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PubMed1993

Human T cell leukemia virus type I infection and chronic myelopathy.

The central nervous system (CNS) pathology of HTLV-I associated myelopathy or tropical spastic paraparesis (HAM/TSP) is reviewed, based mainly on 12 autopsy cases of Japanese HAM/TSP with a serological confirmation of HTLV-I infection. The essential histopathological feature of HAM/TSP is a chronic progressive inflammatory process heralded by parenchymal infiltration of memory CD4 cells. The inflammation involves both the grey and white matter of the spinal cord, and progresses for more than three years after the onset of neurological symptoms, resulting in preferential degeneration of the white matter. In cases with a history of more than nine years, however, the spinal cord lesions appears degenerative rather than inflammatory. Both the inflammation and the white matter degeneration are most conspicuous in the lower thoracic cord. The lateral funiculus is always and most severely affected. Although the parenchymal tissue degeneration is not confined to any particular long tracts, symmetrical degeneration of the lateral pyramidal tract is evident in all cases. The involvement of the posterior and anterior funiculi is variable and neurons are relatively well preserved. Since evidence for HTLV-I infection in the CNS is limited to detection of proviral DNA by the polymerase chain reaction (PCR) and isolation of the virus from CSF cells, autoimmune nature of the disease is suspected, but is supported by ample evidence for derangements of the host immune system compatible with those of autoimmune diseases. Recent studies on induction of white matter degeneration in the rat with a topographical similarity to human HAM/TSP is also briefly reviewed. However, in the rat disease, inflammatory cell infiltrations are inconspicuous.

Animals↗

PubMed1989

Corticofugal axonal degeneration in rats after middle cerebral artery occlusion.

We used the Fink-Heimer method to study degenerating corticofugal axons after unilateral middle cerebral artery occlusion in 14 adult male Long-Evans hooded rats. Axonal degeneration in the pyramidal tracts was prominent at 1-3 weeks, manifesting in well-defined silver-impregnated axonal bundles coursing from the internal capsule to the pyramids and crossing completely to the contralateral spinal cord. In half of eight rats examined at 1-3 weeks, the cortical infarct included the forelimb region of the sensorimotor cortex, and degenerating corticospinal axons could be traced to the lower cervical segments; in rats with involvement of the hindlimb cortical area as well, axonal degeneration extended to the lumbosacral segments. Terminal degeneration products were present in the forebrain, midbrain, and brainstem within 2 days after arterial occlusion; the number of degenerating terminals peaked at 7 days and decreased gradually thereafter up to 6 weeks. Dense terminal degeneration was observed in the trigeminal nuclear complex of all seven rats studied at 2 and 7 days. In these seven rats, five had small cortical infarcts, and silver-impregnated terminals were observed in the lateral reticular formation; in two rats with large cortical lesions, terminal degeneration was prominent in the medial reticular formation as well. We conclude that infarcts produced by middle cerebral artery occlusion cause axonal degeneration in the brainstem and spinal cord. The Fink-Heimer method may be useful for evaluating the rat middle cerebral artery occlusion model.

Animals↗

PubMed1992

Electrophysiological assessment of spinal cord lesions by means of transcranial cortical stimulation.

Central Motor Conduction Time (CMCT) was assessed in 30 healthy volunteers and 22 patients with spinal cord lesions due to compressive, degenerative and demyelinating disease. To obtain the CMCT, electrical Transcranial Stimulation and Percutaneous Spinal Stimulation or F wave calculations were employed. Pyramidal Tract (PT) conduction was always abnormal in the clinically impaired corticospinal tracts of all the studied patients. This results correlated with the degree of muscle weakness specially in those having compressive lesions. Subclinical evidence of pyramidal damage was also observed in two patients with Multiple Sclerosis. As opposed to the other groups, patients with degenerative spinal disease, showed essentially symmetric abnormalities. An important overlap of CMCT slowness was seen among the three studied groups, suggesting that this isolated clue is not valuable enough for aetiological suspicion. Double muscle responses due to single TCS were obtained, during rest, in some patients from each group, but never in controls. This pathological feature, not reported by others, could represent the excitation of indirect corticospinal connections, partially responsible for the residual motor function after PT damage.

Adolescent↗

PubMed1981

Modulation of proprioceptive transcortical reflexes in the cat with a penicillin epileptic motor focus.

Mechanisms responsible for the triggering of paroxysmal events by proprioceptive afferents, previously described in the monkey with a chronic epileptic focus, were studied in more detail in the cat with a penicillin focus. To analyse the topical organization of this reflex triggering, the focus was restricted to very small areas of the motor cortex; in this study only pericruciate areas were considered in which stimulation elicited a motor response in one of the several forelimb muscles tested, and which received afferents from that muscle. When the focus was located in the post-sigmoid gyrus, stimulation (usually by stretch) of the given (target) muscle first elicited a cortical spike following the evoked response, and secondly a late phasic EMG response (about 40 msec latency) quite distinct from purely spinal reflexes. Cortical spikes and late EMG responses were closely correlated, especially considering their probability of occurrence or their parallel latency fluctuations. In most cases, this effect was limited to the muscle whose motor area had been treated with penicillin: stretching muscles in the vicinity was ineffective, nor were these muscles activated when the target muscle was stimulated. Evidence is given for the participation of a transcortical reflex in the generation of the late phasic response and for the involvement of the pyramidal tract in this reflex.

Animals↗

PubMed1979

Pyramidal infarction in the medulla: a cause of pure motor hemiplegia sparing the face.

We present a case with an infarct limited to the right pyramidal tract in the medulla. The lesion lay approximately 1 cm below the pontomedullary junction. On the basis of this case and three previously reported cases of medullary pyramidal infarction, there is defined a syndrome of severe hemiplegia with relative sparing of the face, tongue and articulation, minimal sensory loss, and good recovery. The hemiplegia is initially flaccid and later spastic. Transient symptoms, referable to the tegmentum of the medulla, occur at the onset, and reflect ischemia in the deeper territory of a paramedian penetrating vessel.

Brain↗

PubMed1989

Syringomyelia extending to the basal ganglia. Case report.

A 10-year-old girl was admitted to the hospital with complaints of progressive right hemiparesis and sensory disturbance. Magnetic resonance imaging revealed a Chiari Type I malformation and syringomyelia from T-10 to C-1. The syrinx extended from the medulla to the right putamen along the pyramidal tract.

Basal Ganglia↗

PubMed1991

[Pallido-pyramidal syndrome: an unrecognized entity].

A female teenager, without familial history, presented, since the age of 13 years, with gradually worsening pyramidal signs and a parkinsonian syndrome controlled by L-Dopa in small doses. The clinical complex was suggestive of the pallido-pyramidal syndrome, an entity which was individualized in 1954 by Davison on the basis of 5 young patients who had pyramidal signs and a parkinsonian syndrome. In only one of these patients a pathological study was carried out, disclosing a non specific degeneration without inclusions, involving the pallidum, substantia nigra and pyramidal tract. We hope that this report will encourage other authors to report similar cases, since only the study of new cases will determine whether the pallido-pyramidal syndrome is a true entity.

Adolescent↗

PubMed2000

MR imaging and proton MR spectroscopy in adult Krabbe disease.

We present the MR imaging findings in four patients (two pairs of siblings from two unrelated families) with adult Krabbe disease. In the first family, clinical presentation mimicked familial spastic paraplegia. Their MR images showed selective, increased signal intensity on T2-weighted sequences along the corticospinal tracts, most prominently in the proband and barely detectable in her brother. Proton MR spectroscopy showed increased choline and myo-inositol in the affected white matter. In the second family, the clinical presentation differed in that the signs of pyramidal tract involvement were asymmetrical, with concomitant asymmetry on MR images in one. In adults, Krabbe disease may present on MR imaging with selective pyramidal fiber involvement.

Adult↗

PubMed1966

Organization of neurones in the cat cerebral cortex that are influenced from group I muscle afferents.

1. Neurones in the Group I projection area of the first sensori-motor cortex were investigated with extra- and intracellular technique.2. The majority of the neurones influenced by volleys in Group I afferents of contralateral forelimb nerves received exclusively excitation, but some received exclusively inhibition, and some mixed excitation and inhibition.3. The Group I influenced cells were usually found 500-1500 mu beneath the cortical surface.4. The EPSPs and IPSPs evoked from Group I afferents had a steep rising phase and a slow, approximately exponential decay. The duration was sometimes more than 50 msec. The EPSP evoked by a maximal Group I volley was often formed by a small number of large unitary EPSPs.5. Latency measurements indicate that the majority of the Group I activated neurones were monosynaptically excited from the thalamic fibres, and hence constitute the fourth-order neurones in the Group I projection system. The latencies of the IPSPs suggest a disynaptic linkage with thalamic fibres. Hence, the exclusively inhibited cells would constitute fifth-order neurones. It is suggested that most or all of the fourth-order neurones are inhibitory.6. The convergence of excitation and/or inhibition to individual cells was usually extensive and included effects not only from muscle groups working at different joints but also effects from antagonistic groups at the same joint. In addition cutaneous afferents contributed synaptic actions which had a longer latency than the synaptic actions from Group I afferents.7. The neurones influenced from Group I afferents were not antidromically activated on stimulation of the pyramidal tract.

Animals↗

PubMed2001

Increased intracortical facilitation in patients with autosomal dominant pure spastic paraplegia linked to chromosome 2p.

There are at least seven clinically indistinguishable but genetically different types of autosomal dominant pure spastic paraplegia (ADPSP). In this study we investigated electrophysiological characteristics in patients with ADPSP linked to chromosome 2p (SPG4). Twelve patients from six different families with ADPSP linked to chromosome 2p and 15 control persons were included. Electromyography (EMG), motor and sensory nerve conduction, and motor evoked potentials using single and paired transcranial magnetic stimulation (PTMS) was performed. From the peripheral nervous system we found signs of motor and sensory axonal neuropathy. Motor evoked potentials disclosed greatly reduced corticospinal tract conduction velocity and amplitude of evoked potentials to the lower extremities indicating that the very marked spasticity predominantly seems to rely on dysfunction of the fast conducting axons of the pyramidal tract. PTMS showed an increased intracortical facilitation (ICF), which may reflect an impaired function of gamma-aminobutyric acid (GABA)-controlled interneuronal circuits in the motor cortex, alternatively an increased glutamatergic transmission or a compensatory recruitment of a larger number of neurones with corticospinal projections.

Adult↗

PubMed1992

Recovery of distal skills after neonatal lesion of the sensorimotor cortex in the cat.

The cytoarchitectonic cortical areas containing the cells of origin of the pyramidal tract were unilaterally removed from kittens during the first postnatal month. After 5 months, the distal skills of these operated animals were analyzed using a food retrieving task. After an initial deficit, cats achieved the same performance in grasping and wrist movement with the limb contralateral to the lesion as with the opposite limb. The duration of the deficit was dependent on age at the time of lesion. Recovery of distal skills after neonatal lesion is discussed with regard to the low degree of maturity of the corticospinal tract in newborn cat.

Aging↗

PubMed2002

Basic mechanisms of TMS.

Transcranial magnetic stimulation (TMS) is now established as an important noninvasive measure for neurophysiologic investigation of the central and peripheral nervous systems in humans. Magnetic stimulation can be used for stimulating peripheral nerves with a similar mechanism of activation as for electrical stimulation. When TMS is applied to the cerebral cortex, however, some features emerge that distinguish it from transcranial electrical stimulation. One of the most important features is designated the D and I wave hypothesis, which is now widely accepted as a mechanism of TMS of the motor cortex. Transcranial electrical stimulation excites the pyramidal tract axons directly, either at the initial segment of the neuron or at proximal internodes in the subcortical white matter, giving rise to D (direct) waves, whereas TMS excites the pyramidal neurons transsynaptically, giving rise to I (indirect) waves. There are still other phenomena with mechanisms that remain to be elucidated. First, not only excitatory effects but also inhibitory effects can be elicited by TMS of the cerebral cortex (e.g., the silent period and intracortical inhibition). The inhibitory effect may also be used to investigate cerebral functions other than the motor cortex, such as the visual, sensory cortices, and the frontal eye field, from which no overt response like the motor evoked potential can be elicited. Second, there is an abundance of intraregional functional connectivities among different cortical areas that can also be revealed by TMS, or TMS in combination with neuroimaging techniques. Last, repetitive transcranial stimulation exerts a lasting effect on brain function even after the stimulation has ceased. With further investigation of the neural mechanisms of TMS, these techniques will open up new possibilities for investigating the physiologic function of the brain as well as opportunities for clinical application.

Brain↗

PubMed1996

Corticospinal collaterals to medullary cardiovascular nuclei in the rat: an anterograde and a retrograde double-labeling study.

There is little evidence allowing the hypothesis of the existence of direct pathways from the sensorimotor cortex (SMC) to main cardiovascular medullary nuclei: the dorsal motor nucleus of the vagus (DMV), the nucleus of the solitary tract (NTS) and the rostral ventrolateral medulla (RVLM). The purpose of this study was to identify in the rat direct SMC-NTS/DMV and-RVLM projections descending through the pyramidal tract (PT) and corticospinal neurones projecting to spinal somatic centers and sending collaterals to the NTS/DMV and the RVLM. The first group of animals (N = 15) received injections of anterograde tracers into the SMC: wheat germ agglutinin conjugated to horseradish peroxydase (WGA-HRP) or rhodamine-conjugated dextran (DR). In the second group (n = 35), retrograde tracers were injected: fluorogold (FG) into the NTS/DMV or into the RVLM and DR into the lateral thoracic cord (Th2-Th4). Anterograde transport of WGA-HRP and DR allowed corticofugal fibers to be followed inside the PT ipsilaterally to the site of cortical injection and showed bilateral labeled projections to the NTS/DMV and RVLM. After retrograde transport, bilateral FG or DR labeled cells were distributed in the SMC, mainly in the medial (AGm) and lateral (AGl) agranular cortex. After spinal and bulbar injections, double-labeled cells were distributed in same cortical areas. After injections in RVLM, 49% of labeled cells showed a double-labeling in the frontal cortex (rostral AGm and premotor cortex) while only 24% were observed in the posterior SMC (caudal AGl). On the contrary, when injections were done in NTS/DMV, double-labeled neurons were respectively of 11% in the frontal cortex and 4% in the posterior SMC. In the present work it was shown that the SMC sent direct projections to bulbar cardiovascular nuclei by means of fibers descending through the PT and corticospinal collaterals. The hypothesis which may be drawn from this study is that cortical motor areas probably program cardiovascular adjustments, preparatory or concomitant to the control of striate muscles.

Animals↗

PubMed1976

Bladder and urethral innervation in multiple sclerosis.

Bladder and urethral innervation was studied in 52 patients with multiple sclerosis using a signal tracing technique (evoked reflex latency measurement). The majority of the patients showed prolonged signal transit times indicative of demyelinating plaques localised to the lumbosacral spinal cord. Futhermore, impairment of the corticospinal innervation of the pudendal nucleus was found in 29 patients indicating lesions of the pyramidal tract.

Adult↗

PubMed1977

Task dependence of slowing after pyramidal lesions in monkeys.

The effect of lesions in a medullary pyramid was studied in two experiments. (a) Monkeys were trained to press a key with a rear-projected circle, presented together with different numbers of keys with ellipses. Two to eight choices were presented in a random sequence. Discrimination was measured with a titration schedule, and short choice reaction times were reinforced selectively. Choice reaction time and the function relating it to the number of choices were unaffected by lesions reducing the area of a transverse section of the pyramid up to 93%. (b) A repetitive response controlled by a fixed-ratio schedule was performed simultaneously with a holding response with the other hand, and the two hands changed function after each food pellet. Lesions reducing the pyramid only 25% increased interresponse times of the phasic response with the contralateral hand. Experiment 1 and previous studies are interpreted to indicate that slowing after pyramidal lesions is dependent on behavioral context. Experiment 2 showed that a simple repetitive movement is affected when the rate is high. The static response was more clearly affected than the phasic response, which indicates a role for the pyramidal tract in posture.

Animals↗

PubMed1991

Corticospinal potentials after electrical and magnetic stimulation in man.

The present report deals with our study of the descending volley evoked by both electrical and magnetic transcranial stimulation in man. We discuss the differences of these two techniques specifically as regards the latency and amplitude of evoked potentials. In both cases, electrodes were placed either in the epidural space or directly on the spinal cord. Following electrical stimulation, the descending volley consisted of an early wave which appeared at low stimulation intensity and increased in amplitude and decreased in latency when the strength of the stimulus was increased. At high stimulation intensities the early wave was followed by later waves which travel at the same speed as the initial wave. By delivering paired cortical stimuli, the early wave evoked by the test stimuli is present at 1-msec interval and progressively recovered with longer intervals. The recovery cycle of the later waves is also extremely short. Following magnetic stimulation, the descending volley also consisted of an initial wave followed by later waves. The initial wave has a slightly longer latency, a higher threshold and a smaller amplitude than the early wave evoked by electrical stimulation. The results are discussed with reference to the D and I waves recorded from the pyramidal tract in animals.

Adult↗

PubMed1991

The corticospinal tract attains a normal configuration in the absence of myelin: observations in jimpy mutant mice.

The corticospinal projection was examined in dysmyelinated, jimpy mice and in unaffected littermates following cortical injections of either wheat germ agglutinin conjugated to horseradish peroxidase or biocytin. Corticospinal axons in both phenotypes traverse the medulla within a well-defined pyramidal tract, decussate within several fascicles at the spinomedullary junction, and extend down the spinal cord in a compact bundle in the ventral-most part of the dorsal funiculus. Very few labeled fibers are seen separated from the main bundle. This normal configuration of the corticospinal tract is attained despite the virtual absence of CNS myelin in jimpy mice. It seems unlikely then that the myelin normally present in fiber bundles adjacent to this relatively late emerging projection can significantly influence pathway selection during its development.

Animals↗

PubMed1991

Dementia of frontal lobe type and motor neuron disease. A Golgi study of the frontal cortex.

Neuropathological findings in a 38 year old patient with dementia of frontal lobe type and motor neuron disease included pyramidal tracts, myelin pallor and neuron loss, gliosis and chromatolysis in the hypoglossal nucleus, together with frontal atrophy, neuron loss, gliosis and spongiosis in the upper cortical layers of the frontal (and temporal) lobes. Most remaining pyramidal and non-pyramidal neurons (multipolar, bitufted and bipolar cells) in the upper layers (layers II and III) of the frontal cortex (area B) had reduced dendritic arbors, proximal dendritic varicosities and amputation of dendrites as revealed in optimally stained rapid Golgi sections. Pyramidal cells in these layers also showed depletion of dendritic spines. Neurons in the inner layers were preserved. Loss of receptive surfaces in neurons of the upper cortical layers in the frontal cortex are indicative of neuronal disconnection, and are "hidden" contributory morphological substrates for the development of dementia.

Adult↗