An observational study in Multiple Sclerosis, sponsored by Assiut University. Status unknown. Open to participants aged 18 Years to 60 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2020-07-27.
Sponsored by Assiut University · Observational
Multiple sclerosis (MS) MS is a chronic disease containing the inflammatory, demyelinating, anddegenerative processes of the central nervous system. The inflammation, microglial activation, astrocyticgliosis, demyelination, and somewhat axonal loss inwhite matter and grey matter was present in the brainsof the patients with MS . Moreover, MS patientspresented a reduction in the cerebral blood flow (CBF)affecting both grey and white matter in positronemission tomography (PET) studies.
MS is the most common autoimmune disorder of the central nervous system. As of 2010, the number of people with MS was 2-2.5 million (approximately 30 per 100,000) globally, with rates varying widely in different regions. MS affects approximately 1000000 people between 17 and 65 years old world wide, the projected prevalence rate of MS for the white US population was 191 per 1000000 and the incidence rate was 7.3 per 1000000 persons .
the contribution of neurodegenerative processes in the disease pathogenesis has been increasingly recognized, especially with respect to possible mechanisms of progression. These may include axonal degeneration, mitochondrial injury, energy failure, hypoxia, oxidative damage, iron accumulation or global cerebral hypoperfusion . Interestingly, Cerebral vasomotor reactivity (CVMR) in MS may be impaired as well.
Although the cause of CVMR impairment in MS is not clear, several potential factors mightcontribute to this phenomenon.
For the purpose of clarity,we divide them into (1) vascular factors, (2) glial factors, and (3)neuronal factors:
Vascular factor
Blood-brain barrier (BBB) disruption might be anotherfactor contributing to CVMR impairment in neurodegenerative disorders. CVMR impairment could also be caused by an increase inthe concentration of vasoconstrictive agents. For instance,endothelin-1 (ET-1) - a potent vasoconstrictor, is overexpressed in the cerebral vessels of MS and elevated in both serumand cerebrospinal fluid of patients with MS.
Glial factors
Reactive astrocytes, i.e. hypertrophied astrocytes that overexpress GFAP (glial fibrillary acidic protein) have been described in virtually all CNS disorders including MS . they could also contribute to CVMR impairment through the production of ET-1 and possibly other vasoconstrictors Another way in which glial cells could contribute to the impairment of CVMR might be associated with their involvement in oxidative stress pathways. Glial pathology may also cause BBB dysfunction.
It has been shown that cholinergic projections originating from the nucleus basalis induce cerebral vasodilation directly through the release of acetylcholine and indirectly through the stimulation of NO-releasing interneurons . there is evidence of a cholinergic deficit in MS.
From a clinical point of view, reduced white and gray matter CBF in patients with MS has thus far been associated with cognitive manifestations.
Cognitive impairment occurs in 40 to 65% of patients with MS and can have a considerable impact on occupational and social life. also reduced deep gray matter perfusion in MS negatively correlated with fatigue.
Cerebrovascular reactivity (CVR) is an inherent indicator of the dilatory capacity of cerebral arterioles for a vasomotor stimulus for maintaining a spontaneous and instant increase of CBF) in response to neural activation. The integrity of this mechanism is essential to preserving healthy neurovascular coupling. Transcranial Doppler ultrasound (TCD) is defined as a non-invasive ultrasound procedure to evaluate the changes in cerebral blood flow velocity (CBFV) . The high temporal resolution and non-invasive nature of TCD make it a useful tool in the assessment of integrative cerebrovascular function in terms of cerebral reactivity, autoregulation and neurovascular coupling (NVC).
Multiple sclerosis (MS) MS is a chronic disease containing the inflammatory, demyelinating, anddegenerative processes of the central nervous system[FrischerJMet al, 2009]. The inflammation, microglial activation, astrocyticgliosis, demyelination, and somewhat axonal loss inwhite matter and grey matter was present in the brainsof the patients with MS [Wegner C et al, 2006]. Moreover, MS patientspresented a reduction in the cerebral blood flow (CBF)affecting both grey and white matter in positronemission tomography (PET) studies [Sun X et al, 1998].
MS is the most common autoimmune disorder of the central nervous system[Berer K et al,2014]. As of 2010, the number of people with MS was 2-2.5 million (approximately 30 per 100,000) globally, with rates varying widely in different regions. [Milo R et al ,2010] MS affects approximately 1000000 people between 17 and 65 years old world wide, the projected prevalence rate of MS for the white US population was 191 per 1000000 and the incidence rate was 7.3 per 1000000 persons [Mayr WTet al, 2003]. Another study of prevalence of Multiple Sclerosis in Egypt in age group >17years in a population number 21774 was about 13.74 per 100000 [El-Tallawy HNet al, 2013].
The contribution of neurodegenerative processes in the disease pathogenesis has been increasingly recognized, especially with respect to possible mechanisms of progression. These may include axonal degeneration, mitochondrial injury, energy failure, hypoxia, oxidative damage, iron accumulation or global cerebral hypoperfusion [Mahad DH et al, 2015, D'haeseleer M et al, 2015]. Interestingly, Cerebral vasomotor reactivity (CVMR) in MS may be impaired as well.
Although the cause of CVMR impairment in MS is not clear, several potential factors mightcontribute to this phenomenon.
For the purpose of clarity,we divide them into (1) vascular factors, (2) glial factors, and (3) neuronal factors:
Vascular factor
Blood-brain barrier (BBB) disruption might be anotherfactor contributing to CVMR impairment in neurodegenerative disorders [Alvarez JI, et al, 2013]. CVMR impairment could also be caused by an increase inthe concentration of vasoconstrictive agents. For instance,endothelin-1 (ET-1) - a potent vasoconstrictor, is overexpressed in the cerebral vessels of MS and elevated in both serumand cerebrospinal fluid of patients with MS [Haufschild T, et al,2001, D'haeseleer M, et al,2013].
Glial factors
Reactive astrocytes, i.e. hypertrophied astrocytes that overexpress GFAP (glial fibrillary acidic protein) have been described in virtually all CNS disorders including MS [Ben Haim L, et al, 2015]. they could also contribute to CVMR impairment through the production of ET-1 and possibly other vasoconstrictors Another way in which glial cells could contribute to the impairment of CVMR might be associated with their involvement in oxidative stress pathways [Haider L et al, 2011]. Glial pathology may also cause BBB dysfunction [Alvarez JI, et al, 2013].
It has been shown that cholinergic projections originating from the nucleus basalis induce cerebral vasodilation directly through the release of acetylcholine and indirectly through the stimulation of NO-releasing interneurons [Hamel E. et al, 2006] there is evidence of a cholinergic deficit in MS [Kooi E-J, et al, 2011].
From a clinical point of view, reduced white and gray matter CBF in patients with MS has thus far been associated with cognitive manifestations [-Inglese M, et al, 2008, D'Haeseleer M et al, 2013].
Cognitive impairment occurs in 40 to 65% of patients with MS and can have a considerable impact on occupational and social life [Amato MP, et al, 2001]. also reduced deep gray matter perfusion in MS negatively correlated with fatigue [Vucic S, et al, 2010].
Cerebrovascular reactivity (CVR) is an inherent indicator of the dilatory capacity of cerebral arterioles for a vasomotor stimulus for maintaining a spontaneous and instant increase of CBF) in response to neural activation. The integrity of this mechanism is essential to preserving healthy neurovascular coupling. Transcranial Doppler ultrasound (TCD) is defined as a non-invasive ultrasound procedure to evaluate the changes in cerebral blood flow velocity (CBFV) [Powers J et al,2009]. The high temporal resolution and non-invasive nature of TCD make it a useful tool in the assessment of integrative cerebrovascular function in terms of cerebral reactivity, autoregulation and neurovascular coupling (NVC).
3,460 studies on the registry are indexed under Multiple Sclerosis; 661 are open to participants now.
This study's planned enrollment of 50 is below the median of 100 across 1,016 observational studies indexed under Multiple Sclerosis.
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All patients are subjected to the following:
Laboratory tests:
CBC-KFT-LFT-Na-K-PT-PC-INR..
MRI brain and spinal cord:
To confirm diagnosis of MS by experienced neuro-radiologist.
Visual Evoked potential:
Help to confirm diagnosis (detect central demyelination and disseminated in space), VEP was performed using the Nihon Kohden model). MEB-7102 (Nihon Kohden Corp., Tokyo, Japan).
Exclusion Criteria:
30 patients were diagnosed with MS according to revised MacDonald's criteria 2017 \& collected from Neuropsychiatry department in Assuit university hospital
Radiation: mri
30 healthy volunteers subjects matched with age, sex \& education level were recruited from outpatient clinic neuropsychiatry department and included only if they had no current or previous history of any neurological illness and their neurological examination was free
Radiation: mri
mri brain \& spinal cord
evaluate cerebrovascular changes in patients with MS byTCD, which is an easy applicable and non-invasivebedside technique
Time frame: 1 year
No study locations are listed for this record.
Plan to share: No
No publications or documents are linked to this record.
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Assiut University