Case of transient global amnesia-like syndrome after recreational cold-water swimming
- 1 Older people's unit, Royal United Hospitals NHS Foundation Trust, Bath, UK
- 2 Population Health Sciences, University of Bristol, Bristol, UK
- Correspondence to Dr Matthew D Smith; matthew.smith@bristol.ac.uk
Abstract
We document a case of a transient global amnesia (TGA)-like syndrome following open water swimming. This case was atypical for TGA, in that symptoms were prolonged and ischaemic infarct was considered within the differential. MRI did not demonstrate any changes associated with acute ischaemia although did show a mild degree of small vessel change. With amnesia taking greater than 24 hours to resolve, we have labelled this case to be a TGA-like syndrome, provoked by the commonly reported TGA precipitant of cold water immersion. The possibility of a tiny, strategic infarct causing these symptoms was considered and antiplatelet therapy commenced.
Background
In 1801, Dr James Currie described the beneficial effects of cold water immersion in the treatment of typhus fever in his work entitled ‘Dr. Currie on the Affusion of Cold Water’.1 Currie ‘stripped him [the afflicted individual] naked and threw four or five gallons of sea water on him, dried him and put him to bed’. When the fever returned, he repeated the procedure; ‘I threw water again over him with the same happy effect’. He likely recognised the phenomenon of after drop where core temperature can further reduce on exiting the water.2 Now 221 years later, immersion in cold water is undergoing somewhat of a revival as a recreational activity in the form of cold-water swimming.3 Enthusiasts swim in bodies of water that range from small artificial lakes to oceans, proclaiming benefits to mental and physical health in addition to overall well-being, beyond that of simply swimming.4 Despite these benefits the possibility of hypothermia is a risk, particularly where water temperature is extremely low, where immersion is prolonged or where the swimmer’s physiology is unable to compensate and adapt. We describe a case of prolonged but self-limiting neurological dysfunction following a session of open water swimming, manifesting as a transient global amnesia (TGA)-like syndrome.
Case presentation
A woman in her 70s was brought to the emergency department (ED) via ambulance with acute confusion and hypothermia (34°C) after an organised session of open water swimming in a purposely flooded ex-quarry. She was normally well with no active co-morbidities and had regularly swam in open water for the past few months. On this occasion, she attended a supervised class (water temperature: 13°C) wearing a wetsuit and was seen to have left the class prematurely after 30 min. She was found shortly afterwards hyperventilating, shivering and acutely confused. First aiders reported she was not oriented to time or place and there were concerns from bystanders that she had mild right-sided weakness of her arm and face. It was not possible to ascertain the exact nature and duration of these symptoms as a collateral history could not be obtained. There was no loss of consciousness or loss of personal identity. She had no signs of physical injury. Her medical history composed of poliomyelitis as a child (with no sequelae) and a Holmes-Adie pupil resulting from a viral infection 20 years prior. She took no regular medications. She was a non-smoker and drank three units of alcohol a week. She was fully independent.
Paramedics attended by which point there was no sign of the mild weakness. She was conveyed to the ED and on arrival her temperature was 34°C, as measured with a tympanic temperature probe. The remainder of her observations were within normal limits and with external active rewarming her temperature increased to 36.4°C. Despite successful rewarming, she remained confused and this was predominantly amnestic where she was unable to recall any events since that morning and her content of speech was repetitive. This was, therefore, suggestive of anterograde amnesia with retrograde amnesia for the immediate past. There was no suggestion of specific dysphasia of speech or word generation and there were no other neurological symptoms noted from admission to the ED. On examination, her cardiovascular and respiratory systems were normal. Her pupils were 5 mm, with the right pupil sluggish to respond to light. Her cranial nerve, upper and lower limb examinations were normal with no deficit in power, tone, co-ordination or sensation. She scored 4/10 on Abbreviated Mental Test (AMT-10) and 6/12 on the 4 'A’s Test (4AT).
Investigations
A 12-lead ECG indicated left axis deviation with a complete right bundle branch block, as well as T-wave inversion in leads V5 and V6, in sinus rhythm. In the absence of chest pain and using previous ECG for comparison, no further immediate management was deemed necessary. A chest radiograph indicated normal appearances of the heart and lungs. Blood tests were reassuring with a normal white cell count (9.8×109/L), haemoglobin (144 g/L) and normal biochemistry (including a sodium of 141 mmol/L). A random glucose was 6.8 mmol/L and a venous blood gas demonstrated a pH of 7.378, a pCO2 of 5.91 kPa and a lactate of 1.53 mmol/L. CT imaging of the patient’s brain demonstrated no intracranial haemorrhage or space occupying lesion with minimal small vessel ischaemic change. An MRI of the brain with diffusion weighted imaging was subsequently performed (figure 1) indicating no restriction of diffusion or haemorrhage but again suggesting a mild degree of small vessel vascular change.
Coronal flair (A) and sagittal diffusion weighted imaging (DWI) sequences (B) of temporal lobes from MRI scan.
Differential diagnosis
In the context of acute confusion and anterograde amnesia following cold-water swimming, a working diagnosis of TGA was made but it was recognised that in light of the history of possible right-sided weakness, an acute ischaemic stroke needed to be excluded. The history of having been swimming in cold water yielded further consideration of watershed infarcts having occurred secondary to fluid shifts. Therefore, the MRI brain imaging was expedited to identify cerebral ischaemia. The differentials, also considered, included a prolonged postictal state from an unwitnessed focal seizure, toxic encephalopathy, migrainous process (the patient had a history of typical migraines around the menopause 10 years prior) or concussion following an unwitnessed head injury. Exercise-induced hyponatraemia is another consideration,5 although in this case serum sodium was demonstrated to be normal. Focal seizure was also felt unlikely given the hypothermia and history, and an electroencephalogram (EEG) was not performed.
A diagnosis of exclusion, TGA secondary to hypothermia was deemed the most likely causative mechanism underlying the patient’s presentation initially. The possibility of neurological deficit in the form of weakness warranted consideration but was never professionally witnessed or elicited and therefore was challenging to corroborate. The possibility that the patient had suffered from an ischaemic event even with normal MRI findings could not be entirely excluded. However, the clinical picture of amnesia in isolation occurring following cold water immersion, TGA remained the most likely diagnosis at this time.
Treatment
Initial treatment involved passive rewarming with warm clothes and a hot drink, as well as external active rewarming with a Bair Hugger and electric blankets. She was admitted under the medical team recognising the risk of ‘after drop’ where body temperature continues to drop due to central return of cool peripheral blood.
Once cerebral haemorrhage had been excluded with the CT head, she was initially treated with a single dose of 300 mg aspirin while awaiting the MRI scan. The normal MRI scan made an ischaemic event less likely and the specialist stroke team agreed with the working diagnosis of TGA. Aspirin (75 mg daily) was commenced in case of transient ischaemic attack (TIA). A formal stroke work-up was not undertaken given the low probability of a preventable cause of stroke with the cold water being the precipitating factor. The mainstay of treatment for TGA is supportive, so the patient was monitored in hospital, including repeated cognitive testing and with neurological observations, until the symptoms of confusion and amnesia resolved.
Outcome and follow-up
The patient spent 2 days in hospital, for which approximately 30 hours she remained amnestic and unable to recall the events leading up to or including the swim. Over this period, however, she gradually became oriented to time, person and place and a Mini-ACE (addenbrooke's cognitive assessment) assessment performed prior to discharge gave a result of 30/30. The patient did not, at any point, recover the memories of the day of the event. She was discharged back home. The final diagnosis was a TGA-like syndrome (given the duration of >24 hours amnesia) with antiplatelet cover being initiated given the possibility that a subtle vascular event had occurred not visible on imaging. Counselling was provided on the risks of open water swimming and performing this safely. At 18 months, she still is unable to recall the events of the day in question and now tends to enjoy swimming in heated environments.
Discussion
Ice-swimming has been long established in countries with colder climates. Established in 2009, the International Ice Swimming Association hosts frequent competitions.6 During the COVID-19 pandemic, cold-water swimming has increased in profile and popularity with features in mainstream media purported to range from improved health to mending broken hearts.7 8 Putative benefits assessed scientifically include improved cardiovascular,9 endocrine10 and immune function4 but these findings have not been consistent nor substantiated in large scale, high quality studies.
Cold water can be tolerated for short periods of time, particularly when body temperature is maintained by exercise while immersed.11 However, cold water or swimmers without adequate clothing such as a wetsuit can experience hypothermia quickly.12 The physiological changes that occur with ageing and with some co-morbidities render older individuals less able to tolerate lower temperatures and continued cooling leads to eventual circulatory collapse and cardiac arrest.13 Initial exposure to cold water also leads to a neurogenic ‘cold-shock’ response of abnormal respiration with an acute rise in of blood pressure,14 despite an individual acclimatising and having a successful swimming session. Other health hazards include acute pulmonary oedema associated with hypothermia and issues with water quality leading to infection.12 A water temperature of 25°C has been described as normothermic for individuals exercising in water,15 and a minimum of 18°C has been suggested for elite marathon swimming.11 Notably the water temperature was 13°C in the case of our patient.
TGA affects between 3.4 and 10.4 per 100 000, primarily occurs in people in later life.16 Accepted criteria define that amnesia cannot last longer than 24 hours (see the Hodges and Warlow criteria, Box 1),17 and hence our case has been labelled as a ‘TGA-like syndrome’. Other ‘atypical TGA’ cases have been described previously, including the involvement of sensorimotor deficits and prolonged amnestic periods beyond 24 hours.18 The cause of TGA is not understood and multiple proposed aetiologies have been suggested ranging from vascular to migrainous mechanisms,16 which may also encompass atypical TGA cases within a potentially broader clinical spectrum. Rarely a similar presentation can be seen in other well defined conditions, such as epilepsy (transient epileptic amnesia) and the increased use of MRI has demonstrated in numerous studies, a subset of patients who exhibit diffusion weighted changes after presenting with apparent TGA.19
Criteria proposed by Hodges and Warlow for diagnosis of transient global amnesia17
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Attacks must be witnessed and information available from a capable observer who was present for most of the attack.
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There must be clear-cut anterograde amnesia during the attack.
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Clouding of consciousness and loss of personal identity must be absent, and the cognitive impairment limited to amnesia (ie, no aphasia, apraxia, etc).
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There should be no accompanying focal neurological symptoms during the attack and no significant neurological signs afterwards.
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Epileptic features must be absent.
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Attacks must resolve within 24 hours.
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Patients with recent head injury or active epilepsy (ie, remaining on medication or one seizure in the past 2 years) are excluded.
Exposure to cold has been described as a precipitating factor in a number of case reports and descriptive studies of individuals with TGA. This is most commonly described around cold water immersion (recreational, experimental or reason undocumented),20–24 as well a case documenting TGA following exposure to cryotherapy (extremely cold dry air),25 and a case while sailing in the rain.26 Another case is described of an individual experiencing TGA after swimming underwater, having held their breath for 1 min (intentionally, without near-drowning).27 However, the nature and temperature of the water body are not disclosed and the case considered to be secondary to hypoxia by the authors.
This case was clearly associated with exposure to cold and is a somewhat archetypal scenario of cold water immersion followed by amnesia. However, in this case infarct remained a concern, especially given the prolonged nature of the amnesia and brief report of weakness but was considered less likely given the lack of acute infarction on MRI (performed while cognitively symptomatic) and precipitating circumstances with proven hypothermia. However, antiplatelet medications were commenced for secondary prevention to address this possibility. Although metabolic neuronal changes in the patient’s hippocampus resulting from cold exposure were hypothesised to be the most likely cause of her symptoms, it is also possible that the hyper-acute change in physiology from cold-shock response (hypertension) may have provoked transient endothelial dysfunction. Ischaemia may have occurred in a critically affected site, with a degree of small vessel disease seen on the MRI suggesting mild cerebrovascular dysfunction and the hippocampal neurons particularly vulnerable similarly as in TGA. Subclinical cerebrovascular dysfunction affecting this region may also have provoked the response seen in our patient purely due to the compromise associated with hypothermia.
Patient’s perspective
I started coming out of my fog in the late afternoon on the day of my episode when someone was asking me if I knew where I was and looking around I realised I was in hospital, although I had no recollection of how I got there. It took me some time to piece things together as my swimming stuff was there, so I got out of bed to feel the wetsuit and realised it was wet, so I thought I must have been in the water, but I couldn’t remember anything about it. I cannot remember anything about getting ready that morning, driving to the centre or anything during the day. Gradually I came to and became aware of staff asking me questions about the date, etc. I wrote some texts saying over and over ‘It’s all a bit of a mystery’ and I have relied on other people filling in the gaps telling me what happened. I still have no memory of the day but have not experienced any long term effects. I am just extremely grateful for the way I was looked after both at the centre and in the hospital.
Learning points
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Cold-water swimming is increasingly enjoyed by many as a recreational activity.
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Future research that seeks to further delineate the purported benefits of cold-water swimming will also serve to better qualify and quantify the risks involved.
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In cases of atypical transient global amnesia (eg, lasting more than 24 hours), the possibility of ischaemia should be considered and in the setting of normal imaging, the risk-benefit assessment of preventative (antiplatelet) treatment should be carefully considered.
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Enthusiasts should be aware of the risk of hypothermia and appropriate safety measures and mitigations should be implemented when swimming in cold water.
Ethics statements
Patient consent for publication
Footnotes
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Contributors RF drafted the manuscript and lead the writing of this case report. MMS provided further drafting of the manuscript. EH reviewed the manuscript.
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Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
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Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
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Competing interests EH: Grants: National Institute of Health Research Health Technology Assessment Grant; Elizabeth Blackwell Institute Health Data Strand; Engineering and Physical Sciences Research Council (EPSRC); Robotics and Everyday Life Award; Research for Patient Benefit (RfPB) Programme; Alzheimer’s UK Pump Priming Award. British Geriatrics Society; The Gatsby Foundation. Consulting and Honoraria: Kyowa Kirin; Abbvie; Luye; Medicys. Meetings and travel: Ever; Bial; Abbvie. Advisory boards: Kyowa Kirin; Bial; Abbvie. Commercial: Xeropoint. MMS: Honoraria: teaching provided on behalf of AbbVie. RF: none.
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Provenance and peer review Not commissioned; externally peer reviewed.
- © BMJ Publishing Group Limited 2023. No commercial re-use. See rights and permissions. Published by BMJ.
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