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PubMed1998

[Disturbance of deep sensation in medial medullary syndrome. Topographical localization of medial lemniscus in the medulla oblongata].

Medial medullary infarction is characterized by ipsilateral hypoglossal nerve palsy with contralateral hemiparesis and disturbance of deep and discriminative sensory perception. We examined the extent and distribution of disturbances in deep sensation and compared the findings with the lesion location in the medial lemniscus detected by MRI in 3 patients with medial medullary infarction. We classified the lesion location into 2 groups; type I and type II. Type I was ventral to the middle medial lesion of the medial lemniscus, and type II was ventral to the dorsal medial lesion. In our series, type I (Case 1) impairment of the three kinds of deep sensations was more severe in the lower extremities than in the up-per extremities. In type II (Cases 2, 3) the severity or impairment in the upper extremities was moderate or severe and nearly equal to that in the lower extremities. There was no difference in the severity of impairment for the four kinds of discriminative sensations. In the literature, type I (8 patients) impairment of position sense in deep sensation was found in 1 of 7 patients in the upper extremities and 5 of 7 patients in the lower extremities. Impairment of vibration sense was found in 1 of 7 patients in the upper extremities and in all patients in the lower extremities. In type II (14 patients) severe impairment of position and vibration sense in deep sensation was found in 3 patients in the upper extremities equal to that in the lower extremities. There was no tendency in the severity of impairment of four kinds of discriminative sensations. Including our 3 cases and 22 in the literature, impairment of deep sensation was more severe in the lower extremities than in the upper extremities in type I (9 patients) and the extent was none (7), mild or moderate (2) in the upper extremities, mild (2), moderate (1), severe (2), obscure (4) in the lower extremities, while in type II (16 patients) the severity in the upper extremities was nearly equal to that in the lower extremities and the extent was none (1), mild or moderate (1), severe (5), obscure (9) in the upper extremities, none (2), mild or moderate (1), severe (6), obscure (7) in the lower extremities. It is concluded that hemiparesis appeared with lesions located in the pyramidal tract of the medulla, hemiparesis and disturbance of deep sensation in the upper and lower extremities, predominantly in the lower extremities with the lesion of the pyramidal tract to the middle of medial lemniscus in the medulla, hemiparesis and disturbance of the upper and lower extremities deep sensation with lesions of the pyramidal tract to the whole of the medial lemniscus in the medulla. Evaluating deep sensation of the upper and lower extremities is useful for speculation of the lesion location in the medial lemniscus in medial medullary infarction.

Cerebral Infarction↗

PubMed1986

Collaterals of corticospinal and pyramidal fibres to the pontine grey demonstrated by a new application of the fluorescent fibre labelling technique.

Selective visualization of collaterals of corticospinal and pyramidal fibres to the pons in cat was obtained by retrograde transport of the fluorescent tracer fast blue (FB) through the stem fibres. Unilateral FB injections in the cervical cord and the pyramidal tract respectively produced soft blue fluorescent labelling of pyramidal fibres and of fibres and structures resembling 'terminals' in the pontine grey: contralateral to the spinal injections and ipsilateral to the pyramidal injections. These labelled elements were concluded to represent collaterals of corticospinal and pyramidal fibres because (a) their distribution corresponded to that of the pericruciate corticopontine fibres, (b) their labelling was prevented when the FB injections were preceded by a transection of either the cerebral peduncle or the pyramidal tract which lesions also prevented the FB labelling of the distal parts of the transected axons. Similar findings were obtained when using wheat germ agglutinin-horseradish peroxidase. In other experiments FB-labelling of pyramidal collaterals was combined with retrograde labelling of pontine neurones projecting to the contralateral anterior lobe of the cerebellum using diamidino yellow dihydrochloride as the second tracer. The distributions of the retrogradely labelled neurones and of the pyramidal collaterals in the pontine grey showed an almost complete overlap indicating that these collaterals mainly establish connections with the cerebellar anterior lobe.

Amidines↗

PubMed1988

[Pure spastic hemiplegia of pyramidal origin].

The relationship between the interruption of the human pyramidal tract and its attendant clinical manifestations has been a matter of concern to neurologists and neurosurgeons for over a century. We presently report three cases of unilateral pyramidal tract ischemic lesions within the cerebral hemispheres who presented with a contralateral pure spastic hemiplegia syndrome. In none could we find any disturbance in the somatosensitive evoked potentials of the four limbs. The review of some cases on record since the time of Charcot and Erb has made it clear that the pyramidal syndrome is a valid clinical concept which should be qualified according to the particular animal species one is referring to. In man, it manifests itself by paresis, hyperactive muscular reflexes, spasticity and Babinski sign. Based on this evidence we propose the idea of a "differential control" exerted by the pyramidal tract upon the segmental neuronal pool as its key mode of normal functioning.

Adult↗

PubMed1994

Recording an identified pyramidal volley evoked by transcranial magnetic stimulation in a conscious macaque monkey.

A descending volley in response to non-invasive transcranial magnetic stimulation has been recorded from the pyramidal tract in a conscious monkey and identified by means of a collision test. The short latency of the earliest wave was inconsistent with a trans-synaptically mediated activation of pyramidal tract neurones. Considerable variability in the size of this wave was seen in response to a constant stimulus, and isoflurane anaesthetic was shown to depress it markedly. These results are consistent with direct activation of pyramidal tract neurones at a site close to the cell body.

Animals↗

PubMed1977

Microiontophoretic studies of the effects of cylic nucleotides on excitability of neurones in the rat cerebral cortex.

1. Responses of cerebral cortical neurones to the microiontophoretic application of acetylcholine, noradrenaline, cyclic adenosine 3',5'-monophosphate (cyclic AMP) and cyclic guanosine 3',5'-monophosphate (cyclic GMP) were examined.2. The application of acetylcholine and cyclic GMP to identified pyramidal tract neurones resulted in an increased frequency of firing in a large number of cells. Upon application of both substances to cells which could not be identified as pyramidal tract cells, a reduction in the frequency of spontaneous firing was sometimes observed.3. Careful current controls had no effect on the cells discussed here, indicating that the observed responses were not due to the iontophoretic currents. Also, the electro-osmotic ejection of cyclic GMP (outward current) produced similar changes of cell firing to those which followed iontophoretic application (inward current).4. The microiontophoretic application of atropine resulted in a blockade of acetylcholine responses while leaving responses to cyclic GMP unaffected. This suggests that cyclic GMP was not acting indirectly by releasing acetylcholine from presynaptic endings.5. Ejection of cyclic GMP from solutions containing calcium ions produced responses comparable to those produced by cyclic GMP alone. It is unlikely therefore that cyclic GMP was causing excitation by chelating calcium.6. Applications of noradrenaline and cyclic AMP produced a reduction in the spontaneous discharge rate of most neurones tested.7. Phosphodiesterase inhibitors such as ICI 63,197 caused a potentiation of the noradrenaline responses of pyramidal tract neurones.8. 5'-adenosine monophosphate produced a powerful depression of all cells to which it was applied. This action was blocked by aminophylline, suggesting the effect was mediated through an adenosine receptor. Responses to cyclic AMP were usually not abolished, but were reduced by about 50% in amplitude.9. These results are consistent with the hypothesis that cyclic AMP may mediate some neuronal effects of noradrenaline and cyclic GMP may mediate some effects of acetylcholine. The results are also consistent with the suggestion that the two nucleotides may sometimes mediate opposite cellular responses to humoral stimuli.

Acetylcholine↗

PubMed1975

Relationship of neuronal discharges in the precentral gyrus of monkeys to the performance of arm movements.

Recordings have been made from 162 pyramidal tract neurones which discharged bursts of nerve impulses in characteristic temporal association with performances of a stereotyped motor task by monkeys. Clinical evaluation of the relationship between discharges of the neurones and free movement led to the view that each cell's firing was associated with a characteristic aspect of movement performance and the contraction of a particular group of muscles. Quantitative evaluation of these relationships led to the conclusion that coding of the recruitment of motor units to the movement task could have been conferred by the number of pyramidal tract neurones discharging to those motoneurone targets. A ramp of "recruitment" of pyramidal tract neurones preceded the development of a ramp of force by about 100 msec. This general conclusion was supported by the observations made in a single animal in which orderly discharge of precentral neurones in relation to a sterotyped movement performance was clearly evident.

Animals↗

PubMed1996

Role of the motor cortex in the control of visually triggered gait modifications.

One important aspect of locomotor control is the ability of an animal to make anticipatory gait modifications to avoid obstacles, by stepping either around them or over them. This paper reviews some of the evidence that suggests that the motor cortex is one of the principal structures involved in the control of such anticipatory gait modifications in cats, in particular when they are triggered by a visual signal. Evidence for this statement is provided both from experiments in which the motor cortex has been lesioned or inactivated and from studies in which the activity of motor cortical neurones has been recorded during locomotor tasks in which visual information is required to ensure the correct positioning of the paw or an appropriate modification of the limb trajectory. Inactivation of small regions of the motor cortex with the GABA agonist muscimol results in changes in the limb trajectory so that cats hit an obstacle instead of stepping over it as they do normally. A similar disruption of the hindlimb trajectory is seen following lesions of the spinal cord at T13 that interrupt the corticospinal tract. The results from cell recording studies are complementary in that they show that the activity of many identified pyramidal tract neurones increases when the cat is required to modify the forelimb or hindlimb trajectory to step over obstacles. We suggest that the major function of this increased discharge frequency is to regulate the amplitude, duration, and temporal pattern of muscle activity during the gait modification to ensure an appropriate modification of limb trajectory. We further suggest that different groups of pyramidal tract neurones are involved in regulating the activity of groups of synergistic muscles active at different times in the gait modification. For example, some groups of pyramidal tract neurones would be involved in ensuring the appropriate and sequential activation of the muscle groups involved in the initial flexion of the elbow, while others would be active prior to the repositioning of the paw on the support surface. We discuss the possibility that the motor cortical activity seen during locomotion is the sum result of a feedforward signal, which provides visuospatial information about the environment, and feedback activity, which signals, in part, the state of the interneuronal pattern generating networks in the spinal cord. The way in which the resulting descending command may interact with the basic locomotor rhythm to produce the gait modifications is discussed.

Animals↗

PubMed1978

The Babinski sign and the pyramidal syndrome.

The presence or absence of a Babinski sign can be puzzling, but in the light of existing pathological studies it is more fruitful to consider which pyramidal tract fibres release it than whether they release it. This was investigated clinically, by looking for correlations with other reflex changes and with motor deficits in the leg. A survey of 50 patients with a unilateral Babinski sign and six patients who lacked it in spite of other pyramidal tract signs was supplemented with follow-up of the patients who had acute lesions. Appearance of the Bibinski sign proved to depend on the interaction of two factors: (1) activity (not necessarily hyperactivity) in the segmental pathways of the flexion synergy; (2) a motor deficit of the foot, in some cases consisting only in an impairment of rapid foot movements, and probably representing a disturbance of direct pyramidal tract projections to distal motoneurones.

Female↗

PubMed2005

Brainstem and cerebellar changes after cerebrovascular accidents: magnetic resonance imaging.

We illustrate the various types of secondary degeneration in the brainstem and/or cerebellum detected on magnetic resonance (MR) images obtained after cerebrovascular accidents. The changes include: (a) ipsilateral nigral degeneration after striatal infarction; (b) Wallerian degeneration of the pyramidal tract in the brainstem after supratentorial pyramidal tract or motor cortex injury; (c) Wallerian degeneration of the corticopontine tract in the brainstem after frontal lobe infarction; (d) ipsilateral brainstem atrophy and crossed cerebellar atrophy due to an extensive supratentorial lesion; (e) ipsilateral superior cerebellar peduncle atrophy, contralateral rubral degeneration, contralateral inferior olivary degeneration and ipsilateral cerebellar atrophy after dentate nucleus hemorrhage; (f) ipsilateral inferior olivary degeneration after pontine tegmentum hemorrhage; (g) bilateral wallerian degeneration of the pontocerebellar tracts after ventromedial pontine infarction or basis pontis hemorrhage; and (h) ipsilateral cerebellar atrophy after middle cerebellar peduncle hemorrhage.

Adult↗

PubMed1984

The postnatal development of corticotrigeminal projections in the cat.

The postnatal development of corticotrigeminal projections was studied in kittens following 3H-amino acid injections into the face area of the primary somatosensory cortex. Corticofugal axons grow into the brainstem and form the pyramidal tract prenatally. Corticotrigeminal projections begin to develop at the end of the first postnatal week. The earliest corticotrigeminal axons grow out of the pyramidal tract caudally and project into laminae III-V of the spinal trigeminal (Vs) nucleus caudalis. During the second postnatal week, corticotrigeminal axons grow out of the pyramidal tract in a caudal to rostral sequence and project up to the ventromedial borders of Vs-interpolaris, Vs-oralis, and to the principal trigeminal nucleus. Corticotrigeminal axons pause at the periphery of these nuclei for 1-2 days before penetrating the trigeminal neuropil and forming terminal arborizations in a centripetal direction. Coincident with the development of cortical projections to the principal trigeminal nucleus, some of the labeled axons which were in lamina III of Vs-caudalis project into lamina I and terminate. This sequence of development of corticotrigeminal projections closely parallels, albeit at a later time, the sequence of formation of the trigeminal nuclei, suggesting that the temporal sequence of cytogenesis of trigeminal neurons may be a factor which regulates their order of innervation by afferents. Corticotrigeminal projections develop bilaterally and, during the second postnatal week, are relatively equal in density in the ipsilateral and contralateral nuclei. Many of the ipsilateral corticotrigeminal projections are lost, however, after the second postnatal week, so that by the fourth postnatal week, corticotrigeminal projections are mainly contralateral and adultlike in their distribution. It remains to be determined whether the transience of ipsilateral corticotrigeminal projections is due to selective elimination of axon collaterals or to neuronal death.

Animals↗

PubMed1985

The transient corticospinal projection from the occipital cortex during the postnatal development of the rat.

The transient occipital cortical component of the pyramidal tract which we previously had identified during the postnatal development of the rat (Stanfield et al., '82) has been studied with anterograde as well as retrograde techniques. A continuous band of retrogradely labeled layer V neurons which spans the entire cortex including the occipital cortex is seen following injections of the fluorescent marker Fast Blue into the pyramidal decussation during the first postnatal week. No labeled cells are found in the occipital cortex following similar injections made on postnatal day 20 (P20), although such injections label many neurons in the more rostral cortical fields. However, if the Fast Blue injection is made on P2 and the animal is allowed to survive until P25 a large number of Fast Blue-labeled layer V neurons is found in the occipital cortex, even though an acute, second injection of the retrograde tracer Nuclear Yellow made into the pyramidal decussation shortly before the animal is killed results in no occipital cortical labeling. When Fast Blue injections confined to the mid- or upper-cervical spinal cord are made on P4 and the animals are killed on P9, again many retrogradely labeled neurons are found in the occipital cortex. Further, when injections of 3H-proline or wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) confined to the occipital cortex are made during the first 2 postnatal weeks, anterogradely transported label is seen within the pyramidal tract. At all stages examined the amount of such label and its caudal extent are less than that seen following similar injections into the parietal or frontal cortex. The greatest extent of the labeled occipital cortical fibers is reached at about the end of the first postnatal week and the number of these fibers seems to peak at about this same time. At this stage many of these labeled axons extend for a considerable distance down the spinal cord with some reaching as far caudal as lower lumbar levels, and at this stage some of these labeled occipital corticospinal fibers enter into the spinal gray. Over the next week the number of occipital cortical fibers in the pyramidal tract rapidly decreases and by P17 occipital cortical injections of 3H-proline or WGA-HRP result in virtually no transported label caudal to the pons.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1983

Low threshold motor effects produced by stimulation of area preinsularis (2 pr.i) of the secondary sensory cortex in the cat; input-output relationship.

Intracortical microstimulation (ICMS) delivered to area 2 perinsularis (area 2 pr. i) of the second somatosensory cortex, SII, elicited contralateral distal limb movements with threshold currents as low as 2 microA. The effective sites for a particular movement were located in a small area within the depth of the cortex extending along the direction of the radial fibers. Neurons in an area for a particular movement generally received peripheral input from the skin overlying the muscle to which the area projected. ICMS in area 2 pr.i produced powerful monosynaptic as well as disynaptic activation of pyramidal tract neurons, suggesting that the effect was mediated by the pyramidal tract. Ablation of the motor cortex did not eliminate or otherwise reduce the low threshold responses from area 2 pr.i suggesting that the described effect is independent of the motor cortex.

Animals↗

PubMed2006

Microstructural development of human brain assessed in utero by diffusion tensor imaging.

BACKGROUND: Diffusion-weighted MR imaging (DWI) has been shown to be a great tool to assess white matter development in normal infants. Comparison of cerebral diffusion properties between preterm infants and fetuses of corresponding ages should assist in determining the impact of premature ex utero life on brain maturation. OBJECTIVE: To assess in utero maturation-dependent microstructural changes of fetal cerebral white matter using diffusion tensor MR imaging. MATERIALS AND METHODS: An echoplanar sequence with diffusion gradient (b=700 s/mm(2)) applied in six non-colinear directions was performed between 31 and 37(+3) weeks of gestation in 24 fetuses without cerebral abnormality on T1- and T2-weighted images. Apparent diffusion coefficient (ADC) and fractional anisotropy (FA) were measured in the white matter. RESULTS: Mean ADC values were 1.8 microm(2)/ms in the centrum semiovale, 1.2 microm(2)/ms in the splenium of the corpus callosum and 1.1 microm(2)/ms in the pyramidal tract. The paired Wilcoxon rank test showed significant differences in ADC between these three white matter regions. Mean FA values were 1.1%, 3.8% and 4.7%, respectively, in the centrum semiovale, corpus callosum and pyramidal tract. A significant age-related decrease in ADC and an increase in FA towards term were demonstrated in the pyramidal tract and corpus callosum. CONCLUSION: Diffusion tensor imaging in utero can provide a quantitative assessment of the microstructural development of fetal white matter. Anisotropic parameters of the diffusion tensor should improve with technical advances.

Anisotropy↗

PubMed1999

[Neuropathology of amyotrophic lateral sclerosis--from basic findings to topics].

Amyotrophic lateral sclerosis (ALS) is a relentlessly progressive neurodegenerative disease that selectively affects upper and low motor neurons (UMNs and LMNs). The remaining LMNs show, in addition to normal appearance, a variety of cell pathology such as central chromatolysis, atrophy of the cell body and processes, Bunina bodies, and ubiquitinated hyaline and skein-like inclusions. Ultrastructural studies of the last two profiles indicate their processing by lysosomes. Whether apoptosis is responsible for motoneuronal death in ALS or not remains to be determined. In Klüver-Barrera (KB) staining, the pyramidal tracts in ALS usually appear normal at the pons in spite of their obvious pallor at the lower levels, leading to the dying-back hypothesis. However, axonal staining in such cases reveals obvious loss of large axons in the pontine pyramidal tracts, a finding inconsistent with the hypothesis. Similarly, in cases of motoneuron disease with the pyramidal tracts well stained by KB method, therefore, 'spinal progressive muscular atrophy (SPMA)', axonal staining demonstrated patent loss of large axons there. Thus, reappraisal seems to be required for previously reported SPMA cases, whose pathological diagnosis used to be made by KB staining alone.

Amyotrophic Lateral Sclerosis↗

PubMed1976

Timing of the responses in the motor cortex of monkeys to an unexpected disturbance of finger position.

Monkeys were trained with food rewards to hold the wrist and fingers of their right hand in a flexed posture and maintain force with the finger tips against an isometric lever for a number of seconds. Once the animal had learned to produce a reliable performance of the task an assembly was attached to the skull through which microelectrodes could be introduced into the precentral cortex to record the activity of single neurones. Neurones whose activity was correlated with the force of finger flexion were studied; some of these could be identified as pyramidal tract neurones by their response to electrical stimulation in the medullary pyramids. While the monkey was flexing against it, the lever was sometimes suddenly released so that the fingers flexed without resistance. This unexpected disturbance was often followed by a change in the discharge of precentral neurones, although the monkey had not been trained to respond to the release in any particular way. On release of the lever the discharge of a given cortical neurone might either increase or decrease, and the direction of this change could not be predicted from the behaviour of the neurone during the isometric task. The most common response was an increase in cortical cell firing in neurones whose natural discharge was associated with the active development of force. The discharge of pyramidal tract neurones changed 25-50 msec after the sudden unexpected peripheral disturbance. Earlier changes were seen in some other neurones situated within the precentral gyrus and in the anterior bank of the central sulcus.

Animals↗

PubMed1978

Operant conditioning of tonic firing patterns from precentral neurons in monkey neocortex.

This report presents a single neurons operant conditioning paradigm which allows the quantification of operant control between neurons and monkeys. The operant task is for the monkey to change firing patterns of the neuron from phasic to tonic. In 60 neurons conditioned after the protocol had been standardized the following results were obtained. (1) For a fixed interspike interval target range, the time off target may be considered error, and this may be used as a parameter with which to judge operant neuronal control. (2) The degree to which the monkey could control a neuron was not correlative with the neuron's initial firing rate, firing rate variance, or pattern. (3) Neurons coactivated by distal arm muscle groups were, as a group, more highly controlled in comparison to neurons coactivated by proximal muscle groups. (4) Pyramidal tract neurons, as a group, appear more accurately controlled than non-pyramidal tract neurons. (5) The role of proprioception in response acquisition is discussed.

Animals↗

PubMed2000

Acute myelitis after asthma attacks with onset after puberty.

A poliomyelitis-like illness after asthma attacks has been found and is called asthmatic amyotrophy (Hopkins' syndrome). All of the previously reported cases were under 13 years of age. Three patients are described who developed acute myelitis after asthma attacks at 15, 22, and 73 years of age. All of them showed acute flaccid monoparesis, and needle EMG disclosed denervation potentials in the relevant muscles. In addition, in the two adult patients the sensory or pyramidal tracts were involved, and evoked potential studies confirmed an involvement of the pyramidal tracts in one of them. This 22 year old patient showed a second episode of monoparesis in the other limb after another asthma attack. All three patients had no significant changes in their antiviral antibody titres, whereas every patient had hyperIgEaemia and allergen specific IgE. These findings suggest that asthmatic amyotrophy can develop after puberty and that patients who develop this disease in adulthood seem to show both a widespread involvement of the spinal cord and a more varied course.

Acute Disease↗

PubMed1988

Morphology of pyramidal neurones in monkey motor cortex and the synaptic actions of their intracortical axon collaterals.

1. Pyramidal neurones in the precentral motor area of the monkey were studied using intracellular techniques. Pyramidal tract neurones (PTNs) were identified by antidromic activation from the cerebral peduncles or medullary pyramids. Orthodromic responses were recorded in PTNs and in other pyramidal neurones when antidromic volleys were set up by stimulation of the peduncles or pyramids. The neurones were then labelled by intracellular ionophoresis of horseradish peroxidase and their morphology examined. All neurones studied were identified as pyramidal cells according to their morphology. 2. Six pyramidal neurones located in lamina V were well stained; they included two fast PTNs and two slow PTNs. The morphology of all pyramidal neurones in this lamina (fast PTNs, slow PTNs and those pyramidal cells that were not antidromically characterized) was essentially similar. A single apical dendrite branched as it ascended and its terminals arborized subpially. Numerous lateral and oblique dendrites branched from the apical dendrites in lamina V and near its border with lamina III: short basal dendrites arborized in the vicinity of the soma in lamina V. Long basal dendrites had a wider field of arborization in lamina V and sometimes extended into lamina VI. 3. Three to five collaterals arose from the axon of lamina V cells in the cortex and arborized in laminae V and VI. Short collateral branches arborized in the vicinity of the soma in the region of the basal and lateral dendrites. Long collateral branches could be traced over long distances (often more than 1 mm). One pyramidal neurone in this lamina (a fast PTN) lacked short collateral branches from the axon. 4. Four pyramidal neurones in lamina III were stained well. The dendritic morphology of all these neurones was similar. Apical dendrites branched as they ascended and terminated subpially. Lateral and basal dendrites formed a column of dendritic branches around the soma. No long basal dendrites were seen. 5. The number and arborization of intracortical collaterals from the axon of lamina III cells varied widely; from three to twelve collaterals arose from the axon. The biggest arbor of collateral branches involved all the cortical laminae and was about 3 mm wide mediolaterally, while the smallest arbor was restricted mainly to lamina III in the vicinity of the soma. One neurone in this lamina also lacked short collateral branches from the axon. 6. Antidromic volleys from the pyramidal tract evoked excitatory responses in fast PTNs, predominantly inhibitory responses in slow PTNs and either excitatory or inhibitory responses in other pyramidal neurones in lamina V.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗