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PubMed2003

Human embryonic germ cell derivatives facilitate motor recovery of rats with diffuse motor neuron injury.

We have investigated the potential of human pluripotent cells to restore function in rats paralyzed with a virus-induced motor neuronopathy. Cells derived from embryonic germ cells, termed embryoid body-derived (EBD) cells, introduced into the CSF were distributed extensively over the rostrocaudal length of the spinal cord and migrated into the spinal cord parenchyma in paralyzed, but not uninjured, animals. Some of the transplanted human cells expressed the neuroglial progenitor marker nestin, whereas others expressed immunohistochemical markers characteristic of astrocytes or mature neurons. Rare transplanted cells developed immunoreactivity to choline acetyltransferase (ChAT) and sent axons into the sciatic nerve as detected by retrograde labeling. Paralyzed animals transplanted with EBD cells partially recovered motor function 12 and 24 weeks after transplantation, whereas control animals remained paralyzed. Semi-quantitative analysis revealed that the efficiency of neuronal differentiation and extension of neurites could not account for the functional recovery. Rather, transplanted EBD cells protected host neurons from death and facilitated reafferentation of motor neuron cell bodies. In vitro, EBD cells secrete transforming growth factor-alpha (TGF-alpha) and brain-derived neurotrophic factor (BDNF). Neutralizing antibodies to TGF-alpha and to BDNF abrogated the ability of EBD-conditioned media to sustain motor neuron survival in culture, whereas neutralizing antibodies to BDNF eliminated the axonal outgrowth from spinal organotypics observed with direct coculture of EBD cells. We conclude that cells derived from human pluripotent stem cells have the capacity to restore neurologic function in animals with diffuse motor neuron disease via enhancement of host neuron survival and function.

Alphavirus Infections↗
PubMed2005

Spinal cord diffusion tensor imaging and fiber tracking can identify white matter tract disruption and glial scar orientation following lateral funiculotomy.

Diffusion tensor magnetic resonance imaging (DTI) provides data concerning water diffusion in the spinal cord, from which white matter tracts may be inferred, and connectivity between spinal cord segments may be determined. We evaluated this potential application by imaging spinal cords from normal adult rats and rats that received cervical lateral funiculotomies, disrupting the rubrospinal tract (RST). Vitrogen and fibroblasts were transplanted into the surgical lesion at time of injury in order to fill the cavity. At 10 weeks, animals were sacrificed; the spinal cords were dissected out and then imaged in a 9.4-Tesla magnet. DTI tractography demonstrated the disruption of the rubrospinal tract axons while indicating which axon tracts were preserved. Additionally, DTI imaging could identify the orientation of glial processes in the gray matter adjacent to the site of injury. In the injured animals, reactive astrocytes in adjacent gray matter appeared to orient themselves perpendicular to white matter tracts. In summary, DTI identified not only white matter disruption following injury, but could distinguish the orientation of the accompanying glial scar.

Animals↗
PubMedDate not supplied

High b-value q-space analyzed diffusion-weighted MRS and MRI in neuronal tissues - a technical review.

This review deals with high b-value q-space diffusion-weighted MRI (DW-MRI) of neuronal tissues. It is well documented that at sufficiently high b-values (and high q-values) neuronal water signal decay in diffusion experiments is not mono-exponential. This implies the existence of more than one apparent diffusing component or evidence for restriction. The assignment of the different apparent diffusing components to real physical entities is not straightforward. However, the apparent slow diffusing component that was found to be restricted to a compartment of a few microns, if originating mainly from a specific pool and if assigned correctly, may potentially be used to obtain more specific MR images with regard to specific pathologies of the CNS. This review examines the utility of analyzing high b-value diffusion MRS and MRI data using the q-space approach introduced by Callaghan and by Cory and Garroway. This approach provides displacement probability maps that emphasize, at long diffusion times, the characteristics of the apparent slow diffusing component. Examples from excised spinal cord, where the experimental conditions for which the q-space analysis of MR diffusion data was developed can be met or approached will be presented. Then examples from human MS patients, where q-space requirement for the short gradient pulse is clearly violated, are presented. In the excised spinal cord studies, this approach was used to study spinal cord maturation and trauma, and was found to be more sensitive than other conventional methods in following spinal cord degeneration in an experimental model of vascular dementia (VaD). High b-value q-space DWI was also recently used to study healthy and MS diseased human brains. This approach was found to be very sensitive to the disease load in MS, compared with other conventional MRI methods, especially in the normal appearing white matter (NAWM) of MS brains. Finally, the potential diagnostic capacity embedded in high b-value q-space analyzed diffusion MR images is discussed. The potentials and caveats of this approach are outlined and experimental data are presented that show the effect of violating the short gradient pulse (SGP) approximation on the extracted parameters from the q-space analysis.

Algorithms↗
PubMed2004

A novel DNA enzyme reduces glycosaminoglycan chains in the glial scar and allows microtransplanted dorsal root ganglia axons to regenerate beyond lesions in the spinal cord.

CNS lesions induce production of ECM molecules that inhibit axon regeneration. One major inhibitory family is the chondroitin sulfate proteoglycans (CSPGs). Reduction of their glycosaminoglycan (GAG) chains with chondroitinase ABC leads to increased axon regeneration that does not extend well past the lesion. Chondroitinase ABC, however, is unable to completely digest the GAG chains from the protein core, leaving an inhibitory "stub" carbohydrate behind. We used a newly designed DNA enzyme, which targets the mRNA of a critical enzyme that initiates glycosylation of the protein backbone of PGs, xylosyltransferase-1. DNA enzyme administration to TGF-beta-stimulated astrocytes in culture reduced specific GAG chains. The same DNA enzyme applied to the injured spinal cord led to a strong reduction of the GAG chains in the lesion penumbra and allowed axons to regenerate around the core of the lesion. Our experiments demonstrate the critical role of PGs, and particularly those in the penumbra, in causing regeneration failure in the adult spinal cord.

Animals↗
PubMed1998

Autocrine hepatocyte growth factor provides a local mechanism for promoting axonal growth.

In this report, we describe a novel local mechanism necessary for optimal axonal growth that involves hepatocyte growth factor (HGF). Sympathetic neurons of the superior cervical ganglion coexpress bioactive HGF and its receptor, the Met tyrosine kinase, both in vivo and in vitro. Exogenous HGF selectively promotes the growth but not survival of cultured sympathetic neurons; the magnitude of this growth effect is similar to that observed with exogenous NGF. Conversely, HGF antibodies that inhibit endogenous HGF decrease sympathetic neuron growth but have no effect on survival. This autocrine HGF is required locally by sympathetic axons for optimal growth, as demonstrated using compartmented cultures. Thus, autocrine HGF provides a local, intrinsic mechanism for promoting neuronal growth without affecting survival, a role that may be essential during developmental axogenesis or after neuronal injury.

Animals↗
PubMed1989

Regrowth of calcitonin gene-related peptide (CGRP) immunoreactive axons from the chronically injured rat spinal cord into fetal spinal cord tissue transplants.

Fetal spinal cord tissue was transplanted into either a hemisection or complete transection lesion site at lumbar levels of the adult rat spinal cord that had been produced 3, 6, or 11 weeks prior to grafting. Tissue sections containing the graft and adjacent regions of the host spinal cord were processed for calcitonin gene-related peptide immunoreactivity (CGRP-IR) 2-6 months later. Numerous CGRP-IR axons within laminae I, II, V and X of the host spinal cord were observed crossing the graft-host interface as they spread diffusely throughout the caudal-rostral extent of the transplants. Many of these immunolabeled axons terminated in a distinct bouton-like formation. These results indicate that within the chronically injured spinal cord at least one-specific neuronal population retains the potential for regrowth in a long-term injury condition and that this capacity for axonal elongation can be sustained by the presence of fetal spinal cord tissue grafts.

Animals↗
PubMed2004

Amiloride increases neuronal damage after traumatic brain injury in rats.

OBJECTIVE: It is well known that traumatic brain injury (TBI) decreases brain free magnesium (Mg) concentration, and that administration of Mg salts after TBI restores concentration of Mg in brain and improves functional outcome. In the presence of hemorrhage, administration of Mg salts exacerbates the injury process and worsens outcome. An alternative to administration of Mg salts may be to prevent cellular loss of Mg with use of amiloride, which inhibits the Na(+)/Mg(2+) exchange. METHODS: In the present study, male, adult Sprague-Dawley rats were injured using the impact acceleration model of diffuse TBI and administered either 100 mols/kg i.v. amiloride, or an equal volume of 50% DMSO/saline, 30 minutes (min) after injury. RESULTS: Amiloride did not improve functional outcome (motor or cognitive outcome) after TBI relative to vehicle treated controls. Histologically, treatment with amiloride significantly increased hippocampal caspase-3 expression (apoptosis), axonal swellings in the medulla and the degree of dark cell change (cell stress) in the cortex. Phosphorus NMR demonstrated that amiloride did not increase free Mg concentration after injury. CONCLUSIONS: Thus, amiloride is ineffective in preventing Mg loss after TBI when administered 30 min after trauma. Moreover, by administering amiloride after the TBI-related Mg decline has already been initiated, it may exacerbate injury by, in part by inhibiting Na(+)/Mg(2+) antiport and preventing entry of Mg back into the cell, and also by inhibiting other Na(+) linked transporters.

Amiloride↗
PubMed1991

[The application of in vivo diffusion weighted magnetic resonance imaging to intracranial disorders].

We have developed a magnetic resonance (MR) spin echo method to obtain diffusion weighted imaging using motion-probing gradient (MPG) pulses in one or three orthogonal directions before and after a 180 degree pulse. Phantom models containing water and acetone, normal volunteers and patients with brain tumors, brain edema and infarction were examined. Experimental models of brain edema including triethyltin intoxication and cold injuries were also examined in Wistar rats. MRI was performed at a 1.0-T clinical machine or a 4.7-T experimental machine using spin echo pulse sequences with or without additional MPGs on one or three orthogonal axes. The one direction method was useful to define diffusion anisotropy of myelinated axonal fibers in white matter. Faster diffusion was detected in the white matter parallel to the direction of MPGs. On the other hand, slower diffusion was detected perpendicular to the direction of MPGs because the myelin sheath restricted water diffusion. The three orthogonal gradients method was useful to demonstrate the difference in the diffusion coefficients in various diseases due to its larger total gradient strength. The clear distinction between the cytotoxic edema, which revealed slower diffusion, and the vasogenic edema, which revealed faster diffusion, was demonstrated in the experimental models using diffusion weighted image. In the clinical cases, faster diffusion was demonstrated in the brain tumor and perifocal vasogenic edema, which was in agreement with the results in the experimental models of rats. Brain tumors such as low grade astrocytoma with microcysts and perifocal vasogenic edema have very wide extracellular space.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Diffuse brain damage of immediate impact type. Its relationship to 'primary brain-stem damage' in head injury.

In a neuropathological analysis of 151 fatal non-missile head injuries, there were 19 cases with focal lesions in the dorsolateral quadrant of the brain-stem in the corpus callosum, and histological evidence of diffuse damage to white matter. Eight of these cases had not experienced a high intracranial pressure during life. All 19 cases had been rendered unconscious at the moment of impact and had remained so or in the persistent vegetative state until death. It is therefore concluded that diffuse damage to white matter may occur as a primary event at the moment of impact, that is, it is one type of immediate impact damage to the brain. It is also concluded that this type of damage is the pathological basis of 'primary brain-stem injury' since in no patient thought clinically to have sustained 'primary brain-stem injury' were abnormalities confined to the brain-stem. Since no patient with this type of brain damage recovered consciousness after injury, it is probable that diffuse damage to white matter is the most important single factor governing the outcome in a patient who sustains a non-missile head injury.

Adolescent↗
PubMed2001

A new model for diffuse brain injury by rotational acceleration: II. Effects on extracellular glutamate, intracranial pressure, and neuronal apoptosis.

The aim of this study is to monitor excitatory amino acids (EAAs) in the extracellular fluids of the brain and to characterize regional neuronal damage in a new experimental model for brain injury, in which rabbits were exposed to 180-260 krad/s2 rotational head acceleration. This loading causes extensive subarachnoid hemorrhage, focal tissue bleeding, reactive astrocytosis, and axonal damage. Animals were monitored for intracranial pressure (ICP) and for amino acids in the extracellular fluids. Immunohistochemistry was used to study expression of the gene c-Jun and apoptosis with the terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) technique. Extracellular glutamate, glycine, and taurine increased significantly in the hippocampus within a few hours and remained high after 24 h. Neuronal nuclei in the granule layers of the hippocampus and cerebellum were positive for c-Jun after 24 h. Little immunoreactivity was detected in the cerebral cortex. c-Jun-positive neuronal perikarya and processes were found in granule and pyramidal CA4 layers of the hippocampus and among the Purkinje cells of the cerebellum. Also some microglial cells stained positively for c-Jun. TUNEL reactivity was most intense at 10 days after trauma and was extensive in neurons of the cerebral cortex, hippocampus, and cerebellum. The initial response of the brain after rotational head injury involves brain edema after 24 h and an excitotoxic neuronal microenvironment in the first hour, which leads to extensive delayed neuronal cell death by apoptosis necrosis in the cerebral cortex, hippocampus and cerebellum.

Acceleration↗
PubMed1993

A model for axonal propagation incorporating both radial and axial ionic transport.

We present an axonal model that explicitly includes ionic diffusion in the intracellular, periaxonal, and extracellular spaces and that incorporates a Hodgkin-Huxley membrane, extended with potassium channel inactivation and active ion transport. Although ionic concentration changes may not be significant in the time course of one action potential, they are important when considering the long-term behavior (seconds to minutes) of an axon. We demonstrate this point with simulations of transected axons where ions are moving between the intra- and extracellular spaces through an opening that is sealing with time. The model predicts that sealing must occur within a critical time interval after the initial injury to prevent the entire axon from becoming permanently depolarized. This critical time interval becomes considerably shorter when active ion transport is disabled. Furthermore, the model can be used to study the effects of sodium and potassium channel inactivation; e.g., sodium inactivation must be almost complete (within 0.02%) to obtain simulation results that are realistic.

Action Potentials↗
PubMed2003

Neuroprotective effects of nitrone radical scavenger S-PBN on reperfusion nerve injury in rats.

The nitrone-based free radical scavengers have potent neuroprotective activities in models of stroke in which oxidative stress plays a key role in its development. We examined the effects of S-PBN (sodium 4-[(tert-butylimino) methyl]benzene-3-sulfonate N-oxide), a spin trap nitrone, on reperfusion injury in rat peripheral nerves. Immediately after the onset of 4-h ischaemia in rat right hindlimb, S-PBN was administered via mini-osmotic pumps, containing 2 ml of S-PBN (1.2 M), inserted subcutaneously. S-PBN, in addition, was given by a single injection (50 mg/kg BW, i.p.). Mean plasma concentrations of S-PBN were significantly greater in S-PBN-treated rats than in controls after 24, 48 and 72 h of reperfusion. Pump and dosing solution analysis indicated that the rats received between 82 and 99% of the target S-PBN concentration. Morphology in sciatic, tibial and peroneal nerves was assessed after 4 h of ischaemia followed by 72 h and 7 days of reperfusion. After 72 h of reperfusion, saline-treated control rats showed endoneurial oedema at the thigh level and diffuse axonal degeneration of myelinated nerve fibres distally. S-PBN-treated nerves were normal or revealed less severe abnormalities in myelinated fibres after 72 h and 7 days of reperfusion, when compared with those in saline-treated control nerves. Morphometrically, the frequency of abnormal myelinated fibres at calf levels was significantly less in S-PBN-treated nerves than in controls. In conclusion, post-ischaemic administration of S-PBN exhibits substantial neuroprotective properties in ischemia/reperfusion nerve injury.

Animals↗
PubMed2002

Magnetic resonance imaging of multiple sclerosis.

Although conventional magnetic resonance imaging (cMRI) is widely used for diagnosing multiple sclerosis (MS) and monitoring disease activity and evolution, the correlation between cMRI and clinical findings is far from strict. Among the reasons for this "clinical-MRI paradox," a major role has been attributed to the limited specificity of cMRI to the heterogeneous pathological substrates of MS and to its inability to quantify the extent of damage in the normal-appearing tissue. Modern quantitative MRI techniques have the potential to overcome some of the limitations of cMRI. Metrics derived from magnetization transfer and diffusion-weighted MRI enable one to quantify the extent of structural changes occurring within and outside macroscopic MS lesions with increased pathological specificity over cMRI. Magnetic resonance spectroscopy can add information on the biochemical nature of such changes, with the potential to improve significantly our ability to monitor inflammatory demyelination and axonal injury. Finally, functional MRI might provide new insights into the role of cortical adaptive changes in limiting the clinical consequences of white-matter structural damage. This review outlines the major contributions given by MRI-based techniques to the diagnostic work-up of MS patients, to the understanding of the pathobiology of the disease, and to the assessment of the effects of new experimental treatments.

Contrast Media↗
PubMed1990

Sensory nerve evoked responses in spinal cord injury.

Previous studies have documented the presence of fibrillations, positive waves, and decreased motor evoked response amplitudes in spinal cord injury (SCI) subjects. The purpose of this study was to further evaluate sensory nerve status in this population. Twenty-eight subjects with SCI for at least five months and evidence of spasticity were included. Sural sensory and tibial motor evoked response amplitudes were measured. The mean sural sensory amplitude was 8.0 +/- 5.9 microV (normal = 15.0 +/- 5.3 microV). The mean tibial motor amplitude was 5.1 +/- 4.3 mV (normal = 11.7 +/- 3.8 mV). In six subjects with significantly reduced sural sensory amplitudes, more extensive electrodiagnostic testing was performed. These studies showed diffusely decreased lower extremity sensory and motor evoked response amplitudes and diffuse positive waves and fibrillations in no particular distribution. Thus, subjects with SCI may have sensory as well as motor nerve abnormalities. An intact connection between the second order and primary sensory neuron may be necessary for maintenance of axonal integrity of the primary neuron.

Adolescent↗
PubMed1990

Disruption of cellular elements and water in neurotoxicity: studies using electron probe X-ray microanalysis.

Regulation of elements and water in nerve cells is a complex, multifaceted process which appears to be vulnerable to neurotoxic events. However, much of our knowledge concerning the potential role of elements in nerve cell injury is limited by the relatively gross level of corresponding analyses. If we are to confirm and understand the proposed role, more precise and detailed information is needed. As indicated in this commentary, research employing electron probe microanalysis and digital X-ray imaging has begun to provide this necessary information. Recent EPMA studies of nerve and glial cells in the peripheral and central nervous systems have shown that each cell type and their corresponding morphologic compartments exhibit unique distributions of elements and water. The use of microprobe analysis has allowed us to document precisely how elements and water redistribute in morphological compartments of damaged nerve cells. Accumulating evidence from EPMA studies suggests that, rather than being an epiphenomenon, intracellular changes in diffusible elements might mediate the functional and structural consequences of neurotoxic insult. It is also evident from this research that elements other than Ca might play a pertinent role in the injury response and that changes in intraneuronal elemental composition might develop according to a specific temporal pattern, e.g., transection-induced sequential alterations in axonal K, Na, Cl, and Ca. Therefore, rather than conducting end-point studies, longitudinal investigations are necessary to define the sequential pattern of elemental perturbation associated with a given neurotoxic event. Such research can also help identify the role of individual elements in the injury response. Future microprobe studies should be combined with measurements of ion levels (e.g., using fura-2 or ion selective electrodes) to provide a comprehensive and dynamic view of elemental deregulation. In addition, parallel biochemical studies should be performed to determine mechanisms of elemental disruption and possible biochemical and metabolic consequences of this disruption. Although evidence presented in this commentary suggests that each type of neurotoxic event produces a characteristic pattern of decompartmentalization, further work is necessary to confirm this possibility. Finally, based on a presumed involvement of elements in nerve injury, efforts are currently underway in several laboratories to develop appropriate pharmacological therapies for certain chemical- and trauma-induced neuropathological conditions (Dretchen et al., 1986; El-Fawal et al., 1989; Beattie et al., 1989).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2003

Intraputamenal infusion of GDNF in aged rhesus monkeys: distribution and dopaminergic effects.

Site-specific delivery of trophic factors in the brain may be important for achieving therapeutic efficacy without unwanted side effects. This study evaluated the site-specific infusion of glial cell line-derived neurotrophic factor (GDNF) into the right putamen of aged rhesus monkeys. After 4 weeks of continuous infusion at a rate of 22.5 microg/day, GDNF had diffused up to 11 mm from the catheter openings in the putamen into the rostral putamen, internal capsule, external capsule, caudate nucleus, and globus pallidus. Anisotropic flow along the external capsule tracts carried GDNF into the anterior amygdaloid area. Backflow of GDNF along the catheter track from the frontal cortex infiltrated juxtaposed corpus callosal and cortical tissue. GDNF was carried by retrograde transport to dopamine neurons in the ipsilateral substantia nigra, stimulating an 18% increase in the number of tyrosine hydroxylase (TH)-positive dopamine neurons and a 28% increase in dopamine neuron perikaryal size. Also, TH-positive fiber density was increased in the ipsilateral globus pallidus, caudate nucleus, and putamen. Anatomic effects from GDNF stimulation of the dopaminergic system were restricted to the ipsilateral hemisphere. Retrograde GDNF labeling was also present in a few TH-positive neurons in the locus coeruleus and a large cluster of TH-negative neurons in the ventral anterior thalamus. Anterograde transport of GDNF was evident in axons in the pyramidal tract from the cerebral peduncle to the caudal spinal cord. Tissue injury from the intraparenchymal catheter and continuous infusion was confined primarily to a narrow zone surrounding the track and was mild to moderate in severity.

Aging↗
PubMed2006

White and gray matter development in human fetal, newborn and pediatric brains.

Brain anatomy is characterized by dramatic growth from the end of the second trimester through the neonatal stage. The characterization of normal axonal growth of the white matter tracts has not been well-documented to date and could provide important clues to understanding the extensive inhomogeneity of white matter injuries in cerebral palsy (CP) patients. However, anatomical studies of human brain development during this period are surprisingly scarce and histology-based atlases have become available only recently. Diffusion tensor magnetic resonance imaging (DTMRI) can reveal detailed anatomy of white matter. We acquired diffusion tensor images (DTI) of postmortem fetal brain samples and in vivo neonates and children. Neural structures were annotated in two-dimensional (2D) slices, segmented, measured, and reconstructed three-dimensionally (3D). The growth status of various white matter tracts was evaluated on cross-sections at 19-20 gestational weeks, and compared with 0-month-old neonates and 5- to 6-year-old children. Limbic, commissural, association, and projection white matter tracts and gray matter structures were illustrated in 3D and quantitatively characterized to assess their dynamic changes. The overall pattern of the time courses for the development of different white matter is that limbic fibers develop first and association fibers last and commissural and projection fibers are forming from anterior to posterior part of the brain. The resultant DTMRI-based 3D human brain data will be a valuable resource for human brain developmental study and will provide reference standards for diagnostic radiology of premature newborns.

Adult↗
PubMed2005

Quantitative diffusion tensor imaging in cerebral palsy due to periventricular white matter injury.

Periventricular white matter injury (PWI) is a major form of brain injury observed in congenital hemiparesis. The aim of this study is to determine the usefulness of diffusion tensor imaging (DTI) and fibre tracking in delineating the primary and secondary degenerative changes in cerebral white matter and deep grey matter in patients with spastic cerebral palsy due to PWI and to look for any possible reorganization of the axonal architecture. Five hemiparetic cerebral palsy patients (median age 14 years) with known PWI were prospectively studied with DTI of the brain at 1.5T and quantitatively compared with five age and sex matched controls. Fibre tracts for various corticofugal, thalamocortical and association tracts were generated and analysed for the DTI fibre count and for diffusion parameters. A region of interest based analysis was performed for the directionally averaged mean diffusivity (D(av)) and fractional anisotropy (FA) values in various white matter locations in the brain and the brainstem and in the deep grey matter nuclei. Group statistics were performed for these parameters using Mann-Whitney U-test comparing the affected sides in patients with either side in controls and the unaffected side in hemiparetics. There was significant reduction in DTI fibre count on the lesional side involving corticospinal tract (CST), corticobulbar tract (CBT) and superior thalamic radiation in the patient group compared with controls. Also there was an increase in DTI fibre count in the unaffected side of the hemiparetic patients in CST and CBT, which reached statistical significance only in CBT. The corpus callosum, cingulum, superior longitudinal fasciculus and middle cerebellar peduncle failed to show any significant change. ROI measurements on the primary site of white matter lesion and the thalamus revealed a significant increase in D(av) and decrease in FA, suggesting primary degeneration. The CST in the brainstem, the body of corpus callosum and the head of caudate and lentiform nuclei showed features of secondary degeneration on the affected side. The CST on the unaffected side of hemiparetics was found to have a significant decrease in D(av) and an increase in FA. Thus the degeneration of various motor and sensory pathways, as well as deep grey matter structures, appears to be important in determining the pathophysiological mechanisms in patients with congenital PWI. Also evidence suggesting the reorganization of sensorimotor tracts in the unaffected side of spastic hemiparetic patients was noted.

Adolescent↗