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PubMedDate not supplied

Effects of selective spinal cord lesions on the spinal motor evoked potential (MEP) in the rat.

The effects of selective spinal cord lesions on the motor evoked potential (MEP) in 21 rats were investigated. No significant change in peak amplitude was observed following lesions of the pyramidal tract. There was a significant decrease in peaks 1 and 2 with ventral funiculi lesions. All 4 peaks of the MEP were significantly reduced following lesions of the lateral funiculus. The most marked decrease in peak amplitude followed lateral funiculi lesions that involved the lateral grey of the spinal cord. In one animal where the lesion was confined to the grey matter in the cord there was a marked decrease in all peaks of the MEP. In 3 additional animals interruption of the descending tracts of the spinal cord via bilateral hemisections of the spinal cord failed to completely abolish the MEP. Increases in peak latency were also noted following spinal lesions. In some animals the increase in latency occurred in the absence of significant peak amplitude changes. The findings in this study refute the previously held position that the MEP in the rat arises from pyramidal tract activation. The role of the reticulospinal and propriospinal tracts in the generation and propagation of the MEP are discussed.

Animals↗

PubMed1982

[Encephalitis of the basel ganglia associated with mumps].

Two weeks after epidemic parotitis a 10-year old boy developed an acute extrapyramidal syndrome together with pyramidal tract signs but without impairment of consciousness. The CSF showed mild pleocytosis. The CT of the brain exhibited a well defined circumscribed and symmetrical swelling and hypodensity of the basal ganglia and of the internal capsule. Only slight and transient dysrhythmia was to be found in the EEG. Therapy with Prednisolone, Biperidene and Tiapride resulted in regression of symptoms. But one year later rigor and pyramidal tract signs remained evident in spite of intensive physiotherapy and logopaedic measures. Residual symmetric atrophia of the basal ganglia became evident in the CT by dilatation of the anterior horns of the lateral ventricles caused by lacking of the vault of the caudate nuclei heads.

Basal Ganglia Diseases↗

PubMedDate not supplied

Red nucleus: past and future.

The red nucleus has greatly interested scientists for almost a century. This can be explained by the fact that problems of general interest are encountered when studying this nucleus. Some of them are outlined in this paper, such as the phylogenetic evolution of the rubrospinal tract, the respective roles of the rubrospinal and pyramidal tracts in the execution of various types of movements, and the respective roles of these two tracts in movement automatization.

Animals↗

PubMedDate not supplied

[Spinocerebellar ataxias type 1 and 2: comparison of clinical, electrophysiological and magnetic resonance evaluation].

BACKGROUND AND PURPOSE: Spinocerebellar ataxias type 1 (SCA1) and type 2 (SCA2) belong to neurodegenerative disorders of autosomal dominant inheritance, genetically and clinically heterogeneous, caused by the expansion of CAG trinucleotides. Trunk and limb ataxia, dysarthria, dysphagia, gaze palsy, sensory and motor axonal neuropathy are the dominant features in both entities. The aim of the study was to evaluate the differences between genotype and phenotype based on clinical and electrophysiological assessment of the visual, auditory pathways, and EEG alterations in comparison with the cerebellar and brain atrophy in MRI. MATERIAL AND METHODS: 44 patients with SCA1 and 24 cases with SCA2 confirmed molecularly were examined neurologically and using the International Cooperative Ataxia Rating Scale (ICARS). A correlation of clinical symptoms and signs, and CAG repeat numbers with EEG, visual (VEP) and brainstem auditory (BAEP) evoked potentials, and MRI alterations were evaluated. RESULTS: A statistically significant negative correlation between the age of disease onset and number of CAG repeats in both types of SCA was found. Examined patients with SCA2 were younger, with longer disease duration and more pronounced cerebellar and brain atrophy in MRI. We found a significant correlation between ICARS and CAG repeats in this group. The dysphagia, pyramidal tract involvement and depressive reaction were significantly frequent in SCA1 patients. However in SCA2 patients, the peripheral nerve damage and extrapyramidal signs were more prominent. The amplitude of P100 visual evoked potentials was significantly lower in SCA1 patients and negatively correlated with CAG repeats. CONCLUSIONS: These results provide further evidence for the phenotypic differences of genetically defined SCA1 and SCA2 patients, expressed by more frequent involvement of the pyramidal tract and depression reaction in SCA1, in contrast to peripheral nerve involvement and extrapyramidal signs in the clinical feature of SCA2 phenotype. Furthermore, atrophy of the brain and cerebellum revealed in MRI was more pronounced than electrophysiological functional alterations, especially in SCA2. The decreased amplitude of P100 VEP in SCA1 patients was the only electrophysiological parameter differentiating between both groups of patients.

Adult↗

PubMed1989

[MR images of wallerian degeneration--relation between the time and MR findings of wallerian degeneration].

On magnetic resonance (MR) images, wallerian degeneration of the pyramidal tract can be demonstrated as an abnormal intensity showing prolonged T1 and T2 relaxation times corresponding to the corticospinal tract, and/or as shrinkage of the ipsilateral cerebral peduncle and pons. We evaluated 150 cases with supratentorial cerebrovascular accident (CVA) and found the above findings in 35 patients (hematoma 21, infarction 14). The time interval between the ictus of CVA and manifestation of wallerian degeneration on MR images was evaluated. In all 35 cases the foci of CVA located at or extended into the motor cortex, the corona radiata of the pyramidal tract or the posterior limb of the internal capsule. Abnormal signal intensity appeared as early as 5 weeks after ictus and was observed in all 17 cases after 10 weeks. Ipsilateral shrinkage of the cerebral peduncle and the pons has appeared 13 months after ictus. MR appears to be the most useful modality for early detection of waller degeneration.

Cerebrovascular Disorders↗

PubMed1994

[MRI of paraventricular white matter lesions in amyotrophic lateral sclerosis--analysis by diffusion-weighted images].

Magnetic resonance images in some cases of amyotrophic lateral sclerosis (ALS) revealed abnormal signals in both the paraventricular white matter and in the posterior limbs of the internal capsule. We examined T2- and diffusion-weighted MR images of these lesions in 18 cases of ALS. There were symmetrical high-signal areas in the posterior limbs of the internal capsule in all of the cases. The high-signal areas in the internal capsule corresponded to the pyramidal tracts in the anatomical atlas by Talairach. In 5 of the cases of ALS, T2- weighted MR images showed discrete paraventricular white matter lesions as well. The mean age of the ALS patients with paraventricular white matter lesions was higher than that of the ALS patients without such lesions. Proton densities calculated from the conventional MR images were higher in both the capsular and paraventricular lesions. The diffusion coefficients perpendicular to the pyramidal tract in the internal capsula lesions were within the normal range, where as the diffusion coefficients in the paraventricular lesions were increased in all directions. Thus, diffusion anisotropy was lost in the paraventricular lesions. These findings are similar to those observed in the white matter lesions of cerebro-vascular origin. As a result, the pathology of the paraventricular lesions in ALS was confirmed to be different from that of the internal capsular lesions.

Aged↗

PubMed1998

[A case of late adult-onset dentatorubral-pallidoluysian atrophy (DRPLA) successfully treated with V-P shunt operation].

A 44-year-old Japanese man was diagnosed as having late adult-onset dentatorubral-pallidoluysian atrophy (DRPLA), whose CAG repeats in the DRPLA gene were 60 and 15. He developed gait disturbance, limb ataxia, pyramidal tract signs, dementia, and psychiatric symptoms including character changes within a few years of the above diagnosis. His T 2-weighted brain MRI showed symmetric high-signal lesions in the cerebral white matter and brain stem, in addition to cerebellar, brain stem, and cerebral cortical atrophy. Since the results of RI cisternography indicated that he manifested the clinical features of normal pressure hydrocephalus (NPH), V-P shunt operation was done. In a week after the operation, his gait disturbance, pyramidal tract signs, dementia and psychiatric symptoms were remarkably improved. White matter lesions have been thought to be concomitant with late adult-onset DRPLA patients, but some of these patients may have characteristics of NPH pathophysiology.

Adult↗

PubMed1987

Fetal cortical transplants in the cerebral hemisphere of newborn rats: a retrograde fluorescent analysis of connections.

Fetal cerebral neocortex (E15-17) was grafted into the cortex of newborn (0-1 day old) rats. In some animals the tissue was grafted just caudal to cortical aspiration lesions made immediately prior to grafting. At maturity, transplant efferents were examined by use of the retrogradely transported fluorescent dyes Fast Blue and Diamidino Yellow. Dyes were principally injected in various combinations into the host pyramidal tract decussation and into cervical and lumbar spinal cord levels. In addition some of these animals received injections into the host cortex opposite the transplant, into the ipsilateral thalamus or into the transplant. Transplants were recovered in 26 of 30 animals, and they were typically larger in recipients sustaining aspiration lesions. Histologically, transplants commonly demonstrated laminar patterns that resembled normal cortical supra- and infragranular laminae. Numerous retrogradely-labeled neurons were counted within transplants after injections of fluorescent tracers into the host pyramidal tract decussation or cervical spinal cord. These cells were often located appropriately in areas resembling infragranular layers. Retrogradely labeled neurons were also found within transplants after injections into the host cortex or thalamus. Additionally, numerous host neurons were labeled after Diamidino Yellow injections into the transplant. These findings demonstrate an exchange of connections between host and transplant and suggest the establishment of normal connection patterns.

Animals↗

PubMed1998

[What does the Babinski sign have to offer 100 years after its description?].

One hundred years after its description, the Babinski sign remains a faithful and precise indicator of dysfunction in the pyramidal tract. Unlike a normal plantar reflex, which is a local reflex (S1), the Babinski sign is an integral part, though with its own specificity and thus value, of the defense reflectivity of the lower limbs. It should be triggered, preferably in the lateral region of the foot, by a non-painful stimulation. The characteristic response is a dorsal flexion of the greater toe by recruitment of the extensor hallucis. The pathological response is related to a dysfunction involving a precise fraction of the pyramidal tract (van Gijn. 1996), responsible for a monosynaptic stimulation of the extensor hallucis motor neurons, but also, via interneurons, for inhibition of the extensor hallucis. Its relationship with defense reflexes is certain (Walshe, etc.) put quite complex. We refer here to the "fanning" sign or Babinski "equivalents", plantar areflexia, peripheral "pseudo-Babinski", responses obtained by stimulating the plantar aspect of the foot in the newborn, and to global hyperflexion. We also discuss the role of the Lundberf dorsal reticulospinal tract.

Brain Diseases↗

PubMed2001

Activation of cerebellar climbing fibres to rat cerebellar posterior lobe from motor cortical output pathways.

1. The activation of climbing fibres projecting to the posterior lobe cerebellar cortex by focal stimulation of the cerebral corticofugal pathway was investigated in anaesthetised rats. Large climbing fibre responses were evoked in parts of crus II and paramedian lobule by stimulation of corticofugal fibres. Lesions of the pyramidal tract just rostral to the inferior olive substantially reduced these responses, suggesting that they were not mediated by relays in the rostral brainstem. 2. By comparison of latencies of climbing fibre responses evoked from different locations in the corticofugal pathway, the conduction velocities of the corticofugal fibres that mediate the responses were estimated to be 1.9 +/- 0.3 m s(-1) (mean +/- S.E.M.). The fastest conducting corticofugal fibres were estimated to conduct significantly faster (18.7 +/- 2.3 m s(-1)). 3. Climbing fibre responses with similar form and cerebellar distribution were evoked from sites in the pyramidal tract rostral and caudal to the inferior olive. This suggests that at least a proportion of the fibres that activate climbing fibres are corticospinal fibres. 4. Lesions of the dorsal column nuclei did not affect the climbing fibre responses evoked in crus II, and produced a relatively small reduction of the responses in the paramedian lobule. This implies that the climbing fibre responses were not exclusively mediated via the dorsal column nuclei. 5. Corticofugal evoked climbing fibre responses were mapped across the cerebellar hemisphere. At some sites they were co-localised with responses evoked by limb afferents. On the basis of limb afferent inputs and other work, these zones were tentatively identified as being functionally equivalent to the c1, c2 and d zones described in the cat.

Animals↗

PubMedDate not supplied

[Familial cerebellar ataxia: clinical, radiological and electrophysiological findings].

A family with cerebellar ataxia of late onset occurring in four generations was observed. Neurological abnormalities included signs of cerebellar ataxia, pyramidal tract damage and damage to the peripheral motor neuron. Computerized tomography demonstrated in five out of six studied patients an image suggesting olivo-ponto-cerebellar atrophy. In the cerebellar structures, brainstem and cerebral hemispheres evidence of atrophy was detected. No correlation was demonstrated between the intensity of the clinical signs and the progression of changes in CT image. Electrophysiological investigations demonstrated changes compatible with damage to the motor and sensory fibres in the peripheral nerves and signs suggesting damage to the spinal motor neurons and pyramidal tract. These observations confirm the multilevel development of the process. The use of similar diagnostic methods will permit a more accurate classification of cerebellar ataxia and obtaining of better information for prognostication of individual cases.

Adult↗

PubMed1992

[A case of chronic toluene intoxication with abnormal MRI findings: abnormal intensity areas in cerebral white matter, basal ganglia, internal capsule, brain stem and middle cerebellar peduncle].

We reported a case of 21 years old man of chronic toluene intoxication with abnormal intensity areas on MRI in cerebral white matter, basal ganglia, internal capsule (especially posterior limb), brain stem and middle cerebellar peduncle. The patient developed various neurological abnormalities such as blurred vision, ataxic speech, gaze evoked horizontal nystagmus, bilateral pyramidal tract sign and limb ataxia after 8 years sniffing of thinner (mainly toluene). MRI examination revealed diffuse high intensity areas in cerebral white matter on T1 weighted image. On T2 weighted image, high intensity areas of deep cerebral white matter, internal capsule (especially posterior limb), cerebral peduncle, ventral pons and middle cerebellar peduncle were noted. Basal ganglia (caudate nucleus, lenticular nucleus and thalamus) were displayed as low intensity area on T2 weighted image. These high intensity areas of internal capsule, brain stem and middle cerebellar peduncle on T2 weighted image would be significant for understanding pyramidal tract sign and cerebellar sign of this case. On the basis of neuropathological descriptions of chronic toluene intoxication, these high intensity areas of T2 weighted image were presumed to be demyelinating lesions of the central nervous system.

Adult↗

PubMed1988

Pediatric acquired immunodeficiency syndrome. Neurologic syndromes.

Central nervous system (CNS) dysfunction was documented in 61 of 68 infants and children with symptomatic human immunodeficiency virus infection. The most frequent manifestations included acquired microcephaly, cognitive deficits, and bilateral pyramidal tract signs. Lymphoma of the CNS, cerebrovascular accidents, and CNS infection caused by conventional pathogens were documented in only ten children (15%). Neurologic deterioration in 11 children was subacute but steadily progressive; in 31 the course was more indolent and began with a plateau. Of these 31 children, 13 had further neurologic deterioration and the conditions of three improved. Seventeen children had a static course with cognitive deficits (seven children) or cognitive plus neurologic impairment (ten children). Neuroradiologic studies in the children with a subacute progressive or plateau course disclosed cerebral atrophy, white matter abnormalities, and calcification of the basal ganglia. Postmortem findings included variable degrees of inflammatory response, multinucleated cells, calcific vasculopathy, and pyramidal tract degeneration. Computed tomographic studies of the children with a static course were normal or showed mild atrophy, but poor brain growth was documented by serial head circumference measurements.

Acquired Immunodeficiency Syndrome↗

PubMed1989

[Motor and cortical sensory evoked potentials by magnetic stimulation].

Motor evoked potentials (MEP) by magnetic stimulation on the scalp and the spinous processes of the 7th cervical (C 7) and 5th lumbar (L 5) vertebrae were studied in 20 normal subjects and 10 patients with the pyramidal tract lesions. The magnetic stimulator composed of two flat helical coils with mean inner diameters of 12.0 and 2.2 cm. The evoked muscle action potentials were recorded from the thenar muscle in the hand and abductor hallucis muscle in the leg. The mean peak latencies of MEP recorded from the thenar muscle were 22.1 +/- 1.7 and 12.8 +/- 0.9 msec at the stimulations on the scalp and C 7, respectively. The central motor conduction time (CMCT) between the cortex and C 7 was 9.1 +/- 1.1 msec. On the other hand, the peak latencies of MEP were 41.0 +/- 3.2 and 21.6 +/- 2.3 msec at the stimulations on the scalp and L 5, respectively. CMCT between the cortex and L 5 was 19.3 +/- 2.3 msec. The patients with pyramidal tract involvements showed delayed peak latencies or absent MEP. The cortical somatosensory evoked potentials (SEP) by the noninvasive magnetic stimulation on the levels of Th 10, Th 12 and L 5 spines, gluteus and ankle were studied in 20 normal subjects and 7 patients with neurological diseases. Cortical components P 2 and N 2 were recorded clearly in all normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1992

'Fatigue' in patients with multiple sclerosis. Motor pathway conduction and event-related potentials.

Ten patients with a definite diagnosis of multiple sclerosis and complaints of "fatigue" were studied using (1) reaction times and event-related potentials accompanying the performance of auditory memory tasks (target detection, verbal short-term memory) and (2) motor conduction velocities of the pyramidal tract elicited by cerebral and cervical magnetic stimulation. Patients were studied when "rested" and when fatigued. Reaction times of the patients when rested were significantly delayed in the short-term memory but not the target-detection tasks when compared with normal controls. When patients were fatigued, their reaction times became significantly longer in all tasks compared with when they were rested. Event-related potentials in these tasks consist of N1/P2 sensory components and P3a and P3b cognitive components. The N1 component latency was longer and P3a and P3b amplitudes were reduced in patients compared with controls. Fatigue in patients with multiple sclerosis was accompanied by a shortening of P3a latency and an increase in P3a and P3b amplitudes compared with these measures when patients were rested. Pyramidal tract conduction velocities did not differ between rested and fatigued conditions. Thus, fatigue in patients with multiple sclerosis was associated with a slowing of performance (reaction time) on memory tasks, whereas brain potentials reflecting neural events of stimulus encoding and classification were either unchanged or paradoxically speeded up in latency in the fatigued compared with the rested conditions. We postulate that, in patients with multiple sclerosis, fatigue affects neural processes acting after stimulus evaluation but before activation of the primary motor pathways.

Adult↗

PubMed1994

Calcium accumulation following middle cerebral artery occlusion in stroke-prone spontaneously hypertensive rats.

Delayed neuronal damage in the ischemic region of the rat brain following middle cerebral artery (MCA) occlusion in stroke-prone spontaneously hypertensive rats was studied. The distribution of neuronal damage was determined by 45Ca autoradiography. Accumulation of 45Ca was observed in the corpus callosum and ipsilateral cerebral cortex immediately following MCA occlusion. After 3 days of occlusion, 45Ca had accumulated in the ipsilateral pyramidal tract, the ventral posterior nucleus of the thalamus, and the lateral portion of the striatum. Significant accumulation of 45Ca was observed in the same areas after 7 and 14 days of occlusion. Next the effect of MK-801 on accumulation of 45Ca after MCA occlusion was examined using the same technique. MK-801 (0.5-10 mg/kg i.v.) or saline was administered 15 min before MCA occlusion, and volumes of accumulation of 45Ca were calculated 1 week after ischemic insults. MK-801 significantly reduced 45Ca uptake in the cortex, striatum, and thalamus. Furthermore, there was a strong statistical correlation between the volume of accumulation of 45Ca in the cortex and that in the thalamus (r = 0.8974; p < 0.001; n = 25). We speculate that delayed neuronal damage in the corpus callosum, ipsilateral pyramidal tract, and thalamus may be caused by secondary neuronal degeneration. However, neuronal damage in the striatum, a segment not supplied by the MCA, may be related to excessive release of glutamate.

Animals↗

PubMed1976

Undernutrition in the developing rat: effect upon myelination.

Long-Evans rats were undernourished from birth by removing the mother from the sucling rats for part of each day; the undernutrition was continued after weaning till 60 days of age by restricting the daily food intake. Brain development was monitored by histologic and selected biochemical analyses coordinated with an ultrastructural morphometric analysis of the pyramidal tract of 30-day-old rats. Brain and body growth were already reduced after 10 days of undernutrition. At 20 days of age, the peak of myelination in the controls, the body and brain weights of the undernourished rats, compared to the controls, were reduced by 25 and 60%, respectively, and by the end of the study (60 days), the brain and body weights were reduced by 30 and 70%, respectively. Morphometric analysis indicated that the proportion of myelinated axons was significantly reduced in starved (34%) relative to control (43%) animals. Fiber analysis revealed that not only were the myelin sheaths thinner in the undernourished rats, but that the sheath was disproportionately reduced relative to the axon diameter. Chemical analysis on a whole brain basis demonstrated a greater than 60% deficit in the relatively myelin-specific galactolipids. (Whole brain analysis included regions more severely affected than the morphometrically analyzed pyramidal tract.) We also obtained evidence for both a delay in the initiation and a general retardation of myelinogenesis. The promyelinating fibers (axons with one or two non-compacted myelin lamellae) still constituted 4.5% of the myelinated fibers in the undernourished animals at 30 days but had declined to 0.3% in the controls. Analysis of the fabtty acids of cerebroside and sulfatide (lipids enriched in myelin) demonstrated in the undernourished group a pattern characteristic of a younger animal. Thus, the effect of undernutrition on the developing rat appears to be one of inhibited and somewhat retarded myelination. These effects were most likely due to a reduction in the number of myelinating glia formed and the restricted capacity of those which form to generate myeline lamellae.

Age Factors↗

PubMed2000

[A patient with marked immunodeficiency in an HTLV-I carrier: a case report].

We report a 49-year-old man who was an HTLV-I carrier with an immunodeficiency state and intracranial pyramidal tract lesion revealed by MRI. He was born in Hokkaido and was admitted to our hospital because of fluminant hepatitis. On admission, neurologic examination revealed exaggerated deep tendon reflexes including the jaw jerk; the plantar response was flexor. Laboratory examination revealed decrease in the number of lymphocytes and CD4-positive lymphocytes in the peripheral blood and CD4/CD8 ratio was consistently low, indicating the presence of cellular immunodeficiency state. Serum anti-HTLV-I antibody was markedly increased but he did not have HTLV-I associated myelopathy (HAM). He had no underlying disease which would cause immunodeficiency state such as adult T-cell leukemia (ATL) or HIV infection. We concluded that the HTLV-I carrier state induced his immunodeficiency. During the course, he developed retrobulbar neuritis. T2 weighted cranial MRI revealed high signal lesions in the bilateral corona radiata, posterior limb of the internal capsule, and the pontine base, corresponding to the location of the pyramidal tracts. His hospital course was complicated by opportunistic infections such as Pneumocystis carinii pneumonia, cytomegalovirus infections, and meningitis, and died of multiple organ failure 7 months after the admission. Cellular immunodeficiencies in ATL patients are well known. Intracranial central nervous system (CNS) lesions in HAM patients are also mentioned. Recently coincidence of ATL and HAM in the same patients has also been reported. Asymptomatic HTLV-I carriers may have a latent immunodeficiency state and/or CNS lesions. We shall have to be alert about the presence of such carriers.

Carrier State↗