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PubMed1993

A new inherited prion disease (PrP-P105L mutation) showing spastic paraparesis.

We report the clinicopathological findings of 5 patients with an inherited prion disease with a codon 105 (Pro to Leu) mutation. All of the patients had a spastic gait disturbance and progressive dementia without either cerebellar signs, myoclonus, or periodic synchronous discharges. Autopsy of 3 patients revealed numerous amyloid plaques in the cerebral cortex, especially in the motor cortex and the frontal lobe where neuronal loss and severe gliosis were observed in the absence of spongiform changes. The cerebellum was preserved histologically except for only a few amyloid plaques. The pyramidal tracts in the brainstem and spinal cord showed vacuolated changes and a loss of myelin, but no prion protein accumulations. Thus, the prion protein codon 105 mutation is considered to correspond to a new variant of the Gerstmann-Sträussler syndrome with spastic paraparesis.

Adult↗

PubMed1995

Striatal dopaminergic denervation in pallidopyramidal disease demonstrated by positron emission tomography.

Pallidopyramidal disease is a rare disease of young patients in which they manifest a parkinsonian syndrome and pyramidal signs. Pallidopyramidal disease has been attributed to a degeneration of the pallidum and the pyramidal tract, although only 1 patient has been studied postmortem. In the present report, [18F]fluorodopa positron emission tomography in 2 patients showed a marked dopaminergic denervation of the striatum, suggesting that this disease corresponds more to a nigropallidopyramidal dysfunction.

Adolescent↗

PubMed1997

Friedreich-like ataxia with retinitis pigmentosa caused by the His101Gln mutation of the alpha-tocopherol transfer protein gene.

The alpha-tocopherol transfer protein (alpha-TTP) is a cytosolic liver protein that is presumed to function in the intracellular transport of alpha-tocopherol, the most biologically active form of vitamin E. We studied 4 unrelated patients with autosomal recessive Friedreich-like ataxia who had isolated vitamin E deficiency. A point mutation was identified in all of them at position 101 of the gene for alpha-TTP, where histidine (CAT) was replaced with glutamine (CAG). Three of the 4 patients developed retinitis pigmentosa subsequent to the onset of ataxia. Neurological symptoms included ataxia, dysarthria, hyporeflexia, and decreased proprioceptive and vibratory sensations. Electrophysiological and pathological examinations showed that the cardinal sites affected were the central axons of dorsal root ganglion cells and the retina, with minor involvement of the peripheral sensory nerve, optic nerve, and pyramidal tract. The vitamin E tolerance test performed showed that the absorption of vitamin E was normal but that its decrease from the serum was accelerated. Oral administration of vitamin E appeared to halt the progression of visual and neurological symptoms. We propose a new treatable syndrome of Friedreich-like ataxia and retinitis pigmentosa caused by a defect in the alpha-TTP gene.

Aged↗

PubMed1981

Some effects of protein-calorie undernutrition on the developing central nervous system of the rat.

Some effects of undernutrition were noted in the brains of 21-day-old pups undernourished from birth by being reared by nursing dams fed on a low protein diet. As compared to the normally fed control pups, the body weight, brain weight, and thickness of the parietal neocortex and paravermal cerebellar cortex were significantly lower in the undernourished pups (p less than 0.001), while the thickness of the cortices of the dentate gyrus and hippocampus CA3 only reached significance at the 5% level. Again, as compared to the control pups, the number of spines per unit length on the distal dendritic segments of the pyramidal cells of lamina III of the parietal neocortex and of the hippocampus CA3 reached significance at the 5% level whereas that of the granule cells of dentate gyrus and Purkinje cells of the paravermis did not reach significance at the 5% level. The myelination of the pyramidal tract and spinal trigeminal tract in the lower medulla was less advanced in the undernourished pups. To date, the demonstration of precise functional correlates for the observed changes of morphological and physiological parameters in animals subjected to undernutrition has been elusive. An approach that may lead to unraveling this problem is suggested in a discussion of relating sources of input to the specific dendritic segments where the spine counts were made.

Animals↗

PubMed1978

Atlas of the distribution of monoamine-containing nerve cell bodies in the brain stem of the cat.

The distribution and morphological characteristics of monoamine (MA)-containing neuronal somata in the brain stem of kittens and of adult cats were studied by means of the Falck-Hillarp histofluorescence method. This investigation has shown, among other things, that in the midbrain of the cat the catecholamine (CA) perikarya are chiefly confined to the pars compacta of the substantia nigra, the ventromedial tegmental area, the nucleus linearis rostralis and the nucleus parabrachialis pigmentosus. Numerous CA neurons are also present in the dorsolateral part of the pontine tegmentum but also within the nucleus subcoeruleus, in nuclei lemnisci lateralis dorsalis and in nuclei parabrachialis lateralis and medialis. In the medulla, a few CA neuronal somata are lying near the hypoglossal nucleus whereas a larger number of CA cell bodies occur at the level of nucleus reticularis lateralis and in nucleus paragigantocellularis lateralis. On the other hand, most of the serotonin (5-HT) perikarya are confined to the raphe nuclei of the brain stem: nuclei raphe dorsalis, centralis superior, raphe pontis, raphe magnus, raphe pallidus and raphe obscurus. Some 5-HT neuronal somata are also found lateral to the pyramidal tract and to the inferior olivary complex. The various similarities and differences in respect to the pattern of the topographical distribution of MA neurons in the brain stem of the cat as compared to that of other mammals are discussed.

Animals↗

PubMed1982

Regional (14C) 2-deoxyglucose uptake during vibrissae movements evoked by rat motor cortex stimulation.

Repetitive left mystacial vibrissae movements were produced by electrical stimulation of right motor cortex (MI) were a bipolar electrode in the alert, unanesthetized rat. Regional increases of (14C) 2-deoxyglucose (2DG) uptake were mapped autoradiographically during these left vibrissae movements. Uptake of 2DG increased in a 2-4-mm-diameter area about the stimulating electrode in right MI and in a smaller region in left MI cortex. Columnar increases of 2DG uptake occurred bilaterally in somatosensory cortex in the face region of somatosensory cortex (SI). Bilateral increases of 2DG uptake occurred subcortically in dorsolateral caudate-putamen (CP) and subthalamic nucleus. Primary right-sided increases of 2DG uptake occurred in other basal ganglia structures including dorsal globus pallidus (GP), posterior, entopeduncular nucleus (EPN), ventrolateral substantia nigra pars reticulata (SNr), and anterolateral substantia nigra pars compacta (SNc). Uptake of 2DG increased on the right side of the following thalamic regions: much of the ventrolateral (VL) nucleus, particularly dorsally; the anterodorsal reticular nucleus; dorsolateral posteromedial (POm) nucleus; the ventromedial nucleus; and dorsolateral parafasicular nucleus. The anterior and ventral posterior portions of VL were not activated. Caudal to thalamus right-sided 2DG uptake increased in the medial, ventral, and lateral pontine nuclei, deep layers of superior colliculus, lateral deep mesencephalic nucleus (DMN), and nucleus cuneiformis (NCU). UPtake of 2DG increased in right rostral parvocellular and red nucleus in a few animals. Discrete portions of the right internal capsule and right medial pyramidal tract increased 2DG uptake during MI stimulation. Uptake of 2DG increased on the left side of the brain during right MI stimulation in the left lateral nucleus (NL) of cerebellum and in several discrete regions of left cerebellar hemisphere granule cells including anterior paravermis, lobulus simplex, crus II, and the paramedian lobule. Uptake of 2DG increased in left nucleus of the spinal tract of the trigeminal nerve (ntV) ventrally in subnuclei interpolaris and oralis. Left lateral portions of the facial nucleus were activated in a few animals. The lateral portions of the facial nucleus are known to project to vibrissae musculature. All of the above structures may be involved in the motor-sensory processing responsible for vibrissae movements. Regions not previously suggested to play a major role in vibrissae movements include DMN and NCU. Though NCU has been called the "locomotor center" it may play a role in facial movements as well. Polysynaptic activation of GP, EPN, NL, and cerebellar hemisphere occurred since no connections between MI and these regions exist. A pathway from ntV to POm to MI and SI is suggested to provide proprioceptive input to motor-sensory cortex from the moving vibrissae since neither the principal trigeminal sensory nucleus nor the ventrobasal nucleus of the thalamus increased 2DG uptake during MI stimulation.

Animals↗

PubMed1986

Development of projections from somatic motor-sensory areas of neocortex to the diencephalon and brainstem in the North American opossum.

The development of projections from somatic motor-sensory areas of neocortex to the diencephalon and brainstem was studied by using the orthograde transport of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) in a series of pouch-young opossums. The opossum was chosen for study because it is born in a very immature state, 12 days after conception, and has a protracted postnatal development. Cortical axons form a cerebral peduncle by at least postnatal day (PD) 10, a medullary pyramid by estimated PD (EPD) 17, a pyramidal decussation by EPD 26, and reach the first cervical segment of the spinal cord by EPD 29. Cortical axons innervate diencephalic nuclei and perhaps the substantia nigra by EPD 17, but do not grow into more caudal brainstem nuclei until EPD 26. The first brainstem areas innervated by cortical axons are the mesencephalic and rostral pontine tegmentum and parts of the pontine gray adjacent to the pyramidal tract (EPD 29). By EPD 31, cortical axons project to additional areas of the pontine gray, the gigantocellular reticular formation, the medial accessory olive, and the cuneate nucleus. Cortical innervation of the red nucleus and superior colliculus begins at EPD 31 but is not well developed until EPD 35. Cortical axons do not innervate the parvicellular reticular formation or the sensory trigeminal nuclei until EPD 35. Evidence for transient cerebrocerebellar axons was also found.

Animals↗

PubMed1987

Serotonin- and substance P-containing projections to the nucleus tractus solitarii of the rat.

The objective of the present study was to determine the location of the neurons that give rise to serotonin- and substance P-containing terminals in the nucleus tractus solitarii. This was done by injecting rhodamine-filled latex microspheres into the nucleus tractus solitarii of rats to retrogradely label neuronal cell bodies and by processing sections from the brains of these animals to determine whether the labelled neurons contained serotonin or substance P immunoreactivity. Serotonin-immunoreactive neurons that projected to the nucleus tractus solitarii were found in the nucleus raphe magnus, nucleus raphe obscurus, nucleus raphe pallidus, and in the ventral medulla, lateral to the pyramidal tract. Substance P-immunoreactive neurons that projected to the nucleus tractus solitarii were found in similar areas but were proportionately less numerous in the nucleus raphe magnus and proportionately more numerous in the nucleus raphe pallidus. It is concluded that neurons in the medullary raphe nuclei, some of which presumably utilize serotonin or substance P as a neurotransmitter, could regulate autonomic function via direct projections to the nucleus tractus solitarii.

Afferent Pathways↗

PubMed1990

Calcium-binding proteins, parvalbumin- and calbindin-D 28k-immunoreactive neurons in the rat spinal cord and dorsal root ganglia: a light and electron microscopic study.

The distribution of two calcium-binding proteins, parvalbumin (PV) and calbindin-D 28K (CaBP), was studied by the peroxidase-anti-peroxidase immunohistochemical method at the light and electron microscopic level in the rat spinal cord and dorsal root ganglia. The possible coexistence of these two proteins was also investigated. PV-positive neurons were revealed in all layers of the spinal cord, except lamina I, which was devoid of labelling. Most of the PV-positive cells were found in the inner layer of lamina II, lamina III, internal basilar nucleus, central gray region, and at the dorsomedial and ventromedial aspects of the lateral motor column in the ventral horn. Neuronal processes intensely stained for PV sharply delineated inner lamina II. With the electron microscope most of them appeared to be dendrites, but vesicle containing profiles were also found in a smaller number. CaBP-positive neurons appeared to be dispersed all over the spinal gray matter. The great majority of them were found in laminae I, II, IV; the central gray region; the intermediolateral nucleus; and in the ventral horn just medial to the lateral motor column. Laminae I and II were densely packed with CaBP-positive punctate profiles that proved to be dendrites and axons in the electron microscope. A portion of labelled neurons in lamina IV and on the ventromedial aspect of the lateral motor column in the ventral horn disclosed both PV- and CaBP-immunoreactivity. All of the funiculi of the spinal white matter contained a large number of fibres immunopositive for both PV and CaBP. The highest density of CaBP-positive fibres was found in the dorsolateral funiculus, which was also densely packed with PV-positive fibres. PV-positive fibres were even more numerous in the dorsal part of the dorsal funiculus. The territory of the gracile funiculus in the brachial cord and that of the pyramidal tract in its whole extent were devoid of labelled fibres. In the thoracic cord, the dorsal nucleus of Clarke received a large number of PV-positive fibres. Dorsal root ganglia displayed both PV- and CaBP-immunopositivity. The cell diameter distribution histogram of PV-positive neurons disclosed two peaks--one at 35 microns and the other at 50 microns. CaBP-positive cells in the dorsal root ganglia corresponded to subgroups of small and large neurons with mean diameters of 25 microns and 45 microns, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2006

Coherent corticomuscular oscillations originate from primary motor cortex: evidence from patients with early brain lesions.

Coherent oscillations of neurons in the primary motor cortex (M1) have been shown to be involved in the corticospinal control of muscle activity. This interaction between M1 and muscle can be measured by the analysis of corticomuscular coherence in the beta-frequency range (beta-CMCoh; 14-30 Hz). Largely based on magnetoencephalographic (MEG) source-modeling data, it is widely assumed that beta-CMCoh reflects direct coupling between M1 and muscle. Deafferentation is capable of modulating beta-CMCoh, however, and therefore the influence of reafferent somatosensory signaling and corresponding neuronal activity in the somatosensory cortex (S1) has been unclear. We present transcranial magnetic stimulation (TMS) and MEG data from three adult patients suffering from congenital hemiparesis due to pre- and perinatally acquired lesions of the pyramidal tract. In these patients, interhemispheric reorganization had resulted in relocation of M1 to the contralesional hemisphere, ipsilateral to the paretic hand, whereas S1 had remained in the lesioned hemisphere. This topographic dichotomy allowed for an unequivocal topographic differentiation of M1 and S1 with MEG (which is not possible if M1 and S1 are directly adjacent within one hemisphere). In all patients, beta-CMCoh originated from the contralesional M1, in accordance with the TMS-evoked motor responses, and in contrast to the somatosensory evoked fields (SEFs) for which the sources (N20m) were localized in S1 of the lesioned hemisphere. These data provide direct evidence for the concept that beta-CMCoh reflects the motorcortical efferent drive from M1 to the spinal motoneuron pool and muscle. No evidence was found for a relevant contribution of neuronal activity in S1 to beta-CMCoh.

Adult↗

PubMed2002

Alzheimer's disease with spastic paresis and cotton wool type plaques.

We reviewed Alzheimer's cases with spastic paresis and cotton wool type plaques in five Japanese and nine Caucasian cases. Most were early onset familial Alzheimer's disease with presenilin 1 mutations. The cotton wool type plaques were related to extremely high production of A beta 42, due mainly to presenilin 1 mutations and low immune responses. Cotton wool plaques were numerous in the entire central nervous system, including basal ganglia, brainstem and even in spinal cord. Cotton wool type plaques were composed of slightly electron dense synaptic structures, but amyloid fibrils were rarely found. Such a high accumulation of A beta 42 may cause degeneration of the pyramidal tract and basal ganglia from an early stage of Alzheimer's disease.

Adult↗

PubMed1976

Brachium conjunctivum-red nucleus synaptic system in the baboon.

Electrophysiological properties of the brachium conjunctivum-red nucleus (BC-RN) synaptic system were studied in barbiturate-anesthetized baboon (Papio). Topographic recordings from the mesencephalon demonstrated that most of the BC-evoked activity was restricted to an area histologically identified as red nucleus; however, some brachium-evoked activity was recorded from the surrounding mesencephalic reticular formation. Short latency BC-evoked activity was also recorded from the pons in the region of nucleus reticularis tegmenti pontis. The majority of the BC fibers were found to conduct at a rate of 44 m/sec; a second group of BC fibers with a slower conduction velocity of 23 m/sec was also observed. Brachium-evoked responses recorded from magnocellular and pravicellular RN neurons were short latency responses consistent with monosynaptic activation of these RN neurons by the BC fibers. The BC-RN synaptic system was found to be a very secure synaptic system and could transmit activity at high rates of stimulation with little or no failure. The responsiveness of the BC fibers was found to be similar to that of optic nerve fibers and pyramidal tract fibers, both of which have been characterized as being similar to peripheral A fibers. The responsiveness of the BC-RN synaptic system began to decrease 5 msec after a single or repetitive transmission and was reduced to about 50% of normal responsiveness at 34 msec. This period of reduced postsynaptic responsiveness was associated with a reduction in presynaptic input to RN and suggest that a disfacilitation at the level of the deep cerebellar nuclei may be in part responsible for the subnormal responsiveness of the BC-RN synaptic system.

Animals↗

PubMed1991

Regional variation in the abundance of axonal cytoskeletal proteins.

The relative abundance of several axonal cytoskeletal proteins was determined by immunoassay at various sites in the peripheral and central nervous systems of adult rats. Within the peripheral nervous system, the ratio of tubulin to neurofilaments was greatest for nerves composed of unmyelinated axons and least for nerves with large myelinated axons. MAP1 protein was more prominent in unmyelinated fibers; conversely tau proteins were relatively more abundant in large myelinated axons. An immunochemical index of neurofilament phosphorylation was less for unmyelinated fibers than for myelinated ones. In the fimbria-fornix, pyramidal tract, and superior cerebellar peduncle, similar trends were observed: small axons had more MAP1, less tau, and a greater ratio of tubulin to neurofilament proteins. The phosphorylation index was greatest for the superior cerebellar peduncle, the tract with the largest axons. The immunochemical index of neurofilament phosphorylation was greater for the optic nerve than for axonal tracts in the brain proper. These results suggest that development of large myelinated axons is associated with greater neurofilament content, neurofilament phosphorylation, and with greater abundance of tau proteins in the CNS and the PNS; however, quantitative aspects of these relationships differ in the PNS and the CNS.

Animals↗

PubMed2002

Postoperative management of Vim DBS for tremor.

Stimulation of the ventralis intermedius (Vim) is a treatment of severe tremor from various origins. The adjustment of electrical parameters is done when the lesion-like effects of the implant disappear. Each contact is assessed successively, by using a constant pulse width of 60 microsec and a frequency of 130 Hz or above and progressively increasing the voltage. At the same time, the tremor and possible side effects are monitored. The most frequent side effects are paresthesias, dysarthria, muscle contractions related to stimulation of the pyramidal tract, and cerebellar syndrome. Medications have to be adjusted slowly, and often, particularly in case of Parkinson's disease, it is difficult to decrease the dosage. It is important to teach the patient to switch the stimulator on or off and check that it is working. Patients need to be seen within the 3 months after implant, then occasionally according to the effect. In the long-term, some patients will develop some rebound of tremor when they switch off and/or some tolerance to the effect of the stimulator, which can be difficult to manage. In case of Parkinson's disease, motor fluctuations and dyskinesias, that does not respond to Vim stimulation, can occur.

Antiparkinson Agents↗

PubMed2005

Is sphincter electromyography a helpful investigation in the diagnosis of multiple system atrophy? A retrospective study with pathological diagnosis.

Sphincter electromyography (spEMG) is often used as an ancillary test when multiple system atrophy (MSA) is suspected. Our aim was to determine the clinical features associated with spEMG being performed, the influence of the result on the final clinical diagnosis, and its utility as a clinical investigation. A retrospective audit of all cases in the Queen Square Brain Bank between 1989 and 2002 was performed. The clinical features and diagnostic accuracy were compared between patients in whom spEMG was performed and those in whom it was not. From 845 sets of complete clinical records, we identified 37 (4.4%) cases that had been investigated with spEMG. Thirty of these cases had a pathological diagnosis of MSA. Of these 30, 24 had abnormal spEMGs, 5 had a borderline result, and only 1 had a normal spEMG. Sixty-six cases had pathologically proven MSA but no spEMG. Those investigated with spEMG were younger at disease onset (P < 0.001), more frequently male (P = 0.03), and more likely to have had other investigations performed. They had a greater incidence of pyramidal tract signs at final clinical diagnosis, and the final clinical diagnostic accuracy was higher (P = 0.04). Due to the retrospective nature of the study, balanced populations for calculation of sensitivity and specificity were not available. In this selected series of pathologically confirmed cases, investigation with spEMG was one of several factors associated with improved clinical diagnostic accuracy. A normal spEMG is unlikely in pathologically proven MSA, at least in cases with a mean symptom duration of more than 5 years when the test is performed.

Adult↗

PubMed2006

Behavioral models of Parkinson's disease in rodents: a new look at an old problem.

The circuitry important for voluntary movement is influenced by dopamine from the substantia nigra and regulated by the nigrostriatal system. The basal ganglia influence the pyramidal tract and other motor systems, such as the mesopontine nuclei and the rubrospinal tract. Although the neuroanatomical substrates underlying motor control are similar for humans and rodents, the behavioral repertoire mediated by those circuits is not. The principal aim of this review is to evaluate how injury to dopamine-mediated pathways in rodents gives rise to motor dysfunction that mimics human Parkinsonism. We will examine the behavioral tests in common use with rodent models of Parkinson's disease and critically evaluate the appropriateness of each test for detecting motor impairment. We will show how tests of motor performance must be guided by a thorough understanding of the clinical symptoms accompanying the disease, the circuitry mediating dopamine deficits in rodents, and familiarity with the rodent behavioral repertoire. We will explain how investigations in rodents of skilled forepaw actions, including placing, grooming, or foot faults, have clear correlates in Parkinson's disease, and are, therefore, the most sensitive ways of detecting motor impairment following dopamine loss from the basal ganglia of rodents.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1995

Motor function in a patient with bilateral lesions of the globus pallidus.

This study describes the long-term deficits of a patient who, after a toxic encephalopathy, sustained extensive bilateral damage to both segments of the globus pallidus (GP) and the right substantia nigra (SN). There were no signs of lesions of the pyramidal tracts or of other motor structures. The most obvious deficits were an abnormal gait with an exaggerated knee extension and a tendency to fall slowly, especially when pushed backward. In contrast, Romberg's test on an unstable platform was normal, as were long-latency leg reflexes induced by perturbations. Inadequate anticipatory and compensatory postural responses, in particular across the hip and knee joints, and slow movements seemed responsible for the falls. Muscle tone was normal but reflex studies showed signs of abnormal facilitation and inhibition at various levels of the neuraxis. We conclude that the GP and SN lesions caused defective input to premotor cortical and brain stem target zones. Dysfunctioning of these zones leads to improper control of the descending ventromedial motor system responsible for locomotion, postural control, and reflex status. The deficits in upper extremity motor performance included delayed and slow movements, inaccurate amplitudes of ballistic responses, a lack of predictive control, and deficits in bimanual coordination. Sensory feedback, proprioceptive more than visual, played a powerful compensating role in rapid aiming movements. Regional blood flow (studied using 15(O)2) was reduced in multiple frontal cortical regions, among which are the hand areas of the supplementary and premotor cortex. We hypothesize that this reflected impaired functioning of these areas, caused by defective bilateral output from GP and SN, and resulting in the motor deficits of the arm and hand.

Adult↗

PubMed2006

HIV-1 encephalopathy among perinatally infected children: Neuropathogenesis and response to highly active antiretroviral therapy.

HIV-1 encephalopathy among perinatally infected children in the United States was initially defined by a classic triad of findings that included: (1) developmental delay, (2) secondary or acquired microcephaly, and (3) pyramidal tract neuromotor deficits. The most severe form of this disorder typically occurred among young children who developed rapidly progressive disease in concert with profound immunosuppression, and Pneumocystis jiroveci pneumonitis (PCP). The neuropathogenesis of this disorder appears to involve a cascade of viral products, various cytokines and chemokines, and neurotransmitters which promote ongoing inflammation, excitation, and overstimualtion of the N-methyl-D-aspartate type receptor (NMDAR) system. These subsequently lead to neuronal injury and death secondary to apoptosis or necrosis, astrocytosis, as well as dentritic and synaptic damage. The frequency of the most severe forms of encephalopathy among children has dropped dramatically since the introduction of highly active antiretroviral therapy (HAART). Of concern, however, is the possibility that a more insidious form of this disorder may be occurring presently among older vertically infected children as a result of inadequate penetration of HAART agents into the cerebrospinal fluid (CSF). This paper will review what published data there is as yet that bears on this question.

AIDS Dementia Complex↗