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PubMed2004

Cognitive and motor functioning in a patient with selective infarction of the left basal ganglia: evidence for decreased non-routine response selection and performance.

Focal damage to the basal ganglia is relatively rare, and little is known about the cognitive effects of damage to specific basal ganglia structures. A 28-year-old, highly educated male (patient RI) sustained a unilateral left ischemic infarction involving primarily the putamen and secondarily the head of the caudate and the anterior internal capsule. Two detailed neuropsychological assessments, at 3 and 16 months post-infarction, revealed that a majority of cognitive abilities were spared. RI's general intelligence, simple attention, concept formation, cognitive flexibility, and explicit memory were unaffected. Select cognitive abilities were affected, and these appeared to be related to direct involvement of the putamen and/or to indirect disruption of circuits between the basal ganglia and frontal lobes. Consistent with involvement of the left putamen, RI showed micrographia with his right hand. Interestingly, his micrographia was context-dependent, appearing only when verbal expression was involved (e.g., present when writing spontaneously, but not when copying sentences or when drawing). Evidence of disruption to frontal systems included variably decreased sustained attention, mildly decreased ability to generate words and to generate ideas, and significantly impaired abstraction ability in both verbal and visual modalities. Although there are several possible interpretations for these findings, this pattern of cognitive and motor functioning is consistent with neuroimaging research suggesting that the frontal/subcortical circuit between the putamen and frontal motor areas plays a role in non-routine response selection and performance.

Adult↗
PubMed2004

Early movement impairments in a patient recovering from optic ataxia.

Since Balint's first description, optic ataxia has been considered as a pure visuomotor impairment produced by a lesion of the posterior parietal cortex. Beyond general agreement on the parietal involvement in visually guided behaviour, the exact role of the dorsal posterior parietal cortex in the temporal aspects of visuomotor control remains unclear. Recent evidence has indicated a specific involvement of the parietal cortex in the on-line visual guidance of movement. Here, we report the motor performance of, GT, a patient recovering from an optic ataxia due to a right focal lesion of the dorsal posterior parietal cortex. When asked to reach and grasp, with his left contralesional hand, different sized objects, located at different positions from his body, GT showed an apparently complete recovery from optic ataxia. However, the early kinematic aspects of GTs prehension movement were not normally tuned either by intrinsic or extrinsic visual properties of objects. At variance with both an age-matched control group and a neurological patient with a right internal capsule lesion and no sign of optic ataxia, GTs latencies to peak wrist acceleration and peak velocity were not modulated by object location. A similar defective pattern was present in GTs grasping component where, despite the sparing of the classical scaling of grip aperture, object size did not modulate the peak velocity of grip aperture. These results constitute evidence that the posterior region of the dorsal parietal cortex, besides playing a role in the on-line control of movement execution may also be involved in the programming of early kinematics parameters.

Aged↗
PubMed2004

Subacute sclerosing panencephalitis: a cause of acute vision loss.

A 4-year-old male presented with only acute vision loss. His neurologic examination, funduscopic examination, and pupils were normal. Cranial magnetic resonance imaging revealed abnormal hyperintense, bilaterally symmetric lesions (on T(2)-weighted and fluid-attenuated inversion recovery, images) in bilateral optic radiations, pulvinar region in the thalami, crus posterior of internal capsules, periventricular white matter, and unilaterally left anterior pons. Elevated measles antibody titers in the cerebrospinal fluid confirmed the diagnosis of subacute sclerosing panencephalitis. Vision loss improved and cranial magnetic resonance imaging findings regressed,but myoclonic jerks and deterioration began 7 months later. The diagnosis of subacute sclerosing panencephalitis should be considered in cases with acute vision loss resulting from cortical blindness even when classical findings of the central nervous system do not exist.

Acute Disease↗
PubMed2006

Diffusion tensor imaging in early Alzheimer's disease.

Our aim was to investigate the extent of white matter tissue damage in patients with early Alzheimer disease (AD) using diffusion tensor magnetic resonance imaging (DTI). Although AD pathology mainly affects cortical grey matter, previous magnetic resonance imaging (MRI) studies showed that changes also exist in the white matter (WM). However, the nature of AD-associated WM damage is still unclear. Conventional and DTI examinations (b=1000 s/mm(2), 25 directions) were obtained from 12 patients with early AD (Mini Mental State Examination [MMSE] score=27, Grober and Buschke test score=33.2, digit span score=5.6) and 12 sex- and age-matched volunteers. The right and left mean diffusivity (MD) and fractional anisotropy (FA) of several WM regions were pooled in each patient and control, and compared between the two groups. Volumes of the whole brain and degree of atrophy of the temporal lobe were compared between the two groups. In AD, MD was increased in the splenium of the corpus callosum and in the WM in the frontal and parietal lobes. FA was bilaterally decreased in the WM of the temporal lobe, the frontal lobe and the splenium compared with corresponding regions in controls. Values in other areas (occipital area, superior temporal area, cingulum, internal capsule, and genu of the corpus callosum) were not different between patients and controls. No correlations were found between the MMSE score and the anisotropy indices. Findings of DTI reveal abnormalities in the frontal and temporal WM in early AD patients. These changes are compatible with early temporal-to-frontal disconnections.

Age Factors↗
PubMed2004

Brain arrest neurological outcome scale (BrANOS): predicting mortality and severe disability following cardiac arrest.

BACKGROUND: To create a predictive scale of neurological outcome following cardiac arrest (CA) that incorporates radiological and clinical markers of brain injury. METHODS AND RESULTS: Brain arrest neurologic outcome scale (BrANOS) is a prospective 16-point scale. It consisted of three variables: (1) duration of arrest (DAR), (2) reversed Glasgow coma scale (GCS), and (3) Hounsfield unit (HU) ratio on non-contrast CT scan of the head. Reversed GCS score was defined as 15-GCS (best GCS in the first 24 h). HU ratio was defined as the density ratio of the caudate nucleus over the posterior limb of the internal capsule measured on unenhanced CT scan of the brain. We identified 32 comatose patients who had: (1) CT scan performed within 48 h of event; (2) no previous history of either coma, severe head trauma, cardiac arrest or stroke. Primary outcome was defined as alive or dead. Secondary outcome was the Glasgow outcome score recorded on discharge. Patient demographics were collated from retrospective chart review. Patients' mean age was 63 +/- 3 years (mean +/- S.E.M.); 44% were females. Mortality rate was 81%. Mean DAR was 21 +/- 2 min. Survivors had a significantly lower BrANOS score (8 +/- 2 points) compared to non-survivors (13 +/- 1) (P = 0.006). BrANOS was a strong predictor of mortality alone (ROC = 0.86) and mortality with severe disability combined (ROC = 0.9). The scale had a 100% specificity and positive predictive value. CONCLUSIONS: BrANOS is a reliable predictor of neurological outcome following CA. It is the first scale to incorporate clinical and radiological markers of brain injury.

Adult↗
PubMed2006

Cerebral grey, white matter and csf in never-medicated, first-episode schizophrenia.

We report the first voxel-based morphometric (VBM) study to examine cerebral grey and white matter and cerebrospinal fluid (CSF) using computational morphometry in never-medicated, first-episode psychosis (FEP). Region-of-interest (ROI) analysis was also performed blind to group membership. 26 never-medicated individuals with FEP (23 with DSM-IV schizophrenia) and 38 healthy controls had MRI brain scans. Groups were balanced for age, sex, handedness, ethnicity, paternal socio-economic status, and height. Healthy controls were recruited from the local community by advertisement. Grey matter, white matter, and CSF: global brain volume ratios were significantly smaller in patients. Patients had significantly less grey matter volume in L and R caudate nuclei, cingulate gyri, parahippocampal gyri, superior temporal gyri, cerebellum and R thalamus, prefrontal cortex. They also had significantly less white matter volume in the R anterior limb of the internal capsule fronto-occipital fasciculus and L and R fornices, and significantly greater CSF volume especially in the R lateral ventricle. Excluding the 3 subjects with brief psychotic disorder did not alter our results. Our data suggest that fronto-temporal and subcortical-limbic circuits are morphologically abnormal in never-medicated, schizophrenia. ROI analysis comparing the schizophrenia group (n=23) with the healthy controls (n=38) confirmed caudate volumes were significantly smaller bilaterally by 11%, and lateral ventricular volume was significantly larger on the right by 26% in the patients. Caudate nuclei and lateral ventricular volume measurements were uncorrelated (Pearson correlation coefficient 0.30, p=0.10), ruling out the possibility of segmentation artefact. Ratio of lateral ventricle to caudate volume was bilaterally significantly increased (p<0.005, 2-tailed), which could represent an early biomarker in first-episode, never-medicated schizophrenia.

Adolescent↗
PubMed2006

Ferroportin in the postnatal rat brain: implications for axonal transport and neuronal export of iron.

This study mapped the distribution of ferroportin in the developing rat brain using Wistar rats aged postnatal (P) days P7, P21, and P70 (adult). Ferroportin immunoreactivity was observed in neurons throughout the CNS regardless of the age of the animals studied. The neuronal labeling was detected in both perikarya, and axons and dendrites. The labeling intensity within the neurons varied among the different ages of the rats with an overall higher ferroportin immunoreactivity seen at P21, particularly in axons and white matter tracts. The neuronal labeling was high in the neocortex, striatum, hippocampus, brain stem nuclei, deep cerebellar nuclei, catecholaminergic neurons, and reticular nuclei, and particularly high in neurons of the mesencephalic trigeminal nucleus and medial habenular nucleus. In axonal tracts, ferroportin immunoreactivity was high in fibers of the internal capsule, fimbria, mamillothalamic tract and the habenulo-interpedunculo pathway. Slight ferroportin immunoreactivity was observed in oligodendrocytes and differentiating macrophages that invade the postnatal brain. The finding of a pronounced content of ferroportin in axons of the developing brain are in keeping with the idea of elevated axonal transport and export of iron possibly because of higher metabolic needs.

Animals↗
PubMed2006

Clinical and electrophysiological features of epilepsy in Italian patients with CLN8 mutations.

Neuronal ceroid lipofuscinoses (NCLs) are characterized by epilepsy, visual failure, psychomotor deterioration, and accumulation of autofluorescent lipopigment. CLN8 mutations result in Northern epilepsy and Turkish variant late infantile NCL. We describe the clinical and neurophysiological findings of three patients with CLN8 mutations from Italy. In these patients, the onset of epilepsy occurred between 3 and 6 years of age, with myoclonic, tonic-clonic, and atypical absence seizures. Electroencephalograms revealed focal and/or generalized abnormalities. In all cases, blindness and progressive attenuation of the electroretinogram were observed. Magnetic resonance imaging revealed cerebral and cerebellar atrophy, thinning of the corpus callosum, deep white matter hyperintensity, and hyperintensity of the posterior limb of internal capsules. Skin biopsy revealed lysosomal storage in the cytoplasm of fibroblasts. The clinical picture of our cases resembles that of the Turkish patients and clearly differs from that of Northern epilepsy, which is marked by a prolonged course without myoclonus and visual loss. Definition of the clinical spectrum of this condition will aid in its recognition and have implications for diagnosis and genetic counseling.

Child↗
PubMed2000

Immunolocalization of p38 MAP kinase in mouse brain.

p38 has been implicated to play a critical role in regulating apoptosis in PC12 and cerebellar granule cells, and is inactivated in cultured fetal neurons in response to insulin. Though p38 is activated in microglia after ischemia, the physiological functions of p38 in the brain are not well understood. As a first step to elucidate the physiological functions of p38 in the central nervous system, we raised a polyclonal antibody against p38 and performed immunohistochemical examination to demonstrate the localization of p38 in mouse brain. Strong p38 immunoreactivity was apparent in fiber bundles including the olfactory tract, anterior commissure, corpus callosum, cingulum, internal capsule, stria terminalis, fimbria and alveus hippocampi, fornix, stria medullaris, optic chiasm and optic tract. Although similar regions were stained with both anti-p38 and anti-neurofilament antibodies, intense p38 immunoreactivity was often observed in myelin sheath-like structures but not in axons. This is the first demonstration of the localization of p38 in the central nervous system and provides an anatomical basis for understanding physiological roles of p38.

Animals↗
PubMed2003

Identification of neurons containing orexin-B (hypocretin-2) immunoreactivity in limbic structures.

Orexins (hypocretins) are neuropeptides which have recently been identified exclusively within lateral hypothalamic and perifornical neurons, and these orexin (ox) containing neurons appear to have extensive projections to all levels of the neuraxis. In this study, we report the identification of two distinct clusters of neurons containing ox-B-like immunoreactivity within the amygdaloid complex of the rat. A cluster of small to medium size ovoid shaped neurons containing ox-B-like immunoreactivity was found predominantly within the lateral division of the central nucleus of the amygdala (ACe). A second distinct, but smaller group of ox-B labelled neurons with similar shapes and sizes to those in ACe was also identified in the anterior lateral subnucleus of the bed nucleus of the stria terminalis (BST) immediately adjacent the internal capsule, and in an area just ventral to the lateral ventricle. Neurons containing ox-A-like immunoreactivity were not observed in either structure. However, both structures contained ox-A- and ox-B labelled varicose fibers. Unilateral electrolytic lesions of the lateral hypothalamic area that contained ox-A and ox-B neurons did not alter the labelling of either ACe or BST ox-B pericarya. As both the ACe and BST are known to be involved in integrating complex homeostatic mechanisms associated with behaviours, these data suggest that a specific subset of ox-B neurons within the amygdaloid complex may serve as a component of neuronal circuits coordinating these responses.

Animals↗
PubMed2003

Immunohistochemical localization of PDE10A in the rat brain.

PDE10A is a newly identified cAMP/cGMP phosphodiesterase for which mRNA is highly expressed in the mammalian striatum. In the present study, PDE10A protein and mRNA expression throughout the rat brain were determined, using a monoclonal antibody (24F3.F11) for Western blot and immunohistochemical analyses and an antisense riboprobe for in situ hybridization. High levels of mRNA are observed in most of the neuronal cell bodies of striatal complex (caudate n, n. accumbens and olfactory tubercle), indicating that PDE10A is expressed by the striatal medium spiny neurons. PDE10A-like immunoreactivity is dense throughout the striatal neuropil, as well as in the internal capsule, globus pallidus, and substantia nigra. These latter regions lack significant expression of PDE10A mRNA. Thus, PDE10A is transported throughout the dendritic tree and down the axons to the terminals of the medium spiny neurons. These data suggest a role for PDE10A in regulating activity within both the striatonigral and striatopallidal pathways. In addition, PDE10A immunoreactivity and mRNA are found at lower levels in the hippocampal pyramidal cell layer, dentate granule cell layer and throughout the cortex and cerebellar granule cell layer. Immunoreactivity is detected only in cell bodies in these latter regions. This more restricted subcellular localization of PDE10A outside the striatum suggests a second, distinct function for the enzyme in these regions.

Animals↗
PubMed1997

Parvalbumin-containing neurons in the basal forebrain receive direct input from the substantia nigra-ventral tegmental area.

By means of anterograde tracing of Phaseolus vulgaris-leucoagglutinin (PHA-L) it was determined if parvalbumin-immunoreactive neurons in the basal forebrain receive a direct synaptic input from the A9-A10 dopaminergic nuclei of the substantia nigra and ventral tegmental area. Forebrain sections were processed for immunocytochemical detection of PHA-L and parvalbumin (PV) at light and electron microscopic levels. At the ultrastructural level, PHA-L-labeled terminals were found to establish synaptic contacts with PV-immunoreactive neuronal somata in the ventromedial globus pallidus, the ventral pallidum, the internal capsule, and the substantia innominata. PV-containing neurons in pallidal and adjacent basal forebrain territories are thus directly targeted by presumably A9-A10 dopaminergic neurons and represent a novel aspect of midbrain dopaminergic control of basal forebrain neuronal activity.

Animals↗
PubMed1998

Magnetic resonance imaging shows orientation and asymmetry of white matter fiber tracts.

Apparent diffusion tensor maps of the human brain were acquired with a magnetic resonance imaging sequence (Gudbjartsson, H., Maier, S.E., Mulkern, R.V., M6rocz, I.A., Patz, S., Jolesz, F.A., Magn. Reson. Med. 36 (1996) 509-519). It was shown that the geometric nature of the apparent diffusion tensors can quantitatively characterize the tissue structure. Display of the orientation and directional uniformity of the water diffusion in the brain demonstrated most of the known major anatomical constituents of human white matter. A comparison of corresponding anatomic regions in the white matter of both hemispheres in 24 healthy volunteers revealed that fiber tracts within the anterior limb of the internal capsule have a significantly higher (P < 0.01) measure of alignment in the right hemisphere. This method offers a unique tool for the in vivo demonstration of neural connectivity in healthy and diseased brain.

Anisotropy↗
PubMed1998

Dose-dependent, protective effect of FK506 against white matter changes in the rat brain after chronic cerebral ischemia.

Neuroprotective effects of immunosuppressive agents have been shown in cerebral ischemia. To investigate the role of immunosuppressive agents in chronic cerebral ischemia and to design a drug protocol with safe therapeutic windows, we examined the effects of FK506, a potent immunosuppressive agent, on chronic cerebral ischemia. Both common carotid arteries were ligated in 73 male Wistar rats. Fifty-eight of these rats received a chronic injection of FK506 (0.2, 0.5, 1.0 mg/kg) and the remaining 15 received a vehicle solution injection. Microglia/macrophage was investigated with immunohistochemistry for leukocyte common antigen and major histocompatibility complex, and astroglia was examined with glial fibrillary acidic protein as markers. White matter rarefaction and the number of immunopositive glial cells were assessed from 7 to 30 days after the ligation. In the vehicle-treated animals, there was persistent and extensive activation of the microglia/macrophages and astroglia in the white matter, including the optic nerve, optic tract, corpus callosum, internal capsule, anterior commissure and traversing fiber bundles of the caudoputamen. In the FK506-treated rats, the number of activated microglia/macrophages was significantly reduced in a dose-dependent manner (p<0.01) as compared to the vehicle-treated rats. Rarefaction of the white matter was also inhibited by FK506 in a dose-dependent manner (p<0. 01). Thus, a clinically-relevant dosage of FK506 attenuated both glial activation and white matter changes in chronic cerebral ischemia in the rat. These results indicate a potential use for FK506 in cerebrovascular diseases.

Animals↗
PubMed1992

Pure topographical disorientation due to a deep-seated lesion with cortical remote effects.

Lesions producing pure topographical disorientation syndromes are classically located either in the right parietal region either in the right parahippocampal gyrus. The patient described in the present study was admitted to hospital after sudden onset of a left hemiparesis. The lesion at CT scan was located in the posterior limb of the right internal capsule. Neuropsychological assessment was normal except for the presence of a major topographical disorientation and of mnestic disturbances for visuo-spatial material leading us to attribute topographical disorientation to a specific loss of topographical memory. Regional cerebral blood flow measurements disclosed a right parietal hypoperfusion. This remote cortical effect could account for the presence of the neuropsychological disorders.

Aged↗
PubMed1995

Within- and between-task dissociations in visuo-spatial neglect: a case study.

We describe a patient, J.B., who suffered an infarction of the right internal capsule and thalamus. There was a pronounced left hemiplegia but no visual field deficit. Investigated at four months and four years post-stroke, there were no signs of left visuo-spatial neglect other than a severe impairment of line bisection. The results on a test of perceptual judgement of the left and right extents of pretransected lines showed mild neglect of the left. The magnitude of this deficit did not predict quantitatively the severity of the patient's rightward deviation on a manual bisection task. Additional data are also reported on perceptual judgements and (manual) bisections of radially-oriented lines.

Cerebral Infarction↗
PubMed1998

A new family of orphan G protein-coupled receptors predominantly expressed in the brain.

The cloning of a cDNA encoding a G protein-coupled receptor homologous to the endothelin type B receptor, but unable to bind endothelin, was recently reported and termed ET(B)R-LP. We report here the isolation of a human cDNA encoding a receptor that is highly related to ET(B)R-LP and which was therefore termed ET(B)R-LP-2. Comparison of the two amino acid sequences revealed 68% overall homology and 48% identity. As is the case for ET(B)R-LP, the new receptor is strongly expressed in the human central nervous system (e.g. in cerebellar Bergmann glia, cerebral cortex, internal capsule fibers). Membranes of HEK-293 cells stably expressing ET(B)R-LP-2 did not bind endothelin-1, endothelin-2, endothelin-3, bombesin, cholecystokinin-8 or gastrin-releasing peptide.

Amino Acid Sequence↗
PubMed1988

Acute extrapyramidal syndrome in methylmalonic acidemia: "metabolic stroke" involving the globus pallidus.

We report four patients with methylmalonic acidemia who developed acute extrapyramidal disease after metabolic decompensation. The neurologic findings resulted from bilateral destruction of the globus pallidus with variable involvement of the internal capsules. This complication was unrelated to a specific gene defect responsible for methylmalonic acidemia or to cyanocobalamin administration. These lesions constitute a "metabolic stroke," probably because of the accumulation of toxic organic acid metabolites, because they cannot be accounted for by hypoxemia or vascular insufficiency.

Adolescent↗