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PubMed2002

Imaging of white matter lesions.

Magnetic resonance imaging (MRI) is very sensitive for the detection of white matter lesions (WML), which occur even in normal ageing. Intrinsic WML should be separated from physiological changes in the ageing brain, such as periventricular caps and bands, and from dilated Virchow-Robin spaces. Genuine WML are best seen with T2-weighted sequences such as long TR dual-echo spin-echo or FLAIR (fluid-attenuated inversion recovery); the latter has the advantage of easily separating WML from CSF-like lesions. Abnormal T2 signal in MRI is not specific, and can accompany any change in tissue composition. In the work-up of WML in small vessel disease, magnetic resonance angiography can be used to rule out (concomitant) large vessel disease, and diffusion-weighted MRI to identify new ischaemic lesions (amidst pre-existing old WML). The differential diagnosis of WML includes hereditary leukodystrophies and acquired disorders. The leukodystrophies that can present in adult age include metachromatic leukodystrophy, globoid cell leukodystrophy, adrenomyeloneuropathy, mitochondrial disorders, vanishing white matter, and cerebrotendinous xanthomatosis. These metabolic disorders typically present with symmetrical abnormalities that can be very diffuse, often with involvement of brainstem and cerebellum. Only the mitochondrial disorders tend to be more asymmetric and frequently involve the grey matter preferentially. Among the acquired white matter disorders, hypoxic-ischaemic causes are by far the most prevalent and without further clinical clues there is no need to even consider the next most common disorder, i.e. multiple sclerosis (MS). Among the nonischaemic disorders, MS is far more common than vasculitis, infection, intoxication and trauma. While vasculitis can mimic small vessel disease, MS has distinctive features with preferential involvement of the subcortical U-fibres, the corpus callosum, temporal lobes and the brainstem/cerebellum. Spinal cord lesions are very common in MS, but do not occur in normal ageing nor in small vessel disease.

Aged↗
PubMed1998

A review on blood pressure and ischaemic white matter lesions.

Hypertension or high blood pressure is constantly reported to be the main risk factors for ischaemic white matter lesions (WMLs). These lesions show the histopathological picture of diffuse demyelination and moderate loss of axons in subcortical structures. The main hypothesis regarding the association between high blood pressure and ischaemic WMLs is that long-standing hypertension causes lipohyalinosis of the media and thickening of the vessel walls with narrowing of the lumen of the small perforating arteries and arterioles which nourish the deep white matter. Episodes of hypotension may then lead to hypoperfusion and hypoxia-ischaemia in the white matter. In line with this, low blood pressure has also been reported to be a risk factor for WMLs. However, also other pathogenetic mechanisms may be involved. Hypertension may cause disturbances in the blood-brain barrier, which may cause lesions in the white matter by cerebral oedema, by activation of astrocytes or by destructive enzymes or other poisons which pass through the damaged vessel walls. The renin-angiotensin system is an example of a system that may be involved in the pathogenesis of both hypertension and arteriosclerosis. Its effector peptide angiotensin II has several blood-pressure-increasing effects, such as direct vasoconstriction and activation of the sympathetic nervous system. It also promotes hyperplasia and hypertrophy in vascular smooth muscle cells. Recently an association between hypertension and Alzheimer's disease has been reported. It is not clear whether this may be the reason for the common occurrence of WMLs in cases of late-onset Alzheimer's disease, as Alzheimer's disease may also cause lesions in the cerebral microvasculature. The association between WMLs and hypertension may thus be mediated through several different pathogenetic pathways.

Animals↗
PubMed1998

The overlap between Alzheimer's disease and vascular dementia: the role of white matter changes.

As there is some overlap between Alzheimer's disease (AD) and vascular dementia (VaD), it can be assumed that some particular features that they have in common are responsible for this overlap. One of the candidates is white matter changes whose presence in variants of the two entities is described in this paper. A common, although much debated, division of AD is into two types, type I usually with early and type II usually with late onset. As to VaD, the division can be based on neuropathological changes and vascular disease mechanisms. In one subtype, 'subcortical white matter dementia', white matter lesions are conspicuous features. The overlap between this subtype and AD type I is small, but the overlap is considerable between the same subcortical subtype and AD type II. In the latter, white matter changes and Alzheimer encephalopathy may interact to produce dementia.

Alzheimer Disease↗
PubMed2002

White matter injury, neural connectivity and the pathophysiology of psychiatric disorders.

Psychiatric disorders are characterized by diverse clinical manifestations that include deficits in cognition, perception, mood and arousal. These complex processes are not mediated by any specific brain region but require the coordinated activity of several areas that are anatomically connected. Impairments in these neural circuits may therefore be expected to result in an attenuation of the functions regulated by them. The white matter provides the structural and physiological substrate of neural circuits in the central nervous system. We propose that injury to the white matter, from diverse biological sources, may compromise neural connectivity by associated axonal injury or impaired conductivity. Either mechanism could result in clusters of signs and symptoms that are currently recognized as psychiatric disorders. The role of white matter impairment in the pathophysiology of psychiatric illness is under-appreciated in the neurosciences. Focused translational research aimed at identifying the links between white matter compromise and specific behaviors are necessary for a more thorough understanding of the etiology of mental illness to emerge.

Adult↗
PubMed2003

Diffuse white matter lesions in carbon disulfide intoxication: microangiopathy or demyelination.

Long-term exposure to carbon disulfide (CS(2)) may induce diffuse encephalopathy with parkinsonism, pyramidal signs, cerebellar ataxia, and cognitive impairments, as well as axonal polyneuropathy. The pathogenic mechanisms of diffuse encephalopathy are unclear, although vasculopathy and toxic demyelination have been proposed. Recently, we have encountered a patient who developed headache, limb tremors, gait disturbance, dysarthria, memory impairment, and emotional lability after long-term exposure to CS(2). The brain magnetic resonance images (MRI) showed diffuse hyperintensity lesions in T(2)-weighted images in the subcortical white matter, basal ganglia, and brain stem. The brain computed tomography perfusion study revealed a diffusely decreased regional cerebral blood flow and prolonged regional mean transit time in the subcortical white matter and basal ganglion. To our knowledge, there have been few reports demonstrating diffuse white matter lesions in chronic CS(2) encephalopathy using brain MRI. In addition, the (99m)Tc-TRODAT-1 single photon emission computed tomography showed a normal uptake of the dopamine transporter, indicating a normal presynaptic dopaminergic pathway. We conclude that diffuse white matter lesions may develop after chronic exposure to CS(2), possibly through microangiopathy. In addition, CS(2) poisoning can be considered as one of the causes of chronic leukoencephalopathy.

Brain↗
PubMed2004

Ultrastructural hippocampal and white matter alterations in mild cognitive impairment: a diffusion tensor imaging study.

Mild cognitive impairment (MCI) is considered to be a transitional stage between normal aging and dementia. In Alzheimer's disease (AD), white matter structural pathology is due to Wallerian degeneration and central angiopathy. However, in MCI patients, the presence and extent of white matter alterations as a possible correlate of impaired memory function and as predictor of subsequent progression to AD is not clarified yet. Diffusion tensor imaging (DTI) reveals the ultrastructural integrity of cerebral white matter tracts. Therefore, it could detect pathological processes that modify tissue integrity in patients with MCI. In our prospective study, conventional and diffusion tensor MR scans were obtained from 14 patients with MCI, 19 patients with AD, and 10 healthy controls. Mean diffusivity (MD) and fractional anisotropy (FA) were measured in temporal, frontal, parietal and occipital white matter regions as well as in the corpus callosum (genu and splenium) and the hippocampus. MCI patients showed higher MD values in the left centrum semiovale (p = 0.013; right: p = 0.026), in the left temporal (p = 0.006), the right temporal (p = 0.014) and the left hippocampal (p = 0.002) region as compared to the control group. FA values of MCI patients and controls did not differ significantly in any region. Compared to controls, AD patients had increased MD values in the left centrum semiovale (p = 0.012), the left parietal (p = 0.001), the right parietal (p = 0.028), the left temporal (p = 0.018), the right temporal (p = 0.011) and the left hippocampal region (p = 0.002). Decreased FA values were measured in the left temporal area (p = 0.017) and in the left hippocampus (p = 0.031) in AD patients compared to controls. FA and MD values did not differ significantly between AD and MCI patients. Elevated MD values indicating brain tissue alterations in MCI patients were found in regions that are typically involved in early changes due to AD, particularly the left hippocampus. The sensitivity of distinguishing MCI patients from controls was 71.4% (with a specificity set at 80%). Therefore, the DTI technique validates the MCI concept, and diffusion tensor MR measurement can be a helpful tool to quantify MCI pathology in vivo.

Aged↗
PubMed2004

Effects of electroconvulsive therapy on frontal white matter in late-life depression: a diffusion tensor imaging study.

This study was conducted to elucidate the effects of electroconvulsive therapy (ECT) on frontal white matter in late-life depressed patients. Diffusion tensor imaging was performed on 8 late-life depressed patients and 12 healthy age-matched controls. The patients were scanned before and after a course of ECT. Fractional anisotropy (FA) was determined in the frontal and temporal regions and the corpus callosum. A significant white matter FA reduction was found in widespread frontal and temporal brain regions in patients with depression before ECT treatment compared with controls. A significant increase in frontal white matter FA was seen following ECT treatment. A course of bilateral ECT ameliorated white matter integrity in frontal brain regions. This suggests a strong relationship with the antidepressant action of ECT.

Age of Onset↗
PubMed2006

Cerebral white matter hyperintensities on MRI: Current concepts and therapeutic implications.

BACKGROUND: White matter hyperintensities (WMH) are commonly observed MRI abnormalities in the elderly, which generally reflect covert vascular brain injury. WMH cumulatively produce substantial neurologic, psychiatric, and medical morbidity. This review provides an overview of current knowledge on vascular WMH, and describes some pharmacological agents that may have a role in mitigating this condition. SUMMARY OF REVIEW: This review has two main focus areas. The first is a discussion of currently available knowledge regarding the public health burden, pathogenesis, and various risk factors associated with the presence of vascular white matter lesions noted on brain MRI. The second section of the article details the mechanistic and clinical basis for promising pharmacological treatment modalities that could potentially prevent progression of ischemic cerebral white matter brain injury. Many of these therapies are already of proven efficacy in preventing recurrent stroke. CONCLUSIONS: Individuals with vascular white matter lesions on MRI may represent a potential target population likely to benefit from secondary stroke prevention therapies.

Age Factors↗
PubMed2006

Thymus involution and cerebral white matter damage in extremely low gestational age neonates.

BACKGROUND: Among newborns who die, those who have cerebral white matter damage are more likely than others to have thymus involution and low thymus weights. OBJECTIVE: We sought to evaluate in a population of preterm newborns who did not die if those who developed a cerebral white matter damage (as defined by an echolucency) are more likely than others to have thymus involution as assessed on chest radiographs. METHOD: The 89 infants whose data were evaluated were born before the 28th week of gestation, had at least one chest radiograph within the first 2 days of life (to determine thymus size), and at least one cranial ultrasonogram to assess for white matter echolucency. RESULTS: Eighty-five percent of these infants had a small thymus within the first 2 weeks of life. Median time to thymus involution in those born before the 26th week of gestation was 36 h, and in those born during or after the 26th week of gestation was 140 h. Infants who developed involution before the median time in their respective gestational age groups were classified as early involuters (group 1) and were compared to their peers with late/no involution (group 2). Infants with an echolucency were more likely to have had early involution than infants without an echolucency (89% vs. 44%) (p = 0.01). This relationship was not distorted by potential confounders. The echolucency odds ratio associated with early thymus involution was consistently above 8 in all strata of the sample. CONCLUSION: These results are consistent with the possibility that early thymus involution and neonatal white matter damage are not independent phenomena and may have common antecedents.

Echoencephalography↗
PubMed1990

Panencephalopathic type of Creutzfeldt-Jakob disease with primary extensive involvement of white matter.

The case of a 66-year-old woman with atypical Creutzfeldt-Jacob disease (CJD) presents several peculiarities. Pathologic examination confirmed a rare CJD case with primary generalized spongiform changes of the white matter and only moderate, but typical changes of the gray matter. Besides an essentially typical clinical course, the patient developed temporary diplopia and vertical eye movement paralysis. Intoxication had been excluded. Isoelectric focusing revealed oligoclonal CSF-IgG. Magnetic resonance imaging studies showed periventricular accentuated flat and striped hyperintense structures. EEG had CJD-typical periodic 1/s synchronous discharges. This case illustrates for the first time that in panencephalopathic type of CJD the cerebral white matter can be involved primarily and more extensively than the gray matter.

Aged↗
PubMed1997

Magnetic resonance imaging of cerebral associative white matter bundles employing fast-scan techniques.

Rapid scan techniques have introduced new sequence parameters as well as novel contrast concepts into everyday magnetic resonance imaging (MRI). In particular contrast characteristics of fast-spin echo (FSE) sequences showed some significant differences when compared to conventional spin echo images. The purpose of this work was to demonstrate the capabilities of FSE MRI in identifying and characterizing the in vivo anatomy of the main cerebral associative systems. Between March and November 1995, 20 healthy adult volunteers (12 males, 8 females, mean age 35 years) were submitted to a cranial MRI examination (1.5 Philips Gyroscan NT). In all cases axial and coronal 2-dimensional FSE T2-weighted and 2-dimensional inversion recovery FSE T1-weighted images were obtained. All MRI images were examined by a neuroradiologist (G. Dal Pozzo) for the depiction of the following compact white matter fiber bundles: anterior commissure, corpus callosum, superior fronto-occipital fasciculus, cingulum, fornix, mammillothalamic tract, uncinate fasciculus, superior and inferior longitudinal fasciculus. All these associative pathways could be well identified on T2-weighted images due to a lower signal intensity with respect to the surrounding white matter. On T1-weighted images only the corpus callosum, the anterior commissure and the fornix could always be identified. Correlation with myelin-specific colorations (Luxol fast blue stains) in anatomic atlases and a review of the literature on the myelinization process during infancy indicate that the short T2 relaxation times of the aforementioned cerebral associative systems may be due to heavy myelination and high fiber density. The correct visualization of interintrahemispheric associative white matter fiber bundles may play an important role in white matter disorders like dys- and demyelinating diseases and in the spreading of vasogenic edema and/or tumor being useful for their staging.

Adult↗
PubMed1994

Periventricular white matter lucency and cerebral blood flow autoregulation in hypertensive patients.

The goal of this study was to elucidate the association between the development of periventricular white matter lucency and autoregulation of cerebral blood flow in hypertensive patients through the arteriovenous oxygen saturation difference method. We studied 51 hypertensive patients who had previously suffered from minor strokes (lacunar infarction, 43; deep basal minor hemorrhage, 8). Patients were divided into three groups based on the findings of periventricular white matter lucency. We measured the absolute value of resting cerebral blood flow using the argon inhalation method, and stepwise reduction of blood pressure was obtained with patients on a tilting table. Intracerebral venous blood sampling was accomplished by direct cannulation into the jugular vein up to the jugular bulb. We calculated several cerebral circulatory parameters, such as cerebrovascular resistance and cerebral oxygen consumption, and also delineated individual autoregulation curves. Cerebrovascular resistance was significantly greater in patients with severe periventricular white matter lucency than in patients without it (P < .05). Impaired autoregulation was also significantly more prevalent in patients with more severe periventricular lesions (P < .05). Multiple regression analysis revealed that the impaired autoregulation was significant and an independent determinant of the severity of such periventricular lesions (R = .34, P < .05). In conclusion, our findings indicated that hypertensive patients with severe periventricular white matter lucency were more likely to have impaired autoregulation of cerebral blood flow and suggest that stricter blood pressure control is required in such patients to prevent deterioration of the cerebral microcirculation.

Aged↗
PubMed2004

White matter hyperintensity on cranial magnetic resonance imaging: a predictor of stroke.

BACKGROUND AND PURPOSE: We have previously reported that several "silent" infarcts found on magnetic resonance imaging (MRI) were a risk factor for stroke. Several recent reports have shown that high white matter grade (WMG) and increasing WMG over time were risk factors for stroke. We tested the hypothesis that high WMG > or =2 was a predictor of risk for stroke, independent of other risk factors. METHODS: We examined the extent of white matter hyperintensity on cranial MRI of 3293 participants from the Cardiovascular Health Study (CHS). The degree of white matter hyperintensity was graded from least severe (grade=0) to most severe (grade=9). Participants were followed-up for an average of 7 years for the occurrence of a stroke. Clinical stroke diagnoses were based on hospital records reviewed by an adjudication committee expert in stroke diagnosis. During this period, 278 strokes occurred. Results The relative risk of stroke increased significantly as the WMG increased. The risk of stroke was 2.8% per year for participants with high WMG (grades > or =5), compared with only 0.6% for participants with grades 0 to 1.Conclusions The risk of stroke with high WMG is independent of traditional stroke risk factors and persists when controlling for MRI infarcts, another subclinical imaging marker of cerebrovascular disease. Assessment of white matter disease may be valuable in assessing future risk of stroke.

Aged↗
PubMed2005

Cilostazol attenuates gray and white matter damage in a rodent model of focal cerebral ischemia.

BACKGROUND AND PURPOSE: To evaluate whether delayed treatment with the antiplatelet agent cilostazol reduces the volume of infarction in the gray and white matter in a rodent model of permanent focal cerebral ischemia and to explore the mechanism of the neuroprotective effect in vivo. METHODS: Cilostazol (30 or 50 mg/kg) or vehicle was administered by gavage 30 minutes and 4 hours after the induction of cerebral ischemia by permanent occlusion of the left middle cerebral artery (MCA). Animals were euthanized 24 hours after MCA occlusion, and the volume of gray matter damage was evaluated by quantitative histopathology. Axonal damage was determined with amyloid precursor protein immunohistochemistry. Dynamic susceptibility contrast MRI was used to assess regional cerebral blood volume (CBV) and cerebral blood flow (CBF). RESULTS: Treatment with the higher dose of cilostazol (50 mg/kg) significantly reduced the volume of gray matter damage and axonal damage in the cerebral hemisphere by 45.0% (P<0.02) and 42.4% (P<0.002), respectively, compared with the control group. Relative CBV in the peri-infarct area after MCA occlusion was significantly increased in the cilostazol-treated group (50 mg/kg) compared with the control group (P<0.05). Relative CBF tended to be higher in the cilostazol-treated group compared with the control group. CONCLUSIONS: Treatment with cilostazol significantly reduced the gray and white matter damage associated with permanent focal ischemia. Cilostazol improved CBV and CBF in the peri-infarct area. The major action of cilostazol is to increase perfusion in the ischemic penumbra.

Animals↗
PubMed1988

White matter signal abnormalities in normal individuals: correlation with carotid ultrasonography, cerebral blood flow measurements, and cerebrovascular risk factors.

We studied 52 asymptomatic subjects using magnetic resonance imaging, and we compared age-matched groups (51-70 years old) with and without white matter lesions with respect to carotid ultrasonography, cerebral blood flow (xenon-133 injection), and cerebrovascular risk factors. In the group with white matter signal abnormalities, we noted a higher frequency of extracranial carotid artery disease, a lower mean gray matter blood flow (F1), and a significant reduction (p less than 0.05) in blood flow of the slow-flowing (F2) compartment. Hypertension, diabetes mellitus, and cardiac diseases (p less than 0.002) were found more often in this group. Our results indicate that a higher incidence of changes known to be associated with an increased risk for stroke exists in the presence of white matter lesions in normal elderly individuals.

Adult↗
PubMed1995

White matter hyperintensities on MRI in the neurologically nondiseased elderly. Analysis of cohorts of consecutive subjects aged 55 to 85 years living at home.

BACKGROUND AND PURPOSE: We undertook this study to evaluate the frequency and risk factors of white matter hyperintensities seen on T2-weighted MR imaging. We examined cohorts of neurologically nondiseased elderly subjects participating in a general-community study, the Helsinki (Finland) Aging Brain Study. Cohorts of consecutive subjects aged 55, 60, 65, 70, 75, 80, and 85 years (n = 20, 18, 20, 18, 19, 18, and 15, respectively; total, n = 128) were divided into a young-old (age < 75 years, n = 76) group and an old-old (age > or = 75 years, n = 52) group. METHODS: Frequency of hyperintensities seen on T2-weighted axial and coronal MR images (0.02 T) was rated using a four-point scale in periventricular and centrum semiovale areas. RESULTS: The majority of the subjects showed only mild white matter hyperintensities, which were more frequent in the periventricular areas. Age was the most important factor to explain the presence of hyperintensities. A logistic regression analysis related periventricular hyperintensities in the entire group to central atrophy (odds ratio [OR], 4.7; 95% confidence interval [CI], 1.7 to 12.9) and silent infarcts (OR, 5.6; 95% CI, 1.0 to 19.8); among the young-old, hyperintensities related to diabetes (OR, 17.0; 95% CI, 1.9 to 154.2) and central atrophy (OR, 14.7; 95% CI, 3.5 to 61.8). Centrum semiovale hyperintensities related in the entire group to cardiac arrhythmia (OR, 4.0; 95% CI, 1.0 to 15.5), central atrophy (OR, 3.9; 95% CI, 1.2 to 12.4), and silent infarcts (OR, 3.6; 95% CI, 1.0 to 12.5). CONCLUSIONS: These mild white matter hyperintensities in the neurologically nondiseased elderly related especially to age and also to concomitant silent infarcts, atrophy, and some vascular risk factors. The known factors, however, explained only part of the variation. The young-old and old-old groups showed different associations. In contrast to former assumptions, the presence of white matter hyperintensities among the aged is likely to be linked to other as yet unidentified age-related factors.

Aged↗
PubMed1995

The significance of cerebral white matter abnormalities 100 years after Binswanger's report. A review.

BACKGROUND: Changes in the cerebral hemispheric white matter are detected with increasing frequency by CT and MRI among persons older than 60 years. The pathogenesis, clinical significance, and morphological substrate of these changes are incompletely understood. Patients who have such neuroimaging abnormalities are sometimes diagnosed with "Binswanger's disease," an eponym that has generated much confusion because of its imprecise meaning. The objectives of this study were to determine whether the term Binswanger's disease merits acceptance as a distinct clinicopathologic entity, to deduce the clinical significance of these white matter abnormalities from the analysis of appropriate publications, and to evaluate studies that correlate in vivo changes in the cerebral white matter with pathological features. SUMMARY OF REVIEW: We evaluated Binswanger's original case description and, after conducting a Medline search, reviewed more than 160 publications, mostly in the English language, on the subject of white matter abnormalities detectable by currently used neuroimaging methods (ie, leukoaraiosis). CONCLUSIONS: Binswanger's original description appears to be insufficient for the purpose of defining a new nosological entity. After evaluating the vaguely outlined pathological correlates described in a few of these subcortical cerebral leukoencephalopathies, we conclude that the clinical significance of leukoaraiosis remains incompletely defined. However, its frequency increases with age independent of other risk factors, and in nondemented subjects leukoaraiosis is associated with deficits in selected cognitive functions. Moreover, leukoaraiosis correlates with an increased risk for the subsequent development of strokes. We make specific suggestions for future studies that may help to clarify this topic.

Aged↗
PubMed1996

Lobar intracerebral hemorrhage model in pigs: rapid edema development in perihematomal white matter.

BACKGROUND AND PURPOSE: The mechanisms underlying brain injury from intracerebral hemorrhage (ICH) are complex and poorly understood. To comprehensively examine pathophysiological and pathochemical alterations after ICH and to examine the effects of hematoma removal on these processes, we developed a physiologically controlled, reproducible, large-animal model of ICH in pigs (weight, 6 to 8 kg). METHODS: We produced lobar hematomas by pressure- controlled infusions of 1.7 mL of autologous blood into the right frontal hemispheric white matter over 15 minutes. We froze brains in situ at 1, 3, 5, and 8 hours after hematoma induction and cut coronal sections of hematoma assessment, morphological brain examination, and immunohistochemical and water content determinations. RESULTS: At 1 hour after blood infusion, "translucent" white matter areas were present directly adjacent to the hematoma. These markedly edematous regions had a greater than 10% increase in water content (>85%) compared with the contralateral white matter (73%), and this increased water content persisted through 8 hours. In addition, these areas were strongly immunoreactive for serum proteins. Intravascular Evans blue dye failed to penetrate into the brain tissue at all time points, demonstrating that this serum protein accumulation and edema development were not due to increased blood-brain barrier permeability. CONCLUSIONS: Experimental lobar ICH in pigs models a prominent pathological feature of human ICH, ie, early perihematomal edema. Our findings suggest that serum proteins, originating from the hematoma, accumulate in adjacent white matter and result in rapid and prolonged edema after ICH. This interstitial edema likely corresponds to the low densities on CT scans and the hyperintensities on T2-weighted MR images that surround intracerebral hematomas acutely after human ICH.

Animals↗