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PubMed2006

Longitudinal magnetic resonance imaging study of rhesus monkey brain development.

To examine early brain development, T1-weighted structural MRI scans of seven rhesus monkeys (Macaca mulatta) were obtained longitudinally between the ages of 1 week and 4 years at 12 age points. Total brain volume, calculated at each age point, increased significantly, by 56%, between 1 week and 4 years. The greatest increase of 22% occurred between 1 week and 1 month, followed by further significant increases between 1 and 2 months, and 3 and 4 months. Gradually smaller increases continued up to 3 years with no further significant changes thereafter. A robust maturation of white matter occurred between 1 week, at which the only easily identifiable fibre tracts were internal capsule and optic radiations, and 3 months, at which most large fibre tracts were visible; only at this age reproducible measurements were possible for all cases. White matter volume increased by 126% between 3 months and 4 years, with the biggest increase between 3 and 4 months (32%) followed by smaller but significant increases up to 4 years. The macaque brain development parallels that of humans by reaching the maximum in total brain volume around the age of sexual maturity (in macaques 3-4 years) and by the increases in white matter continuing beyond this age. The most rapid growth in both total brain volume and white matter from birth to approximately 4 months is consistent with the emergence of various cognitive abilities in macaques at that age.

Age Factors↗
PubMed1982

Aphasia following right striato-insular infarction in a left-handed child: a clinico-radiological study.

The case of six-year-old girl with non-fluent aphasia following a subcortical right-hemispheric cerebrovascular accident is reported. Examination by computerised tomographic scan revealed a right paraventricular area of diminished density involving the internal capsule, lenticular nucleus and the insula. The speech disturbance was followed by typical right-hemispheric signs and by left-channel extinction in dichotic listening tests. The aphasia cleared in two weeks, paralleled by an improvement in left-channel performance, suggesting that language recovery was dependent on right-hemispheric structures.

Aphasia↗
PubMed1986

High density on computed tomography in infantile Krabbe's disease: a case report.

In a child with a compatible clinical presentation and course of illness, Krabbe's disease was proven by white blood-cell galactocerebrosidase estimation in the homozygous range. A CT head scan performed at five months of age revealed symmetrical high density in the thalami, posterior limbs of the internal capsules and corona radiata. It also showed low density in the deep white-matter of the cerebral and cerebellar hemispheres and minor cerebral atrophy. Similar CT findings have been recorded in four other cases of infantile Krabbe's disease, and the authors consider that they are sufficient to alert the clinician to the probability of this diagnosis when the clinical signs are appropriate.

Atrophy↗
PubMed1989

Hypokinesia and rigidity as clinical manifestations of mitochondrial encephalomyopathy: report of three cases.

Three patients are reported with a neurological disorder in which hypokinesia and rigidity were the most prominent clinical signs. On CT scan and MRI, two were found to have bilateral lesions in the striatum, mainly in the putamen, and the third had bilateral lesions in the posterior limb of the internal capsule. Laboratory investigations suggested abnormal pyruvate metabolism in all three cases, which was confirmed to skeletal muscle in two cases. In the third the cause was a NADH dehydrogenase defect. The signs and symptoms, the bilateral striatal lesions in two of the patients, and the abnormal pyruvate metabolism justify a classification of mitochondrial encephalomyopathy, resembling Leigh syndrome. This diagnosis must be considered for infants and children presenting with Parkinsonian signs, and mitochondrial energy metabolism should be investigated.

Adolescent↗
PubMed1998

Acute necrotizing encephalopathy of childhood (infantile bilateral thalamic necrosis): two non-Japanese cases.

This report describes two Spanish cases of acute necrotizing encephalopathy of childhood, a rare disease first described in Japan by Mizuguchi and colleagues. Similar cases have been reported from Taiwan and other countries of the Far East. Two cases have been reported from the UK and one from the USA. The disease affects young children and is characterized by acute encephalopathy after a viral illness, with seizures and decreased levels of consciousness. The hallmark of the disease is diffuse and symmetrical CNS lesions of both thalami, internal capsules, upper brainstem tegmentum, and cerebral white matter. The aetiology is unknown but an infectious or parainfectious process seems likely. Because of the predominant involvement of the thalami, we propose the term 'infantile bilateral thalamic necrosis', a more specific term and one which distinguishes the entity from other basal ganglia diseases in childhood.

Brain↗
PubMed1980

Thiamin deficiency in the lamb: changes in thiamin phosphate esters in the brain.

Concentration of thiamin (unphosphorylated), thiamin monophosphate (TMP), thiamin diphosphate (TDP), and thiamin triphosphate (TTP) were measured in three regions of the brain of seven pairs of lambs. The lambs were maintained on a thiamin-free synthetic diet for 2, 3, or 4 weeks. Controls were pair-fed and supplemented with thiamin. The three brain regions were: (1) dorso-lateral aspect of the cortex [common site for lesions of polioencephalomalacia (PEM)]; (2) pyriform lobe of the cortex (no PEM lesions are found here); (3) white matter of the internal capsule (no PEM lesions found here). The concentration of TTP ina ll three sections of brain was maintained at control values for up to 4 weeks on the thiamin-deficient diet. TDP concentration decreased to 22% of control values in both regions of grey matter after 4 weeks on the diet. Unphosphorylated thiamin and TMP decreased to a smaller extent than TDP.

Animals↗
PubMed1984

Topographical atlas of the gangliosides of the adult human brain.

Forty different brain samples, consisting of neocortical, archicortical, and paleocortical areas; telencephalic, diencephalic, and mesencephalic subcortical nuclei; and the cerebellum as well as some of the corresponding white matter bundles were analyzed with respect to total content of ganglioside-sialic acid and the ganglioside pattern. The total content of gangliosides seems to depend mainly on the proportions of gray and white matter. Thus, neocortical areas, which are rich in gray matter, have a four- to fivefold higher ganglioside content (per milligram of protein) than white matter-rich samples such as optic chiasm, capsula interna, or corpus callosum. White matter-rich regions, although very heterogeneous in ganglioside composition, are further characterized by appreciable amounts of the myelin-enriched GM4. In the neocortex a remarkable degree of regional pattern differences was revealed. In the frontal and parietal areas there is a moderate, and in the temporal region a strong preponderance of sialic acid bound to gangliosides of the a-pathway (GD1a, GM1). In contrast, the occipital cortex favors the b-pathway of ganglioside synthesis (GQ1b, GT1b, GD1b). A predominance of "b-gangliosides" was found in all structures that are related to the visual system (optic chiasm, pulvinar-thalamus, superior colliculi, visual cortex) as well as in the cerebellum and the nucleus ruber. All diencephalic nuclei tend to favor slightly "b-gangliosides," while the mesencephalic nuclei are very heterogeneous in their ganglioside composition. A preponderance of "a-gangliosides" was found in the periamygdalar cortex, putamen, inferior colliculi, substantia nigra, frontal white matter, internal capsule, globus pallidus, basal nucleus of Meynert, and corpus callosum as well as in the frontal, parietal, and temporal cortices. An exceptional predominance of GM1 and GD1a was revealed for the hippocampal archicortex and the amygdala, suggesting a possible functional correlation to glutaminergic synaptic transmission.

Brain Chemistry↗
PubMed2006

Voxel-based optimized morphometry (VBM) of gray and white matter in temporal lobe epilepsy (TLE) with and without mesial temporal sclerosis.

PURPOSE: In temporal lobe epilepsy (TLE) with evidence of hippocampal sclerosis (TLE-MTS) volumetric gray (GM) and white (WM) matter abnormalities are not restricted to the hippocampus but also are found in extrahippocampal structures. Less is known about extrahippocampal volumetric abnormalities in TLE without hippocampal sclerosis (TLE-no). In this study, we used optimized voxel-based morphometry (VBM) with and without modulation with the following aims: (a) to identify WM and GM abnormalities beyond the hippocampus in TLE-MTS and TLE-no; and (b) to determine whether extratemporal WM and GM abnormalities differ between TLE-MTS and TLE-no. METHODS: Optimized VBM of GM and WM with and without modulation was performed in 26 TLE-MTS (mean age, 35.6 +/- 9.7 years), 17 TLE-no (mean age, 35.6 +/- 11.1 years), and 30 healthy controls (mean age, 30.3 +/- 11.1 years). RESULTS: In TLE-MTS, GM/WM volume and concentration reductions were found in the ipsilateral limbic system, ipsi- and contralateral neocortical regions, thalamus, cerebellum, internal capsule, and brainstem when compared with controls. In contrast, no differences of GM/WM volumes/concentrations were found between TLE-no and controls or between TLE-no and TLE-MTS. CONCLUSIONS: In TLE-MTS, optimized VBM showed extensive GM and WM volume reductions in the ipsilateral hippocampus and in ipsi- and contralateral extrahippocampal regions. In contrast, no GM/WM volume or concentration reductions were found in TLE-no. This further supports the hypothesis that TLE-no is a distinct clinicopathologic entity from TLE-MTS and probably heterogeneous in itself.

Adult↗
PubMed1997

Cortical and subcortical white matter damage without Wernicke's encephalopathy after recovery from thiamine deficiency in the rat.

The relative etiologic roles of ethanol and thiamine deficiency in the cortical atrophy and loss of cerebral white matter in chronic alcoholics are uncertain. The present study examined the distribution of degenerating axons within cortical and subcortical tracts 1 week after recovery from early to late symptomatic stages of thiamine deficiency in the absence of ethanol in Sprague-Dawley rats. The brains of rats exposed to an early symptomatic stage of pyrithiamine-induced thiamine deficiency, 12-13 days of treatment, contained degenerating axons in corpus callosum, anterior commissure, external and internal capsules, optic and olfactory tracts, and fornix and mammillothalamic tracts. A dense pattern of degenerating axons was evident in layers III-IV of frontal and parietal cortex. Less intense and more evenly distributed degenerating axons were present in layers IV-VI of frontal, parietal, cingulate, temporal, retrosplenial, occipital, and granular insular cortex. Neuronal counts in mammillary body nuclei and areal measurements of the mammillary body were unchanged from controls and the thalamus was relatively undamaged. In animals reversed at later and more advanced symptomatic stages of thiamine deficiency, 14-15 days of treatment, degenerating axons were found in other cortical regions and hippocampus and there was extensive neuronal loss and gliosis within mammillary body and medial thalamus. These results demonstrate that a single episode of thiamine deficiency can selectively damage cortical white matter tracts while sparing the thalamus and mammillary body and may be a critical factor responsible for the pathological and behavioral changes observed in alcoholics without Wernicke's encephalopathy.

Alcoholism↗
PubMed2000

Acute stroke in very old people: clinical features and predictors of in-hospital mortality.

OBJECTIVES: To examine demographic characteristics, clinical features, neuroimaging data, and outcome of all acute stroke events occurring in individuals aged 85 years or older. DESIGN: Collection of data from a prospective hospital-based stroke registry. SETTING: Between January 1986 and December 1995, the data was collected of 2,000 stroke patients admitted consecutively to the department of neurology ( having 25 beds and an acute stroke unit) of Sagrat Cor-L'Alianza Hospital of Barcelona (an acute care, 350-bed teaching hospital serving a population of approximately 250,000). PARTICIPANTS AND MEASUREMENTS: For the purpose of this study, very old patients (aged 85 years or older) were selected (n = 262). The data of very old stroke patients were compared with the data of patients younger than 85 years of age (n = 1738). Predictors of in-hospital mortality based on clinical and neuroimaging variables were recorded within 48 hours of stroke onset, and outcome variables (medical complications that developed during hospitalization) were assessed by multiple regression analysis. RESULTS: The very old patients showed a significantly greater frequency of atherothrombotic (27.5% vs. 21.9%, P<.05) and cardioembolic infarctions (24.4% vs. 26.3%, P<.001) and a lesser frequency of stroke of unusual cause. Acute stroke in the very old patients was more severe than in patients younger than 85 years of age, with greater rates of in-hospital mortality (27% vs. 13.5%, P<.001), longer duration of hospital stay (22.03+/-29.6 vs. 17.5+/-21.5 days, P<.001), and lesser frequency of absence of neurologic deficit at the time of hospital discharge (21.4% vs. 33.1%, P<.001). Altered consciousness, limb weakness, sensory symptoms, involvement of the parietal lobe and temporal lobe, involvement of the internal capsule (with a protective effect), intraventricular hemorrhage, cardiac events, and respiratory events were selected as independent predictors of in-hospital mortality in the multivariate analysis. CONCLUSIONS: Very old patients with acute stroke showed a differential clinical profile, different frequency of stroke subtypes, and a poorer outcome compared with stroke patients who were younger than 85 years of age. Clinical and neuroimaging factors that are indicative of the severity of stroke and that were available at the time of the initial diagnosis and at the time of the development of cardiac and respiratory complications showed a predominant influence on in-hospital mortality and may help clinicians to establish prognosis more accurately.

Acute Disease↗
PubMed2001

Localization of clinical syndromes using DWI: two examples of the "capsular" warning syndrome.

The capsular warning syndrome (CWS) is a subtype of transient ischemic attack characterized by its recurrent nature, absence of cortical signs, and high probability of early capsular stroke. Currently, standard imaging techniques have identified only internal capsule lesions in this entity. The authors present 2 cases with an otherwise typical CWS in whom a brainstem stroke was detected by diffusion-weighted imaging (DWI). DWI's ability to differentiate between acute and chronic infarcts may assist in more accurate localization of clinical syndromes.

Aged↗
PubMed1982

Prognostic significance of cerebral computed tomography results in supratentorial infarction.

In 69 patients with supratentorial cerebral infarction findings at computed tomography (CT) were related to clinical state on admission and course of recovery. In patients with initial disability of slight to moderate degree CT did not provide prognostically useful information; in patients with severe symptoms at onset location of lesion to the internal capsule or the right parietal lobe and the presence of the mass effect, as single factors or in combination, were ominous CT indicators in terms of functional recovery.

Adult↗
PubMed1991

CT, somatosensory and brainstem auditory evoked potentials in the early prediction of functional outcome in putaminal hemorrhage.

The CT and median somatosensory and brainstem auditory evoked potentials (SEP and BAEP) were studied in 80 patients with spontaneous putaminal hemorrhage for their values in the early prediction of functional outcome. The CT scan was performed within 2 days and EPs within a week after the onset of symptoms. The activities of daily living was assessed at 6 months. Patients with good functional recovery had the following findings: 1) the hemorrhage had not involved the thalamus or the posterior limb of the internal capsule; 2) the SEPs were normal or had prolonged central conduction time; and 3) the BAEP was normal. When the cortical SEPs were absent, the majority of patients were moderately or severely disabled. Attenuation or absence of BAEP wave V always forecast a grave prognosis. It is concluded that the combined use of CT, SEP and BAEP is an objective and reliable method for the early prediction of functional outcome in patients with putaminal hemorrhage.

Activities of Daily Living↗
PubMed1998

Akinetic mutism: a report of three cases.

OBJECTIVES: To report 3 new cases of akinetic mutism, a clinical syndrome defined by silent immobility with preserved visual alertness not accountable by lesion of the areas and/or effector pathways of speech and voluntary movements. MATERIAL AND METHODS: Anatomopathological studies were performed in Cases 1 and 2; clinical follow-up, EEG, angiography and CT scans in Case 3. RESULTS: Case 1: Bipallidal necrosis; Case 2: Left pallidal necrosis with right frontoparietal cortico-subcortical infarction; Case 3: Striato-capsular infarction on the left side, involving the caudate nucleus and the anterior arm of the internal capsule, together with obstructive hydrocephalus. CONCLUSION: The roles of both globus pallidus and prefrontostriatal circuits in the onset of voluntary movements are discussed.

Adult↗
PubMed1995

Post-polio syndrome spinal cord pathology. Case report with immunopathology.

Post-polio syndrome (PPS) describes the clinical onset of progressive muscular weakness many years after survival of acute paralytic poliomyelitis, often in muscle groups clinically unaffected by the original disease process. Prior pathologic descriptions of this often disabling, but not usually fatal, syndrome have been scanty. These have emphasized the presence of persistent or new inflammation in the meninges, spinal cord, and muscles of affected patients. The inflammation suggests several pathogenetic hypotheses, including persistent active poliovirus infection, autoimmune attack on central and peripheral nervous system elements, or increased vulnerability of poliovirus-damaged tissue to new infections. We have recently examined the central nervous system from a PPS patient. The cord showed focal perivascular intraparenchymal chronic inflammatory infiltrates. Immunoperoxidase staining demonstrated that the infiltrates were virtually pure populations of B lymphocytes (immunopositive with antibody L26, and immunonegative with the T cell marker UCHL1 as well as the macrophage marker HAM56). There were rare macrophages (HAM56 immunopositive) and no T cells. The character of the infiltrates suggests that PPS could be an autoimmune disorder mediated by antibodies produced in situ, and not by a cell-mediated process. Additional important pathological features were the presence in the anterior horns of axonal spheroids and of moderate Wallerian degeneration in the lateral columns. The brain was entirely unremarkable, with no detectable cell loss of gliosis in the internal capsules or precentral gyri.

Anterior Horn Cells↗
PubMed1999

The basal forebrain corticopetal system revisited.

The medial septum, diagonal bands, ventral pallidum, substantia innominata, globus pallidus, and internal capsule contain a heterogeneous population of neurons, including cholinergic and noncholinergic (mostly GABA containing), corticopetal projection neurons, and interneurons. This highly complex brain region, which constitutes a significant part of the basal forebrain has been implicated in attention, motivation, learning, as well as in a number of neuropsychiatric disorders, such as Alzheimer's disease, Parkinson's disease, and schizophrenia. Part of the difficulty in understanding the functions of the basal forebrain, as well as the aberrant information-processing characteristics of these disease states lies in the fact that the organizational principles of this brain area remained largely elusive. On the basis of new anatomical data, it is proposed that a large part of the basal forebrain corticopetal system be organized into longitudinal bands. Considering the topographic organization of cortical afferents to different divisions of the prefrontal cortex and a similar topographic projection of these prefrontal areas to basal forebrain regions, it is suggested that several functionally segregated cortico-prefronto-basal forebrain-cortical circuits exist. It is envisaged that such specific "triangular" circuits could amplify selective attentional processing in posterior sensory cortical areas.

Alzheimer Disease↗
PubMed2000

Hemihyperaesthesia and hyperresponsiveness resembling central pain syndrome in a dog with a forebrain oligodendroglioma.

A 4-year-old male Boxer was presented with neurological signs referable to a right forebrain lesion that was confirmed with computed tomography. Whilst characteristic signs of a unilateral forebrain lesion were observed, the dominant and striking finding was a right-sided hemisensory disturbance characterised by hyperaesthesia and hyperresponsiveness. Necropsy revealed a gelatinous mass confined to the right forebrain that was identified histologically as an oligodendroglioma. The lesion was centred on the internal capsule and involved ventral frontal and temporal lobes and the ventrolateral thalamus, including lateral and medial parts of the ventrocaudal nuclear region (ventrobasilar complex) of the thalamus. On clinical and neuroanatomical grounds, the case exhibited features in common with central pain syndrome in human patients with thalamic lesions. These included a somatosensory disorder of hyperaesthesia affecting an entire side of the head and body, behavioural manifestations consistent with spontaneous pain and a lesion involving the ventrobasilar complex. Of interest, the hemisensory abnormality was ipsilateral to the lesion, contrasting with central pain in humans, in which clinical signs are contralateral to analogous lesions. It is suggested that species-specific differences in spinal cord organisation of pain pathways, particularly the greater bilateral projection of nociceptive afferents to thalamic relay nuclei in carnivores, may account for this disparity. Notably, central pain is rare in human patients with brain tumours, even those affecting the thalamus, and this may also be the case in dogs.

Animals↗
PubMed1997

Degeneration of the pyramidal tracts in patients with amyotrophic lateral sclerosis. A premortem and postmortem magnetic resonance imaging study.

To investigate focal hyperintensity in the internal capsule (IC) on magnetic resonance images (MRIs) and its clinical significance, 80 patients with amyotrophic lateral sclerosis (ALS) and 80 sex- and age-matched normal control subjects were studied. On T2-weighted images, hyperintense foci were found in the posterior part of the posterior limb (PL) of the IC in 41 (51%) of 80 control subjects. However, no subject showed increased signal intensities on proton density-weighted images. Hyperintense foci were also observed in the posterior part of the PL of the IC on T2-weighted images in 52 (65%) of 80 ALS patients and on proton density-weighted images in 26 (65%) of 40 ALS patients; the abnormally intense foci were seen at the same anatomical location in the IC as those in the normal control subjects. On postmortem MRI, the abnormally intense foci were found in the posterior part of the PL of the IC in the formalin-fixed brains from 9 ALS patients. Three normal control subjects did not show signal intensity changes on postmortem MRI. On histological examination of 9 ALS brains, distinct myelin pallor and gliosis were found in the posterior third of the PL of the IC. Proton density-weighted images appear to be useful to distinguish neuropathological changes in the corticospinal tract of ALS patients.

Adult↗