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Results for “Pyramidal Tracts”

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PubMed1997

Evolving isolated hand palsy: a parietal lobe syndrome associated with carotid artery disease.

Six patients with cerebral ischaemia who presented evolving isolated hand palsy were studied, five prospectively and one retrospectively. The motor deficit involved only the hand and the wrist in some cases. In almost all cases the motor deficit was pseudo-ulnar. None of them had a Babinski sign, all had mild sensory symptoms or signs in the affected hand. CT and MRI disclosed recent infarctions contralateral to the affected hand, in the white matter of the angular gyrus, in a vascular borderzone. Five had a tight stenosis of the internal carotid artery. The pyramidal tract was anatomically spared in three cases, even considering its parietal origin. Consistent with previous data, our study suggests that the parietal lobe is involved in the control of the motor function of the hand. We propose the existence of a new entity, characterized by an evolving non-pyramidal motor deficit in the hand following infarction of the angular gyrus of the inferior parietal lobe.

Aged↗

PubMed1976

[The ultrastructure of portions of the cat spinal cord gray matter connected to fibers of different descending tracts].

Definite ultrastructural features were found in the regions of the cat spinal grey matter connected with different descending pathways, especially in the structure of dendritic membranes and relative quantities of axon terminals. Two types of destructive changes in myelinated axons and axon terminals in these regions were observed during experimental degeneration of descending fibres. Axon terminals of small size and F-type vesicles were subjected to degeneration after pyramidal tract lesion, while large terminals of both S-type and F-type were affected after sectioning of extrapyramidal tracts.

Animals↗

PubMedDate not supplied

Transcranial magnetic stimulation in an adrenoleukodystrophy patient.

We experienced an 11-year-old boy diagnosed as having adrenoleukodystrophy (ALD), and studied his motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS). He had intellectual and visual impairment, and MRI revealed high intensity of the parieto-occipital white matter. On evaluation of the long tracts, slight spasticity with equivocal Babinski signs was noted: however, the long tracts appeared intact on MRI, and short latency somatosensory evoked potentials (SSEPs) were completely normal. On TMS delivered through a circular coil, MEPs recorded from the relaxed first dorsal interosseous muscle showed that only the duration was significantly prolonged, which may be due to temporal dispersion of descending volleys in the pyramidal tracts, while the latency was not prolonged. TMS in ALD was considered sensitive and useful for detecting subtle involvement of the long tracts.

Adrenoleukodystrophy↗

PubMed2001

Protein thiol oxidation by haloperidol results in inhibition of mitochondrial complex I in brain regions: comparison with atypical antipsychotics.

Usage of 'typical' but not 'atypical' antipsychotic drugs is associated with severe side effects involving extrapyramidal tract (EPT). Single dose of haloperidol caused selective inhibition of complex I in frontal cortex, striatum and midbrain (41 and 26%, respectively) which was abolished by pretreatment of mice with thiol antioxidants, alpha-lipoic acid and glutathione isopropyl ester, and reversed, in vitro, by disulfide reductant, dithiothreitol. Prolonged administration of haloperidol to mice resulted in complex I loss in frontal cortex, hippocampus, striatum and midbrain, while chronic dosing with clozapine affected only hippocampus and frontal cortex. Risperidone caused complex I loss in frontal cortex, hippocampus and striatum but not in midbrain from which extrapyramidal tract emanates. Inhibition of the electron transport chain component, complex I by haloperidol is mediated through oxidation of essential thiol groups to disulfides, in vivo. Further, loss of complex I in extrapyramidal brain regions by anti-psychotics correlated with their known propensity to generate side-effects involving extra-pyramidal tract.

Animals↗

PubMed1997

Wolfram syndrome: a neuropathological study.

Neuropathological examination was carried out on a patient aged 37 years who had suffered from Wolfram syndrome. Atrophy of the olfactory bulbs and tracts, atrophy of the optic nerves and chiasm, loss of neurons in the lateral geniculate nuclei mainly affecting the small cell layers, atrophy of the superior colliculus, loss of fibers in the cochlear nerve and mild loss of neurons in the cochlear nuclei and inferior colliculus, mild olivopontocerebellar atrophy, and demyelination of the pyramidal tracts were the main neuropathological findings. These correlated with anosmia, loss of vision, loss of hearing, cerebellar symptoms and signs, Babinski sign, and clonus, respectively, clinically observed in this patient. Mild neuron loss and gliosis in the preoptic and paraventricular area of the hypothalamus and mild motor neuron loss in the spinal cord did not reach thresholds of impaired function, although loss of neurons in discrete bulbar nuclei might have accounted for the late episode of food aspiration and suffocation. The relationship between memory loss, personality disturbances, and signs of prefrontal release and mild loss of neurons in the anterior and dorso-medial nuclei of the thalamus remains unclear.

Adult↗

PubMed1997

Long tract degeneration in familial sudanophilic leukodystrophy with prominent spheroids.

We describe a family with an autosomal dominant neurodegenerative disorder, three siblings of which were verified by autopsy as having sudanophilic leukodystrophy (SLD). The clinical picture of the family is one of progressive dementia and spastic paralysis. Pathological examinations detected diffuse and patchy white matter lesions and the widespread presence of axonal spheroids in the lesions of all three autopsy patients. Because change was found selectively in the pyramidal tracts and optic radiations, this disease is considered to affect the long tracts systematically. The SLD in the family we studied is distinguished from other leukodystrophies by its clinical and pathological features, indicative that it may be a special type of SLD.

Adolescent↗

PubMed1984

Long-term treatment of cerebrotendinous xanthomatosis with chenodeoxycholic acid.

We studied the effect of chenodeoxycholic acid in 17 patients with cerebrotendinous xanthomatosis. Before treatment, all subjects were symptomatic, with Achilles tendon xanthomas (in 15 of 17), cataracts (in 12 of 17), dementia (in 13 of 17), pyramidal-tract signs (in all 17), cerebellar dysfunction (in 13 of 17), mild peripheral neuropathy (in 7 of 17), electroencephalographic abnormalities (in 10 of 13), and abnormal cerebral computerized axial tomographic scans (in 10 of 12). After at least one year of chenodeoxycholic acid treatment (750 mg per day), dementia cleared in 10 subjects, and pyramidal and cerebellar signs disappeared in 5 and improved in another 8. Peripheral neuropathy was no longer detected in six. The electroencephalogram became normal in five and showed fewer abnormalities in another three subjects. Cerebral computerized axial tomographic scans improved in seven patients; the changes included the disappearance of a cerebellar xanthoma in one case. Concomitantly, mean plasma cholestanol levels declined threefold, and abnormal bile acid synthesis was suppressed. We conclude that long-term therapy with chenodeoxycholic acid may correct the biochemical abnormalities and arrest and possibly reverse the progression of cerebrotendinous xanthomatosis.

Adolescent↗

PubMed1995

[Ubiquitin immunoreactivity in the central nervous system of gracile axonal dystrophy (GAD) mouse].

In order to know the relationship of ubiquitin and axonal degeneration in the central nervous system (CNS) of the gracile axonal dystrophy (GAD) mutant mouse, the immunocytochemical study was performed in the spinal cord, medulla oblongata and brain of normal and GAD mice at 4, 9, 18 and 32 weeks of age. The polyclonal antibodies of ubiquitin were used for this study. The results were as follows: Many ubiquitin-positive dot-like structures (DS) were first observed in the gracile nucleus affected primarily with axonal degeneration. They extended to the gracile fasciculus on the dorsal part of spinal cord in accordance with the dying-back type degeneration. The second-order neurons at Clarke's nucleus were also affected slightly later stages and revealed ubiquitin-positive DS along the posterior spinocerebellar tract and the white matter of certain lobes of cerebellum. In 18th week, the transneuronal degeneration started from the distal axonal ends of the primary sensory neurons came up to the some parts of cortical neurons through the secondary neurons in the thalamus. The ubiquitin-positive DS were detected on the ventral surface of the medulla oblongata and increased progressively in number along the corticospinal (pyramidal) tract of spinal cord which consists of the descending fibers derived from the cortical neurons. These findings suggest that abnormal proteins in the degenerating axons were ubiquitinated rapidly before they accumulated in the preterminal axons whose neuron stems are far away from the place, and that GAD mouse would be a useful animal model to know the mechanism(s) of the naturally occurring transneuronal degeneration from the distal axonal ends of both ascending sensory neurons and descending pyramidal neurons in the CNS.

Animals↗

PubMed1980

Autoradiographic tracing of developing subcortical projections of the occipital region in fetal rabbits.

Thirty rabbit embryos and two neonates (E18-P1) received micropipette injections of 3H-Leucine into the occipital region of one hemisphere and were killed after 0.5--5 hours. Incorporated tracer was demonstrated by autoradiography of serial sections of the brains. The first axons were seen in the intermediate zone of the developing cerebral cortex, on day E20, and by day E22 they reached the internal capsule. The entire cortico-peduncular bundle and a short branch of the superficial (thalamic) bundle were labeled on day E24. On day E25, additional branches directed to claustrum, thalamus (deep bundle), and cerebellum were distinguished. By day E28 the first indications of terminal field development were observed. One day before birth (E30), the neonate pattern of subcortical pathways was fully established and silver grain condensations were present over most of the subcortical target areas. Subcortically, the axons followed preferentially preexisting fiber tracts. There was a period of at least 2--3 days between the arrival of the supplying bundles at the target sites and the onset of terminal field formation: The axon bundles grew first towards more distal targets, and even beyond, before terminal fields developed proximally. Transient axon bundles reaching the cerebellar paraflocculus and traveling along the pyramidal tract and the external and extreme capsules failed to form terminal fields and disappeared around birth. The data suggest that growth of long axonal tracts and the development of terminal fields are separate phenomena possibly regulated by different mechanisms.

Age Factors↗

PubMed2000

Modalities of fatigue in multiple sclerosis: correlation with clinical and biological factors.

Although different factors are probably involved in the etiology of fatigue in multiple sclerosis patients, no definite mechanism has been proposed. We have proposed that fatigue is a complex symptom that includes three clinical different entities (asthenia, fatigability and worsening of symptoms with effort). The goal of this study is to demonstrate if there is a peculiar mechanism for each of the different varieties of fatigue. A control sample of 155 patients (105 women, 50 men) with clinically definite MS was studied. Fatigue was measured using the Fatigue Descriptive Scale (FDS) and the Fatigue Severity Scale (FSS). Treatment, depression, anxiety, sleep and cellular immune status were studied too. Fatigue was a symptom in 118 patients (76.13%); 26 patients (22.03%) described it as asthenia (fatigue at rest); 85 patients (72.03%) as fatigability (fatigue with exercise), and seven patients (5.9%) as worsening of symptoms. The severity of pyramidal involvement was significantly more severe in patients suffering from fatigue; some immunological parameters were associated with fatigue as well. The discriminant analysis of the data shows that some of the immunoactivation parameters are associated with asthenia (F=21.5, P<0.001), and pyramidal tract involvement is associated with fatigability (F=10.5, P<0.001). Sleep disorders, anxiety and depression were linked with fatigue in a few patients. No relationship with treatment was proven. In conclusion, fatigue in MS seems to be a heterogeneous entity. Asthenia and fatigability may be different clinical entities. Certain immunoactivation parameters correlate with the presence of asthenia while pyramidal involvement is associated with fatigability.

Adolescent↗

PubMed1990

Hypoplasia of posterior spinal roots and dorsal spinal tracts with arthrogryposis multiplex congenita.

We report a male infant with arthrogryposis multiplex congenita (AMC) who survived for 19 weeks following birth at 36 weeks gestational age. No heritable or acquired cause of neuromuscular disease was found. He manifested joint contractures of upper and lower extremities, diffuse hypotonia requiring ventilatory support, and areflexia; the general examination also showed facial dysmorphisms, and an ichthyotic rash. Pathological examination of the brain and spinal cord revealed severe hypoplasia of dorsal roots and posterior columns, nondecussation of pyramidal tracts, and anterior horns of an unusual configuration; the brain was normal, and the cerebellum contained Purkinje cell heterotopias. Muscle spindles could not be identified. To our knowledge, these spinal cord abnormalities in association with AMC have not been previously reported, thus raising interesting speculations about the possible role of such abnormalities in the pathogenesis of AMC.

Arthrogryposis↗

PubMed1975

Anterior horn cell disease seen in South India.

Thirty-two patients with clinical evidence of anterior horn cell dysfunction are descirbed. This group of patients could be divided into those with bulbar dysfunction, and those without. Eighth cranial nerve involvement was seen in 10%. The commonest perpheral distribution seen was symmetrical involvement of all four extremities. During the period of follow-up (1 to 5 years) none of the patients without bulbar dysfunction initially developed such symptoms. In all these patients electromyographic evidence of anterior horn cell disease was confirmed. The motor nerve conduction velocities in all of these patients were normal. None of them showed signs of pyramidal tract involvement. Muscle biopsy showed evidence of group fibre atrophy in 10 cases, was normal in 3, and showed a myopathic pattern in 1. Sural nerve biopsy obtained in a single patient was considered histologically normal. Plasma citrate and plasma pyruvate levels obtained in 5 patients of this group, showed elevated values for plasma citrate with normal plasma pyruvate levels. Conspicuous absence of pyramidal signs, elevated plasma citrate, normal plasma pyruvate values and the extremely slow progression suggest that this group of patients are different from other varieties of anterior horn cell dysfunction previously described.

Adolescent↗

PubMed1998

The structural and functional mechanisms of motor recovery: complementary use of diffusion tensor and functional magnetic resonance imaging in a traumatic injury of the internal capsule.

OBJECTIVES: Recovery from focal motor pathway lesions may be associated with a functional reorganisation of cortical motor areas. Previous studies of the relation between structural brain damage and the functional consequences have employed MRI and CT, which provide limited structural information. The recent development of diffusion tensor imaging (DTI) now provides quantitative measures of fibre tract integrity and orientation. The objective was to use DTI and functional MRI (fMRI) to determine the mechanisms underlying the excellent recovery found after a penetrating injury to the right capsular region. METHODS: DTI and fMRI were performed on the patient described; DTI was performed on five normal controls. RESULTS: The injury resulted in a left hemiplegia which resolved fully over several weeks. When studied 18 months later there was no pyramidal weakness, a mild hemidystonia, and sensory disturbance. fMRI activation maps showed contralateral primary and supplementary motor cortex activation during tapping of each hand; smaller ipsilateral primary motor areas were activated by the recovered hand only. DTI disclosed preserved structural integrity and orientation in the posterior capsular limb by contrast with the disrupted structure in the anterior limb on the injured side. CONCLUSIONS: The findings suggest that the main recovery mechanism was a preservation of the integrity and orientation of pyramidal tract fibres. The fMRI studies do not suggest substantial reorganisation of the motor cortex, although ipsilateral pathways may have contributed to the recovery. The initial deficit was probably due to reversible local factors including oedema and mass effect; permanent damage to fibre tracts in the anterior capsular limb may account for the persistent sensory deficit. This study shows for the first time the potential value of combining fMRI and DTI together to investigate mechanisms of recovery and persistent deficit in an individual patient.

Adult↗

PubMed2004

Cerebellar activation of cortical motor regions: comparisons across mammals.

This chapter discusses the nature of mammalian cerebello-thalamo-cortical projections. These play an important role in motor control, but with species differences evident in the innervation patterns of thalamo-cortical (T-C) fibers relaying cerebellar inputs. A phylogenetic comparison of the mode of cerebellar activation of cortical motor regions reveals that cerebellar inputs are relayed by the deep and superficial T-C projections in the cat, but predominately by the latter in rat and monkey. Another difference across mammals is the nature of cerebellar activation of cortical neurons. Fast-conducting pyramidal tract neurons in the cat routinely receive fast-rising EPSPs from the deep cerebellar nuclei (CN). This tendency is not observed in rat and monkey, however. These findings suggest that the responsiveness of cortical output neurons also shows species differences, these having bearing on the development of species-specific motor skills. Common to all three species, however, are fast-rising and large CN-EPSP responses of layer III pyramidal neurons to CN input. It is argued that layer III pyramidal neurons modulate cerebellar input to layer V pyramidal neurons, which latter cells provide command signals from the motor cortex to the lower centers.

Animals↗

PubMed2003

Diffusion tensor MRI of early upper motor neuron involvement in amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative system disorder affecting both upper and lower motor neurons. Despite supportive electrophysiological investigations, the involvement of the upper motor neuron is often difficult to assess at an early stage of disease. Diffusion tensor MRI provides an estimate of the orientation of fibre bundles in white matter on the basis of the diffusion characteristics of water. Diffusivity is generally higher in directions along fibre tracts than perpendicular to them. This degree of directionality of diffusion can be measured as fractional anisotropy. Changes in tissue structure due to degeneration of the corticospinal fibres can lead to a modification of the degree of directionality which can be detected by diffusion tensor MRI. We investigated 15 patients with ALS, six of whom had no clinical signs of upper motor neuron involvement at the time of MRI investigation, but developed pyramidal tract symptoms later in the course of their disease. These patients met the El Escorial criteria as their disease progressed. We found a decrease in fractional anisotropy in the corticospinal tract, corpus callosum and thalamus in all 15 ALS patients, including the patients without clinical signs of upper motor neuron lesion, compared with healthy controls. Regression analysis showed a negative correlation between fractional anisotropy and central motor conduction time obtained by transcranial magnetic stimulation, allowing spatial differentiation between the degenerated corticospinal tract fibres that supply the upper and lower extremities. Thus, diffusion tensor MRI can be used to assess upper motor neuron involvement in ALS patients before clinical symptoms of corticospinal tract lesion become apparent, and it may therefore contribute to earlier diagnosis of motor neuron disease.

Adult↗

PubMed1990

Tracing of Neuronal Connections in the Human Brain by Magnetic Resonance Imaging in vivo.

Axon degeneration after disruption of fibre tracts in the mammalian nervous system is accompanied by myelin breakdown which leads to changes in its magnetic resonance properties. In two patients with pure motor strokes due to small ischaemic lesions restricted to the internal capsule, magnetic resonance imaging disclosed a narrow band of pathological signal increase descending band-like into the brain stem and ascending to the precentral gyrus, which corresponded to the well-known path of the pyramidal tract. The findings suggest that in man anterograde and possibly retrograde fibre degeneration can be traced in vivo by conventional magnetic resonance imaging techniques. Critical conditions are the presence of small, strategically located lesions, appropriate choice of imaging plane, and the interval between time of lesion and of imaging. This demonstration may open a new era for functional neuroanatomy of man.

Journal Article↗

PubMed1998

The pachygyria-polymicrogyria spectrum of cortical dysplasia in X-linked hydrocephalus.

Neural cell adhesion molecules (CAM) play important roles in neural development, neurite outgrowth, axonal guidance, fasciculation and synapse formation. Neuropathological studies of X-linked hydrocephalus (XLH) associated with L1 CAM mutations emphasize marked hypoplasia of the pyramidal tract, agenesis of the corpus callosum and septum pellucidum, and a thin cerebral mantle with hypoplastic white matter, but there are no detailed studies of the cerebral cortex in the literature. We report clinical, neuroimaging, and neuropathological findings in three boys with XLH. All had severe congenital hydrocephalus with marked thinning of the cerebral mantle and severe development disabilities. The brain specimens from the three boys showed both pachygyria and polymicrogyria, hypoplasia of the medullary pyramids, hypoplasia of the corpus callosum, small anterior commissure, hypoplasia and poorly differentiated hippocampi. A small but patent aqueduct was present in all three brains. Despite the extensive cerebral malformations, the cortex in all three brains showed normal-appearing laminar cortical neuronal architecture and absence of gliosis. In XLH, it is likely that the poor developmental outcome of spasticity, contractures and severe mental retardation results from a disturbance of neuronal connectivity, fasciculation, and synapse formation rather than aqueductal stenosis, increased intracranial pressure, or abnormal neuroblast migration.

Antigens, Surface↗

PubMed1990

Central motor conduction in ischaemic and hemorrhagic cerebral lesions.

Electrical Transcranial Cortical Stimulation was performed in 20 healthy volunteers and 14 patients having supra- or infratentorial vascular lesions. Central Conduction Time (CCT) in the Pyramidal Tract (PT) was calculated by subtraction of the Peripheral Conduction Time and the spinal synaptic delay to the Motor Evoked Potential (MEP) latency. Twelve out of fourteen patients showed prolonged MEP latencies or CCTs in the affected corporal segments. Only in 3 cases, 2 with subcortical hematoma and other with bilateral ischaemic lesions, the PT was inexcitable. Two patients, one with a discrete cortical lesion and the other with an hemispheric cerebellar infarct showed no abnormalities in pyramidal conduction. Electrophysiological results showed a good correspondence with the degree of clinical impairment.

Adult↗