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PubMed1977

Effects of voluntary isometric and isotonic activity on late transcortical reflex components in normal subjects and hemiparetic patients.

When the median nerve is stimulated at the wrist during voluntary contraction of m. abductor pollicis brevis (APB) EMG activity of this muscle contains different distinct responses: a direct muscular response (M response), a spinal reflex response (S response) and a third late reflex response, first described by Upton et al. (1971) as a second volitional reflex response (V2). Comparison of this very likely long-loop reflex involving pathways to and from the cortical level (therefore labelled C response) under isometric (hold) and isotonic (move) contraction revealed a strong facilitation of the response under the latter condition. Repetitive trains of stimuli had stronger facilitatory effect on the occurrence of this late reflex response than single stimuli. Cutaneous stimuli of the median nerve afferents did not exhibit M and S responses but definite late excitatory responses with similar latencies to the C responses. In cases of hemiparesis (mild to severe loss of sensorimotor control of finger movements) the C response was diminished, delayed or absent. These findings together with recent primate and human experimental work support the hypothesis of a transcortical stretch reflex. On the premise that muscular as well as cutaneous afferents contribute to the afferent cortical input the late C response can be interpreted as the efferent component. The C response may be a valuable aid in the diagnosis of small lesions of the sensorimotor cortex and internal capsule.

Adult↗

PubMed1985

Medium- and long-latency responses to displacements of the ankle joint in patients with spinal and central lesions.

In order to elucidate further the possible pathways and the functional significance of long-loop reflexes we recorded short-, medium- and long-latency responses from leg muscles in 27 patients with spinal lesions, 20 patients with central lesions of the internal capsule or cerebral hemisphere, and in 18 control patients with frontal or occipital lesions without motor or sensory disturbances. Our normal population included 50 subjects, who were age and sex matched to the patients. The mean latency of the long-latency response (LL) in the anterior tibial muscle was significantly delayed in patients with spinal (164.5 msec) and central lesions (145.1 msec) compared to control patients (123.5 msec) and the normals (125.3 msec). This delay of LL could be observed in patients who exhibited only motor or sensory disturbances or a combination of both. The medium-latency response (ML) was absent in 47% of the records in patients with spinal lesions, mainly on the side which was clinically more affected. Its latency was normal if the response occurred. The integral of the LL response was enlarged in patients with spinal or central lesions, but was also enlarged in the control group. The results indicate that the ML response is segmental, but that its amplitude is modulated by supraspinal structures. The LL response probably corresponds to a transcortical 'reflex.'

Ankle Joint↗

PubMed1988

Changes in pyramidal tract conduction with experimental brain-stem ischaemia in the monkey.

The effect of graded ischaemia on intracranial nerve fibre conduction has not previously been studied quantitatively. We measured pyramidal tract (PT) discharges evoked by electrical stimulation of the ipsilateral motor cortex, together with local blood flow (by hydrogen clearance), in the internal capsule and ventral pons of baboons anaesthetised with alpha-chloralose. Changes in conduction time and amplitude of the motor volley were monitored over this PT segment as it was subjected to progressive ischaemia in controlled stages. Conduction time increased significantly, with attenuation of the volley, at average brain-stem tissue flows below 30 ml/100 g/min. Using paired stimuli, we demonstrated relative refractory and supernormal characteristics of PT conduction. In mild ischaemia, the conduction time of the test response decreased, much more than with single stimulation, and in denser ischaemia it increased, relatively more so at smaller inter-stimulus intervals. The data demonstrate the impairment of conduction in a population of CNS axons with reduced local blood flow and indicate that the transmission of relatively rapid sequences of impulses would be the first aspect of conduction to suffer in ischaemia prior to conduction block.

Animals↗

PubMed1987

A model of embolic cerebral ischemia in the rat.

Experimental studies of embolic cerebral ischemia using the rat are limited by variability in the location, size, and frequency of lesions produced. A technique is described herein which improves the reliability of an established model. Eight male Sprague-Dawley rats underwent injection of the cervical internal carotid artery with 0.1 ml of 1-h-old fragmented autologous blood clot through an external carotid artery cannula. The pterygopalatine artery was ligated prior to embolization. At killing 2 h after embolization, clot was observed in the proximal middle cerebral and posterior cerebral arteries in all animals. Areas of reduced blood flow at 2 h postembolization were assessed by digital image processing of iodo-[14C]antipyrine autoradiographic images. No-flow and low-flow areas were measured for each of approximately 25 serial brain sections with a computerized bit-pad. Volumes were calculated and lesions localized by anatomical reconstructions. No animal sustained a hemorrhagic lesion. One animal sustained only a very small area of ischemia in the internal capsule. Of the remaining seven, all had large regions of ischemia in the middle cerebral distribution involving cortex and basal ganglia. Posterior cerebral involvement was observed in six of the seven animals as well. The contralateral hemisphere was unaffected. Volume values could be calculated for primary vascular distributions. Most variability occurred in the pattern of posterior cerebral involvement. The technique described produces a relatively consistent region of ischemia in the middle and posterior cerebral artery distributions in the rat and is a useful model for the study of cerebral ischemia.

Animals↗

PubMed1990

Horizontal compartmentation in the germinal matrices and intermediate zone of the embryonic rat cerebral cortex.

Cellular compartmentation was studied in the germinal matrices and the intermediate zone of the cerebral cortex of rat embryos that survived for 1 or more days after injection with [3H]thymidine. In contrast to the vertical compartmentation seen in the neuroepithelium with short-survival thymidine autoradiography, sequential-survival autoradiography revealed a horizontal compartmentation both in the germinal matrices and the intermediate zone. In the neuroepithelium of embryos that survived for 24 h, the differentially labeled cells form two distinct horizontal bands. The band overlapping with the mitotic zone is composed of heavily labeled cells, whereas the band overlapping with the synthetic zone is composed of lightly labeled cells. This indicates that there are two proliferative cell populations within the neuroepithelium, one turning over fast and the other more slowly. In the cortical intermediate zone of the same embryos several horizontal bands are present. Of these, the dispositions of two bands of heavily labeled cells--the superior band and the inferior band--were followed for several days. The superior band is apparently composed of glial cells that disperse in the direction of the internal capsule and the corpus callosum. In contrast, the inferior band (which overlaps with the subventricular zone where many cells are horizontally oriented) is apparently composed of sojourning young neurons. The cells of the inferior band resume their migration toward the cortical plate after a pause of 1-2 days. These observations call for a reappraisal of the view that young cortical neurons follow a direct radial path to the cortical plate.

Animals↗

PubMed1992

Is there capacity for anatomical and functional repair in the adult somatosensory thalamus?

The capacity for structural and functional remodeling in damaged adult CNS sensory systems can be studied by replacement of neurons in damaged structures by fetal cells from these anatomical origins. For integration to take place, the replacement paradigm assumes that (a) reconnection of adult host afferent fibers onto developing neurons is possible and (b) that the correct molecular signals exist also in the adult brain for fetal neurons to extend axons and pattern synaptic contacts. We have tried to answer some of these fundamental questions by using neuronal depletion models followed by neuronal replacement in the adult rat CNS (Isacson et al. 1984. Nature (London) 311: 458-460; Isacson et al. 1988. Prog. Brain Res. 78: 13-27; Nothias et al. 1988. Brain Res. 461: 349-354; Peschanski and Isacson. 1988. J. Comp. Neurol. 274: 449-463; Sofroniew et al. 1990. Prog. Brain Res. 82: 313-320). In one such model, kainic acid infusions deplete the ventrobasal complex (VB) of all neurons projecting to the somatosensory cortex, while afferent axons from the lemniscal and monoaminergic systems remain in the area. Direct implantation of fetal neurons (gestation age 15-16) of ventrobasal destination allows reconnection of circuitry to take place at the thalamic level, as studied by anatomical tracers, electron microscopy, and functional 2-deoxyglucose studies, while fetal thalamic VB neurons appear less likely to grow through the internal capsule toward the cortical level.

Aging↗

PubMed1995

CNS distribution and overexpression of neurofilament light proteins (NF-L) in mice transgenic for the human NF-L: aberrant accumulation in thalamic perikarya.

Light microscopic immunocytochemistry with monoclonal antibodies recognizing both murine and human light neurofilament proteins (mNF-L and hNF-L) or hNF-L only was used to examine the distribution of NF-L in the CNS of adult mice, normal or transgenic for the human gene. In normal mice, major fiber bundles were immunoreactive to the first antibody, with few exceptions such as the internal capsule, anterior commissure, and corpus callosum. Strong immunoreactivity was also present in the perikarya of motoneurons in the spinal cord and brainstem, as well as in other brainstem nuclei. Faint cell body staining was visible in layers II, III, and V of the parietal cortex and layers V and VI of the retrosplenial cingulate cortex. In transgenic mice, all forebrain as well as brainstem fiber tracts were intensely immunoreactive to both antibodies. Cell body staining was more intense than in normal mouse and involved additional forebrain and brainstem regions, including extended areas of cerebral cortex. Abnormal cell body labeling was particularly striking in several thalamic nuclei, where numerous darkly stained perikarya were considerably enlarged by accumulated immunoreactive material and exhibited eccentric and fragmented nuclei. At the electron microscopic level, these perikarya were filled with disarrayed filaments displacing all other organelles against the cytoplasmic membrane. Such aberrant accumulation of NF-L was presumably the result of an overexpression in selective subpopulations of CNS neurons. It was compatible with prolonged survival of the animal and could provide a new experimental model of neurodegenerative disease.

Animals↗

PubMed1983

The significance of somatosensory evoked potentials for localization of unilateral lesions within the cerebral hemispheres.

Thirty patients with unilateral lesions of the cerebral hemisphere and clinical signs of an affected somatosensory system (mainly disturbances of kinesthesia and stereoesthesia) were investigated. SEP recordings were abnormal in 27. The degree of sensory loss (especially kinesthesia) correlated well with the SEP abnormalities in 26. These SEP abnormalities could be segregated into 4 groups (types 1-4). A type 1 SEP with pathological evoked potentials from P15 on (but a normal P13/14 complex with ear- or extracephalic reference recordings) correlated with lesions of the thalamus, the internal capsule, and the centrum semiovale. A type 2 SEP characterized by loss or severe attenuation of N20 and the following components was found in patients with lesions of the postcentral gyrus. A variant (type 2a) showed isolated loss of N20, but preserved subsequent components and may be due to lesions restricted to area 3b. A third pattern of SEP abnormality is characterized by a preserved primary cortical response and loss of all the subsequent potentials. It is assumed to correlate with lesions of the parietal association cortex. In only 1 case was a type 4 SEP found, with pathological features from N3 (N55) on, caused by an ischemic stroke in area 39. Loss of all evoked responses after P13/14, including P15, suggests a lesion between thalamus and centrum semiovale. Lesions located close to the postcentral cortex lead to a loss of N20 and a variable cut off of the rising negativity following P15. Preservation of the primary cortical complex and distortion or loss of the later components point to a parietal lesion. Severe disturbances of kinesthesia and stereognosia in patients with a normal primary cortical complex and isolated abnormality of the following potentials suggests that the adjacent association cortex may be important for the perception of this complex somatosensory information. Thus the neuronal activity underlying the primary cortical response does not suffice for perception of motion and for stereoesthesia.

Adult↗

PubMed1986

Selective suppression of neurofilament antigen expression in the hypothyroid rat cerebral cortex.

As an integral component of the cytoskeleton neurofilaments play a central role in the establishment and maintenance of neuronal form. In particular, high neurofilament concentrations are characteristic of many classes of axons in the central nervous system. Isolated neurofilaments from rat brain consist of 3 distinct polypeptides with apparent molecular weights 210K, 160K and 68K. A murine monoclonal antibody, mabN210, has been produced which specifically recognizes an epitope associated with the high molecular weight subunit and this antibody has been used to explore the regulation of neurofilament expression during brain development. It has been shown that in the rat cerebellar cortex, the expression of mabN210-immunoreactivity in basket cell axons is severely suppressed in hypothyroidism while neurofilament antigen expression in other cerebellar axons seems not to require thyroid hormones. In view of the well-known cortical deficits in hypothyroidism, these studies have now been extended to include the developing rat cerebral cortex and selected cortical afferent and efferent axons. In hypothyroid rats there is a marked suppression of mabN210-immunoreactivity in the cerebral cortex and corpus callosum and, to a lesser extent, there is a reduction in staining in the internal capsule. By contrast, hypothyroidism did not reduce mabN210-immunoreactivity in the lateral olfactory tract or the stria medullaris. In rats, serum thyroid hormone starts to rise to adult levels on postnatal day 4. It appears that axons that have attained their mature distribution prior to the onset of thyroid hormone expression are not affected by hypothyroidism whereas mabN210-immunoreactivity is suppressed in those axonal tracts that reach a mature distribution after P4.

Afferent Pathways↗

PubMed1987

Spongiform encephalopathy with extensive involvement of white matter.

We report a proven case of CJD with prolonged clinical course and white matter involvement which consisted of severe, widespread myelin damage in the forebrain and cerebellum but with sparing of the internal capsule. Histologically, there was status spongiosus of the involved white matter with axonal loss, proliferation of hypertrophic astrocytes and scattered and perivascular foamy macrophages. White matter lesions have not been considered to be a significant feature of CJD. In the last few years, however, a few cases have been described with prominent degeneration of cerebral white matter. We believe that our findings corroborate the existence of an entity that at present may only be defined as spongiform panencephalopathy.

Adult↗

PubMed1987

Neurophysiological analysis of ataxia in capsular ataxic hemiparesis.

A quantitative analysis of ataxia and the readiness potential were studied in four cases of ataxic hemiparesis resulting from a small infarct in the posterior limb of the internal capsule. The ataxia appeared to be the result of involvement of the corticopontine tract originating from the precentral region (areas 4 and 6) at this level. The voluntary movements of the affected limbs were characterized by slowness and irregularity similar to those seen in cerebellar ataxia. The weakness per se was not such that it could account for the ataxia. The dentato-rubro-thalamo-cortical system did not appear to be significantly involved on the basis of normal readiness potentials.

Ataxia↗

PubMed1990

Emotional facial paresis with striatocapsular infarction.

Emotional facial paresis (EFP) refers to hemifacial paresis of emotionally evoked or spontaneous smiling or weeping with preserved volitional movements of the face. The anatomical location for this phenomenon has been controversial. We report a 15-year-old boy with EFP. Follow-up MRI demonstrated infarction limited to the head of the caudate, putamen and anterior limb of the internal capsule on the contralateral side. This case lends support for selective damage at a striatal or capsular site in the production of EFP.

Adolescent↗

PubMed1991

Mitochondrial encephalomyopathies: a correlation between neuropathological findings and defects in mitochondrial DNA.

Neuropathological studies were carried out in two patients with mitochondrial encephalomyopathies in whom the underlying lesions in muscle mitochondrial DNA (mtDNA) and respiratory enzyme complexes have been investigated. The first, a man with Kearns-Sayre syndrome, died at the age of 49 years. Autopsy showed an old parietal lobe infarct, diffuse spongiform leukoencephalopathy of cerebral and cerebellar white matter and mild spongiform change in deep grey matter and brainstem nuclei. Heteroplasmy of skeletal muscle mitochondrial DNA with a 3.5 kb mtDNA deletion in one of two mtDNA populations was found. The second case, a woman, suffering from myoclonic epilepsy, cerebellar ataxia, bilateral sensorineural deafness, several 'stroke-like' episodes died at age 52. At autopsy, an old infarct was seen in the L internal capsule. Severe loss of neurons and gliosis were found in the dentate nuclei, moderate changes in the red nuclei and inferior olivary nuclei and mild changes in the substantial nigra and locus coeruleus. In both patients, skeletal muscle biopsy showed numbers of ragged-red fibres and intramitochondrial paracrystalline inclusions at electron microscopy. A defect in the synthesis of the ND5 subunit of the respiratory complex I was suggested in the second patient in whom a diagnosis of MELAS was made.

Adult↗

PubMed1991

Discrete lesions in the sensorimotor control system. A clinical-topographical study of lacunar infarcts.

In 50 patients with computed tomography-verified small, deep, lacunar, infarcts from a prospective stroke registry, we studied the lesion site in relationship with the clinical syndromes pure motor stroke, sensorimotor stroke and ataxic hemiparesis. Seventy per cent (95% confidence interval: 57-83%) of the lesions were located in the posterior limb of the internal capsule or adjacent paraventricular region, affecting the corticospinal tract in pure motor stroke, as well as the thalamocortical tract in sensorimotor stroke, and the cerebellar (dentato(rubro)thalamocortical and corticopontocerebellar) pathways in ataxic hemiparesis. This most frequently involved area is supplied by the anterior choroidal artery, indicating that this artery is the predominant deep, penetrating artery involved in small vessel disease causing lacunar stroke syndromes.

Aged↗

PubMed1992

Immunohistochemical expression of microtubule-associated protein 5 (MAP5) in glial cells in multiple system atrophy.

An immunohistochemical study focusing on glial cells was performed using monoclonal antibodies against microtubule-associated proteins (MAP1, MAP2 and MAP5), transferrin, leukocyte common antigen (LCA) and glial fibrillary acidic protein (GFAP) in 5 cases of multiple system atrophy (MSA) exhibiting olivopontocerebellar atrophy and striatonigral degeneration. An antibody to MAP5, a fetal antigen in developing brain, was strongly demonstrated in the glial cytoplasmic inclusions (GCIs) which have recently drawn a great deal of attention and were observed in all 5 cases of MSA. Moreover, MAP5-positive glial cells (MAP5-Gs) were present in significantly higher number than in the controls in various regions where GCIs were found, predominantly in putamen, substantia nigra, cerebellar white matter and internal capsule. LCA and transferrin, markers of microglia and oligodendroglia, respectively, were immunohistochemically detected in some MAP5-Gs. GFAP, on the other hand, was not expressed in MAP5-Gs at all. These findings suggest that MAP5-Gs consist of reactive microglia and oligodendroglia. Our study is the first to demonstrate immunohistochemical detection of MAP5 in glial pathological changes in MSA.

Aged↗

PubMed1994

A single report of hemiplegic arm stretching related to yawning: further investigation using apomorphine administration.

We observed a stroke patient with an infarct of the internal capsule interrupting the pyramidal tract who stretched his hemiplegic arm during spontaneous and apomorphine-induced yawning. The putative mechanism by which yawning can induce the paradoxical motor response of the plegic arm in the patient might be the functional efficiency of a pathway projecting directly from the stimulated basal ganglia to lower motor systems in the brainstem.

Apomorphine↗

PubMed1996

Micturitional disturbance after acute hemispheric stroke: analysis of the lesion site by CT and MRI.

Micturitional histories and urodynamic studies were performed in 72 acute hemispheric stroke patients. Within 3 months from the onset, 53% of the patients had urinary symptoms including irritative as well as obstructive, and the most common symptom was nocturnal urinary frequency in 36%, which was followed by urge urinary incontinence in 29% and difficulty of voiding in 25% of the patients. We found a correlation between micturitional disturbance with hemiparesis (p <0.05) and not with hemianopsia (p <0.05). Micturitional disturbance was more common in lesions of the frontal lobe (p <0.05) than in those of the occipital lobe. Brain CT or MRI in symptomatic patients showed lesions of anterior and medial surface of the frontal lobe, anterior edge of the paraventricular white matter, genu of the internal capsule and large lesions of putamen or thalamus. Urodynamic studies of 22 symptomatic patients revealed various findings in 91% of them, including detrusor hyperreflexia in 68%, detrusor-sphincter dyssynergia (DSD) in 14% and uninhibited sphincter relaxation in 36%. Patients with urinary retention had atonic cystometrogram and DSD. Detrusor hyperreflexia was noted in lesions of the frontal lobe as well as the basal ganglia, uninhibited sphincter relaxation in the frontal lobe, and detrusor-sphincter dyssynergia common in the basal ganglia. Above findings seem to indicate that anteromedial frontal lobe and its descending pathway, and the basal ganglia seem to be mainly responsible for supranuclear types of pelvic and pudendal nerve dysfunction in our patients with stroke.

Adult↗

PubMed1996

Bilateral perioral sensory symptom after unilateral stroke: does it have a localizing value?

Bilateral perioral sensory dysfunction due to unilateral cerebral lesion is rare, and has been thought to be caused by midline brainstem lesions. Six patients are described herewith, with bilateral perioral sensory symptoms due to unilateral strokes that do not involve the mid-brainstem region. Brain-computed tomographic scan and magnetic resonance imaging demonstrated unilateral cerebral strokes in the thalamus, posterior limb of the internal capsule, basal ganglia, fronto-parietal cortex and the insular-frontal subcortical area. This observation suggests that bilateral perioral sensory symptoms do not have a localizing value. Possible pathogenetic mechanisms for this sign are discussed.

Aged↗