Brain Iron Deposition In Patients Research Articles

Correlation of brain iron deposition and freezing of gait in Parkinson's disease: a cross-sectional study.

Quantitative susceptibility mapping (QSM) is a novel imaging method for detecting iron content in the brain. The study aimed determine whether the iron deposition in the brains of people with Parkinson's disease (PD) is correlated with freezing of gait (FOG). We retrospectively collected the data of 24 patients with PD from the Movement Disorders Program and 36 healthy controls (HCs) from January 2021 to December 2021. Clinical assessments included mental intelligence scales, Parkinson rating scales, motor-related scales, and clinical gait assessments. All exercise scales and gait assessments were performed in the "ON" and "OFF" states. Magnetic resonance imaging (MRI) data were collected using 3-dimensional fast low-angle shot sequences. We chose the bilateral red nucleus, substantia nigra, thalamus, putamen, caudate nucleus, and globus pallidus as regions of interest for QSM analysis. The iron deposition in the substantia nigra of the PD group was significantly higher than that of the HC group (P<0.01). In the PD group, the iron deposition in the substantia nigra of patients with FOG was significantly higher than that in patients without FOG (P=0.04). The iron deposition in the substantia nigra was positively correlated with the New Freezing of Gait Questionnaire (P=0.03). The scores for depression and anxiety of the PD group were significantly higher than those of the HC group, while the Berg balance scale score was significantly lower (P<0.01). The iron deposition in the substantia nigra of patients with PD is increased compared with that of controls and is associated with FOG. QSM can be used to detect brain iron deposition in patients with PD, which would help to explore the mechanism of abnormal neurobiological activity in FOG.

Altered brain iron deposition in patients with minimal hepatic encephalopathy: an MRI quantitative susceptibility mapping study

To explore the use of quantitative susceptibility mapping (QSM) in assessing changes in brain iron deposits and their association with cognitive function in patients with minimal hepatic encephalopathy (MHE). The study cohort comprised 27 cases with hepatitis B-associated cirrhosis with MHE (MHE group), 25 with hepatitis B-associated cirrhosis without MHE (NMHE group), and 25 healthy controls (HC group). Iron deposits in the bilateral frontal white matter, caudate nucleus (CN), putamen, globus pallidus, thalamus, red nucleus, substantia nigra (SN), hippocampus, and dentate nucleus were measured by QSM. The associations between iron deposition with the time taken to complete number connection tests A (NCT-A) and the score on digital-symbol test (DST) were analysed. Susceptibility values differed significantly in the bilateral CN, left thalamus, right SN, and left hippocampus in the MHE group compared with the other groups and were positively associated with the times taken to complete the NCT-A in the bilateral CN, left thalamus, and right SN and negatively associated with DST scores in the bilateral CN, left TH, and left HP. Reduced cognitive function in MHE patients was significantly associated with abnormally increased iron deposition in certain brain areas. The quantification of brain iron deposition by QSM may thus be an objective and accurate means of evaluating MHE.

Quantitative Susceptibility Mapping of Brain Iron Deposition in Patients With Recurrent Depression.

Objective Recurrence is the most significant feature of depression and the relationship between iron and recurrent depression is still lack of direct evidence in vivo. Methods Twenty-one patients with depression and twenty control subjects were included. Gradient-recalled echo, T1 and T2 images were acquired using a 3.0T MRI system. After quantitative susceptibility mapping were reconstructed and standardized, a whole-brain and the regions of interest were respectively analyzed. Results Significant increases in susceptibility were found in multiple recurrent depression patients, which involved several brain regions (frontal lobes, temporal lobe structures, occipital lobes hippocampal regions, putamen, thalamus, cingulum, and cerebellum). Interestingly, no susceptibility changes after treatment compared to pre-treatment (all p>0.05) and no significant correlation between susceptibility and Hamilton Depression Rating Scale were found. Besides, it was close to significance that those with a higher relapse frequency or a longer mean duration of single episode had a higher susceptibility in the putamen, thalamus, and hippocampus. Further studies showed susceptibility across the putamen (ρ2=0.27, p<0.001), thalamus (ρ2=0.21, p<0.001), and hippocampus (ρ2=0.19, p<0.001) were strongly correlated with total course of disease onset. Conclusion Brain iron deposition is related to the total course of disease onset, but not the severity of depression, which suggest that brain iron deposition may be a sign of brain damage in multiple recurrent depression.

Relationship between the state coagulation system, protein and fat metabolism, and Brain iron deposition in patients with cerebral small vessel disease

Brain iron deposition correlates with clinical manifestations of cerebral small vessel disease. Excessive iron load leads to the formation of free radicals, and nervous tissue damage. The main damaging effect of hydroxyl radicals is due to conversion of soluble fibrinogen to insoluble fibrin. There is also a possible relationship between the functional state of the liver and the early manifestations of cardiovascular disease. Objective: to investigate the relationship between the parameters of coagulation system, liver functional state, fat and protein metabolism, and brain iron deposition in patients with cerebral small vessel disease in the presence of hypertension and cerebral atherosclerosis. Materials and methods: 80 patients with diagnosed cerebral small vessel disease were selected. Patients were divided into two groups, depending on the severity of brain iron deposition. All patients underwent MRI in the T1-WI, T2-WI, TIRM, DWI, and SWI sequences. Determination of the coagulation system parameters and the biochemical analysis were carried out during routine blood test. Results: using a double-sample t test, it was determined that patients with severe brain iron deposition had higher levels of urea, triglycerides, and prolonged thrombin time. With the logistic regression analysis adjusted by the age and sex, levels of urea and the length of thrombin time were determined as the independent risk factors for severe brain iron deposition. For urea OR 1.87, CI 95% 1.31-2.65 (p = 0.02), for thrombin time OR 1.55, CI 95% 1.06-2.26 (p = 0.02). For these parameters, the risk increased when assessing only patients with ALT levels&gt; 15 U / l. For such patients, the relationship between thrombin time and brain iron deposition increased significantly: OR 2.11, CI 95% 1.20-3.71 (p = 0.01). In this study no relationship was found between the indicators of fat metabolism, levels of fibrin and iron deposition. There is a probable relationship between the brain iron deposition and the state of coagulation system, protein metabolism and liver functional state in patients with cerebral small vessel disease.

Characterizing Brain Iron Deposition in Patients with Subcortical Vascular Mild Cognitive Impairment Using Quantitative Susceptibility Mapping: A Potential Biomarker.

The presence and pattern of iron accumulation in subcortical vascular mild cognitive impairment (svMCI) and their effects on cognition have rarely been investigated. We aimed to examine brain iron deposition in svMCI subjects using quantitative susceptibility mapping (QSM). Moreover, we aimed to investigate the correlation between brain iron deposition and the severity of cognitive impairment as indicated by z-scores. We recruited 20 subcortical ischemic vascular disease (SIVD) patients who fulfilled the criteria for svMCI. The control group comprised 19 SIVD patients without cognitive impairment. The SIVD and control groups were matched based on age, gender, and years of education. Both groups underwent QSM using a 3.0T MRI system. Susceptibility maps were reconstructed from in vivo data, which were acquired with a three-dimensional spoiled gradient recalled sequence. Then, regions of interest were drawn manually on the map of each subject. The inter-group differences of susceptibility values were explored in deep gray matter nuclei, including the bilateral pulvinar nucleus of the thalamus, head of caudate nucleus, globus pallidus, putamen, hippocampus, substantia nigra, and red nucleus. The correlations between regional iron deposition and composite z-score, memory z-score, language z-score, attention-executive z-score and visuospatial z-score were assessed using partial correlation analysis, with patient age and gender as covariates. Compared with the control, the svMCI group had elevated susceptibility values within the bilateral hippocampus and right putamen. Furthermore, the susceptibility value in the right hippocampus was negatively correlated with memory z-score and positively correlated with language z-score. The susceptibility value in the right putamen was negatively correlated with attention-executive z-score in the svMCI group. However, composite z-score were unrelated to susceptibility values. Our results suggest that brain iron deposition has clinical relevance as a biomarker for cognition. In addition, our results highlight the importance of iron deposition in understanding svMCI-associated cognitive deficits in addition to conventional MRI markers.

No evidence for increased brain iron deposition in patients with ischemic white matter disease

Besides specific iron accumulation in some neurodegenerative disorders, increased iron deposition in cerebral deep gray matter (DGM) is found in multiple sclerosis. As this is considered largely a white matter (WM) disease, we speculated that patients with more severe ischemic WM hyperintensities (WMH) might also have an increased iron concentration in DGM structures and tested this assumption by using magnetic resonance imaging–based quantitative R2* relaxometry. WMH severity was measured in 61 patients with acute transient neurological symptoms (mean age: 71.5 ± 8.3 years) undergoing 3-Tesla magnetic resonance imaging. Despite a 6-year higher age of patients with more severe (i.e., early confluent or confluent) WMH, their DGM R2* rates did not differ from patients with punctate or no WMH. In the globus pallidum, R2* rates were even lower in patients with severe WMH. WMH volume was not correlated with R2* levels in any of the analyzed DGM structures. These findings argue against WM damage per se causing increased DGM iron deposition in multiple sclerosis and suggest no role of iron accumulation in ischemic small vessel disease.

Quantifying brain iron deposition in patients with Parkinson's disease using quantitative susceptibility mapping, R2 and R2*

PurposeTo evaluate the sensitivity and specificity of quantitative magnetic resonance (MR) iron mapping including R2, R2* and magnetic susceptibility to differentiate patients with Parkinson's disease (PD) from healthy controls. Materials and MethodsThirty (30) healthy controls (HC) (64±7years old) and 20 patients with idiopathic PD (66±8years old) were studied using a 3T MR imaging scanner. R2 maps were generated from GRASE sequence while R2*, and quantitative susceptibility mapping (QSM) were obtained from a conventional multi-echo gradient-echo sequence. R2, R2* and relative susceptibility (Δχ) values of structures in the basal ganglia were measured for each patient and control. An analysis of sensitivity and specificity and unpaired t-test was applied to the two groups. ResultsA significant difference (p<0.05) was found for R2 and ∆χ values in the substantia nigra as a whole and in the pars compacta for PD patients. The R2* values were different significantly (p<0.05) only on the substantia nigra pars compacta. QSM presented the highest sensitivity and specificity to differentiate the two populations. ConclusionThe QSM map was the most sensitive quantitative technique for detecting a significant increase of iron for PD. The highest significant difference between controls and patients was found in the substantia nigra pars compacta using QSM.

Quantitative measurement of brain iron deposition in patients with haemodialysis using susceptibility mapping.

To compare the susceptibility of different brain structures in patients with haemodialysis with that in healthy controls using susceptibility mapping and explore the correlations with neuropsychiatric tests and clinical parameters. Fifty three patients with haemodialysis and forty-five age-and sex-matched healthy controls were recruited in this prospective study. Susceptibility maps (SM) were reconstructed from original phase data and used to compare the susceptibility of different brain structures between patients and healthy controls. The SM was compared with iron predictions from a classic cadaver brain study. Spearman's correlation and stepwise multiple regression analysis between susceptibility and neuropsychiatric tests and clinical parameters were calculated. In patients with haemodialysis, the susceptibility of the bilateral caudate head, putamen, substantia nigra, red nucleus and dentate nucleus were significantly higher than those in healthy controls (P < 0.01). There was positive correlation between susceptibility both from normal controls and patients and iron concentration from a classic post-mortem brain study (both r = 0.900, both P = 0.037). In patients with haemodialysis, the susceptibility of the left putamen (r = 0.944), right putamen (r = 0.882) and right thalamus (r = 0.852) were correlated to dialysis duration (all P < 0.05). The susceptibility of the left caudate head (r = -0.415) and right caudate head (r = -0.311) were mildly negatively correlated with neuropsychiatric test scores (all P < 0.05). In summary, our findings indicated that increased brain iron deposition does occur in patients with haemodialysis and correlated with duration of dialysis.

Decreased Serum Hepcidin Concentration Correlates with Brain Iron Deposition in Patients with HBV-Related Cirrhosis

PurposeExcessive brain iron accumulation contributes to cognitive impairments in hepatitis B virus (HBV)-related cirrhotic patients. The underlying mechanism remains unclear. Hepcidin, a liver-produced, 25-aminoacid peptide, is the major regulator of systemic iron metabolism. Abnormal hepcidin level is a key factor in some body iron accumulation or deficiency disorders, especially in those associated with liver diseases. Our study was aimed to explore the relationship between brain iron content in patients with HBV-related cirrhosis and serum hepcidin level.MethodsSeventy HBV-related cirrhotic patients and forty age- sex-matched healthy controls were enrolled. Brain iron content was quantified by susceptibility weighted phase imaging technique. Serum hepcidin as well as serum iron, serum transferrin, ferritin, soluble transferrin receptor, total iron binding capacity, and transferrin saturation were tested in thirty cirrhotic patients and nineteen healthy controls. Pearson correlation analysis was performed to investigate correlation between brain iron concentrations and serum hepcidin, or other iron parameters.ResultsCirrhotic patients had increased brain iron accumulation compared to controls in the left red nuclear, the bilateral substantia nigra, the bilateral thalamus, the right caudate, and the right putamen. Cirrhotic patients had significantly decreased serum hepcidin concentration, as well as lower serum transferring level, lower total iron binding capacity and higher transferrin saturation, compared to controls. Serum hepcidin level negatively correlated with the iron content in the right caudate, while serum ferritin level positively correlated with the iron content in the bilateral putamen in cirrhotic patients.ConclusionsDecreased serum hepcidin level correlated with excessive iron accumulation in the basal ganglia in HBV-related cirrhotic patients. Our results indicated that systemic iron overload underlined regional brain iron repletion. Serum hepcidin may be a clinical biomarker for brain iron deposition in cirrhotic patients, which may have therapeutic potential.

Quantitative T2* Magnetic Resonance Imaging for Evaluation of Iron Deposition in the Brain of β-Thalassemia Patients

Iron overload is a common clinical problem in patients with β-thalassemia major. The purpose of this study was to assess the presence of excess iron in certain areas of the brain (thalamus, midbrain, adenohypophysis and basal ganglia) in patients with β-thalassemia major and evaluate the association with serum ferritin and liver iron content. A cross-sectional study on 53 patients with β-thalassemia major and 40 healthy controls was carried out. All patients and healthy controls underwent magnetic resonance imaging (MRI) examinations of the brain and liver. Multiecho fast gradient echo sequence was used and T2* values were calculated based on the Brompton protocol. Correlations between T2* values in the brain with T2* values in the liver as well as serum ferritin levels were investigated. There were no significant differences between patients and healthy controls with respect to age and sex. Patients had significantly lower T2* values in basal ganglia (striatum), thalamus and adenohypophysis compared to controls while there were no differences in the midbrain (red nucleus). There were no significant correlations between liver T2* values or serum ferritin with T2* values of basal ganglia (striatum), thalamus and adenohypophysis in patients or healthy controls. There were no significant correlations between T2* values of adenohypophysis and thalamus or basal ganglia (striatum) while these variables were significantly correlated in healthy controls. Serum ferritin and liver iron content may not be good indicators of brain iron deposition in patients with β thalassemia major. Nevertheless, the quantitative T2* MRI technique is useful for evaluation of brain iron overload in β thalassemia major patients.

Quantitative assessment of brain iron by R2* relaxometry in patients with clinically isolated syndrome and relapsing–remitting multiple sclerosis

Background Increased iron deposition has been implicated in the pathophysiology of multiple sclerosis (MS), based on visual analysis of signal reduction on T2-weighted images. R2* relaxometry allows to assess brain iron accumulation quantitatively. Objective To investigate regional brain iron deposition in patients with a clinically isolated syndrome (CIS) or relapsing–remitting MS (RRMS) and its associations with demographical, clinical, and conventional magnetic resonance imaging (MRI) parameters. Methods We studied 69 patients (CIS, n = 32; RRMS, n = 37) with 3T MRI and analyzed regional R2* relaxation rates and their correlations with age, disease duration, disability, T2 lesion load, and normalized brain volumes. Results Basal ganglia R2* relaxation rates increased in parallel with age (r = 0.3–0.6; P < 0.01) and were significantly higher in RRMS than in CIS (P < 0.05). Using multivariate linear regression analysis, the rate of putaminal iron deposition was independently predicted by the patients’ age, disease duration, and gray matter atrophy. Conclusions Quantitative assessment by R2* relaxometry suggests increased iron deposition in the basal ganglia of MS patients, which is associated with disease duration and brain atrophy. This technique together with long-term follow-up thus appears suited to clarify whether regional iron accumulation contributes to MS morbidity or merely reflects an epiphenomenon.