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 Table of Contents  
LETTER TO EDITOR
Year : 2020  |  Volume : 40  |  Issue : 5  |  Page : 244-247

Postural instability due to right hemisphere stroke and the role of cognitive functions


1 Department of Neurology, Yozgat City Hospital, Yozgat, Turkey
2 Department of Physical Therapy and Rehabilitation, Yozgat City Hospital, Yozgat, Turkey
3 Department of Psychology, Yozgat City Hospital, Yozgat, Turkey
4 Department of Psychiatry, Yozgat City Hospital, Yozgat, Turkey

Date of Submission06-Aug-2019
Date of Decision13-Feb-2020
Date of Acceptance24-Mar-2020
Date of Web Publication25-May-2020

Correspondence Address:
Dr. Halil Onder
Department of Neurology, Yozgat City Hospital, Yozgat
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jmedsci.jmedsci_143_19

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How to cite this article:
Onder H, Keskin S, Ozyurek O, Yassa A. Postural instability due to right hemisphere stroke and the role of cognitive functions. J Med Sci 2020;40:244-7

How to cite this URL:
Onder H, Keskin S, Ozyurek O, Yassa A. Postural instability due to right hemisphere stroke and the role of cognitive functions. J Med Sci [serial online] 2020 [cited 2020 Oct 28];40:244-7. Available from: https://www.jmedscindmc.com/text.asp?2020/40/5/244/284950



Dear Editor,

A 55-year-old female patient with a history of hypertension and diabetes mellitus presented with a severe gait impairment that had developed following an ischemic stroke of the inferior division of the right middle cerebral artery 2 months previously. She exhibited no motor paralysis or cerebellar disturbances, so she was referred to the neurology department for the investigation of other possible etiologies of the gait problem.

On neurological examination, the patient was found to be cooperative and fully orientated. Remarkably, the visual field examinations showed visual field loss on the left side of the vertical midline. The findings of the motor and cerebellar investigations were within normal limits. However, the sensory investigations revealed hypoesthesia over the whole left side of the body, and the sensory and visual neglect subtypes were also present. In addition, the patient's deep tendon reflexes were normoactive, while her pathological reflexes (Babinski sign, Hoffman sign, etc.,) were absent, which indicated that the pyramidal tract was not disturbed. However, the patient could not mobilize without support due to experiencing a severe imbalance. Her postural stability was severely impaired (she scored four points on the Retropulsion test, as defined by the Movement Disorder Society-Unified Parkinson's Disease (PD) Rating Scale). Due to the severe postural instability, she had fallen several times over the past 2 months, which had left her with a significant fear of falling [Videos 1-2]. Based on these findings, the patient's gait pattern was evaluated as being a dyspraxic gait accompanied by severe postural instability, which had occurred due to a recent stroke affecting the right temporoparietal lobe. The findings of the cranial magnetic resonance imaging (MRI) showed a diffusion restriction in the right temporal lobe, superior parietal lobule, and angular gyrus [Figure 1]. However, a chronic ischemic lesion in the right occipital lobe was also identified [Figure 2]. The findings of the etiological investigations concerning the early-onset stroke, including computed tomography brain/neck angiography, echocardiography, and rhythm Holter, were all within normal limits. Yet, tests concerning the patient's vasculitis biomarkers revealed positive results for antinuclear antibody anticardiolipin antibody immunoglobulin G (IgG), and beta-2 glycoprotein IgG.
Figure 1: Diffusion-weighted imaging sequences showing high signal in the right superior (white arrows), middle (blue arrow), and inferior temporal gyrus (red arrow) and superior parietal lobule (ragged arrows)

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Figure 2: T2-weighted magnetic resonance imaging sequences performed 2 months after stroke, showing ischemic lesion in the right temporoparietal lobe (arrows) and sequela lesion in the right occipital lobe (thick arrows)

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Following interconsultation with the rheumatology department, a diagnosis of antiphospholipid syndrome (as the etiological agent behind ischemic stroke) was established and warfarin treatment was initiated. Besides, based on published data highlighting the importance of supraspinal control and certain cognitive functions during locomotion, further cognitive tests were performed to determine the specific cognitive profile of the postural instability and gait dyspraxia observed in our patient. She scored 20 points on the standardized mini-mental state examination. The patient could only count four numbers forward and count backward from two-digit numbers, which indicated a severe impairment in her attention and executive functions. In addition, she scored 12 points on the Benton Face Recognition Test (two standard deviations below the mean), which indicated an impairment in relation to object discrimination that is likely associated with the injury to her right posterior hemisphere, especially the parietal and occipito-parietal lobes. Furthermore, she could not perform any task included in the judgment of the line orientation test. Remarkably, she scored zero points on the watch drawing test, and she could not even copy elementary figures [Figure 3]. Furthermore, the single letter cancellation test revealed both a left-sided visual deficit and visual spatial neglect [Figure 4].
Figure 3: The imaged showing the performance of the patient in the clock drawing test (a) and figure copying test (b)

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Figure 4: The single letter cancellation test result of the patient showing the left-sided visual deficit and visual spatial neglect

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  Discussion Top


In our patient, the findings of the motor and cerebellar examinations were all within normal limits. Although the presence of left-sided hemihypoesthesia was determined, we classified the gait pattern and postural instability of the patient as a higher-level gait disorder, which could be associated with disturbances in the supraspinal control center of locomotion. Higher-level gait disorders (or gait dyspraxia) represent rather less common subtypes, and this particular type of gait disorder being triggered by a stroke is even rarer in the literature.

In our previous reports, two cases with gait dyspraxia in whom the causative lesion sites included the right occipital lobe were illustrated.[1],[2] However, in this newly reported patient, postural stability was the most prominently disturbed function, and it was the main component of both the dyspraxia and the falling problems. Therefore, we prefer to define the patient as having “postural instability due to stroke.” A disruption in postural control can be involved in clinical manifestations during the acute and chronic phases of stroke.[3],[4] The study by Peurala et al. found that patients with left hemiparesis and right hemisphere stroke experienced postural disturbances more prominently.[3] However, despite this finding, the responsible anatomical regions and the cognitive correlates of postural instability in stroke patients have not yet been investigated in detail.

On the one hand, postural instability is recognized as a cardinal motor symptom of PD, which usually emerges during the later stages of the disease. On the other hand, it can also be present in other neurological diseases, including Parkinson-plus syndromes, normal pressure hydrocephalus, vascular  Parkinsonism More Details, and Alzheimer's disease.[5] Postural instability appears as a tendency to be unstable when standing, and a person experiencing postural instability may easily fall backward if slightly jostled. It is considered to be one of the most disabling symptoms of PD due to its causal association with an increased risk of falling.[6] A substantial body of literature has recognized the relationship between global cognitive dysfunction and the motor symptoms of postural instability/gait disturbance in PD.[7],[8],[9] In addition, PD patients with the postural instability/gait disturbance subtypes have been shown to be at a higher risk of developing dementia.[9] In the crucial report by Uc et al., poorer visuospatial abilities and diminished executive functioning were both found to be associated with worse gait and postural instability in PD patients without dementia.[10] In the recent report by Kelly et al., the impairment of global cognition and different aspects of executive functioning was found to be associated with more severe postural instability symptoms. For this reason, the authors hypothesized the existence of multiple neural pathways that contribute to the associations between cognition and postural instability/gait disturbance symptoms in patients with PD.[11] Wang et al. confirmed the results of Kelly et al. in their large-group of patients with PD.[11],[12]

However, to the best of our knowledge, no large-scale study has yet addressed the cognitive profile of postural instability in patients with vascular dyspraxia. In our previous reports, two cases with vascular dyspraxia accompanied by right occipital infarcts were illustrated.[1],[2] However, postural instability was not the most prominent finding and widespread cognitive tests (as in this case) were not performed. Taken together, we believe that this case represents a crucial illustration in this regard. In accordance with the results of reports concerning PD patients, a widespread cognitive impairment (most prominently in the visuospatial functions as well as in the attention and executive functions) was determined in our index cases.

A major discussion may be the possible role of a primary sensory deficit of left-sided visual defect and neglect in the disturbed locomotion pattern of the patient. However, there was no asymmetrical impairment in her gait and the prominent disturbance was the postural instability which suggest a disruption of more complex cognitive networks related with the right hemisphere functions rather than the injury of primary sensory modalities.

In conclusion, through the illustration of this rare case, we discuss the potential role of widespread cognitive control in the execution of postural stability and locomotion. Future reports of larger case series including patients with postural instability of vascular origin may provide crucial contributions regarding our understanding of the physiology of locomotion.

Consent for publication

Informed consent form has been obtained.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Onder H, Buyuk F. Gait dyspraxia due to right occipital infarct. J Mov Disord 2019;12:54-6.  Back to cited text no. 1
    
2.
Onder H. Dyspraxic gait due to right posterior cerebral artery stroke. J Neurosci Rural Pract 2018;9:162-4.  Back to cited text no. 2
[PUBMED]  [Full text]  
3.
Peurala SH, Könönen P, Pitkänen K, Sivenius J, Tarkka IM. Postural instability in patients with chronic stroke. Restor Neurol Neurosci 2007;25:101-8.  Back to cited text no. 3
    
4.
Corriveau H, Hébert R, Raîche M, Prince F. Evaluation of postural stability in the elderly with stroke. Arch Phys Med Rehabil 2004;85:1095-101.  Back to cited text no. 4
    
5.
Adkin AL, Frank JS, Jog MS. Fear of falling and postural control in Parkinson's disease. Mov Disord 2003;18:496-502.  Back to cited text no. 5
    
6.
Michałowska M, Fiszer U, Krygowska-Wajs A, Owczarek K. Falls in Parkinson's disease. Causes and impact on patients' quality of life. Funct Neurol 2005;20:163-8.  Back to cited text no. 6
    
7.
Poletti M, Frosini D, Pagni C, Baldacci F, Nicoletti V, Tognoni G, et al. Mild cognitive impairment and cognitive-motor relationships in newly diagnosed drug-naive patients with Parkinson's disease. J Neurol Neurosurg Psychiatry 2012;83:601-6.  Back to cited text no. 7
    
8.
Verbaan D, Marinus J, Visser M, van Rooden SM, Stiggelbout AM, Middelkoop HA, et al. Cognitive impairment in Parkinson's disease. J Neurol Neurosurg Psychiatry 2007;78:1182-7.  Back to cited text no. 8
    
9.
Williams-Gray CH, Foltynie T, Brayne CE, Robbins TW, Barker RA. Evolution of cognitive dysfunction in an incident Parkinson's disease cohort. Brain 2007;130:1787-98.  Back to cited text no. 9
    
10.
Uc EY, Rizzo M, Anderson SW, Qian S, Rodnitzky RL, Dawson JD. Visual dysfunction in Parkinson disease without dementia. Neurology 2005;65:1907-13.  Back to cited text no. 10
    
11.
Kelly VE, Johnson CO, McGough EL, Shumway-Cook A, Horak FB, Chung KA, et al. Association of cognitive domains with postural instability/gait disturbance in Parkinson's disease. Parkinsonism Relat Disord 2015;21:692-7.  Back to cited text no. 11
    
12.
Wang YX, Zhao J, Li DK, Peng F, Wang Y, Yang K, et al. Associations between cognitive impairment and motor dysfunction in Parkinson's disease. Brain Behav 2017;7:e00719.  Back to cited text no. 12
    


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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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