Psychiatry and Clinical Neurosciences 2012; 66: 618–621
doi:10.1111/j.1440-1819.2012.02399.x
Short Communication
Peduncular hallucinosis secondary to central
pontine myelinolysis
Mark Walterfang, MBBS, PhD, FRANZCP,1,2* Anita Goh, BSc, DPsych,1,3
Ramon Mocellin, MBBS, MSc, MPM, FRANZCP,1,2 Andrew Evans, MBBS, MD, FRACP1 and
Dennis Velakoulis, MBBS, MMed, DMedSci, FRANZCP1,2
1
Neuropsychiatry Unit, Royal Melbourne Hospital, 2Melbourne Neuropsychiatry Centre, University of Melbourne and North
Western Mental Health and 3Academic Unit for Psychiatry of Old Age, University of Melbourne, Melbourne, Australia
Peduncular hallucinations are generally associated
with lesions in the midbrain. They have rarely been
associated with central pontine myelinolysis, a condition associated with rapid alterations in serum
sodium and chronic alcoholism. Described herein
is the case of a 46-year-old man who developed
typical peduncular hallucinations, whose imaging
demonstrated central pontine myelinolysis. After
alcohol cessation and neuroimaging resolution, the
patient’s hallucinatory phenomena abated.
OMPLEX VISUAL HALLUCINATIONS (CVH)
can result from a variety of processes that disturb
the transmission, processing and modulation of
visual information.1 We describe a case of CVH
resulting from central pontine myelinolysis (CPM),
in which both the hallucinosis and the pontine lesion
resolved concomitantly.
walls, mostly during periods of low light. Figures
would approach him and stare. These periods were
not during periods of alcohol withdrawal, and did
not occur on the periphery of sleep. He described
some memory problems and reported drinking half
to one bottle of spirits per day. He denied other
substance use. He began to drink during a period of
depression following divorce 10 years previously, but
had not used alcohol for more than 1 week. His
blood alcohol level at assessment was zero.
On mental state examination, he was cooperative
and language was intact with no word-finding
difficulty/thought disorder. He described complex
visual hallucinations, in addition to simple auditory
hallucinations of male voices. Insight was limited.
Neurological examination indicated no focal signs
other than reduced vibration sensation and proprioception peripherally, broad-based gait and positive
pout/palmomental reflexes. He scored 57/100 on
the Neuropsychiatry Unit COGnitive assessment
tool (NUCOG),2 with greatest deficits in memory,
attention and executive functioning; a score on the
NUCOG of <70 is consistent with moderate–severe
cognitive impairment. Formal neuropsychological
assessment indicated low average premorbid
function, and difficulties with self-monitoring,
C
CASE REPORT
A 46-year-old alcoholic man presented because of
auditory and visual hallucinations. For some years,
he heard multiple derogatory male voices saying he
would be shot. He had been treated with 10 mg/day
olanzapine for 3 years.
He also reported a 6-month history of complex
visual hallucinations of Lilliputian figures, small malformed animals and faces, that moved in and out of
*Correspondence: Mark Walterfang, MBBS, PhD, FRANZCP,
Neuropsychiatry Unit, Level 2, John Cade Building, Royal Melbourne
Hospital, Melbourne, Vic. 3050, Australia.
Email: mark.walterfang@mh.org.au
Received 31 January 2012; revised 17 June 2012; accepted 20 June
2012.
618
Key words: alcohol, hallucinations, myelinolysis,
peduncular, pons.
© 2012 The Authors
Psychiatry and Clinical Neurosciences © 2012 Japanese Society of Psychiatry and Neurology
Psychiatry and Clinical Neurosciences 2012; 66: 618–621
Hallucinations due to pontine myelinolysis 619
P
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7
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Figure 1. Magnetic resonance imaging at (top) first presentation and (bottom) follow up. (Left) Sagittal T1 shows hypointensity
in the pons, while (middle) axial FLAIR and (right) T2 images show hyperintensity; note significant resolution at 30 months.
abstraction and mental flexibility in addition to
memory retrieval, attention, and psychomotor speed
impairments. Visuospatial skills were intact.
He had elevated mean corpuscular volume and
elevated g-gluteryl transferase consistent with recent
heavy alcohol intake. Serum sodium was normal.
Magnetic resonance imaging (MRI) of the brain
(Fig. 1) showed central cystic high signal within the
pons, without extra-pontine change (Fig. 2). Computed tomography done 8 months earlier showed no
pontine lesions. Overall, the imaging findings suggested recent CPM, superimposed on the likely
central effects of chronic alcohol use. His hallucinosis
responded to 10 mg per day of olanzapine, and
alcohol abstinence.
The patient was reassessed 30 months later. At this
time, he had not consumed alcohol for 12 months,
and continued antipsychotic treatment. Auditory
hallucinations continued intermittently. He had,
however, not experienced visual hallucinations for 12
months. His NUCOG score had improved to 77/100,
particularly in attention and executive function,
and neurologically he demonstrated only mild
antipsychotic-related parkinsonism. Neuropsychological assessment showed improvements in attention and working memory skills, executive function,
and memory retention. On MRI, there was a significant resolution of his pontine lytic lesion with an
area of increased signal, indicating residual gliosis.
Informed consent to report his presentation was
provided.
DISCUSSION
Peduncular hallucinosis (PH) was first described in a
mesencephalic lesion, with visual hallucinations of
colorfully attired people and groups of children that
occurred during low light.3 It has since been associated with pathology in the pons, midbrain and thalamus.1 Hallucinations in PH result from alterations to
© 2012 The Authors
Psychiatry and Clinical Neurosciences © 2012 Japanese Society of Psychiatry and Neurology
620 M. Walterfang et al.
Psychiatry and Clinical Neurosciences 2012; 66: 618–621
Figure 2. Axial T2-weighted magnetic resonance imaging demonstrating a lack of basal ganglia
hyperintensity at baseline.
the ascending reticular activating system that intersects with the retinogeniculocalcarine pathways, particularly at the level of the thalamus.1 Frequent
hallucinatory content includes animals, (Lilliputian)
people, deformed or frightening faces, or tessellated
patterns and landscapes and commonly co-occur
with significant impairments in memory, confabulation, impaired attention and executive dysfunction.4
Central pontine myelinolysis is a condition
characterized by the destruction of myelin in the
pons, but may be accompanied by extra-pontine
(striatal, thalamic and cerebellar) demylination.5
First described in patients with chronic alcohol
abuse and malnourishment, it is also associated with
rapidly corrected hyponatremia, and liver and renal
transplantation. Approximately one-third of patients
completely recover, one-third have minor deficits,
and one-third are left with major motor or cognitive
deficits.6 Associated with rapid osmotic electrolyte
shifts, it may be subsequent to oligodendrocyte sensitivity to osmotic stress, and local white matter anatomical features in the pons.7 Motor features range
from paraparesis, dystonia, dysphagia, and seizures
or it may be asymptomatic. Neuropsychological findings include attentional, memory and executive disturbance.8 Diagnosis is generally confirmed on MRI,
with hypointense T1- and hyperintense T2-weighted
lesions.6 Preventing rapid correction of hyponatremia
is paramount in management. It may improve significantly with supportive care, usually over a period of
months,9 with a resolution of imaging lesions.
Psychotic symptoms have rarely been described in
association with CPM. One alcoholic patient developed symptoms during the timeframe of alcohol
withdrawal,10 and another with auditory hallucina-
tions and delusions 3 months after initial presentation;11 both also had extrapontine (basal ganglia)
lesions. Catatonia without psychosis has been
described,12 but may be difficult to differentiate from
profound dystonia. The present case differs from
these reports, involving predominantly complex
visual phenomena consistent with a peduncular hallucinatory syndrome. The disruption of myelinated
tracts in the pons is likely to have resulted in impairments to ascending fibers from the reticular activating
system to the thalamus, thus resulting in disturbed
transmission through the retinogeniculocalcarine
tract.1 The co-resolution of both clinical and MRI
features with sustained abstinence suggests their
causal association.
This is the first presentation of typical PH associated with CPM. It illustrates the importance of
thorough delineation of the psychopathology of psychotic symptoms, particularly when presentations are
atypical, and also highlights the need for careful
selection and interpretation of neuroimaging in
psychotic presentations in which there are atypical
features.
ACKNOWLEDGMENT
The authors declare no conflict(s) of interest.
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© 2012 The Authors
Psychiatry and Clinical Neurosciences © 2012 Japanese Society of Psychiatry and Neurology