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PubMed2002

Autosomal dominant palatal myoclonus and spinal cord atrophy.

We report a new family with palatal myoclonus, pyramidal tract signs, cerebellar signs, marked atrophy of the medulla oblongata and spinal cord, and autosomal dominant inheritance. These findings were almost identical with those in patients previously reported to have histopathologically confirmed adult-onset Alexander disease. Recently, heterozygous point mutations in the coding region of glial fibrillary acidic protein (GFAP) in patients with an infantile form of Alexander disease have been reported. We found a new heterozygous amino acid substitution, Val87Gly in exon 1 of GFAP, in the affected individuals in this family but not in 100 spinocerebellar ataxia (SCA) patients and 100 controls. Therefore, this family might have new clinical entities related to adult-onset Alexander disease and GFAP mutation.

Amino Acid Substitution↗

PubMed1999

Sporadic amyotrophic lateral sclerosis of long duration mimicking spinal progressive muscular atrophy: a clinicopathological study.

We report an autopsy case of amyotrophic lateral sclerosis (ALS) clinically diagnosed as spinal progressive muscular atrophy (SPMA). The patient was a Japanese woman without hereditary burden. She developed muscle weakness of the distal part of the left lower extremity at age 42, followed by muscle weakness and atrophy of the right lower extremity and upper extremities. At age 57, she needed transient ventilatory support. Slight weakness in the facial muscles and fasciculation of the tongue appeared at age 60. At age 61, she died of sudden respiratory arrest. During the clinical course, neurological examination revealed neither Babinski signs nor hyperreflexia. The neuropathological examination revealed not only neuronal loss with gliosis in the facial nucleus, hypoglossal nucleus, and anterior horns of the spinal cord, but also loss of Betz cells and degeneration of the pyramidal tracts. Based on these clinicopathological findings and review of literature, we conclude that sporadic ALS mimicking SPMA is present.

Amyotrophic Lateral Sclerosis↗

PubMed1976

The syndrome of detrusor-sphincter dyssynergia.

The syndrome of detrusor-sphincter dyssynergia is described in a series of patients with a variety of neurological diseases. Bladder function studies using cystometry, sphincter electromyography and electromyelography revealed that sphincter dyssynergia may be associated with detrusor hyperreflexia as well as detrusor areflexia. Impaired function of the pyramidal tracts was documented in all patients and the majority showed impaired segmental innervation of the bladder and urethra.

Adolescent↗

PubMed2003

Coordination of fingertip forces during precision grasping in multiple system atrophy.

While the pathology and autonomic nervous system components of multiple system atrophy (MSA) have been well described, little is known about the associated motor dysfunction. One prominent feature of MSA is parkinsonism, although ataxias and pyramidal tract signs are frequently present. To investigate the nature of motor deficits in MSA, a natural grip-lift movement requiring a precision grasp was used to examine force coordination. Subjects were asked to grasp an instrumented object using the fingertips of the thumb and index finger and lift it 10 cm above the table surface. Subjects with MSA demonstrated a prolonged duration between object contact and initiation of the lifting drive that increased with the weight of the object. During this period these subjects produced large grasping forces generating a significant portion of the eventual grip force employed to hold the object. In contrast, control subjects generated grip and load forces in parallel after establishing contact with the object. Therefore, subjects with MSA showed a disrupted performance on both the sequential (grasp, then lift) and simultaneous (grip and load force development) portions of this task. Only after initiation of the vertical lifting drive did subjects with MSA generate forces in a similar manner to control subjects. These findings demonstrate that subjects with MSA exhibit a disrupted coordination of grasp and could suggest a general deficit in motor control resulting from multi-focal neural degeneration.

Adaptation, Physiological↗

PubMed2003

Independent digit movements and precision grip patterns in 1-5-month-old human infants: hand-babbling, including vacuous then self-directed hand and digit movements, precedes targeted reaching.

Previous work has described human reflexive grasp patterns in early infancy and visually guided reaching and grasping in late infancy. There has been no examination of hand movements in the intervening period. This was the purpose of the present study. We video recorded the spontaneous hand and digit movements made by alert infants over their first 5 months of age. Over this period, spontaneous hand and digit movements developed from fists to almost continuous, vacuous movements and then to self-directed grasping movements. Amongst the many hand and digit movements observed, four grasping patterns emerged during this period: fists, pre-precision grips associated with numerous digit postures, precision grips including the pincer grasp, and self-directed grasps. The finding that a wide range of independent digit movements and grasp patterns are displayed spontaneously by infants within their first 5 months of age is discussed in relation to the development of the motor system, including the suggestion that direct connections of the pyramidal tract are functional relatively early in infancy. It is also suggested that hand babbling, consisting of first vacuous and then self-directed movements, is preparatory to targeted reaching.

Aging↗

PubMed2004

[Multiple sclerosis associated with neurofibromatosis type I].

Association between neurofibromatosis type 1 (NF-1) and multiple sclerosis (MS) has been very rarely described. We report the case of a 40-year-old woman presenting familial NF-1 who had café au lait spots and cutaneous neurofibromatosis since childhood. Five years earlier, she experienced a first episode of unilateral optic neuritis, recurrent sensory and motor disturbances, then gait ataxia and pyramidal tract dysfunction with progressive walking impairment. Altered evoked potentials, CSF analysis and cerebral MRI findings were consistent with the diagnosis of MS (secondary progressive form after relapsing-remitting phase). We review major demographic, clinical and laboratory data of MS associated with NF-1 and discuss about the potential pathophisiological mechanisms implied.

Adult↗

PubMed2005

[Aicardi-Goutieres syndrome: an oft unrecognised familial early-onset encephalopathy].

INTRODUCTION: Aicardi-Goutieres syndrome, first described in 1984, is a progressive infantile familial encephalopathy featuring cerebral calcifications, mainly of the basal ganglia, cerebral white matter abnormalities and cerebrospinal fluid lymphocytosis. Most of the patients present with severe developmental retardation, microcephaly, abnormal eye movements, pyramidal tract signs, and prominent dystonic movements. An elevated level of interferon-alpha in the CSF is a constant feature, particularly during the first stages of the disease course. One locus has been mapped on chromosome 3p21 in about half of the families so far studied. PATIENTS: and results. We report two new French cases and discuss the limits of the clinical syndrome, the differential diagnosis and issues raised by the pathophysiological mechanisms involved. The major concern is to separate this condition from intrauterine infections because of the genetic and therapeutic consequences. A number of other questions remain unanswered. For example, we still do not know today at what age the absence of features like CSF lymphocytosis, and possibly absence of calcifications, rules out the diagnosis of the condition. The origin of the vasculitis lesions is not known, but seems to be related to dysregulation of interferon production and secretion. CONCLUSION: Currently about 75 patients have been reported, even though many more probably exist. The study of this syndrome can contribute to the understanding of some mechanisms of CNS calcification and in a broader perspective to that of chronic encephalopathies with dysregulation of immune mechanisms.

Age of Onset↗

PubMed1989

What is the role of the supplementary motor area in movement initiation?

The hierarchical position of the supplementary motor area (SMA) relative to the primary motor cortex is discussed on the basis of neurological observations and of animal experiments. In the last 10 years evidence has accumulated, especially from studies on the human brain, that the supplementary motor area is a hierarchically superior structure involved in the processes of movement initiation. Single unit studies in subhuman primates also revealed neuronal populations related to aspects of movement preparation rather than to the movement per se. However, we report that a surprisingly large subpopulation of SMA neurones has features classically found in the primary motor cortex (MI). These MI-like neurones precede movement onset by a relatively short interval. The occurrence of such "short-lead neurones" was somewhat higher in MI, but the histograms of lead-times were completely overlapping in the two areas. Taken together with the fact that the SMA is microexcitable and is part of the origin of the pyramidal tract, these findings suggest that the SMA functions also in parallel with MI as concluded by Woolsey and coworkers (1952). Finally, the SMA and MI are reciprocally interconnected, a situation which is not unlike that of the cortical visual areas.

Animals↗

PubMed1982

Basilar impression and platybasia in osteogenesis imperfecta tarda.

Osteogenesis imperfecta, a rare, genetically transmitted disorder of bone, is known to be associated with the development of basilar impression and platybasia. These deformities of the base of the skull may cause neurosurgical abnormalities secondary to compression of the brainstem and hydrocephalus. The case is presented of a young boy with a family history of osteogenesis imperfecta tarda who suffered respiratory arrest during hospitalization. Cranial nerves and pyramidal tract signs were demonstrated. Roentgenograms showed severe basilar impression and hydrocephalus. Decompression of the brainstem and shunting were performed with improvement in the patient's neurological status. This case represents a rare by significant central nervous system complication of osteogenesis imperfecta. Early recognition and implementation of aggressive treatment are important if irreversible neurological deficits are to be avoided.

Adolescent↗

PubMed1982

Scope of a technique for electrical stimulation of human brain, spinal cord, and muscle.

Brief high-voltage electrical shocks from a special low-output-resistance stimulator, delivered through electrodes on the skin, can excite human muscle directly (not by way of the nerves) and can also excite the motor cortex, the visual cortex, and the spinal cord. Possible applications of the technique include measurement in muscle disorders of the latency relaxation and of the excitability and contractility of muscle without the interposition of nerve fibres or the neuromuscular junction; measurement of conduction velocity in the pyramidal tract; and the detection of neuropathy in the nerves to the external sphincter ani.

Action Potentials↗

PubMed1986

Lathyrism: evidence for role of the neuroexcitatory aminoacid BOAA.

Lathyrism, a form of motoneuron disease induced by excessive consumption of th legume Lathyrus sativus (chickling pea), presents as signs of pyramidal tract involvement. Primate feeding studies show that beta-N-oxalylamino-L-alanine (BOAA), a potent neuroexcitatory aminoacid in the chickling pea, induces corticospinal dysfunction similar to that seen in animals consuming a fortified diet of this legume. BOAA, a potent agonist of the excitatory neurotransmitter glutamate, is likely to be causally associated with lathyrism in man.

Adolescent↗

PubMed2002

Prognosis of ischemic internuclear ophthalmoplegia.

OBJECTIVES: To determine the prognosis of internuclear ophthalmoplegia (INO) caused by infarction. DESIGN: Multicenter, retrospective observational case series. PARTICIPANTS: Thirty three patients with ischemic-related INO. METHODS: Chart review of clinical details. MAIN OUTCOME MEASURE: Resolution of diplopia in primary position. RESULTS: Of the group, 78.8% demonstrated resolution of diplopia in primary position with an average time to resolution of 2.25 months. The presence of associated neurologic symptoms (vertigo, ataxia, dysarthria, facial palsy, pyramidal tract signs) correlated with a worse prognosis for resolution of diplopia. When performed magnetic resonance imaging (MRI) demonstrated the causative infarct in only 52% of cases; the presence of an MRI-demonstrable lesion was not significantly associated with prognosis for resolution. CONCLUSIONS: Similar to ischemic ocular motor palsies, most ischemic-based INO become asymptomatic in primary position over 2 to 3 months. The presence of associated features correlated with persistent diplopia. MRI has limited yield in demonstrating the causative infarct.

Aged↗

PubMed2001

Improving axonal growth and functional recovery after experimental spinal cord injury by neutralizing myelin associated inhibitors.

Injuries of the spinal cord often result in an irretrievable loss of motor and sensory functions of all body parts situated below the lesion site. Functional recovery is restricted mainly due to the limited regeneration and plasticity of injured axons in the adult central nervous system. Over the last few years different experimental approaches have led to axonal growth and functional benefits in animal models. This review focuses on the effects of the neutralization of myelin-associated neurite growth inhibitors, in particular Nogo-A, using the monoclonal antibody IN-1. Acute mAb IN-1 treatment of adult CNS lesioned rats results in extensive plastic changes of neuronal connections and regenerative fiber growth. In two different lesion paradigms (i.e. pyramidal tract lesion and incomplete spinal cord lesion in adult rats), the mAb IN-1-treated animals always showed a higher degree of recovery in various behavioral tests. These observations, together with electrophysiological results, suggest that neuronal CNS circuits of mAb IN-1-treated animals can be rearranged, and that sprouting and regenerating axons form functionally meaningful connections.

Animals↗

PubMed1999

Multiple single unit recording in the cortex of monkeys using independently moveable microelectrodes.

Simultaneous recording from multiple single neurones presents many technical difficulties. However, obtaining such data has many advantages, which make it highly worthwhile to overcome the technical problems. This report describes methods which we have developed to permit recordings in awake behaving monkeys using the 'Eckhorn' 16 electrode microdrive. Structural magnetic resonance images are collected to guide electrode placement. Head fixation is achieved using a specially designed headpiece, modified for the multiple electrode approach, and access to the cortex is provided via a novel recording chamber. Growth of scar tissue over the exposed dura mater is reduced using an anti-mitotic compound. Control of the microdrive is achieved by a computerised system which permits several experimenters to move different electrodes simultaneously, considerably reducing the load on an individual operator. Neurones are identified as pyramidal tract neurones by antidromic stimulation through chronically implanted electrodes; stimulus control is integrated into the computerised system. Finally, analysis of multiple single unit recordings requires accurate methods to correct for non-stationarity in unit firing. A novel technique for such correction is discussed.

Animals↗

PubMed1999

Neurological correlates of depressive symptoms in Alzheimer's disease and vascular dementia.

BACKGROUND: Organic brain disease such as dementia or stroke is associated with depression. In dementia, depressive symptoms are common where there is evidence of vascular disease and in Alzheimer's disease they often coexist with extrapyramidal signs. METHOD: In a study of 60 patients with Alzheimer's disease and 39 patients with vascular dementia, depressive symptoms were rated using the Cornell Scale for Depression in Dementia. Neurological signs were assessed and severity of cognitive impairment was measured with the Mini-Mental State Examination. RESULTS: Depressive symptoms were more severe in vascular dementia. Pyramidal tract signs had no relationship to depression in either type of dementia. In vascular dementia, extrapyramidal and grasp reflexes were strongly related to the severity of depression, and were associated with neurovegetative features. In Alzheimer's disease, extrapyramidal signs were the strongest independent predictor of the severity of depression. CONCLUSION: Depressive symptoms are more severe in vascular dementia compared to Alzheimer's disease and were related to neurological abnormalities.

Aged↗

PubMed1997

Immunohistochemical localization of type-II (AT2) angiotensin receptors with a polyclonal antibody against a peptide from the C-terminal tail.

A polyclonal antibody has been prepared against a synthetic peptide derived from the C-terminal tail of the cloned rat AT2 angiotensin receptor, corresponding to amino acid residue 341-351. The antibody was of high titer and displayed monospecific activity toward the synthetic peptide in the ELISA assay. Western blot analysis indicated that the antiserum recognised only a single protein band with a mean apparent molecular mass of 75.4 kDa in the rat adrenals. Immunohistochemical studies with affinity purified antibody localised immunoreactive AT2 angiotensin receptor in medulla cells of the adrenals. Immunoreactivity was also observed in pyramidal tract, but no specific immunoreactivity can be detected in regions of rat brain that are known to express AT2 angiotensin receptors, including inferior olive, locus coeruleus and cerebellum.

Adrenal Glands↗

PubMed1996

GABAergic characteristics of transcallosal activity of cat motor cortical neurons.

GABAergic characteristics of transcallosal activity of cat pyramidal tract neurons (PTNs) and non-PTNs (nPTNs) were studied with stressing on GABAB receptors. PTNs and nPTNs were further classified into group 1 (< 10 ms) and group 2 (> 10 ms) based on the latency upon transcallosal stimulation. However, mainly the results of group 1 neurons were presented here, due to the small number of group 2 neurons. GABA, bicuculline, CGP 35348 and phaclofen were iontophoretically applied. The spike number to 20 trials of transcallosal stimulation was 8.9 +/- 4.3 (mean +/- S.D.) for group 1 PTNs (n = 14) and 10.4 +/- 4.5 for group 1 nPTNs (n = 38) under the control conditions. CGP 35348, phaclofen and bicuculline significantly increased the spike numbers in both cases. The increase was greater for nPTNs than for PTNs. GABA decreased them. The transcallosal latency was 3.9 +/- 1.1 ms for PTNs under the control conditions. CGP 35348, phaclofen and bicuculline significantly shortened the latency, and GABA elongated it. The transcallosal latency for nPTNs under the control conditions was 2.7 +/- 1.2 ms. This was significantly shortened by application of CGP 35348, phaclofen or bicuculline. GABA restored it. In conclusion, CGP 35348, phaclofen and bicuculline increased spike discharge and shortened the latency upon transcallosal stimulation for both group 1 PTNs and nPTNs.

Animals↗

PubMed1998

Neural repair of the injured spinal cord by grafting: comparison between peripheral nerve segments and embryonic homologous structures as a conduit of CNS axons.

To study the differences between peripheral nerve (PN) and embryonic homologous CNS structures as a conduit for CNS axons, spinal cord segments in neonatal rats were removed at the mid-thoracic level and PN or embryonic spinal cord (ESC) segments were grafted into the vacancy. Neural connections across the graft were examined by the anterograde and retrograde tracing methods. Anterogradely labeled pyramidal tract fibers entered the PN segment meanderingly and were dispersed; most stopped at the caudal end of the graft. Although a small fraction of fibers re-entered the host spinal cord, they terminated near the graft-host interface without further extension. By contrast, similarly labeled fibers entering the ESC segments crossed the graft and extended further to reach the lumbar segments. The fibers were defasciculated in the graft but became fasciculated and oriented dorsally near the caudal end of the graft, and descended in the normal path. Consistent with these findings, the retrograde tracing study revealed that in animals with ESC segment grafts but not in those with PN segment grafts, many neurons in the upper brain structures were labeled with Fast Blue that was injected into the lumbar enlargement. The difference between the two kinds of graft as a conduit for CNS axons is likely to be due to differences in matching growing axons and their guidance cues through the graft-host interface.

Animals↗