ORIGINAL ARTICLE

Self-Injurious Behavior in a Patient With Dementia
A Case Report and Literature Review
Elmar Gardizi, PhD, Emily MacKillop, PhD, and Gagan Gaind, MD

Abstract: Self-injurious behavior (SIB) has frequently been associated with
psychiatric illness and neurological lesions as means of reducing tension or diverting from pain. However, these explanations did not capture the complexity
of SIB in the case of Mr. X, a 62-year-old patient who ingested his fingers in
his sleep where cognitive testing was valuable in informing diagnosis. Mr. X's
SIB was severe enough that he had chewed beyond the middle phalanx for most
of his fingers. Clinical symptoms included daytime sleepiness, hypnogogic hallucinations, and bradykinesia. His cognitive profile revealed declines in his intellectual functioning as well as visuospatial and executive deficits in the context
of preserved attention, language, and memory. His cognitive and clinical presentation suggested that Mr. X had a neurodegenerative disorder, which may have contributed to his SIB. We believed that the most probable diagnosis may have been rapid
eye movement behavioral sleep disorder in the context of Lewy bodies dementia.
Key Words: Autophagia, self-mutilation, dementia, rapid eye movement
sleep disorder, case study
(J Nerv Ment Dis 2019;207: 6–11)

elf-injurious behavior (SIB) in humans is defined as the “destruction of one's own body tissue in the absence of intent to die”
(Nock, 2009). It can manifest in a variety of forms including but not
limited to cutting, burning the skin, banging head and limbs, picking
at wounds, and chewing body parts (Winchel and Stanley, 1991). The
etiology of SIB is believed to stem from either psychological or biological causes. The psychological model of SIB posits that this behavior
develops as a means of reducing tension by providing an outlet for
affect regulation and may also emerge secondary to communication
difficulties, social isolation, and disturbances in reality testing. It has
been reported within the context of anxiety, obsessive compulsive
disorder (OCD), schizophrenia, borderline personality disorder, depression, Tourette disorder, bulimia nervosa, autism, and intellectual disability (e.g., Birrer et al., 1993; Dulit et al., 1994; Favaro and Santonastaso,
1997; Hood et al., 2004; Pacan et al., 2009; Schlozman, 1998; Wells
et al., 1998). For a more comprehensive review of the psychosocial
causes of SIB, the reader is encouraged to refer to Klonsky (2007) and
Nock (2009).
SIB stemming from purely biological causes has been less frequently reported in the literature and remains poorly understood. Frost
et al. (2008) described the occurrence of finger-chewing behavior in
five persons between the ages of 45 to 68 years with C5 to C6 spinal
cord injury (SCI). Four of five individuals sustained their injuries as a
result of high velocity accidents; however, they were not assessed for
traumatic brain injury, and none of the individuals participated in

S

Department of Psychiatry and Behavioural Neurosciences, McMaster University, St
Joseph's Healthcare Hamilton, Hamilton, Ontario, Canada.
Send reprint requests to Elmar Gardizi, PhD, Department of Psychiatry and
Behavioural Neurosciences, McMaster University, St Joseph's Healthcare
Hamilton, 100 West 5th St, Hamilton, Ontario L9C 0E3, Canada. E‐mail:
egardizi@stjoes.ca.
Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
ISSN: 0022-3018/19/20701–0006
DOI: 10.1097/NMD.0000000000000924

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neuropsychological testing. Their psychiatric history was unremarkable, and most of the individuals denied any pain in the area targeted
by their SIB. On average, SIB began 3.8 years after their initial injuries, and in the most severe cases, continued to persist until all of the individual's fingers were autoamputated or their teeth were removed.
Similarly, Nino and Singareddy (2013) described the case of a
47-year-old man with a history of C5 quadriplegia sustained 20 years
prior secondary to a motor vehicle accident who engaged in SIB. He
had severe snoring and fatigue, multiple awakenings, and nocturnal
breathing difficulties. He was diagnosed with obstructive sleep apnea
(OSA) and was treated using a bilevel positive airway pressure machine,
which resolved his sleep difficulties. He was seen for a follow-up evaluation 8 weeks later, which revealed significant improvement in his
nocturnal awakenings, daytime sleepiness, and complete resolution of
snoring. More importantly, his finger-biting behavior resolved once his
sleep difficulties were addressed.
Michopoulos et al. (2012) presented the case of a 66-year-old
man with a history of diabetes mellitus who was engaging in severe
finger mutilation. This patient was also immobilized on a wheelchair
for the last 2 years, albeit he did not have an SCI. His medical history
included end-stage renal failure, for which he was receiving hemodialysis and coronary artery bypass operation 6 years prior. His fingerchewing behavior emerged 1-year after his surgery and resulted in the
loss of the terminal phalanges of all fingers in both hands. He had been
gradually losing sensation in his fingers over the last 2 to 3 years due to
his diabetic neuropathy. He participated in neuropsychological testing,
which demonstrated an IQ in the reference range and cognitive functioning within expected limits for most domains. However, he also
underwent a head computed tomography (CT) scan, which found “serious brain atrophy.” There was no objective evidence of obsessive
compulsive tendencies, although the patient did describe his fingerchewing behavior as a bad habit and admitted experiencing an urge to
bite his fingers without the ability to resist. He did not initially respond
to pharmacological or behavioral interventions; however, he was
eventually placed on a course of haloperidol and provided with a soft
silicon mouth guard upon discharge. At 8-month follow-up, the authors
noted that the patient continued to present with SIB, although it was
less severe.
Given the scarcity of documented SIB in the literature and the
variety of contexts in which it can arise, many questions remain regarding the etiology of this self-destructive behavior, particularly when a
biological origin is being considered. One of the more widely accepted
theories is that SIB can develop secondary to neurological injury (e.g.,
SCI) and may serve the purpose of distracting from central or peripheral nerve pain (Dahlin et al.,1985; Mailis, 1996). On the other hand, some
cases of SIB can occur in the absence of pain, which has led others to
propose that SIB may be used to experience some level of sensory stimulation. This explanation, referred to as the deafferentation theory, has
been studied in individuals with tetraplegia, and it has been used to explain why persons who experience sensory deprivation due to physical
disability may prefer high ventilator volumes or demonstrate excessive
need for oral gratification (Frost et al., 2008). Although these theories
have received the most support, they do not completely capture the
complexity of SIB. Consequently, a neuropsychologist can be at a loss

The Journal of Nervous and Mental Disease • Volume 207, Number 1, January 2019
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The Journal of Nervous and Mental Disease • Volume 207, Number 1, January 2019

when encountering individuals who engage in SIB. These gaps in our
understanding of SIB were highlighted by the case of Mr. X, which
was unique compared with other cases that have been reported in the
literature. Given the rarity of his case and the opportunity to thoroughly
examine Mr. X, we believed that disseminating the results of our assessment would increase our understanding regarding potential biological
factors that may contribute to the emergence of SIB in certain populations.

REPORT OF CASE
Mr. X was a 62-year-old right-handed white man with a complex
medical and psychiatric history who was referred for a neuropsychological assessment to assist with differential diagnosis and treatment
planning. Information regarding his case was gathered from a clinical
interview with Mr. X, review of documentation in his medical record,
collateral interview with his sister, and consultation with his attending
psychiatrist. Mr. X had been admitted to the ER of a local hospital after
he was found with severe self-inflicted injuries to his fingers. He was
delirious upon arrival with urosepsis, hypercalcemia, and renal impairment secondary to dehydration. His Montreal Cognitive Assessment
(Nasreddine et al., 2005) score at the time of admission was 12/30,
which improved to 22/30 after his delirium resolved, and he was subsequently transferred to a tertiary mental health facility where he was seen
by our team to assess his SIB. Mr. X was unable to recall most details
when he was queried regarding the night of the event. He exhibited 4
to 6 hours anterograde amnesia for the incident, recalling that he was
struggling to fall asleep because it was too warm and moved into the
living room from the bedroom. According to the EMS report, he was
found at approximately 4 a.m. by his personal support worker with
blood on his hands and face after chewing his fingers. He sustained significant injuries to his fingers, having chewed beyond the middle phalanx for 8/10 fingers, with exception to his index finger and thumb on
his left hand. Although Mr. X had reduced sensation in his extremities,
he did not have complete sensory loss, which was tested at the time of
the interview by asking him to identify which hands and fingers were
being touched while closing his eyes. He reported that the finger-biting
behavior began approximately 1 year prior and was perplexed about the
origin and occurrence. He denied any obsessive thoughts or compulsions to chew his fingers and reported that it only occurred when he
slept. Over the few months before the assessment, he also reported seeing images (black and white) of his deceased sister and extant friend at
the end of his bed upon waking, which he described as “startling.” He
was unable to recall whether he had experienced any nightmares over
this time.
Mr. X was admitted to the inpatient unit at our hospital for approximately 1 month. He underwent a comprehensive medical workup
during the course of his admission, which included psychiatric and neuropsychological assessment. He also underwent sleep studies and neuroimaging including EEG, CT, and magnetic resonance imaging (MRI)
scans. The results of the EEG revealed abnormal activity with the presence of frontal intermittent rhythmic delta activity, which was thought
to be in keeping with a nonspecific metabolic/toxic encephalopathy.
His CT scan revealed multifocal subcortical deep and periventricular
foci abnormalities in keeping with chronic microangiopathic changes.
His MRI scan was significant for white matter hypoattentuation primarily affecting the frontal lobes, which seemed to have been more pronounced on the right side of the brain. It should be noted, however,
that data obtained from the scans, especially his MRI results, were significantly degraded due to movement artifacts. Mr. X underwent two
sleep studies, neither of which was able to provide insight or additional
information regarding the etiology of his finger-chewing behavior. In
fact, during his most recent sleep study, which occurred 2 months before his hospital admission, the sleep specialist openly acknowledged
that he was quite perplexed and asked Mr. X for permission to take

Self-Injurious Behavior Dementia

pictures of his injuries (see Figures 1A and B) so that he could consult
with his psychiatrist colleagues.
During his hospital course, Mr. X continued to engage in nocturnal finger-biting behavior even after his initial delirium resolved. His
treatment team attempted a number of preventative strategies, including
the application of an aversive agent denatonium benzoate to deter him
from biting his fingers as well as wrapping both of his hands to provide
additional protection. One initial hypothesis was that the behavior
stemmed from an underlying parasomnia; however, a trial of topiramate
provided negligible benefit. Mr. X was then placed on a trial of olanzapine
with the hope that this would assist with sleep and impulse control. Despite these interventions, the finger-biting behavior continued to persist.
His medication was eventually switched to risperidone, which seemed
to have a positive effect as the patient did not engage in finger-biting
behavior for eight consecutive nights. At this time, a meeting with the
patient and his family was held, and he was discharged after they voiced
clear desire to leave the hospital and understanding of the situation and
risks involved. Mr. X, his family, and treatment providers felt comfortable that the necessary home health care supports were put in
place before his discharge.
Approximately 1 month after being discharged, Mr. X was admitted to the hospital again after he was found with decreased levels
of consciousness, which was thought to be secondary to a pressure ulcer
infection. His condition deteriorated, and he suffered a full cardiac arrest and was placed in intensive care unit. Mr. X was intubated and
subsequently regained consciousness to the extent that he was able
to contribute to his own care. He was extubated, and after discussion
with the patient and his family, it was decided that no more intubation
was to occur. Unfortunately, a few days later, Mr. X's right lung collapsed due to the accumulation of secretions, and despite best efforts

FIGURE 1. A and B, Mr. X's mutilated hands. Note: These pictures
were taken before Mr. X's hospital admission. His injuries were much
more severe by the time we had the opportunity to see him.

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The Journal of Nervous and Mental Disease • Volume 207, Number 1, January 2019

Gardizi et al.

by his physicians to suction his right lung, he became bradycardic and
passed away. His final cause of death was described as respiratory
failure secondary to pneumonia.

RELEVANT BACKGROUND INFORMATION
Mr. X was a C4 quadriplegic secondary to severe spinal stenosis
since 1995, which required multiple surgical interventions. He had been
diagnosed with OSA more than 10 years prior and used a nasal continous
positive airway pressure machine at a pressure of 10 cm. He was obese
and reported having hyperlipidemia and low blood pressure. His family
medical history included Alzheimer dementia (AD) in his aunt and
mother (age 90 years) who lived in a long-term care facility at the time
of the assessment. His father was deceased. His sister died of cancer
unexpectedly a few months before his admission. There was no evidence of longstanding anxiety or OCD that interfered with daily life
or functioning or prior behavioral abnormalities.

Attention
Aspects of Mr. X's attention were within expected limits including his basic attention, working memory, and processing speed.

Language
With exception to his vocabulary skills, which were mildly impaired, most of Mr. X's language functioning was preserved including
his category fluency and confrontation naming skills.

Executive Functioning
His problem-solving and reasoning skills were intact, and there
was no evidence of perseverative tendencies. However, his phonemic
fluency was mildly to moderately impaired, and he also demonstrated a tendency to make an elevated number of intrusive and
false-positive errors on a list learning test, which was suggestive of problems with impulsivity.

Memory
BEHAVIORAL OBSERVATIONS
Mr. X was seen over the course of several sessions on an acute
mental health inpatient unit. He presented as an obese man who was casually dressed and appeared his stated age. He was easily engaged and
pleasant throughout the course of the assessment. His comprehension
was intact and his speech was normal for rate, rhythm, and prosody,
and his thought content was clear and goal oriented. He was in an electric powered wheelchair, which allowed for extra mobility given his severe spinal stenosis. The control panel of the wheelchair also gave him
the opportunity to move around using his index finger and thumb
without having to completely grasp the wheels with his hands. Mr. X
provided sufficient effort throughout the course of the assessment as
demonstrated by his performance on stand-alone and embedded measures of effort. It was notable that Mr. X's levels of alertness waxed
and waned quite drastically, especially on the first day of testing when
he was seen in the morning. For instance, he frequently fell asleep during the middle of a test (i.e., vocabulary and matrix reasoning subtests
of the Wechsler Adult Intelligence Scale, Fourth Edition [WAIS-IV]) or
midsentence during the clinical interview. Of note, he fell asleep during
untimed tests so the impact on his performance was minimal, albeit the
instructions had to be repeated (e.g., “tell me what this word means”).
Furthermore, for the matrix reasoning, he was administered an alternative version of the test to ensure that his initial performance was not
solely due to being drowsy.

COGNITIVE TEST RESULTS
Test results were interpreted through comparison of obtained
scores with published normative data sets (see Table 1). Wechsler (2011)
norms were used to describe performance on tests of intellectual functioning while Heaton et al., (2004) norms were used to describe performance on tests of cognitive functioning.

Orientation
Mr. X was oriented for person, place, time, and situation.

Intellect
Full-scale IQ was in the extremely low range that represented a
significant decline from his premorbid level of intellectual functioning,
which was estimated to be in the average range. His intellectual profile
was characterized by a verbal-visual split whereby he demonstrated a
tendency to perform more poorly on visually mediated tests compared
with verbally mediated tests. This pattern of performance was also
observed across specific domains of cognition.
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With respect to learning and memory, Mr. X's immediate and delayed memory for verbal information (i.e., stories and word lists) was in
the average range.

Visual-Spatial
The most prominent feature of Mr. X's cognitive profile was pervasive visuospatial deficits. Specifically, his visual reasoning and visual
perception ranged from mildly to moderately impaired to severely
impaired while his visual organization was average to low average.
Mr. X's visuospatial difficulties extended to his learning and memory
for visual information. For instance, when Mr. X was required to learn
and recall a number of visual designs that were presented to him, his
immediate recall fell in the mildly impaired range while his delayed recall was worse, falling in the mildly to moderately impaired range. His
ability to retain visual information over time fell in the mildly to moderately impaired range, which was suggestive of rapid forgetting. It
should be noted that he demonstrated significant visual learning difficulties despite his vision and visual constructional ability being intact.

DISCUSSION
The etiology of SIB has generally been ascribed to psychological
or biological causes. To this end, there were several discrepancies between the psychological model of SIB and the case of Mr. X. To begin
with, Mr. X did not have a documented history of significant psychiatric
illness and had not been involved with the mental health system before
his inpatient admission. In addition to a lack of preexisting psychiatric
difficulties, Mr. X continued to deny any psychiatric symptoms despite
the severity of his SIB. He reported that his mood was generally fine,
and there was no indication to believe that his symptoms of anxiety were
significant enough to contribute to his SIB. Mr. X also denied any obsessive thoughts or compulsions to engage in SIB, in fact, he was not aware
of when he would engage in SIB because it would only occur when he
was asleep. Mr. X's self-report during the clinical interview was further
corroborated by his responses on a screening measure of psychological
functioning, whereby his profile revealed no significant symptoms of
depression, anxiety, and/or stress at the time of his admission (Depression
Anxiety Stress Scales, Lovibond and Lovibond, 1995). Taken together, we
were confident in concluding that the etiology of Mr. X's SIB was unlikely related to underlying psychological factors.
In contrast, there was some overlap between Mr. X's case and
other persons with SCI. Similar to Mr. X, none of the patients described by Frost et al., 2008, Michopoulos et al., (2012), and Nino and
Singareddy (2013) had a significant psychiatric history, and there was
no evidence to suggest that depression or anxiety were playing a role in
the development and maintenance of their SIB. Furthermore, most of
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The Journal of Nervous and Mental Disease • Volume 207, Number 1, January 2019

Self-Injurious Behavior Dementia

TABLE 1. Neurocognitive Data for Mr. X
Domain
Intellectual functioning
Attention

Functional Area
Premorbid Intellectual Functioning
Global intellectual functioning
Simple attention
Working memory
Processing speed

Executive functioning

Alternation/switching
Impulsivity

Memory

Language

Visuospatial processing

Concept formation
Perseveration
Phonemic fluency
Verbal acquisition, verbal learning
Verbal delayed recall
Verbal delayed recognition

Visual acquisition
Visual learning
Visual delayed recall
Visual delayed recognition discrimination
Vocabulary
Confrontation naming
Semantic fluency
Visual reasoning

Visual organization

Test

Standard Score

TOPF
WASI-II (2 Subtest IQ)
WAIS-IV digit span forward
WAIS-IV digit span backward
WAIS-IV digit span sequencing
DKEFS color naming
DKEFS word reading
DKEFS category switching (total correct)
DKEFS inhibition switching
DKEFS inhibition
CVLT-II intrusions
CVLT-II false-positives
WCST: # categories, total errors, % conceptualization
WCST perseveration
DKEFS system letter fluency
WMS-III logical memory immediate recall
Logical memory stories delayed recall
Logical memory % retention
CVLT-II (list) 1st trial
CVLT-II total words learned
CVLT-II list short delayed recall
CVLT-II list long delayed recall
CVLT-II recognition discrimination
BVMT-R trial 1
BVMT-R total
BVMT-R delayed recall
BVMT-R delayed recognition discrimination
WASI-II vocabulary
BNT
DKEFS category fluency
WAIS-IV matrix reasoning
WASI-II matrix reasoning
JLO
HVOT
WAIS-IV puzzles

92
70*
62
85
95
95
95
85
95
95
70*
62*
88
90
70*
100
100
90
70*
86
100
92
85
82
81
70*
77–81
80
56
90
62*
70*
67*
100
85

Note: Standard scores below 85 considered impaired based on normative data from Heaton et al. (2004).
*Standard score of 70 or below, which corresponds to two standard deviations below the mean.
TOPF indicates test of premorbid functioning; WASI-II, Wechsler Abbreviated Scale of Intelligence Second Edition; DKEFS, Delis-Kaplan Executive Function
System; CVLT-II, California Verbal Learning Test Second Edition; WCST, Wisconsin Card Sorting Test; WMS-III, Wechsler Memory Scale Third Edition; BVMTR, Brief Visual Memory Test Revised; BNT, Boston Naming Test; JLO, Judgment of Line Orientation Test; HVOT, Hooper Visual Organization Test.

the patients denied any pain in the affected area, and they were quite
insightful and forthcoming in discussing their SIB. This seems to lend
support to the deafferentation theory, which would suggest that Mr. X
may have engaged in SIB as a means of providing psychological or
physiological stimulation in compensation for his neurological deficits
and diminished sensory experience.
Nonetheless, while there was overlap between the circumstances
surrounding Mr. X's SIB and the few cases, which have been described in the literature, there are important discrepancies that cannot
be overlooked. To begin with, most of the SIB reported in the literature
emerged shortly after the individuals sustained their neurological injuries. Conversely, Mr. X's SIB emerged nearly 20 years after he became
nonambulatory. The case reported by Nino and Singareddy (2013) was
most similar to Mr. X given that their patient was also quadriplegic and
had a history of OSA. However, unlike Mr. X, this patient's SIB resolved

after OSA diagnosis and treatment. In addition, Mr. X's SIB would only
occur when he was asleep, and therefore, he would have no recollection
of engaging in the behavior upon waking.
Finally, we believe that neuropsychological testing was critical in
understanding the etiology of Mr. X's SIB because the assessment findings demonstrated that he had exhibited significant intellectual and
cognitive decline compared with premorbid levels of functioning. To
our knowledge, the neurocognitive data of only one other patient with
SIB has been reported in the literature, and his profile was unremarkable (Michopoulos et al., 2012). These inconsistencies suggest that
the differentiation theory alone may not entirely capture the complexity
of Mr. X's SIB and that alternative explanations warrant investigation.
To this end, Mr. X's cognitive profile strongly suggests that he
had a neurodegenerative disorder, which may have contributed to his
SIB. His risk factors (e.g., obesity, hyperlipidemia, OSA, and family

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Gardizi et al.

The Journal of Nervous and Mental Disease • Volume 207, Number 1, January 2019

history of neurodegenerative disease) in combination with abnormal
findings on neuroimaging were consistent with a diagnosis of vascular
dementia. Vascular-related changes primarily isolated to the right frontal
lobe may partially explain visuospatial impairments observed on testing.
Also considered was dementia of the Lewy bodies type (DLB), which is
characterized by visuospatial and executive deficits in the context of preserved memory and language (Connor et al., 1998; Galasko et al., 1996).
Our confidence in this diagnosis was initially lower because a number of
confounding factors made it difficult to assess the core clinical features of
DLB (McKeith et al., 2017). More specifically, fluctuations in his levels
of arousal (i.e., daytime sleepiness) may have resulted from his OSA
while his visual hallucinations were hypnopompic in nature compared
with DLB where visual hallucinations are typically recurrent and well
formed (McKeith et al., 2017). Furthermore, it was believed that his
motor symptoms were the result spinal stenosis rather than being related to parkinsonism, which is typical of DLB. Nonetheless, motor
symptoms were unable to be fully assessed given his hemiplegia.
On the other hand, a stronger argument could be made that
Mr. X's clinical presentation was in keeping with a rapid eye movement
behavioral sleep disorder (RBD). This parasomnia is associated with
prominent motor activity and dreaming, which can often be quite frightening and lead to injury (Boeve et al., 2004). The average age of onset for
RBD is 61 with 87% male preponderance (Olson et al., 2000), and behaviors typically emerge during the latter half of the sleep cycle as it appeared to our patient. RBD can be misdiagnosed as OSA as many of the
symptoms including loud snoring and excessive daytime sleepiness can
be identical. Furthermore, hypnogogic/hypnopompic hallucinations are
also observed in patients with RBD (Nightingale et al., 2005; Takata
et al., 1998). The most accurate method for diagnosing RBD is by using
a simultaneous video/polysomnogram (PSG), although there are many
limitations in using this procedure. Specifically, few sleep clinics have
the staff with expertise and the equipment to conduct this type of evaluation (Boeve et al., 2004), and even in cases where a simultaneous
video/PSG examination may be available, there is no guarantee that
complex dream activity will be captured over a single night of recording. One of the features of RBD, which can assist in differential diagnosis, is its comorbidity with neurodegenerative illness. However, this
predilection is not the same for all types of neurodegenerative disorders
as there are no published reports of RBD within the context of AD
(without DLB), Pick disease, frontotemporal dementia, progressive
nonfluent aphasia, semantic dementia, corticobasal degeneration, progressive subcortical gliosis, and argyrophilic grain disease (Boeve
et al., 2004). Conversely, research suggests that at least 50% of patients
with DLB have RBD (Boeve et al., 2004; McKeith et al., 2005).
When this information is taken into consideration, the possibility
that Mr. X's SIB partly stemming from RBD within the context of DLB
increases. Both diagnoses appear to be the most reasonable in terms of
explaining the combination of his cognitive impairments, behavioral
symptoms, and the nocturnal nature of his SIB. At discharge, the plan
for Mr. X was to undergo neuropsychological reassessment in 6 months
in addition to RBD evaluation, which he had not participated in previously. Unfortunately, Mr. X passed away approximately 2 months
after being discharged from pulmonary pneumonia, which prevented
us from following up with him. Furthermore, he did not undergo a
postmortem autopsy, which would have provided a more conclusive
diagnosis of dementia. Although we believe that a neurodegenerative
process was occurring and contributing to the symptom presentation,
we acknowledged that it is difficult to establish a direct link between
Mr. X's neurocognitive profile and his SIB. However, we would argue
that this would be impossible given the complexity of his case and the
low base rate of SIB reported in the literature. Consequently, we felt that
disseminating our results would shed much needed light on this issue,
and at a minimum, allow clinicians to explore the nature of SIB from
different perspectives. To our knowledge, this is the first study to report
nocturnal SIB in the context of a neurodegenerative illness and we
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believe that Mr. X's case speaks to the importance of including neuropsychological testing as part of a comprehensive medical and psychiatric
workup to better understand the etiology and treatment of rare and
unusual symptom presentations.

DISCLOSURES
We certify that none of the authors have any conflict of interest or
received funding from agencies in the public, commercial, or not-forprofit sectors related to this study. We certify that no party has a direct
interest in the results of the research supporting this study or will confer
a benefit on us or on any organization with which we are associated. All
authors have contributed significantly to the work and have had the
opportunity to review and approve the manuscript.

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