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PubMed2003

Rehabilitation of somatic sensation and related deficit of motor control in patients with pure sensory stroke.

OBJECTIVE: To assess the effectiveness of a rehabilitative training program for deficits in somatic sensation and motor control of the hand in patients with pure sensory stroke. DESIGN: Multiple baseline and before-after follow-up trial with behavioral analysis of single cases. SETTING: Rehabilitation unit of a university hospital in Italy. PARTICIPANTS: Four patients were studied: 2 had a unilateral lesion confined to the parietal lobe (patients 1, 2), and 2 had a unilateral lesion of the thalamus (patients 3, 4) that also lapped the posterior limb of the internal capsule. All 4 patients had chronic deficits in somatic sensation and motor control of the contralesional hand. INTERVENTION: Behavioral training consisting of exercises aimed at improving somatic sensation and motor control of the affected, contralesional hand. Thirty treatment sessions, each lasting 50 minutes, were performed. MAIN OUTCOME MEASURES: Somatic deficit was evaluated with 5 tests, and motor control deficit was assessed with 4 tests. One functional test estimated the influence of somatic deficit on daily activities. A visual analog scale (VAS) was also submitted to the patients' relatives to evaluate the amount of use of the affected arm in daily life activities. A baseline was obtained by recording each measure, except for the VAS, 4 times at the first evaluation session. Evaluation sessions were conducted before, after, and 6 months after the end of the experimental treatment. RESULTS: All patients showed a stable baseline in at least 8 of the outcome measures. Patients 1 and 2 significantly improved in 9 and 7 outcome measures, respectively. Patients 3 and 4 improved in 4 and 7 outcome measures, respectively. With the exception of case 3, all patients considerably increased their use of the affected arm during daily life. The improvement was generally stable over a 6-month period, suggesting that the treatment had a long-term effect. CONCLUSIONS: Results suggest the possible effectiveness of our training program for treating somatic and motor control deficits of the hand in patients with cortical or subcortical pure sensory stroke.

Adult↗
PubMed2002

Role of Cajal-Retzius and subplate neurons in cerebral cortical development.

A synaptic network is already formed in the marginal zone of the early telencephalon before the arrival of the first wave of radial migration of neuroblasts from the subventricular zone to form the cortical plate. Cells and fibers forming the marginal zone are mainly the Cajal-Retzius (C-R) neurons and their processes. The origin of these cells is not yet proved but is likely either the median ganglionic eminence or the mesencephalic neuromere. The bipolar or multipolar C-R neurons populate the molecular layer of the fetal cortical plate and are sparse in the adult. Their thick axon emits collaterals for synaptic contact with pyramidal neurons initially in layer 6 and later with in all layers. C-R neurons produce GABA, possibly ACh, several calcium-binding proteins (eg, calmodulin, parvalbumin, calretinin) and several neuropeptides; they are rich in ribosomes. Subplate neurons, beneath the cortical plate, emit pioneer axons in the incipient formation of the internal capsule and also commissural fibers of the early hippocampus. C-R cells express products of the genes RELN, LIS1, and DS-CAM, which mediate radial neuroblast migration and lamination of the cortical plate and important in the pathogenesis of lissencephaly. A subpopulation of C-R neurons also expresses a p53 product implicated in cell survival and apoptosis. In addition to forming the first intrinsic synaptic circuits of the cortical plate and its first afferent and efferent connections with subcortical structures, they may play additional roles in the formation of ocular dominance columns, in regulating neuronogenesis, and in cortical repair. They do not disappear by apoptosis at the completion of cell migration, as was previously thought, but their functional role in the mature brain remains unknown.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1984

Are the amygdaloid projections to the hypothalamic ventromedial nucleus involved in estrous rhythm regulation in the female rat?

The aim of this investigation was to determine whether the corticomedial amygdaloid nucleus (CMA) and its projections to the hypothalamic ventromedial nucleus (VMN) were involved in the regulation of estrous rhythm by the VMN in the rat. It is known (Carrer et al., 1973-1974) that partial VMN lesions caused the occurrence of either 5-day or alternate 4- or 5-day cycles in about 50% of 4-day cyclic female rats and that large lesions induced cycle prolongation in most of the operated animals while hypothalamic dorsomedial nucleus (DMN) lesions left estrous rhythm unmodified. CMA lesions in 4-day cyclic female rats caused the occurrence of either 5-day or alternate cycles with sequence of 4, 5, 4 days, more frequently than in their sham operated counterparts (15/20 vs 3/20). Stria terminalis (ST) lesions placed at its emergence from the CMA or at its horizontal course over the internal capsule induced a higher proportion (10/14 and 9/16, respectively) of females to display changes in cycle duration than did sham operated and unoperated controls as well (10/32 and 7/29, respectively). Combined partial VMN and ST lesions resulted in a 24 hours cycle prolongation or alternate 4- and 5-day cycles in a greater number of females than in those bearing small VMN lesions only (15/18 vs 22/40). A noticeable proportion of CMA, ST and ST + small VMN lesioned females offered more or less prolonged diestrous periods immediately following surgery before resuming estrous cyclicity. It was suggested that the CMA neurons which project fibers to the VMN via the ST are implicated in estrous rhythm regulation in the rat.

Afferent Pathways↗
PubMed2000

A case of leukoencephalopathy with vanishing white matter.

A 6-year old Turkish boy with a recently defined entity: "leukoencephalopathy with vanishing white matter" is described. He was born to consanguinous parents. His psychomotor development was normal till he first presented with fever and generalized tonic-clonic seizures at the age of 2.5, followed by rapid motor and mental deterioration. Decerebrate posture and marked spasticity subsequently developed. The initial MRI examination showed diffuse involvement of white matter, including subcortical U-fibers, with signal intensity parallel to CSF on all sequences. The white matter appeared swollen. The ventricles were slightly enlarged and there was cavum septi pellucidi et vergae. The posterior crus of the internal capsule, external and extreme capsules were affected. Cerebellar hemispheres and vermis showed atrophy. The involvement pattern of brainstem was noteworthy in that pontine tegmentum and cruri cerebri were affected. Follow-up MRI obtained after three years did not show any interval change. Brain biopsy showed thinned cortex with relatively preserved cortical layering and neuronal structure. There was rarefaction of the white matter with cystic degeneration. Fibrillary gliosis and increased number of oligodendroglial cells were observed within the cerebral white matter.

Biopsy↗
PubMed2001

Parenchymal brain injury in the preterm infant: comparison of cranial ultrasound, MRI and neurodevelopmental outcome.

AIM: Magnetic resonance imaging (MRI) is increasingly being used in high-risk preterm neonates. Cranial ultrasound (US) was compared with MRI in preterm patients with parenchymal injury and related to neurodevelopmental outcome. PATIENTS AND METHODS: Studies were performed in 61 patients. Twelve infants with normal US (Group 1) had an MRI within the first 4 weeks of life (early MRI), and 10 also at term age (late MRI). Eight out of 20 infants with intraventricular haemorrhage with parenchymal involvement (IVH + PI) (Group 2) had an early as well as a late MRI and 12 a late MRI. Of the 20 patients with cystic-periventricular leukomalacia (c-PVL) (Group 3), 7 had an early MRI, 1 had an MRI on both occasions and 12 had a late MRI. All 9 children with focal infarction (FI) (Group 4) had a late MRI. RESULTS: MRI was conform with cranial US in Group 1. Early MRI in Group 2 showed contralateral c-PVL in one infant and an additional contralateral occipital parenchymal haemorrhage and blood in the posterior fossa in another infant. Late MRI showed an asymmetrical posterior limb of the internal capsule (PLIC) (n=6), which predicted later hemiplegia. Early MRI in Group 3 showed more cysts (n = 5), punctate white matter lesions (n = 6), lesions in the basal ganglia (n = 1) and once involvement of the cerebellum. Late MRI showed involvement of the centrum semiovale (n = 2) lesions in the basal ganglia (n = 2) and bilateral abnormal signal intensity of the PLIC in 7 infants who all went on to develop cerebral palsy. In Group 4 MRI showed signal intensity changes suggestive of cystic lesions compared to persisting echogenicity on US (n = 3) and an asymmetrical PLIC (n = 5), which predicted hemiplegia in 4. CONCLUSION: Early MRI especially provided additional information in those with c-PVL. MRI at term age could assess the PLIC, which was useful in children with unilateral parenchymal involvement, for prediction of subsequent hemiplegia and, to a lesser degree, in bilateral c-PVL for prediction of diplegia or quadriplegia.

Brain Damage, Chronic↗
PubMed2003

Pyramidal tract damage correlates with motor dysfunction in bilateral periventricular leukomalacia (PVL).

In children with periventricular leukomalacia (PVL), motor dysfunction is thought to be related to involvement of pyramidal tract fibres in the periventricular white matter. The purpose of the present study was to test this hypothesis. Thirteen former preterm adolescents with PVL, ten of whom were suffering from bilateral spastic cerebral palsy, were studied by MRI. The severity of pyramidal tract damage was assessed on semicoronal MRI reconstructions along anatomical landmarks of somatotopy in the precentral gyrus and the internal capsule; for comparison, the overall volume of cerebral white matter (determined by automated volumetry) served as a global measure of lesion severity. The motor dysfunction of each of the four extremities correlated much more strongly with the severity of pyramidal tract damage assessed on the respective MRI reconstruction (range of correlation coefficients, 0.647 to 0.922) than with the total volume of white matter (range of correlation coefficients, - 0.458 to - 0.212; Spearman). These findings corroborate the notion that an involvement of pyramidal tract fibres in the periventricular white matter is indeed a relevant factor for motor dysfunction in children with PVL.

Adolescent↗
PubMed2006

Electrophysiological proof of diffusion-weighted imaging-derived depiction of the deep-seated pyramidal tract in human.

In the living human brain the pyramidal tract (PT) can be displayed with magnetic resonance diffusion-weighted imaging (DWI). Although this imaging technique is already being used for planning and performing neurosurgical procedures in the PT vicinity, there is a lack of verification of DWI accuracy in other areas outside the directly subcortical PT parts. Before definitive electrode placement into the subthalamic nucleus (STN) in patients with Parkinson disease (PD) for chronic stimulation, the stimulation effect on PD symptoms and the side-effects, namely PT activation at the level of the internal capsule (IC), are electrophysiologically tested. To analyze DWI accuracy by matching the stereotactic coordinates of the electrophysiologically proven IC position with these of the DWI-derived IC display, DWI was added to the routine MRI work-up in the stereotactic frame prior to functional surgery in 6 patients. In all of the 10 displayed fiber tracts, concordant findings for imaging and macrostimulation were made. The authors proved for the first time that DWI correctly depicts the deep seated, principle motor pathways in the living human brain. Due to methodical limitations of this study the accuracy of the proven IC display is limited to 3 mm which has proven to be sufficient for the planning and performance of neurosurgical procedures in the vicinity of large fiber tracts.

Adult↗
PubMed1997

MRI assessment of myelination of motor and sensory pathways in the brain of preterm and term-born infants.

A study was performed in 48 neurologically normal preterm and term-born infants, with a postconceptional age at MRI varying between 30 2/7 and 46 weeks and a mean age of 34 2/7 weeks. The purpose of the study was to determine the normal progress of myelination on MRI in that age range. T1- and T2-weighted images of the brain were assessed for changes in signal intensity of white matter relative to gray matter. Multiple sites in the brainstem, cerebellum and cerebral hemispheres were assessed separately. The findings were correlated with the ages of the infants. As judged from relative signal intensities, myelin was present at the post-conceptional age of 30-34 weeks in the following structures: tegmentum pontis (in particular medial lemniscus), superior and inferior colliculi, decussation of the superior cerebellar peduncles, crura cerebri, ventrolateral thalamus, lateral globus pallidus, dorsolateral putamen, dentate nucleus, middle and superior cerebellar peduncles, vermis cerebelli, cortex bordering the central sulcus and hippocampus. Little progress in myelination was noticed up to the post-conceptional age of 46 weeks. Between 34 and 46 weeks, myelin appeared in the lateral part of the posterior limb of the internal capsule and in the central part of the corona radiata and became more prominently visible in the cortex bordering the central sulcus.

Age Factors↗
PubMed1995

Hypoxic ischaemic encephalopathy: early magnetic resonance imaging findings and their evolution.

Eighteen term infants with hypoxic ischaemic encephalopathy (HIE) were studied with serial magnetic resonance imaging of the brain for up to two months following birth. Important early findings included brain swelling, cortical highlighting, diffuse loss of grey/white differentiation and loss of signal in the posterior limb of the internal capsule (PLIC). These signs were easier to identify on T1-weighted spin echo or inversion recovery sequences than on T2-weighted spin echo sequences. Brain swelling was only seen in the first seven days and was present in all grades of HIE. All other signs persisted and were associated with the subsequent development of major structural changes in the brain. The exact pattern of injury was best identified after the first week of life once the signs of brain swelling had cleared.

Asphyxia Neonatorum↗
PubMed1993

[Dynamic cranial CT in ischemic cerebral lesions].

58 patients with recent transient or permanent neurologic deficits of with proven carotid stenoses were examined by dynamic CT at the level of the internal capsule. In the presence of cerebral infarcts there was marked delay in the time/density curve with reduced peaks. Abnormal perfusion could be demonstrated by early examinations before definite morphological changes were seen. With transient ischaemic attacks there were no significant changes in perfusion; in the presence of carotid stenoses the results were variable. The perfusion abnormalities in the hemispheres shown by dynamic cranial CT could be confirmed to some extent by 99mTc-HMPAO-SPECT.

Adult↗
PubMed1995

[Pyrimethamine-sulfadiazine resistant cerebral toxoplasmosis in AIDS].

A 48-year-old man with known HIV infection for 4 years was admitted with a 2-week history of increasing brachio-facial paraesthesiae of the left side of the body and pains in the head and neck. Physical examination also showed discrete slowing of mental activity and oral candidiasis. Toxoplasmosis serology showed a low titre with a borderline IgM titre. Cranial computer tomography showed two confluent contrast medium concentrating foci in the region of the head of the caudate nucleus and the right internal capsule. Because toxoplasmosis encephalitis was suspected, treatment was started with sulfadiazine (1 g four times daily), pyrimethamine (25 mg four times daily), folic acid (15 mg daily) and dexamethasone (8 mg three times daily). After 19 days of treatment there was no clinical improvement, and a check CT scan showed worsening with increased oedema of the cerebellar medulla, compression of the lateral ventricles and a mid-line shift of 5 mm. Since the Sabin-Feldman test titre had increased, and there was no evidence to suggest a lymphoma or a viral or fungal infection, toxoplasmosis resistant to standard therapy was postulated, and treatment was started with clindamycin (600 mg three times daily) and pyrimethamine (25 mg four times daily). The clinical features subsided within 4 days. A further check CT scan 14 days later showed almost complete resolution.

AIDS-Related Opportunistic Infections↗
PubMed1995

[Lacunar cerebral infarction in a young woman].

HISTORY AND FINDINGS: A 29-year-old woman was admitted to hospital with an acute right-sided hemiplegia and sensory disorders, as well as upper right quadrant anopsia. There were no other significant abnormalities. She had previously been healthy and was free of any predisposing risk factors for thromboembolism. Neurological examination elicited a homonymous right upper quadrant hemianopsia, dysesthesia of the right half of the face and hypesthesia and hypalgesia of the right side of the body. In addition there was paresis of the right arm and a positive right Babinski reflex. INVESTIGATIONS: There was no evidence for any underlying haematological, metabolic, infectious or vascular disease. Computed tomography of the head revealed a small hypodense area immediately adjacent to the posterior part of the left internal capsule, compatible with a lacunar infarction, a finding confirmed by magnetic resonance imaging and relating to the area supplied by the thalamic branch of the posterior cerebral artery. Transoesophageal echocardiography demonstrated a patent foramen ovale. TREATMENT AND COURSE: Almost complete regression of all signs occurred within two months on anticoagulation with heparin intravenously for two weeks followed by oral phenprocoumon (Quick's value 30-40%) and intensive physiotherapy. Five weeks after onset of treatment the paresis was obviously regressing and pyramidal tract signs had disappeared. Sensitivity to touch over the right half of the body was still diminished and the homonymous paracentral scotoma still present. CONCLUSION: Lacunar infarction of the brain in young patients has an excellent prognosis, as long as it is treated intensively according to its cause.

Acute Disease↗
PubMed1991

[Listeriosis in malignant diseases].

Listeriosis occurred in two patients, a 46-year-old woman and a 41-year-old man, in the course of an underlying malignant disease. The woman had a metastasizing pancreatic apudoma, requiring partial pancreas resection with splenectomy. After the end of cytostatic treatment she developed headaches and fever up to 40 degrees C. Listeria monocytogenes was demonstrated in the blood and cerebrospinal fluid. She went into coma on the day after hospital admission and, despite antibiotic administration, she died on the fourth day of treatment. The 41-year-old man was suspected of having an angioimmunoblastic lymphoma. Severe haemolytic anaemia (haemoglobin 4.4 g/dl) was treated with glucocorticoids, massive blood transfusions and splenectomy, at first without success. During immunosuppressive treatment with prednisone and cyclophosphamide the haemoglobin rose. But he was still feverish with nocturnal sweating. Neurological symptoms of motor aphasia, cranial nerve deficits and incomplete hemiparesis rapidly developed. Computed tomography revealed a focus in the internal capsule. Blood culture grew Listeria. The focal encephalitis healed with minor sequelae after antibiotic treatment. Both patients had hypogammaglobulinaemia, but no granulocytopenia. It is stressed that listeriosis should be included in the differential diagnosis in cases of septicaemia or cerebral infection occurring in the course of malignant disease.

Adult↗
PubMed1993

New subform of the late infantile form of neuronal ceroid lipofuscinosis.

Clinicopathological studies of a series of nine children with a new subform of Jansky-Bielschowsky disease or late infantile neuronal ceroid lipofuscinosis (LINCL) is presented. The onset of this subform is between 2.5-3.5 years of age with initial neurological symptoms of abnormal motor skills caused by cerebellar and extrapyramidal signs. Soon after dementia, myoclonic seizures are followed. Visual impairment is more clearly seen after the age of 5 or 6 years. The ultrastructural studies of the skin and/or buffy coat showed abundant lysosomal storage of curvilinear profiles, rarely intermixed with fingerprint profiles. The MRI of the head performed in seven cases, showed initially enlargement of the ventricles that is secondary to basal ganglia atrophy and presence of cerebellar and cerebral atrophy. In 4 of 7 cases (Cases 1, 5, 6, 8) abnormalities in the deep white matter showing increased signals of T2-weighted imaging in the periventricular areas of the fronto-parietal region, internal capsule, tracks of the brainstem, and white matter of cerebellum were seen. These abnormalities were also observed by post-mortem neuropathological studies in three cases (nos. 7-9). The MRI in Cases 7 and 9 was not performed. The electrophysiological abnormalities (EEG, ERG, VER) are similar as described in the classical LINCL. Neuropathological studies done in 3 of 9 cases showed generalized brain atrophy and unique type of neuronal cytoplasmic inclusion body in the basal ganglia, brainstem, dentate nuclei, and rarely, cerebral cortex. These large, round neuronal cytoplasmic inclusions were pink in hematoxylin (HE), violet in cresyl violet, and dark blue with Klüver-Barrera method.(ABSTRACT TRUNCATED AT 250 WORDS)

Basal Ganglia↗
PubMed1994

Prediction of outcome in children with congenital hemiplegia: a magnetic resonance imaging study.

The degree of Wallerian degeneration (WD) in the corticospinal tracts seen with magnetic resonance imaging (MRI) was correlated with the distribution and severity of congenital hemiplegia in 20 children aged nine months to nine years. All the children had hemispheric lesions diagnosed with ultrasound in the neonatal period: MRI and clinical assessment were performed from nine months to nine years of age. Hemiplegia was graded as mild, moderate or severe and into predominantly upper or lower limb distribution. WD was assessed by the presence or absence of signal intensity changes in the internal capsule on inversion recovery and spin echo sequences and by the asymmetry of the upper brainstem. The degree of asymmetry was estimated by measuring the cross sectional area (CSA) of the brainstem at three levels and calculating the ratio of the measurements between the side of the lesion and the unaffected side. Infarct size was estimated from the CSA of the infarct at the maximum site of the lesion. Both measurements were correlated with the severity of outcome and the site of involvement. There was a better correlation between severity of outcome and brainstem asymmetry (p = 0.003) than severity of outcome and infarct size (p = 0.02). There was also a significant correlation between upper limb involvement and brainstem asymmetry (p = 0.01). As WD estimated by brainstem asymmetry appears early and is easy to measure, it may be a good marker to estimate later impairment in infants with predominantly unilateral hemispheric haemorrhagic/ischaemic lesions diagnosed in the neonatal period.

Brain Stem↗
PubMed1982

Immunohistochemical distribution of alpha-neo-endorphin/dynorphin neuronal systems in rat brain: evidence for colocalization.

alpha-Neo-endorphin and dynorphin immunoreactivities in rat brain were visualized by double antibody immunofluorescence of frozen sections. Antibodies were used that were specific for their respective antigens. The pattern of neuronal immunostaining produced by alpha-neo-endorphin and dynorphin antisera in adjacent serial sections was completely superimposible. No areas were found in which alpha-neo-endorphin or dynorphin immunoreactivities existed alone. The following brain regions contained alpha-neo-endorphin/dynorphin-immunoreactive fibers and terminals: the median forebrain bundle, the internal capsule, the substantia nigra, the hypothalamus, the nucleus accumbens, the hippocampus, and the medulla oblongata. A few fibers were seen in the cerebral cortex and in the corpus striatum. In many regions, this neuronal fiber system seems to overlap the neuronal system previously described to contain [Met]-/[Leu]enkephalin-immunoreactive material. In brains from colchicine-treated animals, numerous alpha-neo-endorphin/dynorphin-immunoreactive neuronal cell bodies were seen in the supraoptic, retrochiasmatic supraoptic, paraventricular, and magnocellular accessory nuclei of the hypothalamus. It is concluded that alpha-neo-endorphin-like and dynorphin-like immunoreactivities are part of the same neuronal system.

Animals↗
PubMed2003

Clustering and switching in phonemic fluency following pallidotomy for the treatment of Parkinson's disease.

Phonemic fluency impairments have been reported as one of the most consistent cognitive declines following pallidotomy for the treatment of Parkinson's disease. In 39 pallidotomy patients, we evaluated two dissociable processes involved in phonemic fluency: (1) clustering, the ability to generate words within clusters or subcategories, which has been related to intact temporal lobe functioning; and (2) switching, the ability to shift between clusters, which has been related to frontostriatal integrity. We also correlated the location of the lesion in the pallidum and adjacent structures with the effect on phonemic fluency. Pallidotomy patients generated significantly fewer words on phonemic fluency for up to a year following surgery, with a decline in the total number of switches made, rather than a decline in the number of clusters generated. Patients whose lesions on postoperative neuroimaging fell entirely or mostly within the GPi performed worse on switching than patients whose lesions fell half outside of the GPi, either within the GPe or the internal capsule. However, no significant differences were found for lesion location 6 months following surgery. The findings support the hypothesis that the GPi plays a role in cognitive functioning.

Aged↗
PubMed2004

Ketamine blocks non-N-methyl-D-aspartate receptor channels attenuating glutamatergic transmission in the auditory cortex.

OBJECTIVE: To investigate the influence of ketamine on non-N-methyl-D-aspartate (NMDA) receptor-mediated synaptic transmission in the auditory cortex. MATERIAL AND METHODS: Using whole-cell patch-clamp techniques on pyramidal neurons, we studied the effects of ketamine on excitatory post-synaptic potentials (EPSPs) evoked by electrical stimulation of internal capsule fibers in slices of gerbil auditory cortex. RESULTS: After blockade of the slow, NMDA receptor-mediated EPSP component with DL-2-amino-5-phosphonovaleric acid, application of ketamine in a concentration-dependent manner led to a reduction in the amplitude of fast, 6-cyano-7-nitroquinoxalinedione (CNQX)-sensitive EPSPs, accompanied by an increased membrane resistance. Blockade of non-NMDA glutamate receptors with CNQX prevented both effects. CONCLUSION: Ketamine reduces membrane conductance and glutamatergic excitation, in part by blocking alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid receptor channels that may be constitutively active at a low level in slice preparations of auditory cortex.

Action Potentials↗