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At least 1,117 records · Page 62Linked to original sources
PubMed2001

White matter abnormalities in HIV-1 infection: a diffusion tensor imaging study.

Diffuse white matter pallor is the most frequent neuropathological feature of HIV-1 infection and has been found to be particularly prominent in the advanced stages of the disease. The purpose of this study was to determine whether subtle white matter abnormalities can be detected in medically stable, ambulatory HIV-1 patients, in vivo, using diffusion tensor imaging (DTI). DTI is a magnetic resonance imaging (MRI) technique that is uniquely suited for the study of subtle white matter abnormalities. DTI was performed in six HIV-1 patients and nine controls. The two groups were similar in age. Abnormal fractional anisotropy was found in the white matter of the frontal lobes and internal capsules of the HIV-1 patients, in the absence of group differences in mean diffusivity, computed proton density, and computed T2. DTI may be more sensitive than conventional MRI methods for detecting subtle white matter disruptions in HIV-1 disease.

Acquired Immunodeficiency Syndrome↗
PubMed2004

Syringocephaly.

Syringomyelia is associated with Arnold-Chiari Type I malformations. Syringobulbia describes the phenomenon of syrinx extension into the brain stem. Syringocephaly is the further dissection of the fluid-filled cavity into the cerebral peduncles and cerebrum. In this case report, we describe a patient who presented with bulbar, sensory, motor, and coordination deficits both ipsilateral and contralateral to the lesion. This is most likely attributable to the wandering course the syrinx takes as it dissects through the spinal cord and into the internal capsule. This ill-defined syrinx disrupts various nuclei and fasciculi, both pre- and post-decussation, thus explaining the multiple deficits on each side. We initially treated this patient with a suboccipital craniectomy, C1 laminectomy, and duraplasty, which mildly improved his deficits. During follow-up, the patient was then found to have an exacerbation of his symptoms, at which time we performed a VP shunt revision (the patient had a history of hydrocephalus treated by a functioning VP shunt). Approximately 2 weeks after revision of the VP shunt, the patient had worsening of his symptoms, which we treated with a syringopleural shunt. This proved to be the most effective treatment with the greatest clinical improvement. Several months later, however, the patient died secondary to pulmonary disease exacerbated by VP shunt infection. In this paper, we also review the literature regarding the formation and treatment of syringocephaly, a rare and poorly understood entity.

Cerebellum↗
PubMed1998

In vitro and ex vivo autoradiographic studies of nicotinic acetylcholine receptors using [18F]fluoronochloroepibatidine in rodent and human brain.

A fluorine-18-labeled analog of the potent nicotinic agonist epibatidine is a candidate radioligand for positron emission tomographic (PET) studies of nicotinic acetylcholine receptors (nAcChR). Following intravenous administration of [18F]exo-2-(2'-fluoro-5'-pyridinyl)-7-azabicyclo[2.2.1]heptane (NFEP), high uptake in thalamus was visualized in sections of mouse and rat brain by autoradiography using a phosphor imaging device. Binding of [18F]NFEP to rat thalamic homogenate was consistent with a single class of binding site with a Kd value of 71 pM. In vitro autoradiography of thaw-mounted sections of human thalamus revealed a heterogeneous pattern of binding; Bmax values for ventrolateral nucleus, insular cortex and dorsomedial nucleus, and internal capsule were 20, 8, and 3 pmol/cc of tissue, respectively. However, similar Kd values close to 50 pM were calculated for all regions. These studies support the suitability of [18F]NFEP as a radioligand for PET studies of nAcChR in the living human brain.

Animals↗
PubMed1998

Evaluation of acute ischemic stroke using quantitative EEG: a comparison with conventional EEG and CT scan.

The sensitivity of quantitative electroencephalogram (EEG) was compared with that of conventional EEG in patients with acute ischaemic stroke. In addition, a correlation between quantitative EEG data and computerized tomography (CT) scan findings was carried out for all the areas of lesion in order to reassess the actual role of EEG in the evaluation of stroke. Sixty-five patients were tested with conventional and quantitative EEG within 24 h from the onset of neurological symptoms, whereas CT scan was performed within 4 days from the onset of stroke. EEG was recorded from 19 electrodes placed upon the scalp according to the International 10-20 System. Spectral analysis was carried out on 30 artefact-free 4-sec epochs. For each channel absolute and relative power were calculated for the delta, theta, alpha and beta frequency bands and such data were successively represented in colour-coded maps. Ten patients with extensive lesions documented by CT scan were excluded. The results indicated that conventional EEG revealed abnormalities in 40 of 55 cases, while EEG mapping showed abnormalities in 46 of 55 cases: it showed focal abnormalities in five cases and nonfocal abnormalities in one of six cases which had appeared to be normal according to visual inspection of EEG. In a further 11 cases, where the conventional EEG revealed abnormalities in one hemisphere, the quantitative EEG and maps allowed to further localize abnormal activity in a more localized way. The sensitivity of both methods was higher for frontocentral, temporal and parieto-occipital cortical-subcortical infarctions than for basal ganglia and internal capsule lesions; however, quantitative EEG was more efficient for all areas of lesion in detecting cases that had appeared normal by visual inspection and was clearly superior in revealing focal abnormalities. When we considered the electrode related to which the maximum power of the delta frequency band is recorded, a fairly close correlation was found between the localization of the maximum delta power and the position of lesions documented by CT scan for all areas of lesion excepting those located in the striatocapsular area.

Acute Disease↗
PubMed2003

Muscle overactivity and movement dysfunction in the upper motoneuron syndrome.

The upper motoneuron syndrome (UMN) is a collective term that refers to different types of motor behaviors produced by patients who have lesions of the descending corticospinal system. Lesions involving the upper motoneuron, its pathways, and its connections can occur at the level of the cortex, internal capsule, brain stem, or spinal cord. The clinical features of UMN have traditionally been classified as "positive" phenomena, referring to overt behaviors generated by various forms of muscle overactivity, and "negative" phenomena, referring to loss of overt behaviors secondary to impaired muscle activation, impaired control of motor behavior, and impaired motor performance. The clinical impact of UMN on patients is broad and tends to limit functional capacity. The negative and positive signs lead to reduced mobility and limb usage.

Humans↗
PubMed2003

Gender and age effects in structural brain asymmetry as measured by MRI texture analysis.

Effects of gender and age on structural brain asymmetry were studied by 3D texture analysis in 380 adults. Asymmetry is detected by comparing the complex 3D gray-scale image patterns in the left and right cerebral hemispheres as revealed by anatomical T1-weighted MRI datasets. The Talairach and Tournoux parcellation system was applied to study the asymmetry on five levels: the whole cerebrum, nine coronal sections, 12 axial sections, boxes resulting from both coronal and axial subdivisions, and by a sliding spherical window of 9 mm diameter. The analysis revealed that the brain asymmetry increases in the anterior-posterior direction starting from the central region onward. Male brains were found to be more asymmetric than female. This gender-related effect is noticeable in all brain areas but is most significant in the superior temporal gyrus, Heschl's gyrus, the adjacent white matter regions in the temporal stem and the knee of the optic radiation, the thalamus, and the posterior cingulate. The brain asymmetry increases significantly with age in the inferior frontal gyrus, anterior insula, anterior cingulate, parahippocampal gyrus, retrosplenial cortex, coronal radiata, and knee region of the internal capsule. Asymmetry decreases with age in the optic radiation, precentral gyrus, and angular gyrus. The texture-based method reported here is based on extended multisort cooccurrence matrices that employ intensity, gradient, and anisotropy features in a uniform way. It is sensitive, simple to reproduce, robust, and unbiased in the sense that segmentation of brain compartments and spatial transformations are not necessary. Thus, it should be considered as another tool for digital morphometry in neuroscience.

Adolescent↗
PubMed2001

Hypersomnia due to acute disseminated encephalomyelitis in a 5-year-old girl.

A 5-year-old girl suffering from hypersomnia due to acute disseminated encephalomyelitis (ADEM) is reported. Brain CT revealed a large low-density lesion involving the lentiform nucleus, posterior limb of the internal capsule, thalamus, posterior hypothalamus and midbrain in the left side. She was treated with intravenous dexamethazone. After the initial dose of dexamethazone, hypersomnia was dramatically and rapidly improved. A later brain CT study disclosed that the lesion in the brain disappeared. The brain lesion in this case involved the waking center in the brain, which was described by Von Economo. We concluded that hypersomnia in this case was due to ADEM involving the neural mechanism for maintaing wakefulness, probably in the thalamus and posterior hypothalamus. Repeat all night polysomnograpy in this case disclosed prolonged total sleep time and increased amount of stage 3-4 sleep in the hypersomniac state.

Journal Article↗
PubMed2002

Localization of mRNAs for phosphatidylinositol phosphate kinases in the mouse brain during development.

The gene expression for seven phosphatidylinositol phosphate kinases (PIPKs)-types Ialpha, Ibeta, Igamma, types IIalpha, IIbeta, IIgamma, and type III-was examined using in situ hybridization histochemistry, in the mouse brain during normal development. In the embryonic mouse brain, positive expression signals were detected only for the genes encoding PIPK Igamma and PIPK IIbeta in both the cerebral ventricular and mantle zones, with weaker signals in the former zone. On the other hand, the genes encoding all PIPKs were essentially detected in the external granule cell layer which represents the germinal zone for the neuronal granule cells. In the postnatal brain, among the seven PIPKs, the expression for genes encoding PIPK Igamma and IIbeta is evident in most gray matter, while the expression for the other five types was weak in the cortical gray matter and negligible in most non-cortical gray matter such as the diencephalon and brain stem nuclei. While the expression for most PIPKs in the mature hippocampus was distinct, the expression in the CA3 and the dentate gyrus was less definite for the genes encoding PIPK Ialpha and IIgamma, respectively. The distinct expression for the gene encoding PIPK IIalpha was detected in the postnatal white matter such as the cerebellar medulla, the corpus callosum, the hippocampal fimbriae, and the internal capsule.

Animals↗
PubMed2005

Magnetic resonance imaging confirms periventricular venous infarction in a term-born child with congenital hemiplegia.

Magnetic resonance imaging (MRI) of a 5-day-old female born at term with congenital leftsided hemiplegia revealed T2 shortening and T2* signal dropout lining the lateral wall of a focally enlarged right lateral ventricle, reflecting the deposition of haemosiderin or ferritin derived from periventricular venous infarction in utero. This observation strengthens the hypothesis that congenital hemiplegia in children born at term can result from a clinically silent periventricular venous infarction in utero. The loss of shortening of T2 in the right posterior limb of the internal capsule at birth was followed by prolongation of T2 at 1 year. It is important to evaluate the asymmetry of the posterior limb shown by MRI to predict future hemiplegia and enable early therapy.

Cerebral Infarction↗
PubMed2007

A previously undescribed leukodystrophy in Leigh syndrome associated with T9176C mutation of the mitochondrial ATPase 6 gene.

We report two male Taiwanese siblings in whom the T-->C point mutation at nucleotide 9176 of the mitochondrial ATPase 6 gene (m.9176T>C mutation) was associated with early onset hypotonia, lactic acidosis, and death due to respiratory arrest at 7 and 10 months old. Brain MRI showed lesions over diffuse white matter and the bilateral posterior limbs of the internal capsule. The m.9176T>C mutation is suggested as the cause of the bilateral striatal necrosis and Leigh syndrome. However, leukodystrophy in Leigh syndrome associated with m.9176T>C mutation has never been reported before. We suggest that m.9176T>C mutation could be a new aetiology for leukodystrophy in children with Leigh syndrome.

Acidosis, Lactic↗
PubMed1975

Respiratory inhibitory apraxia.

Ten patients have been described showing inability to stop breathing on command, spontaneous respiration and voluntary respiratory stimulation being unaffected. This abnormality not previously described in the literature, we feel should be named respiratory inhibitory apraxia (R.I.A.). The anatomical organization of respiration is briefly reviewed. R.I.A. is often associated with other forms of apraxia or motor impersistence. It is thought that the urinary and bowel incontinence present in some of these cases might also represent a form of inhibitory apraxia. Information is presented which supports the view that respiratory inhibitory apraxia is due to a minor hemisphere lesion, usually deepseated. Our one autopsied case showed a lesion in the descending motor pathways in the internal capsule, in middle cerebral artery branch territory, disconnecting the voluntary respiratory inhibitory center in the cortex in anterior and middle cerebral cortical branch territories.

Aged↗
PubMed1984

Characteristics of EMG responses to imposed limb displacement in patients with vascular hemiplegia.

The segmented EMG activity in flexor carpi radialis to imposed wrist movements was studied in 18 hemiplegic subjects with vascular lesions of the sensorimotor cortex or internal capsule and compared to that in age-matched normal subjects. The segmented EMG activity in the stretched muscle was normalized against the maximum M response elicited by electrical stimulation of its peripheral nerve in hemiplegic and normal subjects. This M response was used to estimate the maximal activity of the motoneuron pool. Twelve of the hemiplegic patients showed a stereotyped abnormal segmentation pattern of the EMG activity characterized by: an increased M1 segment of prolonged duration with both an increased sensitivity to low initial velocities of displacement and an increased slope of the input-output relationship for the range of velocities tested; absent or diminished activity during the interval of the normal M2-3 segment; and a late component not evident in normal subjects. The increased magnitude of the EMG activity during the M1 interval, markedly exceeded the normal range of control values. A method to demonstrate the response distribution of the interrelationship of the magnitude of the M1 segment using two variables (background EMG activity and initial velocity) for individual responses rather than average responses is presented. The results of the study indicate that: the increased excitability, reflected in the enhanced EMG over the M1 segment does not result from increased levels of resting alpha motoneuron activity and may result from disruption of polysynaptic internuncial influences on alpha motoneurons; the absent or diminished activity over the interval of the normal M2-3 segment may partially result from the interruption of a transcortical reflex by the vascular lesions.

Aged↗
PubMedDate not supplied

Prenatal development of axon outgrowth and connectivity in the ferret visual system.

The objective of this study was to determine when the retina, lateral geniculate nucleus (LGN), and striate cortex first send out axons, and first connect with each other, during embryonic development in the ferret. Specifically, we were interested in the timing relationship between axon outgrowth and known temporal patterns of neurogenesis in the LGN and striate cortex. Ferrets (Mustela putorius furo) were selected for study because of their immature developmental state in late gestation and relatively large litters. We examined axon outgrowth from the retina, and anlagen of presumptive LGN and striate cortex between embryonic day 21-30 (E21-E30) using in situ inoculations of two fluorescent lipophilic dyes, DiI and DiA. DiI inoculations were made into the cortex and contralateral thalamus, and DiA inoculations were made into the contralateral eye. Retinal axon termination zones in the diencephalon following the DiA inoculations were used to validate the location of the LGN. Visual cortex and LGN neurogenesis begins at E20 in ferrets. No axon outgrowth could be documented from retina or anlagen of striate cortex and LGN until E24. At E24 some retinal axons reach and cross the chiasm, cortical axons extend some distance within the cortical radiations, and thalamic axons are within the internal capsule. Retinogeniculate, geniculocortical, and corticogeniculate axons extend to their target structures by E27, as evidenced by retrograde labeling in cells of origin. These data suggest that in the ferret retina, and developing LGN and striate cortex, (1) axon outgrowth from each visual area begins within 24-h of each other, after neurogenesis has begun at the source but before it is complete in the target; (2) axons may be generated before parent cell bodies have completed migration; and (3) arriving axons are in a position to influence target structures almost from their inception.

Animals↗
PubMed1995

Nonspecific white matter degeneration following traumatic brain injury.

Morphometric analysis of magnetic resonance (MR) scans in 88 traumatic brain injury (TBI) patients demonstrated significantly larger ventricle-to-brain ratios (VBR) and temporal horn volumes, and significantly smaller fornix-to-brain ratios (FBR) and corpus callosum (CC) area measurements, compared to 73 controls. Additionally, TBI patients were grouped according to Glasgow Coma Scale (GCS) for a within-TBI sample comparison so that severity of injury on brain morphology could be examined. The severe TBI group (GCS = 3-6) differed from the mild and moderate injury groups on measures of the internal capsule, VBR, temporal horn volume, and CC. In a separate analysis wherein the TBI subjects were grouped by degree of fornix atrophy, the group with the smallest fornix size demonstrated the lowest memory performance. Furthermore, anatomic measures correlated with severity of injury, and tests of memory and motor function. Results demonstrate the diffuse nature of degeneration in TBI with more severe injury, and that quantified MR identified morphologic changes relate to neuropsychological outcome.

Adolescent↗
PubMed1998

Methylmalonic acidaemia with bilateral globus pallidus involvement: a neuropathological study.

A 16-month-old boy was hospitalized because of a 1-day history of severe ketoacidosis with lethargy, hypotonia, vomiting, and important dyspnoea. Organic acid assay by gas chromatography-mass spectrometry confirmed the diagnosis of methylmalonic acidaemia (MMA). On the sixteenth day, he developed an acute extrapyramidal disorder. The CT scan of the brain disclosed bilaterally symmetric lucency of basal ganglia. He died at 17 months of age. Post-mortem neuropathological examination, showed severe necrosis with spongiosis, cystic cavitation and numerous lipid-laden macrophages of the globi pallidi, and mild spongiosis of subthalamic nuclei, mammillary bodies, portion of internal capsule adjacent to globus pallidus, superior cerebellar peduncles and tegmentum of brainstem. Pallidal infarction, a focal ischaemic lesion, demonstrates that ischaemia/energy depletion may be important in the etiology of the neuropathology of MMA.

Cobamides↗
PubMed1997

Glial organization and chondroitin sulfate proteoglycan expression in the developing thalamus.

This study examines the early organization of glial cells, together with the expression of chondroitin sulfate proteoglycans in the developing thalamus of ferrets. Glia were identified with antibodies against vimentin and glial fibrillary acidic protein and the chondroitin sulfate proteoglycans were identified by using an antibody against chondroitin sulfate side chains. Our results reveal three striking features of early thalamic development. First, there is a distinct population of glial fibrillary acidic protein-immunoreactive astrocytes (first seen at E30) that resides in the perireticular thalamic nucleus of the primordial internal capsule. These glial fibrillary acidic protein-immunoreactive astrocytes of the perireticular nucleus are transient and form a conspicuous feature of the early developing forebrain. They are first apparent well before any glial fibrillary acidic protein-immunoreactive astrocytes are seen in other regions of the thalamus (at about P8). Further, unlike in other thalamic regions, these peculiar perireticular astrocytes do not express vimentin before they express glial fibrillary acidic protein. Second, in the reticular thalamic nucleus, the radial glial cells express glial fibrillary acidic protein; they are the only ones to do so in the thalamus during development. The glial fibrillary acidic protein-immunoreactive radial glial cells of the reticular nucleus form a rather distinct band across the developing thalamus at these early stages (E30-P1). Finally, and preceding the expression of glial fibrillary acidic protein, the radial glial cells of the reticular nucleus, unlike those in other thalamic regions, are associated closely with the expression of chondroitin sulfate proteoglycans (E20-E30). Later (after E30), the expression of the chondroitin sulfate proteoglycans in the reticular nucleus declines sharply. The significance of this finding is related to the early organization of the cortico-fugal and cortico-petal pathways.

Aging↗
PubMed2002

Apolipoprotein D in the Niemann-Pick type C disease mouse brain: an ultrastructural immunocytochemical analysis.

Enhanced apoD gene expression and abnormally high levels of apoD protein accumulation in the brain have been previously documented as features of the neurodegenerative disorder, Niemann-Pick Type C disease (NP-C). In the present study we have used immunocytochemistry and light and electron microscopy to elucidate the cellular and subcellular distribution of apoD in the Balb/c NIH npc1(-/-) mouse brain. The normal mouse brain demonstrates low levels of apoD-expressing glia particularly in the cerebellar white matter. In contrast, abundant, strongly apoD-immunolabeled cells were observed in select grey matter nuclei, including the globus pallidus, thalamus, and substantia nigra, and in white matter tracts within the internal capsule and cerebellum of NP-C mouse brain. These brains regions have been previously shown to display the most significant neurodegenerative changes in the NP-C mouse. Ultrastructural analysis revealed dense apoD immunoreactivity on the nuclear envelopes of cells that have the morphological features of oligodendrocyte precursor-like cells and light staining on astrocytes. These results define the cellular and subcellular pattern of expression of apoD in NP-C mouse brain and suggest a possible role for this lipocalin in the pathophysiology of this disorder.

Animals↗
PubMed2001

Pterospora floridiensis, a new species of acephaline gregarine (Apicomplexa) from the maldanid polychaete Axiothella mucosa in St. Andrew Bay, Florida.

Pterospora floridiensis, a new species of acephaline gregarine from the body cavity of the bamboo worm Axiothella mucosa (Polychaeta: Maldanidae), is described. The gamont stage is distinctive and possesses a central cytoplasmic mass and two elongate trunks that bifurcate repeatedly and comprise approximately 60% of the total cell length. The gamont averages 198 (50-545) x 71 (25-180) microm (N= 45, 43) from the tip of the trunks to the anterior (the junctional site with the other gamont in syzygy). Gametocysts average 402 (297-545) x 304 (149-495) microm (N = 37). The oöcysts measure 22.5 (20.5-23.5) x 8.3 (7.0-10.0) microm (N = 30) and possess an internal capsule (average length = 13.9 microm, N = 30) containing the sporozoites and aliform wings on the epispore.

Animals↗