Case of recurrent cerebral haemorrhage in an older
adult man who uses dimethylsulfoxide (DMSO) for
self-­management of low mood and pain
Jonathan Olds,1 Mohamed Yousif,2 Oladotun Abidakun,3 Abigail Cannon4
1

Later Life Liaison Psychiatry,
University Hospitals Bristol and
Weston NHS Foundation Trust,
Bristol, UK
2
Department of Medicine,
University Hospitals Bristol and
Weston NHS Foundation Trust,
Bristol, UK
3
Department of Stroke Medicine,
University Hospitals Bristol and
Weston NHS Foundation Trust,
Bristol, UK
4
Department of Geriatric
Medicine, University Hospitals
Bristol and Weston NHS
Foundation Trust, Bristol, UK
Correspondence to
Dr Jonathan Olds;
​jonathan.​olds@​nhs.​net
Accepted 19 January 2021

The residual deficits following the previous haemorrhages were neuropsychiatric and predominantly
arose following bilateral frontal lobe damage;
including anhedonia, mild perseverance, a lack of
executive function and symptoms of depression.
The patient’s motor and sensory functions were
preserved and the patient was discharged home
with a package of care and follow-­up within the
primary care sector with Neurology input. In 2020,
the patient was admitted to hospital with confusion of acute onset and a CT scan of the patient’s
brain revealed a further haemorrhage within the
left frontal lobe. The patient had a history of mild
depression and held health beliefs that were not
consistent with the western medical model. The
BACKGROUND
Dimethylsulfoxide (DMSO) is a colourless, patient declined to use conventional antidepresodourless liquid. The medical uses of DMSO sant medication prescribed by the general practihave generally fallen in to three functional cate- tioner (GP); instead using DMSO that he purchased
gories encompassing tissue/organ preservation, from the internet; believing this to be helping his
penetration-­
enhancing solvent excipients and mood. This was contrary to his GP’s advice and
active pharmaceutical agents, primarily anti-­ concerns raised by his family. The patient described
inflammatory.1 DMSO has been available on the having used DMSO for at least 2 years prior to the
online market; with reported but unsubstanti- first intracerebral haemorrhage. The patient was
ated benefits of use in arthritis. Some studies have admitted to hospital by ambulance after having teleshown that DMSO has toxic effects; for instance, phoned a relative and appeared to be confused. The
it can induce red blood cell haemolysis, reducing patient’s relative was duly concerned and alerted
platelet (PLT) activities and decreasing PLT aggre- the ambulance service. On arrival to the patient’s
gation levels, inhibiting the growth of EAhy926 home, the ambulance crew noted that there was
cells, preventing cell progression from G1 phase to evidence that the patient had used DMSO; despite
S phase and elevating apoptosis rates. Additionally, the advice from his GP and other medical profesit has been reported that DMSO can cause an intra- sionals to stop using it.
cerebral bleed.2
The patient displayed symptoms consistent with
People often use DMSO for arthritic joint pain, a frontal brain injury including marked persefor speeding up wound healing, treating eye condi- verance; as evidenced by compulsively walking
tions such as cataract and glaucoma and for lowering around the ward and pulling alarms in a repetintracranial hypertension. DMSO is usually taken itive manner. There was a marked deficiency of
by mouth or used topically over the skin and in rare executive function as well as hostility and agitaoccasions intravenously.3
tion; consistent with a change in personality.
Through our case report, we wish to reflect on
Social disinhibition was also a feature during the
one of the potentially fatal side effects of DMSO—
patient’s admission.
the ability to induce an intracerebral haemorrhage.

SUMMARY
We present the case of a man in his 70s who had
suffered two separate frontal lobe haemorrhages in the
context of using dimethylsulfoxide (DMSO) to manage
his low mood. The known pathophysiology of DMSO
renders it a likely causative agent of the recurrent
intracerebral haemorrhages. This case highlights the
need for clinicians to robustly enquire about a patient’s
use of over-­the-­counter medications, of non-­prescribed
supplements and other substances, as part of the history.
In addition, the case highlights the potential for highly
debilitating adverse effects from using DMSO.

CASE PRESENTATION
© BMJ Publishing Group
Limited 2021. No commercial
re-­use. See rights and
permissions. Published by BMJ.
To cite: Olds J, Yousif M,
Abidakun O, et al. BMJ Case
Rep 2021;14:e240371.
doi:10.1136/bcr-2020240371

The patient is a man in his 70s who lives alone
with a medical history of two intracerebral haemorrhages (initially left-­
sided frontal intracerebral
haematoma in 2018 and a right-­sided frontal intracerebral haemorrhage in 2019); each individually
affecting the left and right frontal lobes. Otherwise,
the patient had enjoyed good physical health and
worked in an active outdoor profession up until the
second haemorrhage.

INVESTIGATIONS
In 2018, the patient had his first intracerebral
bleed. His head CT scan showed large 4 cm×3.3
cm×3 cm left frontal intracerebral haematoma with
some subarachnoid extension.
After 6 months, the patient had brain MRI and
magnetic resonance angiography (MRA) as a
follow-­up to exclude any underlying causes for the
bleed. MR angiography was reported as normal by
the neuroradiologist and there was no evidence of

Olds J, et al. BMJ Case Rep 2021;14:e240371. doi:10.1136/bcr-2020-240371

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occurred within the frontal lobe which is an uncommon area for
a hypertensive intracerebral bleed.4

Tumour

Many studies showed that brain tumours can present with acute
intracranial bleeds.5–7 The patient’s medical records indicate that
he did not experience any symptoms consistent with malignancy.
Additionally, all the investigations and scans failed to detect any
tumour or malignancy.

Cerebral amyloid angiopathy

Figure 1 CT of the head.
cerebral amyloid angiopathy (CAA) pathology demonstrated no
evidence of arteriovenous malformation.
15 months later, the patient had his second intracerebral bleed
and his head CT revealed a new localised haemorrhage in the
right frontal lobe measuring maximum 4 cm diameter.
On the last admission, a new large 4 cm×3.3 cm×3 cm left
frontal intracerebral haematoma with some subarachnoid extension was found on his head CT scan (figure 1).
Blood tests such as C-­reactive protein (CRP), urea and electrolytes, liver function test and clotting profile were unremarkable.

DIFFERENTIAL DIAGNOSIS
Hypertension

Hypertension is considered to be the most common cause of
intracranial haemorrhage. It usually affects basal ganglia (mainly
putamen), thalamus, pontine and cerebellum. During all the
three intracerebral bleeds, the patient’s blood pressure was
found to be within the normal range and he has never been diagnosed with hypertension. Additionally, all of the three incidences

Learning points
►► Dimethylsulfoxide is increasingly understood to be implicated

in adverse events, including intracerebral haemorrhage.

►► Over-­the-­counter or supplemental medication need to be

considered as potential contributing factors to a patient’s
pathology and need to be enquired about robustly in the
history-­taking.
►► There are significant psychosocial consequences of frontal
brain damage with limited evidence for pharmacological
treatment. Often, medication may need to be tried off-­
license. Consultation with patients and their triangle of care
and consideration and discussion of the aims and potential
limitations of each medication choice are important.
2

CAA is considered as the third most common cause of spontaneous intracerebral haemorrhage after hypertension and
subarachnoid aneurysmal haemorrhage.8 CAA is a deposition of
amyloid beta peptide in blood vessels of the brain and usually
affects the small and medium size vessels. CAA is a degenerative
vasculopathy that is classically associated with lobar intracerebral
or sulcal haemorrhage.8 This patient suffered recurrent frontal
lobar bleed. Furthermore, the prevalence of CAA increases with
age with autopsy studies suggesting a prevalence of about 30% in
60-­year to 69-­year olds and over 50% in the age range from 70
to 89 years. The age of this patient fits perfectly into the higher
prevalence range.9 Although a definitive diagnosis of CAA can
only be made by post-­mortem biopsy, neuroimaging especially
MRI sequence of gradient echo and susceptibility-­
weighted
imaging are useful in detecting microbleeds and deposition
of iron on the brain cortex (cortical superficial siderosis).10 11
However, this patient had multiple brain scans including CT
and MRI, but there was no evidence to support the diagnosis of
amyloid angiopathy.4 10 12

Trauma

Although the patient had a history of an unwitnessed fall in July
2019, the immediate scans did not show any signs of acute intracerebral injury and there was no evidence of any neurological
sequelae.

TREATMENT

The neurosurgical team had made the decision that surgical
intervention was not indicated and therefore conservative
management was commenced. The patient’s blood pressure was
monitored and the systolic pressure was physiologically and
consistently lower than 130 mm Hg. Consistent with recommendations and best practice for patients who have had a stroke,
nutrition and hydration were monitored and optimised.13
The patient’s swallow was not impaired and therefore he was
able to eat and drink without restriction. As with all patients
presenting with a brain haemorrhage, physical rehabilitation was
considered. However, the patient displayed symptoms consistent with a frontal brain injury including marked perseverance,
deficiency of executive function as well as intermittent hostility
and agitation. With the patient’s history of depressive disorder
and previous successful treatment with mirtazapine, we restarted
the mirtazapine on the patient’s admission. Unfortunately, the
patient was not able to engage in a conversation about his mental
state or about the reinstatement of mirtazapine; owing to his
cognitive deficit and it was thus restarted in his best interests after
discussion with the MDT. While objective measures for affective
disorder such as the Brief Assessment Schedule Depression Cards
(BASDEC) were considered, the patient’s cognitive impairment
did not render them appropriate in terms of attaining reliable
diagnostic information. Blood tests revealed no biochemical or
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Case report

endocrine parameter that was deranged and hence potentially
modifiable in terms of improving the patient’s affective state.
Furthermore, primary care records were consulted in order
to add further information to making a best interests decision
around prescribing mirtazapine and the records indicated that
the patient had been experiencing symptoms consistent with
depressive disorder; including anhedonia, fatigue, tearfulness,
disturbed sleep and a lack of appetite for at least 6 weeks prior
to his admission. At times, the patient’s presentation put him
and staff members at risk of physical harm and therefore antipsychotic medication was used in order to try to help with these
symptoms. Initially, we treated the symptoms as if they were
part of a delirium and haloperidol was used, after following the
NICE guidelines for non-­pharmacological techniques in terms
pharmacological techniques
of managing delirium. The non-­
employed included the use of 1:1 nursing care, a well-­lit nursing
bay, management of pain and constipation and optimisation
of food and fluid intake. Furthermore, day/night orientation
was promoted. The diagnosis of delirium was made clinically;
aided by the use of the 4AT test. The 4AT test is a short tool for
delirium assessment and a score of 4 or above suggests presence
of a possible delirium±cognitive impairment. The patient, on
assessment, scored the maximum score of 12 and in the absence
of previous cognitive impairment, the acute onset of symptoms
and the known brain insult, delirium was highly suspected.
Haloperidol had little effect on the patient’s symptoms. There is
a lack of evidence for pharmacological management of psychiatric consequences such as challenging behaviours with frontal
brain injuries. The use of antipsychotics remains of research
interest,14 but the selection of an appropriate medication is
often guided by clinical judgement and the balance of risk versus
potential benefit. Owing to the known prolactinergic effects of
amisulpride as well as its sedative profile, we tried amisulpride
to manage the perseverant and driven behaviours. However,
this had little effect in alleviating the patient’s symptoms and
was hence converted to risperidone, as this has an evidence base
and a license for use in behavioural and psychological symptoms
of dementia (BPSD). While we recognised that the patient did
not have a diagnosis of dementia, the step-­down deterioration
in his cognitive function and behaviours consistent with organic
disease of vascular origin rendered him suitable to warrant the
trial of risperidone.

OUTCOME AND FOLLOW-UP

The risperidone helped with the symptoms of agitation and
aggression, but the perseverant behaviour persisted and at
times the patient was disinhibited and agitated. In order to
meet the patient’s care needs safely while allowing the potential for neurorehabilitation, the patient was discharged from the
acute hospital to nursing residential care with input from the
community older adult psychiatric services to further review the
patient’s mental state and recovery.

DISCUSSION

To our knowledge, published cases of brain haemorrhage in
the context of the use of DMSO are very sparse. A case report
published in 2004 presented a 55-­
year-­
old man who had
presented with three haemorrhagic areas within the brain after
ingesting DMSO.15 In this particular case report, the patient also
had metastatic disease within the brain. This is the first published
case report that we are aware of that demonstrates brain haemorrhage in an otherwise healthy adult male, where DMSO has
been ingested. Clinical guidelines for the management of brain
Olds J, et al. BMJ Case Rep 2021;14:e240371. doi:10.1136/bcr-2020-240371

haemorrhage are comprehensive. However, there is a deficit
in guidelines regarding the pharmacological management of
frontal brain injury with challenging symptoms such as agitation, aggression and sexual disinhibition. The British Association of Psychopharmacology recommends the use of haloperidol
to manage challenging behaviours in the context of delirium
and hence this was the initial medication choice in this case.16
However, haloperidol had little effect on the patient’s symptoms
and therefore we tried amisulpride off-­license with its known
sedative profile, and risperidone, as risperidone has an evidence-­
base and a license for use in BPSD.17 While we recognised that
the patient did not have a diagnosis of dementia, the step-­down
deterioration in his cognitive function and behaviours consistent
with organic disease of vascular origin rendered him suitable to
warrant the trial of risperidone.
Twitter Oladotun Abidakun @ABIDOTUN
Acknowledgements We would like to acknowledge the clinical support of
Dr Clare Holmes; consultant in Stroke Medicine and Head of Care of the Elderly
Medicine at the Bristol Royal Infirmary. We thank Dr Holmes for her support with
regards to the formulation of this case report. We also wish to acknowledge the
clinical care by both the Acute Stroke Team and the Later Life Liaison Psychiatry
team.
Contributors JO and MY contributed equally to this paper and were involved in
the conception and created first draft of the case report. OA and AC provided input
with regard to differential diagnoses and the background to the report as well as
ammending the first draft. All authors contributed to, and are satisfied with the final
submission.
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.
Competing interests None declared.
Patient consent for publication Next of kin consent obtained.
Provenance and peer review Not commissioned; externally peer reviewed.

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