Recovery from Decreased Cerebral Blood Flow in Wernicke’s Encephalopathy Following Abstinence from Alcohol – a Case Report
There have been few reports of recovery from reduced cerebral blood flow (CBF) in patients with Wernicke’s encephalopathy. We report a 70‑year‑old patient with a 2-day history of increased irritability and minimal vocalisation. Neurological examination revealed no abnormal findings. He was diagnosed as having Wernicke’s encephalopathy, because both the blood thiamine concentration and erythrocyte transketolase activity were low. SPECT revealed CBF reduction in many regions of the brain. After thiamine treatment, he reported that he had abstained from alcohol. Two weeks later, all symptoms had resolved completely. SPECT was repeated one month after onset and the CBF reductions observed in the first examination had recovered to almost normal levels. These results suggest that thiamine treatment and abstinence from alcohol can result in recovery from decreased CBF in patients with Wernicke’s encephalopathy, as long as the neurological symptoms are not severe.
Key words: cerebral blood flow – single photon emission computed tomography – Wernicke’s encephalopathy – abstinence from alcohol
Y. Suzuki; K. Ogawa; M. Oishi; T. Mizutani
Division of Neurology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan
Vyšlo v časopise:
Cesk Slov Neurol N 2010; 73/106(2): 187-189
Bylo zaznamenáno několik zpráv o pacientech s Wernickeovou encefalopatií, u kterých došlo k úpravě sníženého mozkového průtoku (CBF). Uvádíme případ 70letého pacienta s anamnézou dvou dnů zvýšené podrážděnosti a nemluvnosti. Při neurologickém vyšetření nebyly zjištěny žádné abnormální nálezy. Byla u něj diagnostikována Wernickeova encefalopatie, protože koncentrace thiaminu v krvi i transketoláza v erytrocytech byly nízké. SPECT odhalila snížení CBF v mnoha oblastech mozku. Po thiaminové léčbě pacient oznámil abstinenci alkoholu. O dva týdny později již nebyly žádné příznaky patrny. Jeden měsíc po nástupu obtíží byla SPECT zopakována; CBF, který byl při prvním vyšetření nižší, se vrátil na téměř normální úroveň. Tyto výsledky naznačují, že léčba thiaminem a abstinence alkoholu mohou vést k vyřešení sníženého CBF u pacientů s Wernickeovou encefalopatií, pokud nejsou neurologické příznaky vážné.
consume alcohol for various reasons. Consumption of alcohol in moderate amounts
(men ~30g/day; women ~20g/day) can help alleviate psychological
stress and promote smooth personal relationships, and these effects may be
pronounced. However, chronic and excessive ethanol consumption (men > 50g/day; women >35g/day) can result in
various neurological diseases, such as cerebellar degeneration, cerebral atrophy, Wernicke’s encephalopathy, Marchiafava‑Bignami disease, spontaneous
intracranial haemorrhage, epilepsy, and peripheral neuropathy. Chronic excessive alcohol consumption has also
been shown to decrease cerebral blood flow (CBF) in various regions of the
brain [1,2]. However, there have been a few reports [3,4] of recovery from
such reduced CBF in patients with Wernicke’s encephalopathy. We report herein
a patient with a history of excessive alcohol consumption in whom
a recovery from reduced CBF was observed following thiamine therapy and
abstinence from alcohol.
The patient was a 70‑year‑old man, by occupation the manager of a small company. He had
consumed more than 2,500ml of beer (5% alcohol by volume) every day
for more than 20 years. He presented at our hospital with a 2-day
history of increased irritability and minimal vocalisation, as reported by his
family. He had ingested little nourishment other than alcohol during the
previous three days due to excessive work‑related stress. While
the patient himself did not feel that anything was wrong, his family reported
that he was more irritable and spoke less than usual. General physical
examination revealed no abnormalities. His temperature at the time of the first
examination was 35.6 °C,
his pulse was 72 beats/min, and his blood pressure was 124/78 mmHg.
On neurological examination, there were no abnormal findings; the disturbed
con-sciousness, ataxia, and diplopia
that usually accompany Wernicke’s encephalopathy
were absent. Laboratory studies revealed that his aspartate aminotransferase
(AST) was 40 (normal range, 8–38) U/l, alanine aminotransferase (ALT)
45 (normal range, 4–44) U/l, blood thiamine concentration 16 (normal
range, 20–50) ng/ml, and erythrocyte transketolase activity 0.61 (normal
range, 0.75–1.30) IU/gHB. Magnetic resonance imaging (MRI) of the head showed
no abnormalities except for slight bilateral frontal lobe atrophy. Three days
after his hospital visit, single photon emission computed tomography (SPECT)
was performed using the 99mTc‑ECD Patlak Plot method
. It revealed reduced CBF in most regions of the brain (Fig. 1A). EEG
revealed background activity of 9 Hz a waves, with a small number of 7 Hz θ waves (Fig. 2A). These
findings appeared to indicate early‑stage Wernicke’s
encephalopathy. The patient was therefore treated with infusions of 100mg of thiamine daily for three days, and was instructed to abstain from
alcohol and eat a well‑balanced diet with vitamin supplements.
Within a few days, he became calmer and began to speak more. Two weeks
later, all symptoms had resolved completely. SPECT was repeated one month after
the first visit to our hospital and revealed that the CBF reductions noted in
most brain regions on the first examination had recovered to almost normal
levels (Fig. 1B). EEG taken one month after onset revealed background activity
of 10 Hz a waves without slow waves (Fig. 2B).
Cerebral glucose metabolism [6,7] and CBF [1,2] are
known to be decreased in chronic alcoholic patients. Decreased regional CBF is
thought to begin before the onset of the neurological and psychiatric symptoms
in chronic alcoholic patients . However, there are a few reports [3,4]
of recovery from such reduced CBF in patients with Wernicke’s encephalopathy.
Meyer et al measured CBF by 133Xe inhalation in nine Wernicke‑Korsakoff syndrome cases (all men; mean daily alcohol consumption,
202 ± 126g; mean duration of alcohol consumption,
25.1 ± 10.9 years) before and three months after treatment and
reported resultant CBF increases of ~25% with improvement of cognitive and
neurological impairments . Benson et al measured CBF by SPECT before and four
months after treatment of a 32‑year‑old woman who presented with severe learning deficits plus impaired
performance . Her daily consumption and duration of alcohol consumption were
unclear. They reported that repeat SPECT showed a return to normal perfusion
in the frontal brain areas, but little improvement in the medial diencephalic
region, although her amnesia remained.
In the present case,
following abstinence from alcohol, the patient’s symptoms disappeared within
one week and the CBF reductions returned to almost normal levels in most brain
regions within one month. These results suggest that abstinence from alcohol
can result in recovery of the decreased CBF in Wernicke’s encephalopathy, as
long as the neurological symptoms are not severe. It is important to advise
such patients to abstain strictly from alcohol and to eat a balanced diet.
Thus, even though the
mechanism still remains unknown, abstinence from alcohol can improve cerebral
metabolism  and vascular smooth muscle contraction . Some reports have
suggested that neurogenesis from neural stem/progenitor cells is
a possible mechanism underlying the structural plasticity in chronic
alcoholic patients . Nixon et al reported that microgliosis could contribute
to volume recovery in non‑neurogenic regions during abstinence from
alcohol in a model of alcohol abuse disorders . These may be
associated with recovery from decreased CBF in Wernicke’s encephalopathy.
In conclusion, thiamine
treatment and abstinence from alcohol can result in recovery from decreased CBF
in patients with Wernicke’s encephalopathy, as long as the neurological
symptoms are not severe.
Accepted for review: 22. 9. 2009
Accepted for print: 21. 1. 2010
Division of Neurology, Department of Medicine
Nihon University School of Medicine
30-1 Oyaguchikami-machi, Itabashi-ku
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