Biochemical and structural magnetic resonance imaging in chronic stroke and the relationship with upper extremity motor function – Full Text

Abstract

Background

Recovery of upper extremity (UE) motor function after stroke is variable from one to another due to heterogeneity of stroke pathology. Structural and biochemical magnetic resonance imaging of the primary motor cortex (M1) have been used to document reorganization of neural activity after stroke.

Objective

To assess cortical biochemical and structural causes of delayed recovery of UE motor function impairment in chronic subcortical ischemic stroke patients.

Methodology

A cross-sectional study with fifty patients were enrolled: thirty patients with chronic (> 6 months) subcortical ischemic stroke suffering from persistent UE motor function impairment (not improved group) and twenty patients with chronic subcortical ischemic stroke and improved UE motor function (improved group). We recruited a group of (16) age-matched healthy subjects. Single voxel proton magnetic resonance spectroscopy (1H-MRS) was performed to measure N-acetylaspartate (NAA) and glutamate+glutamine (Glx) ratios relative to creatine (Cr) in the precentral gyrus which represent M1of hand area in both ipsilesional and contralesional hemispheres. Brain magnetic resonance imaging (MRI) to measure precentral gyral thickness is representing the M1of hand area. UE motor function assessment is using the Fugl Meyer Assessment (FMA-UE) Scale.

Results

The current study found that ipslesional cortical thickness was significantly lower than contralesional cortical thickness among all stroke patients. Our study found that ipsilesional NAA/Cr ratio was lower than contralesional NAA/Cr among stroke patients. UE and hand motor function by FMA-UE showed highly statistically significant correlation with ipsilesional cortical thickness and ipsilesional NAA/Cr ratio, more powerful with NAA/Cr ratio.

Conclusion

We concluded that persistent motor impairment in individuals with chronic subcortical stroke may be at least in part related to ipsilesional structural and biochemical changes in motor areas remote from infarction in form of decreased cortical thickness and NAA/Cr ratio which had the strongest relationship with that impairment.

Introduction

Motor impairment of one side of the body is a major cause of disability in activities of daily living. Recovery from strokes varies from one patient to another due to the heterogeneity of the stroke pathology and rehabilitation strategies. While most stroke patients recover spontaneously, many are left with permanent neurological impairments [1].

Understanding the brain pathologies associated with upper extremity (UE) impairment after stroke, the underlying mechanisms of injury, and the processes associated with recovery is important for achieving good recovery and successful rehabilitation. Advancements in neuroimaging technology have made this possible. Structural and biochemical brain imaging of primary motor cortices has been used to document the reorganization of neural activity after stroke. Ipsilesional and contralesional primary motor cortices, as well as the dorsal premotor cortex, have been identified as areas that can undergo substantial post-stroke neuroplasticity [2].

Single voxel proton magnetic resonance spectroscopy (1H-MRS) is a non-invasive tool to measure the levels of certain metabolites. In acute stroke, the presence of a measurable lactate peak demonstrates a shift from aerobic to anaerobic metabolism in the brain. Previous studies have shown that this is a temporary effect, and levels return to an almost undetectable state within 3 weeks [3].

Biochemical changes have also been observed chronically within ipsilesional normal-appearing grey matter and have been associated with morphological changes in stroke patients [4].

N-Acetylaspartate (NAA) is a metabolite found exclusively in neurons and their processes. It is considered a putative marker of their integrity with specific roles in the central nervous system, including myelin synthesis, neuronal energetics, neuronal osmoregulation, and axonal–glial signaling [5].

In individuals with chronic stroke, lower NAA and higher myo-inositol (an astrocyte marker) concentrations have been reported within ipsilesional and contralesional primary motor cortices [6].

A positive correlation has been drawn between NAA, glutamate (Glu: the principle excitatory neurotransmitter in the human central nervous system), and UE function in a chronic stroke population [7].

Structural changes in regional cortical thickness have also been observed in individuals in the subacute phase (3 months of recovery) after subcortical ischemic stroke and have been linked to functional activation changes in individuals with chronic stroke [89].

The purpose of this study is to assess cortical, biochemical, and structural causes of delayed recovery of UE motor function impairment in patients with chronic, subcortical ischemic stroke.

Subjects and methods

A cross-sectional study with fifty patients were enrolled: thirty patients with chronic (> 6 months) subcortical ischemic stroke suffering from persistent upper extremity motor function impairment (not improved group) and twenty patients with chronic subcortical ischemic stroke and improved upper extremity motor function (improved group).

All patients were recruited from El Sahel Teaching Hospital outpatient clinics.

Inclusion criteria

  1. 1.Eligible right handed patients aged between 50 and 70 years old.
  2. 2.Single clinically diagnosed chronic (> 6 months) subcortical ischemic stroke presented with UE motor impairment at the acute stage.
  3. 3.Radiologically apparent healthy precentral gyrus grey matter.

Exclusion criteria

  1. 1.Patients with disturbed consciousness level.
  2. 2.Patients with aphasia, cognitive impairment, UE apraxia, sensory deficit, or ataxia.
  3. 3.Patients with history of previous stroke.
  4. 4.Patients who had any contraindication for MRI or 1H-MRS.
  5. 5.Patients who underwent neuro-rehabilitation through transmagnetic brain stimulation or transcranial direct current brain stimulation.
  6. 6.Patients with uncontrolled diabetes mellitus.
  7. 7.Patients with chronic renal or hepatic failure.

We recruited right-handed age-matched (16) healthy subject group to be references for our results regarding Egyptian people.

Methods

All participants subjected to:

  1. 1.Full medical history and neurological examination.
  2. 2.Routine lab and imaging.
  3. 3.(1H-MRS) to measure NAA and Glx concentration as ratios of their peak heights to Cr peak height as a stable internal reference (NAA/Cr and Glx/Cr) in ipsilesional and contralesional precentral gyrus which represent the M1 of hand area (landmark of precentral gyrus), determined anatomically by the area that faces and forms the “middle knee” of the central sulcus, located just at the cross point between the precentral sulcus and the central sulcus, which is topographically located at the level of the distal end of the superior frontal sulcus and is therefore also visible on the cortical surface [10] (Fig. 1).
  4. 4.MRI brain to (a) quantify cortical thickness of the precentral gyrus representing the M1of hand area in both ipsilesional and contralesional hemispheres through Picture Archiving and Communication System (PACS), presented in millimeters (mm) and (b) assess white matter disease by fazekas scale which divides the white matter in periventricular (PVWM) and deep white matter (DWM) through fluid attenuated recovery (FLAIR) film with the higher score means more severity.
  5. 5.UE motor function assessment using the Fugl Meyer Assessment (FMA-UE) Scale [11].
  6. 6.Modified rankin scale (mRS) to assess disability degree in stroke patients ranging from 0 to 5 with higher score indicating more disability [12].
figure1
Precentral gyrus, which represents the M1 of hand area (landmark of precentral gyrus), determined anatomically by the area that faces and forms the “middle knee” of the central sulcus, located just at the cross point between the precentral sulcus and the central sulcus, which is topographically located at the level of the distal end of the superior frontal sulcus and is therefore also visible on the cortical surface

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Continue —-> https://ejnpn.springeropen.com/articles/10.1186/s41983-020-00183-2

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