to some depression. However, his preserved ability to learn and retain new things meant that he could return to work and continue to live an independent life.   He was able to re-learn many of the details of his past life, but never remember these as experiences he had had.


Unilateral thalamic stroke

I met Patient TD when he was a 42 year-old inpatient.  He had recently had an infarct in the left anterior thalamic nucleus.  This nucleus is only a few mm wide, but is an important relay node between the hippocampus and mammillary bodies.  The tiny stroke TD suffered resulted in the sudden onset of significant anterograde memory difficulties, with few other noticeable changes.  In the immediate post-stroke period, TD showed almost no retention of events that have taken place in the hospital, who has visited etc., but a good memory for his past life.  There can be improvement in these kinds of cases, but often the recovery is not 100%.  Follow up with TD over the subsequent year indicated that, as a result of ongoing difficulties with retention as well as associated emotional distress, he had to stop working and his relationship ended. 

Eventually and after taking part in cognitive rehabilitation, TD learned a number of strategies and coping mechanisms.  He has since started his own company, has a new partner and is working on a book related to stroke recovery.


The role of memory strategy training

Interventions of various sorts can help patients like these.  For those with very dense amnesia, the focus will likely be on finding individual solutions, adopting routines and maximising the support of lots of external memory aids/carers.  For JG, re-exposure to information and people from this past helped him to re-learn his own history. 

For those with more focal or mild memory issues (e.g., TD), an intervention like MEMORehab is perfect because it can teach one to use several appropriate internal (mental) and external memory aids to substitute for their loss. In fact, for those capable of learning strategies with practice, there is good evidence that this type of intervention is useful in improving memory even long after the onset of a stroke (Miller & Radford, 2014).  I remained in touch with TD for several years after he participated in the face-to-face version of this program. He was very positive about the experience and was keen to share his journey and eventually successful outcome with other young people going through the early stages of stroke recovery. While he felt that his memory had not returned to the pre-stroke level, he was continuing to use some of the strategies he’d learned in the group-based intervention. If such training courses had existed in the 1990s, I might have considered enrolling EM, so that she could learn appropriate memory strategies.


Neuropsychologists tend to focus on the mesial temporal lobe when thinking about memory function.  However, we need to keep in mind that the thalamus makes important contributions to this aspect of cognition. Because of its central location and pivotal role in neuro-connectivity, thalamic damage is often calamitous or fatal. If the damage is more limited, however, and a patient survives a thalamic injury, memory deficits are likely to ensue in a persistent fashion.  Even a tiny change (such as a small infarct) in the thalamus can sometimes have a big effect on memory.  As such, a clinician looking for the cause of a change in memory should always consider what’s happening in the thalamus.



Miller, L.A., Caine, D., Harding, A., Thompson, E.J., Large, M. and Watson, J.D.G. (2001). Right medial thalamic lesion causes isolated retrograde amnesia. Neuropsychologia, 39, 1037-1046.


Miller, L.A., Caine, D., and Watson, J.D.G. (2003).  A role for the thalamus in memory for unique entities.  Neurocase, 9, 504-514.


Miller, L.A. and Harnadek, M.C.S. (1995).  Profound memory impairment after unilateral temporal lobectomy. Epilepsia, 36, Suppl 3, 269.


Miller, L.A. and Radford, K. (2014). Testing the effectiveness of group-based memory rehabilitation in chronic stroke patients.  Neuropsychological Rehabilitation, 24, 721-737.


Radford,K., Say, M., Thayer, Z and Miller, L. (2010) Making the Most of Your Memory: An everyday memory skills program. ASSBI Resources, Sydney.

Scoville W.B. and Milner. B. (1957). Loss of recent memory after bilateral

hippocampal lesions. Journal of Neurology, Neurosurgery and Psychiatry, 20, 11–21.


Tedder, J., Miller, L., Tu, S., Hornberger, M., and Lah, S. (2016). Into the future with little past:  Exploring mental time travel in a patient with damage to the mammillary bodies/fornix. The Clinical Neuropsychologist, 30(2), 334-349.


bottom of page