European Journal of Clinical Nutrition (2013), 12

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CLINICAL CASE REPORT

Delirium as a result of vitamin B12 deciency in a vegetarian

female patient
K Mavromati and O Sentissi
Vitamin B12 deciency can manifest with haematological, gastrointestinal and neuropsychiatric signs. The neuropsychiatric
symptoms may be concurrent or precede the other symptoms. The reported case is a clinical case of delirium due to vitamin
B12 deciency in a female vegetarian patient. The patient was treated with vitamin B12 supplementation. Initially, it was
difcult to diagnose this patient, who presented with delirium that could have been due to multiple causes. The nding
underlines the importance of conducting a complete laboratory test panel for delirium, including the blood levels of
vitamin B12.
European Journal of Clinical Nutrition advance online publication, 17 July 2013; doi:10.1038/ejcn.2013.128
Keywords: delirium; vitamin B12 deciency; vegetarian

INTRODUCTION
Vitamin B12 deciency is a public health problem that affects
B20% of elderly people.1 It can manifest as haematological,
gastrointestinal or neuropsychiatric signs and symptoms
with depression, dementia, catatonia and delirium, which are
considered as precursors.24 Studies have shown a high risk
of depression in elderly women with vitamin B12 deciency
compared with healthy female individuals.5,6
The lack of cobalamin is caused by food cobalamin malabsorption and pernicious anaemia. Dietary causes of vitamin B12
deciency are rare and typically concern elderly people. Strict
vegetarianism can lead to a lack of vitamin B12 ingestion and,
hence, its deciency in the body.5
Neuropsychiatric signs and symptoms secondary to vitamin B12
deciency can be explained by the involvement of vitamin B12, as
well as folate and homocysteine, which are involved in the carbon
transfer metabolism (methylation) required for serotonin production, a crucial step in monoamine synthesis.2
We report the case of a patient for whom the diagnostic and
aetiological work-up indicated delirium secondary to vitamin B12
deciency.

CASE PRESENTATION
Mrs G was a 62-year-old widow of Argentinean origin. She was a
storekeeper and mother of four children and worked at her own
kiosk. She was vegetarian, with a history of a major depressive
episode 5 years ago with complete remission of the episode under
venlafaxine treatment.
She was admitted to the emergency department accompanied
by the police, as she was found wandering lost and confused. She
complained of suffering from insomnia, fatigability and poor
concentration. Following some standard physical and blood tests,
no physical explanation was found to explain her symptoms, and
the patient was taken to our outpatient psychiatric crisis centre.

She presented moderate psychomotor retardation, confusion and

partial disorientation. She had depressed mood and anxiety, poor
concentration and difculty in speech. She also complained of
sleep disturbances for the last few days and fatigue. The memory
decits and insomnia had a rather acute onset over the past days
and presented a uctuation of symptom severity over hours.
A psychometric evaluation demonstrated that the patient
scored 27 on the Montgomery-Asberg Depression Rating Scale
(MADRS) and 22/30 on the Mini Mental Status Examination
(MMSE). We executed a pathologic clock test, and she scored
20 on the Delirium Rating Scale Revised-98 (DRS-R-98) (cutoff
score: 18), indicating delirium with the presence of severe
depressive symptoms and cognitive deciencies.
Upon physical examination, the patient did not present any
pathologic signs or symptoms apart from hypertension (up to
190/110 mm Hg) that required antihypertensive treatment with
ramipril 5 mg. The investigations revealed normal haematological
and ionogram levels. Her serum vitamin B12 level was low at
91 pmol/l (135700 pmol/l), and folic acid was normal at 22.2 mg/l
(4.124 mg/l). Mrs G had a history of vitamin B12 deciency
without presenting neuropsychiatric symptoms at the given time.
The cause of the vitamin B12 deciency was attributed to the
patients strict vegetarianism. We conducted viral and bacterial
screening to exclude an infectious cause of the patients current
status. The serologic results for Lyme were fairly positive for
immunoglobulin M but not immunoglobulin G. The infectious
disease specialist proposed a retest on the subsequent month,
and the results were negative. Other investigations, including
brain magnetic resonance imaging, showed diffused cortical and
subcortical atrophy and some nonspecic abnormalities of the
white matter concordant to the age of the patient. Neuropsychiatric tests, which were conducted 2 weeks after the beginning
of the treatment in our clinic, revealed multiple cognitive
decits that could be explained by either deterioration due to
the patients age or a depressive episode.

Department of Mental Health and Psychiatry, University Hospitals of Geneva, Geneva, Switzerland. Correspondence: Dr SEI Othman, Department of Mental health and psychiatry,
University Hospitals of Geneva, CAPPI Jonction, 35 Rue des bains, Geneva 1205, Switzerland.
E-mail: O.sentissi@hcuge.ch
Received 27 January 2013; revised 8 June 2013; accepted 10 June 2013

Delirium and vitamin B12 deciency

M Katerina et al

2
As no other cause of delirium was found, the patient
was empirically treated with weekly injections of 1000 mg of
cyanocobalamin. The vitamin B12 level was normalised 1 week
later (330 pmol/l). Treatment with escitalopram 10 mg/day was
gradually initiated the week following the rst evaluation, as the
depressive symptoms persisted. A psychiatric examination 2
weeks after the rst evaluation revealed an important diminution
of the cognitive deciency and a partial remission of the
depressive symptoms (MADRS score 22, MMSE 28/30 and
DRS-R-98 4; the clock test was normalised).
Four weeks after the episode, Mrs G presented premorbid
functioning levels, total remission of the depressive symptoms
(MADRS score: 4) and stable mental status; she had already
resumed working on a full-time basis.

lack of other possible causes conrmed our diagnosis of delirium

due to vitamin B12 deciency.10
In conclusion, with this case report, we would like to draw
clinicians attention to vitamin B12 deciency as a reversible cause
of delirium and to the importance of conducting a complete
laboratory work-up for delirium, including the blood levels of
vitamin B12.

CONFLICT OF INTEREST
The authors declare no conict of interest.

REFERENCES
DISCUSSION
We report the case of a patient with delirium for whom
an aetiological investigation indicated a probable vitamin B12
deciency. We emphasise the importance of conducting a wide
range of laboratory tests, including an evaluation of vitamin blood
levels.
The laboratory and clinical examinations we conducted
excluded infectious, vascular, neoplastic, metabolic and endocrine
causes. Our patient had a previous major depressive episode in
addition to high blood pressure, leading to the hypertension
diagnosis, which was considered a predisposing factor of the
delirium.7
The signicant improvement in cognitive function, the return to
a normal level of consciousness and the remission of
her depressive and anxiety symptoms could be explained by
the introduction of the vitamin B12 treatment, rather than
escitalopram at 10 mg/day for only 8 days.8
The remaining multiple cognitive decits were most likely due
to the depressive episode, primary symptoms of dementia or even
the vitamin B12 deciency. Although the results of studies
concerning cobalamin deciency as an aetiology of cognitive
deciency and dementia are controversial, some have shown that
vitamin B12 supplementation can reduce the delirium associated
with dementia in patients with low serum cobalamin levels.9 The
positive clinical response to the substitution treatment and the

European Journal of Clinical Nutrition (2013) 1 2

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