STUDY - Technical - New Dacian's Medicine
Muscle
Weakness, Abnormal Movements and Imbalance
(5)
Translation Draft
Here we are also at the imbalance and the disorders of walking.
Here we are also at the imbalance and the disorders of walking.
I
will start with a boring part, addressed especially to
connoisseurs and practitioners but, also in this post, there
will be interesting "stuff" for any of the readers.
The imbalance is the inability to maintain the intentional orientation of the body in space. It generally manifests as a difficulty in maintaining the vertical posture during standing or walking, a severe imbalance can also affect the ability to maintain posture during the downstate. Patients with imbalance frequently experience feelings of insecurity or instability.
While imbalance or uncertainty are synonymous, instability involves the additional component of spatial orientation damage even as the patient lies. Patients with instability also frequently have vertigo, defined as a rotary motion hallucination.
The imbalance results from damage to the sensory spinocerebellar or vestibular impulses, the integration of these impulses into the brain or cerebellum stem, or from the motor efferevents to the spinal neurons that control the axial and proximal muscles. The position of the head in space is normally detected by the inner ear.
Utricula and bag are sensitive to the static position of the head and acceleration by detecting the direction of gravitational motion and its changes. Semicircular channels are sensitive to rotational motion. These sensations for the static position of the head and for movement are transmitted through the vestibular nerve to the vestibular nuclei of the lower bridge and upper marrow.
Excitatory impulses from the vestibular nuclei are transmitted to the deep fastigial nucleus on the midline of the cerebellum and on the path of the muscular glutamatergic fibers to the cells in the corresponding ipsilateral granular layer of the floculonodular cerebellar cortex. The position of the head towards the limbs and torso is detected by receptors that are responsible for the position of the joints, the movement of the joints and the shortening or elongation of the muscle spindles in the axial and proximal muscles of the limbs.
This sensory impulse is transmitted both along the posterior cord and through the medial woodiscal pathways to the cortex and through the spinocerebellar pathways to the cerebellum. For automatic balance, the sensory protrioceptive influx ascends the spinal cord into the ventral and dorsal spinocerebellar tracts and, for the head position, in the cuneocerebellar tracts.
They enter the cerebellum as excitatory inflows through the muscle glutamatergic fibers to the granular cells in the midline of the ipsilateral vermix of the cerebellar cortex and the ipsilateral fastigial nucleus. The visual impulse, on the path of the mesencephalic tectum, is transmitted to the cerebellum through similar fibers, muscle excitatory.
The midline of the cerebellar cortex and the nuclei are of extreme importance in integrating these impulses and controlling the appropriate motor responses needed to maintain a normal balance. In both the midline and lateral cerebellar cortexes, several types of neural cells mediate these complex interactions.
Purkinje cells of the cortical middle layer are the main eference neurons of cerebellar cortical activity. They have GABA-ergic inhibitory projections to deep cerebellar nuclei. The granular cells of the internal cell layer project an extensive network of axons to the outer molecular layer as parallel fibers, which go (parallel) with the long axis of the foil.
Parallel fibers produce a weak excitatory, glutamatergic influence on the dendrites of many Purkinje cells in the molecular layer and on the basket and star cells, which are interneurons of the molecular layer. Both the cells in the basket and the star cells send inhibitory projections on the Purkinje cells.
The axons of the cells in the basket go perpendicular to the parallel fibers and produce GABA-ergic inhibitions on the bodies of the Purkinje cells just outside the excitation band of the parallel fibers. Thus, the cells in the basket provide a neighborhood antagonism in the cerebellar cortex.
A third inhibitory neuron that acts in the cerebellar cortex is the Golgi cell, which is found at the outer limit of the granular layer. Golgi dendrites are projected towards the molecular layer, where they receive inflow through parallel excitatory fibers. Golgi cells exert GABA-ergic inhibition on granular cells.
The major eference of the cerebellar cortex is the inhibition of deep cerebellar nuclei by Purkinje cells. Deep cerebellar nuclei receive excitatory influx from muscle fibers. The major cerebellar eference for balance comes from the fastigial nuclei to the vestibular nuclei and the reticulated and smaller formation, directly from the Purkinje cells of the median line to the vestibular nuclei.
The vestibular nuclei and the reticulated formation project vestibular and reticulospinal descending afferences on the path of the ventromedial beams to control the axial and proximal muscles of the limbs and torso.
The speed, fluency and integration of limb movements are also controlled by the cerebellum. Proprioceptive spinal feedback from the limbs is projected onto granular cells in the ipsilateral cerebellar cortex and from the interposed ipsilateral nuclei (globos and emboliform) as inflows through muscle glutamatergic fibers.
The major efferent system from the interposed nucleus is to the magnolial portion of the contralateral red nucleus and then to the descending rubrospinal tract, which is the major ventrolateral bulbospinal pathway that facilitates limb movements, partly by activating gamma motor neurons. The lateral cerebellar hemispheres coordinate a complex feedback circuit, which cortically modulates the initiated movement of the limbs.
Motor cortical controls influence the cerebellar hemispheres indirectly through the pontocerebellar muscle fibers and the ascending olivocerebelous fibers. The descending corticopontine fibers excite the ipsilateral pontine. The pontocerebellar fibers cross into the bridge, project themselves to the cerebellum through the middle cerebellar peduncle, and excite the granular cells and the toothed nucleus of the contralateral cerebellar hemisphere.
The lower olivar nucleus in the bulb receives influx from the cortex as collateral from the corticospinal axons and the basal ganglia, the red nucleus and the reticulated formation. Excitatory upward fibers from the lower olivari nuclei cross, pass through the lower cerebellar peduncle and stimulate the Purkinje cells in the lateral cerebellar hemispheres and the toothy nuclei.
Excitatory ascending fibers use aspartate as a neurotransmitter. The eference from the cerebellar hemispheres is transmitted predominantly through the pathway of the tooth nuclei to the parvocellular component of the contralateral red nucleus, to the ventrolateral nucleus of the thalamus and to the motor and premotor cerebral cortex.
Injuries along this circuit cause cerebellar ataxia of the limbs. Sensory ataxia is caused by lesions affecting peripheral sensory fibers, ganglion cells in the dorsal root, posterior cords of the spinal cord, the wood system in the brain stem, the thalamus or parietal cortex.
Impairment of sensory feedback to the cerebellum, basal ganglia and cortex produces sensory ataxia. Sensory ataxia causes imbalance and affects the fluency and integration of movements that can be partially improved by visual feedback.
No more descriptive "techniques"... I'm going to go to the description of walking disorders now.
Walking is one of the most complicated and common motor activities of everyday life. Crucially, all the structures mentioned above participate in normal walking. Step cyclic movements produced by the lombosacrate centers of the spinal cord are altered by cortical influences, from the basal ganglia, brain stem and cerebellum based on proprioceptive, vestibular and visual feedback mechanisms.
We will address the diagnosis and differential diagnosis for the most frequent clinical presentations of imbalance and abnormal gait, starting with examination for imbalance, incoordination and abnormal gait.
Neurological examinations for coordination, balance and gait are typically carried out together. The patient performs different manoeuvres with each member while coordination is evaluated. Finger-toe and heel-knee-tibia maneuvers are taken into observation for signs of incoordination in general and dysmetry in particular.
Dysmetry consists of irregular mistakes as distance and force of limb movements. This is accentuated near the target or place of intent and hence is called intentional tremor. The patient is also asked to keep his arms outstretched against a resistance that is suddenly removed (excessive relaxation indicating a cerebellar dysfunction).
The patient's ability to strike his hands and feet quickly and repetitively is evaluated for speed and rhythmicity. Slow, coarse but rhythmic movements indicate incoordination of interest to the upper motor neuron. Errors in rhythm and irregular speed indicate cerebellar disease, which is most evidently demonstrated by asking the patient to make rapid alternative movements. During attempts to alternately hit the dorsal and palmar surfaces of the hand as quickly as possible, if the rate, pace and regularity of the force cannot be maintained we are dealing with a sign called dysdiadochokesia.
The patient is asked to demonstrate how he combs his hair or washes his teeth in order to assess the ability to initiate and execute a simple sequence of an activity. The balance is examined by putting the patient in orthostatism at rest with his legs glued together. It will be observed whether this position can be maintained, with eyes closed for 5 to 10 seconds.
Accentuating the balance or effective loss of balance are also assessed. If the balance is lost at the moment, it may take some evidence to determine whether the loss is constantly in the same direction. Walking along an uncrowded space, such as a corridor, is observed over the distance of 20 meters or more. Arm sing symmetry and different phases of the walking cycle are observed. Walking is then done on the heels for a few steps, then on the peaks, then in tandem.
The imbalance has several "manifestations". The cerebellar ataxia results from disorders of the cerebellum or its related impulses or efferent projections. Examination frequently helps to locate the anatomical area responsible for ataxia.
Anomalies of the midline cerebellar vermix or flocnonodular lobe are usually revealed during the lifting process from a chair, achieving the vertical position with the legs glued together, or performing other activities during orthostatism. Once the desired position is achieved, the imbalance can be surprisingly gentle. As the walk begins, the imbalance repeats itself.
Patients usually learn to shrink their imbalance by walking with their feet wide apart. The imbalance is not usually lateralized and may be accompanied by symmetrical nystagmus if the floculonodular lobe or its connections is affected. These anomalies of the midline vermix characteristically produce trunccular ataxia (the dysmetry of the lower limbs with intentional tremor may also be present).
Anomalies of the intermediate and lateral portions of the cerebellum typically cause damage to limb movements rather than trunccular ataxia. The interest is asymmetrical, it is frequently lateralized imbalance, usually associated with asymmetric nystagmus.
Clinical signs of cerebellar ataxia of the limbs include dysmetry, intentional tremor, dysdiadookinesia and abnormal relaxation. Muscle tone is frequently reduced modestly, which contributes to abnormal relaxation due to low activity of the segmental reflexes of the spinal cord and also of pendulum reflexes, i.e. a tendency of a tendinous reflex to produce back and forth swings after a single movement.
Offf, I'm tired... We'll continue tomorrow with the vestibular dysfunction imbalance.
The imbalance is the inability to maintain the intentional orientation of the body in space. It generally manifests as a difficulty in maintaining the vertical posture during standing or walking, a severe imbalance can also affect the ability to maintain posture during the downstate. Patients with imbalance frequently experience feelings of insecurity or instability.
While imbalance or uncertainty are synonymous, instability involves the additional component of spatial orientation damage even as the patient lies. Patients with instability also frequently have vertigo, defined as a rotary motion hallucination.
The imbalance results from damage to the sensory spinocerebellar or vestibular impulses, the integration of these impulses into the brain or cerebellum stem, or from the motor efferevents to the spinal neurons that control the axial and proximal muscles. The position of the head in space is normally detected by the inner ear.
Utricula and bag are sensitive to the static position of the head and acceleration by detecting the direction of gravitational motion and its changes. Semicircular channels are sensitive to rotational motion. These sensations for the static position of the head and for movement are transmitted through the vestibular nerve to the vestibular nuclei of the lower bridge and upper marrow.
Excitatory impulses from the vestibular nuclei are transmitted to the deep fastigial nucleus on the midline of the cerebellum and on the path of the muscular glutamatergic fibers to the cells in the corresponding ipsilateral granular layer of the floculonodular cerebellar cortex. The position of the head towards the limbs and torso is detected by receptors that are responsible for the position of the joints, the movement of the joints and the shortening or elongation of the muscle spindles in the axial and proximal muscles of the limbs.
This sensory impulse is transmitted both along the posterior cord and through the medial woodiscal pathways to the cortex and through the spinocerebellar pathways to the cerebellum. For automatic balance, the sensory protrioceptive influx ascends the spinal cord into the ventral and dorsal spinocerebellar tracts and, for the head position, in the cuneocerebellar tracts.
They enter the cerebellum as excitatory inflows through the muscle glutamatergic fibers to the granular cells in the midline of the ipsilateral vermix of the cerebellar cortex and the ipsilateral fastigial nucleus. The visual impulse, on the path of the mesencephalic tectum, is transmitted to the cerebellum through similar fibers, muscle excitatory.
The midline of the cerebellar cortex and the nuclei are of extreme importance in integrating these impulses and controlling the appropriate motor responses needed to maintain a normal balance. In both the midline and lateral cerebellar cortexes, several types of neural cells mediate these complex interactions.
Purkinje cells of the cortical middle layer are the main eference neurons of cerebellar cortical activity. They have GABA-ergic inhibitory projections to deep cerebellar nuclei. The granular cells of the internal cell layer project an extensive network of axons to the outer molecular layer as parallel fibers, which go (parallel) with the long axis of the foil.
Parallel fibers produce a weak excitatory, glutamatergic influence on the dendrites of many Purkinje cells in the molecular layer and on the basket and star cells, which are interneurons of the molecular layer. Both the cells in the basket and the star cells send inhibitory projections on the Purkinje cells.
The axons of the cells in the basket go perpendicular to the parallel fibers and produce GABA-ergic inhibitions on the bodies of the Purkinje cells just outside the excitation band of the parallel fibers. Thus, the cells in the basket provide a neighborhood antagonism in the cerebellar cortex.
A third inhibitory neuron that acts in the cerebellar cortex is the Golgi cell, which is found at the outer limit of the granular layer. Golgi dendrites are projected towards the molecular layer, where they receive inflow through parallel excitatory fibers. Golgi cells exert GABA-ergic inhibition on granular cells.
The major eference of the cerebellar cortex is the inhibition of deep cerebellar nuclei by Purkinje cells. Deep cerebellar nuclei receive excitatory influx from muscle fibers. The major cerebellar eference for balance comes from the fastigial nuclei to the vestibular nuclei and the reticulated and smaller formation, directly from the Purkinje cells of the median line to the vestibular nuclei.
The vestibular nuclei and the reticulated formation project vestibular and reticulospinal descending afferences on the path of the ventromedial beams to control the axial and proximal muscles of the limbs and torso.
The speed, fluency and integration of limb movements are also controlled by the cerebellum. Proprioceptive spinal feedback from the limbs is projected onto granular cells in the ipsilateral cerebellar cortex and from the interposed ipsilateral nuclei (globos and emboliform) as inflows through muscle glutamatergic fibers.
The major efferent system from the interposed nucleus is to the magnolial portion of the contralateral red nucleus and then to the descending rubrospinal tract, which is the major ventrolateral bulbospinal pathway that facilitates limb movements, partly by activating gamma motor neurons. The lateral cerebellar hemispheres coordinate a complex feedback circuit, which cortically modulates the initiated movement of the limbs.
Motor cortical controls influence the cerebellar hemispheres indirectly through the pontocerebellar muscle fibers and the ascending olivocerebelous fibers. The descending corticopontine fibers excite the ipsilateral pontine. The pontocerebellar fibers cross into the bridge, project themselves to the cerebellum through the middle cerebellar peduncle, and excite the granular cells and the toothed nucleus of the contralateral cerebellar hemisphere.
The lower olivar nucleus in the bulb receives influx from the cortex as collateral from the corticospinal axons and the basal ganglia, the red nucleus and the reticulated formation. Excitatory upward fibers from the lower olivari nuclei cross, pass through the lower cerebellar peduncle and stimulate the Purkinje cells in the lateral cerebellar hemispheres and the toothy nuclei.
Excitatory ascending fibers use aspartate as a neurotransmitter. The eference from the cerebellar hemispheres is transmitted predominantly through the pathway of the tooth nuclei to the parvocellular component of the contralateral red nucleus, to the ventrolateral nucleus of the thalamus and to the motor and premotor cerebral cortex.
Injuries along this circuit cause cerebellar ataxia of the limbs. Sensory ataxia is caused by lesions affecting peripheral sensory fibers, ganglion cells in the dorsal root, posterior cords of the spinal cord, the wood system in the brain stem, the thalamus or parietal cortex.
Impairment of sensory feedback to the cerebellum, basal ganglia and cortex produces sensory ataxia. Sensory ataxia causes imbalance and affects the fluency and integration of movements that can be partially improved by visual feedback.
No more descriptive "techniques"... I'm going to go to the description of walking disorders now.
Walking is one of the most complicated and common motor activities of everyday life. Crucially, all the structures mentioned above participate in normal walking. Step cyclic movements produced by the lombosacrate centers of the spinal cord are altered by cortical influences, from the basal ganglia, brain stem and cerebellum based on proprioceptive, vestibular and visual feedback mechanisms.
We will address the diagnosis and differential diagnosis for the most frequent clinical presentations of imbalance and abnormal gait, starting with examination for imbalance, incoordination and abnormal gait.
Neurological examinations for coordination, balance and gait are typically carried out together. The patient performs different manoeuvres with each member while coordination is evaluated. Finger-toe and heel-knee-tibia maneuvers are taken into observation for signs of incoordination in general and dysmetry in particular.
Dysmetry consists of irregular mistakes as distance and force of limb movements. This is accentuated near the target or place of intent and hence is called intentional tremor. The patient is also asked to keep his arms outstretched against a resistance that is suddenly removed (excessive relaxation indicating a cerebellar dysfunction).
The patient's ability to strike his hands and feet quickly and repetitively is evaluated for speed and rhythmicity. Slow, coarse but rhythmic movements indicate incoordination of interest to the upper motor neuron. Errors in rhythm and irregular speed indicate cerebellar disease, which is most evidently demonstrated by asking the patient to make rapid alternative movements. During attempts to alternately hit the dorsal and palmar surfaces of the hand as quickly as possible, if the rate, pace and regularity of the force cannot be maintained we are dealing with a sign called dysdiadochokesia.
The patient is asked to demonstrate how he combs his hair or washes his teeth in order to assess the ability to initiate and execute a simple sequence of an activity. The balance is examined by putting the patient in orthostatism at rest with his legs glued together. It will be observed whether this position can be maintained, with eyes closed for 5 to 10 seconds.
Accentuating the balance or effective loss of balance are also assessed. If the balance is lost at the moment, it may take some evidence to determine whether the loss is constantly in the same direction. Walking along an uncrowded space, such as a corridor, is observed over the distance of 20 meters or more. Arm sing symmetry and different phases of the walking cycle are observed. Walking is then done on the heels for a few steps, then on the peaks, then in tandem.
The imbalance has several "manifestations". The cerebellar ataxia results from disorders of the cerebellum or its related impulses or efferent projections. Examination frequently helps to locate the anatomical area responsible for ataxia.
Anomalies of the midline cerebellar vermix or flocnonodular lobe are usually revealed during the lifting process from a chair, achieving the vertical position with the legs glued together, or performing other activities during orthostatism. Once the desired position is achieved, the imbalance can be surprisingly gentle. As the walk begins, the imbalance repeats itself.
Patients usually learn to shrink their imbalance by walking with their feet wide apart. The imbalance is not usually lateralized and may be accompanied by symmetrical nystagmus if the floculonodular lobe or its connections is affected. These anomalies of the midline vermix characteristically produce trunccular ataxia (the dysmetry of the lower limbs with intentional tremor may also be present).
Anomalies of the intermediate and lateral portions of the cerebellum typically cause damage to limb movements rather than trunccular ataxia. The interest is asymmetrical, it is frequently lateralized imbalance, usually associated with asymmetric nystagmus.
Clinical signs of cerebellar ataxia of the limbs include dysmetry, intentional tremor, dysdiadookinesia and abnormal relaxation. Muscle tone is frequently reduced modestly, which contributes to abnormal relaxation due to low activity of the segmental reflexes of the spinal cord and also of pendulum reflexes, i.e. a tendency of a tendinous reflex to produce back and forth swings after a single movement.
Offf, I'm tired... We'll continue tomorrow with the vestibular dysfunction imbalance.
Restful
and energizing Sunday to prepare you for the coming week!
Don't forget understanding, love and gratitude!
Dorin, Merticaru