Case report

Po Wen Cheng,1 Ruei An Tsai,1 Chien-­Hui Lee,2 Wen-­Ching Chen1
1

General Psychiatry Department,
Yuli Hospital, Ministry of Health
and Welfare, Hualien, Taiwan
2
Department of Neurosurgery,
Buddhist Tzu-­Chi General
Hospital and Tzu-­Chi University,
Hualien, Taiwan
Correspondence to
Dr Wen-­Ching Chen;
​f90841021@​ntu.e​ du.​tw
Accepted 7 November 2023

© BMJ Publishing Group
Limited 2023. Re-­use
permitted under CC BY-­NC. No
commercial re-­use. See rights
and permissions. Published
by BMJ.
To cite: Cheng PW, Tsai RA,
Lee C-­H, et al. BMJ Case
Rep 2023;16:e255286.
doi:10.1136/bcr-2023255286

SUMMARY
A male patient in his 70s with chronic schizophrenia,
who could previously walk independently, developed
a gait disturbance without any significant neurological
deficit. Initially, his short step length and unstable
gait were thought to be related to extrapyramidal
symptoms caused by medication side effects. We
tapered his antipsychotic medication, but the unstable
gait persisted. After 2 weeks of observation, we noted
general weakness with left-­side dominance, leading
us to consider a focal brain lesion despite there being
no recent history of falling or trauma. A CT scan of the
brain showed chronic subdural haematoma and the
patient underwent emergency surgery. After 14 days
of treatment, he was discharged back to the chronic
ward.

CASE PRESENTATION

A male patient in his 70s with chronic schizophrenia, the onset of which occurred in his early
20s, had been in long-­term hospital care in Taiwan
for over 40 years. He had been taking olanzapine
5 mg and valproic acid 400 mg daily for about 3
years and was transferred to the acute ward due
to violent behaviour towards another patient,
which suggested exacerbation of symptoms. After
his admission to the acute ward, we continued to
administer his current psychiatric medication. He
had a relatively stable mood, could cooperate with
ward activity and could walk independently with no
violent behaviour noted. However, he had a short
step length with unstable gait—the typical manifestation of an extrapyramidal gait disturbance—and
leaned forward while walking. He started using a
wheelchair due to his gait disturbance about 1 week
after his transfer to the ward. No seizures, dizziness,
BACKGROUND
headache or recent falling episode was noted on
Extrapyramidal symptoms (EPS) are one of the the ward. Three weeks after being transferred, his
most common adverse effects observed in patients laboratory results showed normal levels of serum
taking antipsychotics. Also referred to as drug-­ sodium, potassium, chloride, calcium, creatinine,
induced movement disorders, the symptoms of blood urea nitrogen, aspartate aminotransferase
EPS include dystonia, akathisia and Parkinsonism. and alanine aminotransferase, as well as normal
In addition, prolonged use of antipsychotics can red and white cell counts. We considered psychicause tardive dyskinesia. Drug-­induced EPS results atric medication side effects related to EPS and thus
from antagonism of dopamine D2 receptors, one tapered and then withheld his psychiatric medicaof the main actions of antipsychotics, especially tion. However, the patient still had general weakin first-­generation drugs such as haloperidol and ness after we withheld his psychiatric medication for
fluphenazine. Although blocking of D2 receptors 7 days. He became bedridden due to general weakin the mesolimbic pathway can improve psychotic ness. We observed no improvement in EPS after
symptoms, blockage of the same receptors in the olanzapine was completely discontinued, and so we
nigrostriatal pathway may result in the unwanted consulted a neurologist for evaluation. Neurologeffects of EPS.1 When the blockage becomes long ical examination showed decreased muscle power
term, overexpression of downstream D2 receptors
may occur to compensate for the lack of dopamine,
which manifests clinically as tardive dyskinesia.2
Treatment usually includes discontinuing the current
antipsychotics, or prescribing anticholinergics such
as biperiden or trihexyphenidyl. EPS can be very
damaging to the patient‘s quality of life and is one
of the major reasons for patients dropping out of
pharmacotherapy, which can directly increase the
risk of relapse and rehospitalisation. Dealing with
EPS is a significant part of clinical practice and a
familiar scenario in the psychiatry field. Medication is not the only cause of EPS, however. Organic Figure 1 (A) Brain CT scan before surgical intervention.
brain injuries,3 for instance, may mimic such symp- The initial CT before surgery revealed chronic subdural
toms. Because of the potentially lethal nature of haematoma at right frontal, temporal and parietal region
brain injuries, timely and correct identification of with midline shift about 9 mm. (B) Brain CT scan after
the cause of symptoms is crucial. Reported here is surgical intervention. The postoperative brain CT revealed
a case of chronic subdural haematoma (SDH) that minimal subdural effusion without midline shift was
manifested as EPS, which was initially approached noted. The trephination surgery relieved mass effect due
as drug-­induced EPS.
to chronic subdural haematoma.
Cheng PW, et al. BMJ Case Rep 2023;16:e255286. doi:10.1136/bcr-2023-255286

1

BMJ Case Rep: first published as 10.1136/bcr-2023-255286 on 1 December 2023. Downloaded from http://casereports.bmj.com/ on April 18, 2024 by guest. Protected by copyright.

Chronic subdural haematoma mimicking
extrapyramidal symptoms

Case report

INVESTIGATIONS

In order to rule out intracranial haemorrhage, infarction or brain
tumour, we arranged for the patient to undergo a CT scan of
the brain.

TREATMENT

Surgical indications for SDH include neurological deficit and
massive mass effect with a midline shift of more than 5 mm. We
arranged emergency trephination of the chronic SDH in the
right parietal region, with a finding of>150 mL dark-­
brown
blood (motor oil like). The right parietal Jackson-­Pratt drainage
tube was removed at postoperative day 2.

OUTCOME AND FOLLOW-UP

The patient was transferred back to the hospital after being
discharged from the medical centre and underwent regular
follow-­up. He regained clear consciousness and can walk and
eat independently.

These symptoms may be misleading in patients with underlying
psychiatric disorders who are taking antipsychotic medication.
Because such movement disturbances are a common concern
in patients who use antipsychotics, as psychiatrists, we initially
considered the disturbance in the present case to be olanzapine-­
related EPS. We did not consider the possibility of a focal
neurological lesion until we consulted the neurologist. The
neurological examination showed decreased muscle power of
the left limbs, a positive left Babinski sign and hyperactive knee
jerk, triceps reflex, and brachioradialis reflex on the left side,
which implied reflex asymmetry, alerting us to the possibility of
a brain lesion.
This case highlights that medications such as antipsychotics
are not the only cause of EPS. An organic brain injury, such as
chronic SDH, may mimic these symptoms. Because chronic SDH
can be lethal, its timely detection and treatment is crucial.

Learning points
► In patients receiving antipsychotic treatment, medication side

effects are often overemphasised when symptoms related to
gait, weakness or alertness are observed.
► Such symptoms may instead be caused by a new medical
condition such as an organic brain injury.
► With a progressing brain injury, timely and correct
identification of the cause of the symptoms is crucial.
► The presence of a focal brain lesion may initially present as a
feature mimicking extrapyramidal symptoms.

Contributors This case was cared by Po Wen Cheng and Rue An Tsai under the
supervision of Wen-­Ching Chen. Surgical intervention was done by Chieu-­Hui Lee.
The report was written and discussed by all co-­authors.
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.

DISCUSSION

The presentation of chronic SDH can vary from no symptoms
to decreased memory, confusion, weakness or numbness of the
arms, legs and face and difficulty in speech and walking. Movement disorders such as Parkinsonism can also be associated with
SDH. Elderly people with subacute progressive Parkinsonism
should therefore undergo CT studies to differentiate it from
primary Parkinsonism.
The aetiology of chronic SDH includes head injury, subdural
effusion, cerebrospinal fluid leakage and spontaneous intracranial hypotension, especially in young-­aged patients to middle-­
aged patients, even without preceding trauma or haematological
disorders.
Surgery is the best treatment option for chronic SDH involving
moderate-­to-­large haematoma with accompanying neurological
deficits. The ideal treatment strategy should be tailored to the
individual patient’s condition. Careful supportive treatment can
be considered if it is well tolerated.4
In the present case, SDH was not diagnosed at our initial
impression due to the lack of neurological deficits and trauma
history. A patient with SDH may also initially present with withdrawn behaviour, the absence of speech, apathy, blunted affect
and poor self-­care, which may be thought to be manifestations
of psychosis.5 Moreover, in many cases of chronic SDH, reversible Parkinson-­like symptoms are the acute presenting feature.6

2

Patient consent for publication Consent obtained directly from patient(s).
Provenance and peer review Not commissioned; externally peer reviewed.
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licenses/by-nc/4.0/.
Case reports provide a valuable learning resource for the scientific community and
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to guide treatment choices or public health policy.

REFERENCES

1 Nevena D, Milica P, Igor J, et al. Second-­generation antipsychotics and extrapyramidal
adverse effects. BioMed Res Int 2014:
2 Burke RE, Fahn S, Jankovic J, et al. Tardive dystonia: late-­onset and persistent dystonia
caused by antipsychotic drugs. Neurology 1982;32:1335–46.
3 Scott O, Hasal S, Goez HR. Basal ganglia injury with extrapyramidal presentation: a
complication of meningococcal meningitis. J Child Neurol 2013;28:1489–92.
4 Yadav YR, Parihar V, Namdev H, et al. Chronic subdural hematoma. Asian J Neurosurg
2016;11:330–42.
5 Kar SK, Kumar D, Singh P, et al. Psychiatric manifestation of chronic subdural
hematoma: the unfolding of mystery in a homeless patient. Indian J Psychol Med
2015;37:239–42.
6 Guppy KH, Khandhar SM, Ochi C. Reversible Parkinson-­like symptoms in patient with
bilateral chronic subdural hematomas and cervical spinal stenosis. World Neurosurg
2018;109:285–90.

Cheng PW, et al. BMJ Case Rep 2023;16:e255286. doi:10.1136/bcr-2023-255286

BMJ Case Rep: first published as 10.1136/bcr-2023-255286 on 1 December 2023. Downloaded from http://casereports.bmj.com/ on April 18, 2024 by guest. Protected by copyright.

of the left limbs, a positive left Babinski sign and hyperactive
knee jerk, triceps reflex and brachioradialis reflex on the left
side. Thus, a focal brain lesion in the right hemisphere was
suspected. The patient was transferred to a general hospital for
further evaluation. A CT scan of his brain showed chronic SDH
in the right frontal, temporal and parietal lobes (figure 1A). He
was then transferred to a medical centre for surgical intervention
by means of trephination of the chronic SDH in the right parietal
region. A follow-­up CT scan of the brain revealed only minimal
subdural effusion without a midline shift (figure 1B). The
drainage tube was removed, following which the patient’s limb
weakness improved. After his surgical stitches were removed, the
patient was discharged and transferred back to the hospital in
stable condition. He is currently in the chronic ward with clear
consciousness and improved muscle power.

Case report
BMJ Case Rep: first published as 10.1136/bcr-2023-255286 on 1 December 2023. Downloaded from http://casereports.bmj.com/ on April 18, 2024 by guest. Protected by copyright.

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Cheng PW, et al. BMJ Case Rep 2023;16:e255286. doi:10.1136/bcr-2023-255286

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