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PubMed2000

Loss of connectivity in Alzheimer's disease: an evaluation of white matter tract integrity with colour coded MR diffusion tensor imaging.

A novel MRI method--diffusion tensor imaging--was used to compare the integrity of several white matter fibre tracts in patients with probable Alzheimer's disease. Relative to normal controls, patients with probable Alzheimer's disease showed a highly significant reduction in the integrity of the association white matter fibre tracts, such as the splenium of the corpus callosum, superior longitudinal fasciculus, and cingulum. By contrast, pyramidal tract integrity seemed unchanged. This novel finding is consistent with the clinical presentation of probable Alzheimer's disease, in which global cognitive decline is a more prominent feature than motor disturbance.

Aged↗
PubMed2000

In vivo fiber tractography using DT-MRI data.

Fiber tract trajectories in coherently organized brain white matter pathways were computed from in vivo diffusion tensor magnetic resonance imaging (DT-MRI) data. First, a continuous diffusion tensor field is constructed from this discrete, noisy, measured DT-MRI data. Then a Frenet equation, describing the evolution of a fiber tract, was solved. This approach was validated using synthesized, noisy DT-MRI data. Corpus callosum and pyramidal tract trajectories were constructed and found to be consistent with known anatomy. The method's reliability, however, degrades where the distribution of fiber tract directions is nonuniform. Moreover, background noise in diffusion-weighted MRIs can cause a computed trajectory to hop from tract to tract. Still, this method can provide quantitative information with which to visualize and study connectivity and continuity of neural pathways in the central and peripheral nervous systems in vivo, and holds promise for elucidating architectural features in other fibrous tissues and ordered media.

Artifacts↗
PubMed2001

Spinal evoked potentials following transcranial magnetic stimulation.

Motor evoked potentials by magnetic stimulation is less invasive and causes no pain as opposed to high current electric stimulation. However, the distribution of the magnetic field generated by the round coil has not been fully studied. In this report, we mapped the extent of the magnetic induction flux density, and then the evoked potentials from the spinal cord were investigated by transcranial magnetic stimulation. We also examined the origin of the evoked potentials obtained by the magnetic stimulation. The following results were obtained. The magnetic induction flux density was at its maximum at the edge of the coil. The potentials consisted of a first negative wave and subsequent multiphasic waves. The first negative wave was similar to a response of the subcorticospinal tract in the lower brain stem, while the subsequent multiphasic waves were similar to those of the pyramidal tract. Although magnetic stimulation has certain advantages over electric stimulation, several problems remain to be solved for the monitoring of motor functions in the clinical settings.

Animals↗
PubMed1988

The pharmacology of excitatory transmission in the rat olfactory cortex slice.

The pharmacology of excitatory transmission in slices of olfactory cortex of the rat, perfused with solution containing picrotoxin, has been studied by assessing the effects of cis-2,3-piperidine dicarboxylate, a nonselective antagonist of excitatory amino acid receptors, 2-amino-5-phosphonopentanoate, a selective antagonist of N-methyl-D-aspartate (NMDA) receptors and 2-amino-4-phosphonobutyrate (APB) and baclofen, which act at APB and GABAB sites, respectively, on evoked surface field potentials. Monosynaptic excitatory transmission was monitored by measuring the amplitude of the N'a'-wave, evoked on stimulation of the lateral olfactory tract, whilst di-/polysynaptic excitatory transmission was evaluated by calculating the areas of the potentials evoked on direct stimulation of the superficial and deep-lying association fibre systems. On the basis of the effects of the drugs in this and earlier studies, it is concluded that: (i) transmission at the lateral olfactory tract-pyramidal cell synapse is mediated by kainate/quisqualate but not NMDA receptors and is regulated by inhibitory APB receptors, located on the tract terminals; (ii) NMDA receptors are involved in mediating excitatory transmission at the synapses of superficial association fibres with the proximal apical dendrites of pyramidal cells with inhibitory APB receptors playing a regulatory role; (iii) transmission at synapses of association fibres with basal dendrites of pyramidal cells, is mediated in part by NMDA receptors with (presynaptic?) GABAB receptors exerting a strong inhibitory influence. These proposed roles of NMDA receptors have been confirmed in experiments in which the effects of magnesium ions on field potentials evoked in slices perfused in magnesium-free solution were monitored.

2-Amino-5-phosphonovalerate↗
PubMed1994

Nitric oxide synthase immunoreactivity in rat pontine medullary neurons.

Nitric oxide synthase immunoreactivity was detected in neurons and fibers of the rat pontine medulla. In the medulla, nitric oxide synthase-positive neurons and processes were observed in the gracile nucleus, spinal trigeminal nucleus, nucleus of the solitary tract, dorsal motor nucleus of the vagus, nucleus ambiguus, medial longitudinal fasciculus, reticular nuclei and lateral to the pyramidal tract. In the pons, intensely labeled neurons were observed in the pedunculopontine tegmental nucleus, paralemniscal nucleus, ventral tegmental nucleus, laterodorsal tegmental nucleus, and lateral and medial parabrachial nuclei. Labeled neurons and fibers were seen in the interpeduncular nuclei, dorsal and median raphe nuclei, central gray and dorsal central gray, and superior and inferior colliculi. Double-labeling techniques showed that a small population (< 5%) of nitric oxide synthase-positive neurons in the medulla also contained immunoreactivity to the aminergic neuron marker tyrosine hydroxylase. The majority of nitric oxide synthase-immunoreactive neurons in the dorsal and median raphe nuclei were 5-hydroxytryptamine-positive, whereas very few 5-hydroxytryptamine-positive cells in the caudal raphe nuclei were nitric oxide synthase-positive. Virtually all nitric oxide synthase-positive neurons in the pedunculopontine and laterodorsal tegmental nuclei were also choline acetyltransferase-positive, whereas nitric oxide synthase immunoreactivity was either low or not detected in choline acetyltransferase-positive neurons in the medulla. The results indicate a rostrocaudal gradient in the intensity of nitric oxide synthase immunoreactivity, i.e. it is highest in neurons of the tegmentum nuclei and neurons in the medulla are less intensely labeled. The majority of cholinergic and serotonergic neurons in the pons are nitric oxide synthase-positive, whereas the immunoreactivity was either too low to be detected or absent in the large majority of serotonergic, aminergic and cholinergic neurons in the medulla.

Amino Acid Oxidoreductases↗
PubMed1992

[A hereditary ataxia associated with hypoalbuminemia and hyperlipidemia--a variant form of Friedreich's disease or a new clinical entity?].

The patients belonged to three different families and were products of consanguineous marriage. The neurological symptoms and signs in these patients began in infancy or childhood and included gait disturbance, horizontal nystagmus, distention tremor of the hands, muscular wasting and sensory impairment of the hands and legs. CT-scan and/or MRI showed atrophy of the cerebellum. Serum biochemical analyses revealed hypoalbuminemia with hyperlipidemia. There were no abnormalities in the heart, liver, kidney, gastrointestinal tract, or endocrine systems. The autopsy revealed degenerative changes in the spinal cord including posterior column and lateral pyramidal tract, as well as in the peripheral nerves and cerebellar cortex. Although we have speculated that the disease presented here would be a clinical variants of Friedreich's disease, it would make a new clinical entity because there was no report about the association to hypoalbuminemia and hyperlipidemia with spinocerebellar degeneration.

Adult↗
PubMed1996

Distribution of high-conductance Ca(2+)-activated K+ channels in rat brain: targeting to axons and nerve terminals.

Tissue expression and distribution of the high-conductance Ca(2+)-activated K+ channel Slo was investigated in rat brain by immunocytochemistry, in situ hybridization, and radioligand binding using the novel high-affinity (Kd 22 pM) ligand [3H]iberiotoxin-D19C ([3H]IbTX-D19C), which is an analog of the selective maxi-K peptidyl blocker IbTX. A sequence-directed antibody directed against Slo revealed the expression of a 125 kDa polypeptide in rat brain by Western blotting and precipitated the specifically bound [3H]IbTX-D19C in solubilized brain membranes. Slo immunoreactivity was highly concentrated in terminal areas of prominent fiber tracts: the substantia nigra pars reticulata, globus pallidus, olfactory system, interpeduncular nucleus, hippocampal formation including mossy fibers and perforant path terminals, medial forebrain bundle and pyramidal tract, as well as cerebellar Purkinje cells. In situ hybridization indicated high levels of Slo mRNA in the neocortex, olfactory system, habenula, striatum, granule and pyramidal cell layer of the hippocampus, and Purkinje cells. The distribution of Slo protein was confirmed in microdissected brain areas by Western blotting and radioligand-binding studies. The latter studies also established the pharmacological profile of neuronal Slo channels. The expression pattern of Slo is consistent with its targeting into a presynaptic compartment, which implies an important role in neural transmission.

Amino Acid Sequence↗
PubMed1994

Clinically silent dysfunction of dorsal columns and dorsal spinocerebellar tracts in hereditary spastic paraparesis.

Hereditary spastic paraparesis (HSP) is a neurodegenerative disorder, of which progressive spastic paraparesis is the clinical hallmark. Given the neuropathological evidence of degeneration of pyramidal tracts, dorsal columns, and dorsal spinocerebellar tracts, it is surprising that sensory symptoms are so indistinct compared to motor symptoms. We investigated the involvement of peripheral conduction and spinal proprioceptive pathways by nerve conduction studies, somatosensory evoked potentials of the median and tibial nerves, and quantitative assessment of the vibration perception thresholds of the hands and feet respectively in 32 patients suffering from HSP and healthy control groups. We did not find peripheral conduction abnormalities in HSP patients. Log-transformed vibration perception thresholds of the feet were abnormal in 13/32 HSP patients and in 0/64 controls (p < 0.00001), while tibial nerve somatosensory evoked potentials were abnormal in 20/32 patients and in 1/17 controls (p = 0.00001). The values for the upper extremities were within normal limits for nearly all subjects. In the HSP group, the neurophysiological disturbances did not correlate significantly with duration or severity of the disease, when age was controlled for, except for median nerve SSEP latency, which was affected by severity (p = 0.0072). We conclude that neurophysiological methods detected proprioceptive, subclinical abnormalities in several HSP patients, which may reflect degeneration of the dorsal columns, and/or dorsal spinocerebellar tracts. Since we found no correlation with several disease variables, the fact that not all HSP patients displayed these abnormalities may be caused by anatomical variations in proprioceptive pathways, rather than by phenotypical heterogeneity.

Action Potentials↗
PubMed1984

Response properties and morphological identification of neurons in the cat motor cortex.

Intracellular recordings and morphological identification of neurons using intracellular HRP staining were performed in the cat motor cortex. By thalamic ventrolateral (VL) or cerebellar nucleus stimulation, pyramidal cells in layer III, fast pyramidal tract neurons (PTNs) and stellate cells in layers II and III were activated with short latency and fast rising EPSPs, while pyramidal cells in layer II and slow PTNs showed longer latency and slow rising EPSPs. This difference may be related to activation through the deep and superficial thalamocortical projections. Although pyramidal cells in layer VI did not respond orthodromically to VL or cerebellar stimulation, some of them proved to receive the recurrent action of PTNs because of the response to stimulation of the cerebral peduncle (CP). One aspinous stellate cell in layer III was activated by CP as well as VL stimulation. This cell was supposed to be an inhibitory interneuron responsible for both recurrent and VL-evoked inhibition.

Animals↗
PubMed2000

Hyper-reflexia without spasticity after unilateral infarct of the medullary pyramid.

Whether or not a lesion confined to the pyramidal tract produces spasticity in humans remains an unresolved controversy. We have studied a patient with an ischemic lesion of the right medullary pyramid, using objective measures of hyper-reflexia, spasticity, and weakness. Electromyographic activity (EMG) of the biceps muscles was recorded under the following conditions: (1) in response to a tendon tap with an instrumental reflex hammer, (2) in response to imposed quick stretch with motion analysis, and (3) during an isometric holding task. Hyper-reflexia of the involved arm in response to tendon tap was shown to be due primarily to an increase in the gain of the reflex arc. No velocity-dependent increase in the response to quick stretch of the involved arm was present. This was consistent with the absence of detectable spasticity on the clinical exam. These findings suggest that a lesion confined to the medullary pyramid can give rise to weakness and hyper-reflexia without causing spasticity. Moreover, these findings suggest that different anatomical substrates may underlie the clinical phenomena of hyper-reflexia and spasticity.

Aged↗
PubMed1992

Electrical stimulation of motor cortex in experimental cortical ischaemia: pyramidal responses at C5 and the surface EMG.

In 7 baboons maintained under propofol anaesthesia, pyramidal tract responses were related to the corresponding peripheral EMG evoked by electrical stimulation of the motor cortex under conditions of focal cortical ischaemia. Pyramidal responses were recorded epidurally at the C5 level and the EMG was recorded from the contralateral hand or foot muscle using subdermal needle electrodes. Cortical ischaemia was produced by transorbital occlusion of the common anterior cerebral artery, and regional cortical blood flow was measured by the hydrogen clearance method. In the normally perfused brain, the later I waves of the C5 response required a lower stimulus strength to elicit them than the earlier I1 wave. It was more difficult to record the EMG from the hand than from the foot following stimulation of the corresponding cortex even though the C5 responses were always obtained in both cases. With moderate ischaemia, the later I waves were selectively abolished, leaving the D and I1 waves. EMG amplitude was significantly correlated with cortical blood flow (r = 0.88, P less than 0.005), and the threshold of cortical flow for the EMG was 10-13 ml/100 g/min. Our results indicate that changes in amplitude of the late I waves and particularly of the EMG are sensitive indicators of cortical ischaemia.

Animals↗
PubMed1999

The bladder cooling reflex and the use of cooling as stimulus to the lower urinary tract.

PURPOSE: We review the physiology of bladder cooling response in experimental animals and humans, and present its clinical usefulness. MATERIALS AND METHODS: We describe experimental studies of the bladder cooling response, and more recent clinical retrospective and prospective studies of the bladder cooling test in adults and children. RESULTS: Studies indicate the existence of a segmental spinal bladder cooling reflex that originates from specific cold receptors in the bladder and urethral walls supplied by unmyelinated C-afferents. The reflex is positive in neurologically normal infants and children until about age 4 years. It becomes negative with further maturation of the nervous system but may be unmasked by pathological processes that disturb the descending neuronal control of normal voiding. A positive test in a patient with an overactive bladder requires further neurourological evaluation. CONCLUSIONS: The bladder cooling response originates from cold receptors within the walls of the lower urinary tract. The cooling response represents a neonatal reflex that may be unmasked by central neuropathology, analogous to the appearance of the Basbinki sign in pyramidal tract lesions. The bladder cooling test is a simple and valuable tool to support the diagnosis of neurourological disorders.

Adult↗
PubMedDate not supplied

[Case of Henoch-Schoenlein purpura with neurological complications].

In a 11-year-old girl with urinary tract infection symptoms and signs of Henoch-Schoenlein syndrome developed with neurological complications in the form of headaches, vomiting slightly marked signs of pyramidal tract and cerebellar damage and severe psychomotor temporal-lobe seizures. These very violent neurological manifestations disappeared completely after control of infection. The authors point out that prognosis in Henoch-Schoenlein syndrome even with such severe neurological complications is good.

Child↗
PubMed1976

[Transfixion of cervical cord by a glass fragment--report of a case (author's transl)].

Stab wound of the spinal cord caused by accident occurred in the home life is rare absolutely. One case of stab wound of the cervical spinal cord caused by penetrated and retained glass fragment within the spinal canal was reported. A 30-year-old woman was hospitarized on August 16, 1971. with complaint of left hemiparesis, gait disturbance and sensory impairment on the right side. A glass door fell down on the patient's neck on April 14, 1971. and one glass fragment was removed from the patient's left neck by one of the patient's family and no immediate spinal cord symptom appeared and no physician was consulted at that time. One and a half month after the injury the patient rod a motor bicycle and pain and severe stiffness in the shoulder and neck, and headache. These subjective symptom disappeared by rest and same subjective symptom repeated in following five days. Three and a half months after the injury the patient found sensation loss in the right foot and gait distrubance appeared. After the sensory impairment extended to the cervical level which was accompanied by left hemiparesis. On examination, the patient was found to have merked weakness of left limbs, spastic gait and severe impairment of touchpain- and thermosensation below the fifth cervical level but deep sensation was preserved. All tendon reflexes showed marked exaggeration and pathological reflexes were proved. Roentgenograms of the cervical spine revealed a long triangular glass fragment which had been retained in the spinal canal between the first and second cervical vertebrae. The air myelogram suggested the glass fragment had transfixed the cervical spinal cord. Laminectomy was performed and the glass fragment which had a shape of a sharp pointed surgical knife was removed by gentle move in the opposite direction of invation. Following removal of the foreign body, the patient's left hemiparesis recovered to normal state at four months after the operation and right sensory impairment also improved. The cervical spinal cord may be injured in the following way: the right lateral spinothalamic tract may be injured by the skewer injury due to glass fragment but injury of the left same tract may be avoided because of oblique direction of penetration of the glass fragment in the spinal cord. On the other hand, the left pyramidal tract may be compressed by glass fragment and not injured, because left hemiparesis recovered very well postoperatively.

Accidents, Home↗
PubMed1989

Motor hemiplegia and the cerebral organization of movement in man. II. The myth of the human extrapyramidal system.

Following a brief review of the concept of extrapyramidal system, clinical and anatomic evidence is presented against its relative prominence in man. It is proposed that the greatest part of those structures traditionally labeled as extrapyramidal effects its respective functional activities by way of the pyramidal tracts themselves. Such structures, centered around the basal nuclei, the cerebellum and possibly, the limbic areas of the prosencephalon are, according to the present suggestion, indeed, pre pyramidal. This model is based upon the clinical analysis of patients and agrees with more than one century of anatomic verifications in human brains, favoring the notion of the singularity of the human brain.

Extrapyramidal Tracts↗
PubMed1998

[Ipsilateral central-type facial palsy and contralateral hemiparesis associated with unilateral medial medullary infarction: a case report].

Clinical pictures of medial medullary syndrome are variable, depending upon the extent of the lesion. Facial palsy has rarely been observed even in medullary infarction. However, central-type facial palsy is usually found contralaterally to the infarct area at the level of the rostral medulla. In the present report, we discuss the pathogenesis of the neurological manifestations in a 57-year-old man with hypertension. The patient presented with mild left facial palsy of central type, right hemiparesis, paresthesia, with deep sensory disturbance of the right extremities. An MRI of the brain showed an infarction localized in the medial region of the left upper medulla. Although the exact course of the supranuclear facial pathways remains controversial, the ipsilateral central facial palsy in this patient is considered to have two possible causes: the interruption of aberrant fibers of the corticobulbar tract, which branch off and swing back at the level of the upper-middle medulla, or the disruption of recurrent ascending fibers from the contralateral pyramidal tract, through decussation.

Cerebral Infarction↗
PubMed1988

Morphology of neurons in area 4 gamma of the cat's cortex studied with intracellular injection of HRP [corrected and issued with original paging in J Comp Neurol 1988 Nov 8;277(2)].

Neurons in laminae II, III, V, and VI of area 4 gamma of the cat motor cortex were studied following intracellular penetration with an HRP-filled micro-electrode. Antidromic and synaptic responses produced by stimulation of the cerebral peduncles and/or of the ventrolateral nucleus of the thalamus were investigated. Horseradish peroxidase was then iontophoresed into the same neurons to allow examination of their detailed morphology. The morphology of pyramidal neurons whose somata were located in a particular lamina was similar but differed from that of pyramidal neurons in other laminae. The modified pyramidal neurons of lamina II had a truncated apical dendrite or did not possess an obvious apical dendrite, even though the ascending dendritic branches were longer and more extensive than the "basal" branches. As was the case for the pyramidal cells in other laminae, the axons of these lamina II modified pyramidal cells descended toward the white matter; their somata were generally pyramidal in shape, and their dendrites were spiny. All pyramidal neurons except some of lamina VI had ascending dendrites which terminated in a tuft in lamina I, subpially. No intracortical collaterals were seen originating from the axons of lamina II or of lamina VI pyramidal neurons. Lamina III pyramidal neurons had extensive short and long axon collaterals which contributed synaptic boutons to all laminae of the cortex. Pyramidal neurons of lamina V had fewer axon collaterals whose synaptic boutons were restricted to laminae V and VI. All somata of pyramidal tract neurons (PRNs), identified by antidromic responses from peduncular stimulation, were located in lamina V, except for one which was located in lamina VI. Recurrent collaterals of pyramidal neurons were activated by peduncular stimulation. Recurrent excitatory postsynaptic potentials (epsps) could be evoked in fast PTNs, slow PTNs, other pyramidal neurons of lamina V, and pyramidal neurons of lamina VI at latencies between 1.3 and 6.25 msec. In some slow PTNs, a recurrent inhibitory postsynaptic potential of long duration was the predominant response. Stimulation of the ventrolateral nucleus of the thalamus resulted in epsps in pyramidal neurons of lamina III, V, and VI at latencies between 1.0 and 5.0 msec.

Animals↗