Research Article
Open Access
The Relationships between Gait Impairments
and Activity Limitations in People with
Depressive and Related Disorders
Include: Depressive Pseudodementia,
Hypochondriasis, Factitious Disorder,
Cognitive Dysfunction and Normal Pressure
Hydrocephalus
Mohammad Reza Dawoudi*
1Turku University of Applied Sciences, Finland.
*Corresponding author: Mohammad Reza Dawoudi, Turku University of Applied Sciences, Finland, Email:
m.reza.dawoudi@abo.fi
Received: February 23, 2018; Accepted: March 08, 2018; Published: March 15, 2018
Citation: Dawoudi MR (2018) The Relationships between Gait Impairments and Activity Limitations in People with Depressive and Related Disorders Include: Depressive Pseudodementia, Hypochondriasis, Factitious Disorder, Cognitive Dysfunction and Normal
Pressure Hydrocephalus Int J Gen Sci 5(1): 1-4. DOI: 10.15226/2377-4274/5/1/00121
Abstract
According to Katzenschlager and Pirker walking speed is a
sensitive indicator of general health status and it associated with life
expectancy in older adults [1]. Accurate pathology diagnosis is the
most important among patients exhibiting neurological disorders
of gait. Several studies have investigated the relationships between
gait dysfunction and participation restrictions in people with
various neurological disorders. Studies show that depression has
been associated with increased risk of gait impairments. This study
reviewed existing evidence on gait dysfunction in neurological disease,
including Depressive, Depressive Pseudodementia, Hypochondriasis,
Factitious disorder, Cognitive dysfunction and Normal Pressure
Hydrocephalus. The aim of this research study is to review the various
neurological factors particularly relevant to depression diseases,
affecting gait impairments.
Keywords: Gait Impairments; Depressive Pseudodementia; Hypochondriasis; Factitious Disorder; Cognitive Dysfunction and Normal Pressure Hydrocephalus.
Keywords: Gait Impairments; Depressive Pseudodementia; Hypochondriasis; Factitious Disorder; Cognitive Dysfunction and Normal Pressure Hydrocephalus.
Introduction
According to Pirker and Katzenschlager ‘the causes of gait
disorders include neurological conditions (e.g. sensory or motor
impairments), orthopedic problems (e.g. osteoarthritis and
skeletal deformities) and medical conditions (e.g. heart failure,
respiratory insufficiency, peripheral arterial occlusive disease
and obesity)’(Pirker, et al.) [1]. Meanwhile, ‘neurological gait
disorders are a common cause of falls and mortality, particularly
amongst the elderly’ (Kaski and Adolfo, et al.) [2]. This study
reviews the neurological aspects of gait impairments (Tan, et al.
& Moon, et al.), with emphasis on Depressive (Brandler, et al. &
Laboni and Flint, et al.), Depressive Pseudodementia (Brenner, et
al.), Hypochondriasis, (Biller, et al.) Factitious disorder (Biller, et
al.), Cognitive dysfunction and Normal Pressure Hydrocephalus
[3,4,5,6,7,8].
Depressive
In 2013 Brandler and et al ‘conducted a crosssectional study of
the relationship between depressive symptoms and gait function,
in an ambulatory community residing sample of 610 older adults
(age 70 and older) who were free of dementia and MDD’(Major
depressive disorder) (Brandler, et al.) [5]. They made conclusion
that ‘increasing depressive symptoms in community residing
older adults are associated with quantitative gait dysfunction
even in the absence of major depression or dementia’ (Brandler,
et al.) [5]. Simultaneously, Lord and et al have found that ‘very
mild depressive symptoms are associated with gait disturbance
in early Parkinson’s disease’ (Lord, et al.) [9]. In other study
(Hausdorff, et al.) have made conclusion that ‘patients with MDD
and patients with bipolar disorder display gait unsteadiness’
(Hausdorff, et al.) [10].
Genetic factors
‘Recent studies have demonstrated impaired balance
performance in patients with major depressive disorder
(MDD)’(Deschamp, et al.) [11]. Multiple ‘genetic factors play
important roles in the development of MDD’ (Major depressive
disorder) according to Lohoff (Lohoff, et al.). 5HTT, 5HTTLPR
(Brown & Harris, et al.) and SLC6A4 genes associate with MDD
across numerous studies (e.g. Brown, et al., Luddington, et al.,
Kuzelova, et al.) [12,13,14].
Depressive Pseudodementia
According to Kennedy: Depressive Pseudodementia is
a term commonly used to describe a condition whereby a
patient experiences a cognitive deficit secondary to a primary
mood disorder. (Kennedy, et al.) [15]. ‘Cognitive deficits in
Pseudodementia are characterized by poor effort and difficulties
with attention and working memory’ (Flemming and Jr, et al.)
[16]. In other word ‘Pseudodementia is a situation where a person
who has depression also has cognitive impairment that looks
like dementia’ ((Steckl C, et al), Reversible Cognitive Disorder
Pseudodementia) [17]. However, there are many studies showing
that gait impairments coexist with depressive pseudodementia.
Genetic Factors
‘Long repeat sequences in the C9ORF72 gene have cropped
up in cases of multiple system atrophy (MSA) and depressive
pseudodementia’ (ALZFORUM, et al.), C9ORF72 Repeats Expand
into New DisordersCause, or Coincidence?) according to Bieniek,
et al. [18].
Hypochondriasis
According to Wilhelmsen Hypochondriasis (Illness anxiety
disorder and Somatic symptom disorder) ‘describes a persistent
preoccupation with the possibility of having one or more
serious and progressive physical disorders’ (Wilhelmsen, et al.),
and ‘defined as a chronic condition distinct from anxiety and
depressive disorders’ (Simon, et al) [19,20]. Hypochondriasis
is distinguishable clinical condition (Hiller, et al.) however,
according to (Weck, et al.) [21,22]. ‘previous experiences with
illness and traumatic childhood experiences did not prove to
be specific risk factors for the development of hypochondriasis’
Hypochondriasis can be accompanied by Major Depressive
Disorder (MDD) (Kapfhammer, et al.). According to Diagnostic and
Statistical Manual of Mental Disorders (DSM5) ‘hypochondriasis
and several related conditions have been replaced by two new,
empirically derived concepts: somatic symptom disorder and
illness anxiety disorder’ (Mayo Clinic.) [23]. There is a strong
correlation between the number of somatic symptoms and the
likelihood of a depression or anxiety diagnosis (Croicu, et al.).
Genetic factors
In 2010 Holliday and et al found that: HTR2A, SERPINA6 and
TPH2 are associated with somatic symptoms score [24].
Factitious disorder
According to (Uzuner, et al.) ‘factitious disorder is
characterized by deliberate production or imitation of physical
or psychological symptoms in order to adopt the sick role’ [25].
‘The etiology of factitious disorder is unclear’ (Osterman, et al.),
however, ‘in the sense that the physical symptoms are prominently
contributed by psychological factors, all somatoform disorders
may be considered to be a subset of psychological factors affecting
a physical condition’(Leight, et al.) [26,27]. According to Guzman
and Correll ‘patients with factitious disorder and comorbid
depression have shown improvement with antidepressant
therapy in addition to psychotherapy’ [28].
Genetic factors
Some studies report genetic estimates in factitious disorder
According to Jaghab and et al (2006) ‘magnetic resonance imaging
(MRI) has detected abnormalities in the brain structure of some
patients with chronic FD, suggesting that there may be biological
or genetic factors in the disorder’ [29]. In recent study Kreisl,
et al. ‘describe the novel constellation of a factitious disorder
presenting as a supposedly genetically confirmed hereditary
disease manifesting with abnormal movements’ [30].
Cognitive Dysfunction
Cognitive dysfunction refer to deficits in attention and
motor perception, learning disability, shortterm and working
memory and processing speed, problem solving functions, visual
or auditory processing deficits (Lam, et al.) [31]. According to
Stout and Paulsen ‘changes to the motor system resulting from
central nervous system damage or disease are virtually always
accompanied by cognitive dysfunction’ [32]. There are a variety
of different types of cognitive dysfunction e.g. ALPS or Adultonset
leukoencephalopathy with axonal spheroids and pigmented
glia, cognitive decline, mild cognitive impairment (Bahureksa,
et al.), and Alzheimer’s disease dementia (Dorfman, et al.)
[33]. Cognitive dysfunction is a common feature of Adultonset
leukoencephalopathy with axonal spheroids and pigmented
glia (ALSP) (Adams, et al.) [34]. This disease is recognized as
both a cognitive and a movement disorder (lkeuchi and et al
2017). Other feature of cognitive dysfunction is Mild Cognitive
Impairment (MCI). In 2015 Callisaya and et al conducted a study
to determine the relationships between cognitive decline and
gait slowing. They made conclusion that ‘decline in nonamnestic
function (specifically executive function) was associated with
decline in gait speed irrespective of the presence of baseline
cognitive impairment’ (Callisaya and et al 2015) [35]. In other
study in 2017 Bahureksa and et al made a conclusion that existing
studies ‘provide evidence that Mild Cognitive Impairment (MCI)
affects specific gait parameters’ (Bahureksa, et al.) [36]. There
are evidences of a direct cause relationship between the mild
cognitive impairment and the development of Alzheimer’s
disease (Roed, et al.).
Genetic factors
According to (Foulds, et al.) ‘AdultOnset Leukoencephalopathy
with Axonal Spheroids and Pigmented Glia (is) caused by a novel
R782G mutation in CSF1R’ [37].
Normal pressure hydrocephalus (NPH)
According to Shprecher and et al (2008) ‘normal pressure
hydrocephalus (NPH) is a syndrome of gait dysfunction and
enlarged cerebral ventricles in the absence of another cause’
[38]. The characteristic psychiatric symptoms of normal
pressure hydrocephalus are dementia and depression (Chopra,
et al.) [39]. In 2016 (Israelsson, et al.) claimed that ‘in many
dementias, depression is overrepresented, but the prevalence of
depression in shunted patients with idiopathic normal pressure
hydrocephalus is unknown’ [40].
Genetic factors
There are increasing evidence that iNPH may have a genetic
component (Korhonen, et al.). In 2016 (Sato, et al.) demonstrated
that a ‘copy number loss in intron 2 of the SFMBT1 gene may be a
genetic risk for shuntresponsive definite iNPH’ [41-45].
Methods and Materials
The narrative reviews of the literatures were conducted
with combination of relevant keywords. We searched the IEEE,
ScienceDirect, Springer, OMICS, PubMed, PubMed Health and
FINNA databases.
Results and Conclusion
There are convincing evidences about the relationship
between gait impairments and Depressive, Depressive
Pseudodementia, Hypochondriasis, Factitious disorder, Cognitive
dysfunction and Normal Pressure Hydrocephalus are improving.
Discussion
This study was reviewed literatures including biological
and psychological aspect. However, Kinesiography is important
functional gait imaging modalities for study the limb mobility
and neural activities. Kinesiography is the interpretation of limb
moment into mathematical form. Combining Kinesiographical
information with biological and psychological aspect of patient
holds promise to produce and improve clinical facility. In this
manner we can apply the image matching methods for the
evaluation of gait impairments in patients with Depressive and
related disorders.
Acknowledgments
The research for this study is financially supported by the
Finno Bio Stock Company in Finland.
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