STUDY - Technical - New Dacian's Medicine
Muscle
Weakness, Abnormal Movements and Imbalance
(4)
Translation Draft
I will continue with dysfunctions of the movement addressing their pathogenesis.
Movement dysfunctions result from basal nuclei disease, subcortical pair structures of gray substance, which form anatomically distinct nuclear groups. They are formed from the caudal nucleus and putamen (which together are called the striated body), the internal and external segments of the pale globe, the subthalamic nucleus and the black substance.
Major interconnections and neurotransmitters involved in basal nuclei circuits are of great importance. Cortical initiated movement is facilitated and competing movements are inhibited by the influence of basal nuclei. The oyster receives organized somatotropic impulses from several cortical areas.
These consist of separate multiple parallel circuits, which include impulses from the frontal, sensory and motor cortex and associated parietotemporooccipital areas (however, only post-central and somatosensory motor projections appear to be directly related to movement.
These projections are glutamatergic and excitatory). The oyster has direct and indirect projections in the major external nuclei of the basal nuclei, pars reticulated of the black substance and in the internal pale globe (also called the pale medial globule). These nuclei also project to the anterior and lateral ventral nuclei of the thalamus by GABA inhibitory neurotransmission.
Talamic currents have excitatory glutamatergic projections in cortical neurons. Thus, the inhibition of the reticulated part of the black substance and the internal pale globe disinhibits the tapamocortical projections that reconsolidate the initiated cortical activity and the arousal of these efferent pathways inhibits the tapamocortic projections for competitive motor responses. The basal core is not projected directly to the spinal cord.
The direct path from the reticulated pars of the black substance to the internal pale globe is GABA-ergic and inhibitory. This direct path then works to facilitate the tamapocratic projections that strengthen the initiated cortical movement. The indirect pathway is more complex and works to inhibit talmamocortical projections to other areas of the motor cortex. The first connection of the indirect path is GABA-ergic, it inhibits activity in the external pale globe, also called the pale lateral globe. The external pale globe transmits GABA-ergic inhibitors to the subthalamic nucleus.
The subthalamic nucleus exerts excitatory glutamatergic feedback on the external pale globe and glutamatergic excitatory impulses on the reticulated pars of the black substance and on the internal pale globe. Thus, the activation of the indirect path increases the effects from the reticulated pars of the black substance and from the internal pale globe, in contrast to the decrease in the effects that occur by activating the direct path.
Direct and indirect pathways are also influenced by pulses from the reticulated pars of the black substance. This dopaminergic aference on the striathas has a net inhibitory effect on the neurons of the direct pathway that predominantly expose dopaminergic D1 receptors and has a net excitatory effect on dopaminergic neurons D2.
The strict also has GABA-ergic feedback inhibitors with compact pars. The striatal activity is further modulated by cholinergic interneurons within the striatum, which are functional antagonists of dopaminergic beams. Behold, I'm done with these descriptions...
Let me move on to the hypokinetic dysfunctions of the movement. The model described explains well the hypokinetic dysfunctions of the movement. The fundamental anomaly in Parkinson's disease lies in the loss of dopaminergic neurons in the compact pars of the black substance. This causes loss of arousal of D1 striatal neurons from the direct pathway and loss of inhibition of D2 striatal neurons in the indirect pathway.
This combination of changes increases the eferences from the reticulated pars of the black substance and from the internal pale globule, which increases the inhibition of talamocortical projections and causes the loss of the facility of the cortical initiated movement. Rest tremor in Parkinson's disease is less explained by this pattern, but can result from the effects on cholinergic interneurons in the striat.
Now, a little bit about hyperkinetic dysfunction of movement. The pathogenesis of Korea in Huntington's disease consists of an initial loss of striatal neurons that expose D2 receptors and a normal GABA-ergic inhibitory projection via the indirect pathway. This disinhibits the external pale globule which, in turn, increases inhibition of the subtalamic nucleus.
Because glutamatergic impulses from the subthalamic nucleus are the primary source of excitation of the reticulated pars of the black substance and the internal pale globe, the loss of this excitation reduces the inhibition of the thalamus and the initiated cortical movements are facilitated without normal feedback control. The pathogenesis of hemibalism is similar, but less complicated, a direct lesion of glutamatergic neurons in the subthalamic nucleus leads to disinhibition of thalacortical projections.
Some movement dysfunctions, such as parkinsonism and Korea, may result from changes in discrete populations of neurons that use a specific neurotransmitter. Such selective vulnerability is commonly present in degenerative neurological diseases, both hereditary and sporadic, and under toxic, nutritional and inflammatory conditions.
Structural disease, which affects more than one cell type, is common only in hemibalism, in which it is almost always found a lesion of the subtalamic nucleus, usually a stroke.
Diagnostic approach and differential diagnosis for frequent clinical presentations of movement dysfunctions are based on different algorithms but, most begin with determining whether movement dysfunction is due to an excess or lack of movement (e.g. hyperkinetic or hypokinetic dysfunction of movement).
From the point of view of hyperkinetic dysfunctions of movement, abnormal involuntary movements are divided into those that are rhythmic and those that are irregular. Those that are rhythmic are called tremors. Tremor is divided into three types: rest tremor, postural tremor and intentional tremor. The resting tremor is maximal at rest and becomes less pronounced with movement.
It is characteristic of parkinsonism, a hypokinetic dysfunction of movement, and is therefore commonly associated with bradykinesis and stiffness in the toothed wheel. A rest tremor that develops acutely is usually due to toxins or dopamine-blocking drugs (such as phenothiazines). If the onset is insidious, the diagnostic approach is the same as for Parkinson's disease.
Postural tremor is maximum when the position of the limbs is actively maintained against gravity, it is reduced by rest and does not increase marked during voluntary movement towards a target. Postural tremor is maximum when the position of the limbs is actively maintained against gravity, it is reduced by rest and does not increase marked during voluntary movement towards a target.
Postural tremor that develops acutely is usually due to toxic or metabolic factors (e.g. hyperthyroidism) or stress. The insidious onset of a postural tremor suggests an essential benign or familial tremor. An intentional tremor is more pronounced during the voluntary movement towards a target and is not present during fasting or at rest. It's a sign of cerebellar disease.
The asterixis, which may at first glance resemble tremor, is an intermittent inhibition of muscle contraction that occurs in metabolic encephalopathy. This leads, for example, to a momentary and repetitive partial flexion of the wrist while attempting the sustained extension of the wrist.
Abnormal involuntary movements that are irregular are further characterized by their speed and place of occurrence and by the possibility of being suppressed voluntarily. The slowest are athetosis and dystonia. Athetosis is a slow contortion, a synuous movement that occurs almost continuously in the distal muscles.
Distonia is a deviation of posture varying slowly, but almost continuously, involving one or more joints (may occur in proximal or distal limbs or in axial structures). Distonia is a more sustained deviation of posture than athetosis, although these two phenomena overlap considerably. Among the rapid irregular movements, nerve tics are controlled with voluntary effort, while the others do not.
Nerve tics frequently appear repetitive in one place, but are sometimes multifocal. Korea, hemibalism and myoclonia are rapid, irregular seizures that cannot therefore be suppressed. Hemibalism is the most distinctive of them. It manifests itself as a sudden and often violent throwing movement of the proximal limb, usually an arm.
Hemibalism usually occurs acutely, due to the infarction of the contralateral subtalamic nucleus, but occasionally occurs subacutely or chronically, due to other lesions of this nucleus. Korea is a rapid, spastic, irregular movement that tends to occur in the distal limbs or in the face, but can also occur in the proximal limbs and axial structures. Acute onset is usually toxic due to excessive therapy with levodopa and dopamine agonists.
In children it can be associated with acute articular rheumatism and in such cases it is designated as Sydenham Korea. The progressive onset in Korea is typical of degenerative neurological diseases, such as Huntington's Korea.
Myoclonia is a fast, short, irregular movement that is usually multifocal. Myoclonia can occur spontaneously at rest, in response to sensory stimuli, or with voluntary movements. It is a symptom that occurs in a wide variety of metabolic and neurological diseases. Posthypoxic intentional myoclonia is a special type of myoclonic syndrome that occurs as a sechele of transient cerebral anoxia.
Myoclonia can result from diseases with lipid storage, encephalitis, Creutzfeldt-Jakob disease or metabolic encephalopathy due to respiratory failure, chronic renal failure, liver failure or electrolyte imbalance. Myoclonia is also a feature of certain types of epilepsy.
There's more to say about hypokinetic movement disorders. These syndromes manifest themselves as bradykinesis, with a mask appearance but facial inexpressivity, loss of associated limb movements during walking and rigid "block" return.
If bradykinesis is associated only with a rest tremor, stiffness in the toothed wheel or impaired postural reflexes (especially with a tendency to fall on the back), Parkinson's disease is considered. If cognitive, language, upper motor neuron, sensory or autonomic signs are also present, there is a degenerative multisystemic neurological disease.
We'll continue tomorrow with everything related to imbalance and walking disorders.
I will continue with dysfunctions of the movement addressing their pathogenesis.
Movement dysfunctions result from basal nuclei disease, subcortical pair structures of gray substance, which form anatomically distinct nuclear groups. They are formed from the caudal nucleus and putamen (which together are called the striated body), the internal and external segments of the pale globe, the subthalamic nucleus and the black substance.
Major interconnections and neurotransmitters involved in basal nuclei circuits are of great importance. Cortical initiated movement is facilitated and competing movements are inhibited by the influence of basal nuclei. The oyster receives organized somatotropic impulses from several cortical areas.
These consist of separate multiple parallel circuits, which include impulses from the frontal, sensory and motor cortex and associated parietotemporooccipital areas (however, only post-central and somatosensory motor projections appear to be directly related to movement.
These projections are glutamatergic and excitatory). The oyster has direct and indirect projections in the major external nuclei of the basal nuclei, pars reticulated of the black substance and in the internal pale globe (also called the pale medial globule). These nuclei also project to the anterior and lateral ventral nuclei of the thalamus by GABA inhibitory neurotransmission.
Talamic currents have excitatory glutamatergic projections in cortical neurons. Thus, the inhibition of the reticulated part of the black substance and the internal pale globe disinhibits the tapamocortical projections that reconsolidate the initiated cortical activity and the arousal of these efferent pathways inhibits the tapamocortic projections for competitive motor responses. The basal core is not projected directly to the spinal cord.
The direct path from the reticulated pars of the black substance to the internal pale globe is GABA-ergic and inhibitory. This direct path then works to facilitate the tamapocratic projections that strengthen the initiated cortical movement. The indirect pathway is more complex and works to inhibit talmamocortical projections to other areas of the motor cortex. The first connection of the indirect path is GABA-ergic, it inhibits activity in the external pale globe, also called the pale lateral globe. The external pale globe transmits GABA-ergic inhibitors to the subthalamic nucleus.
The subthalamic nucleus exerts excitatory glutamatergic feedback on the external pale globe and glutamatergic excitatory impulses on the reticulated pars of the black substance and on the internal pale globe. Thus, the activation of the indirect path increases the effects from the reticulated pars of the black substance and from the internal pale globe, in contrast to the decrease in the effects that occur by activating the direct path.
Direct and indirect pathways are also influenced by pulses from the reticulated pars of the black substance. This dopaminergic aference on the striathas has a net inhibitory effect on the neurons of the direct pathway that predominantly expose dopaminergic D1 receptors and has a net excitatory effect on dopaminergic neurons D2.
The strict also has GABA-ergic feedback inhibitors with compact pars. The striatal activity is further modulated by cholinergic interneurons within the striatum, which are functional antagonists of dopaminergic beams. Behold, I'm done with these descriptions...
Let me move on to the hypokinetic dysfunctions of the movement. The model described explains well the hypokinetic dysfunctions of the movement. The fundamental anomaly in Parkinson's disease lies in the loss of dopaminergic neurons in the compact pars of the black substance. This causes loss of arousal of D1 striatal neurons from the direct pathway and loss of inhibition of D2 striatal neurons in the indirect pathway.
This combination of changes increases the eferences from the reticulated pars of the black substance and from the internal pale globule, which increases the inhibition of talamocortical projections and causes the loss of the facility of the cortical initiated movement. Rest tremor in Parkinson's disease is less explained by this pattern, but can result from the effects on cholinergic interneurons in the striat.
Now, a little bit about hyperkinetic dysfunction of movement. The pathogenesis of Korea in Huntington's disease consists of an initial loss of striatal neurons that expose D2 receptors and a normal GABA-ergic inhibitory projection via the indirect pathway. This disinhibits the external pale globule which, in turn, increases inhibition of the subtalamic nucleus.
Because glutamatergic impulses from the subthalamic nucleus are the primary source of excitation of the reticulated pars of the black substance and the internal pale globe, the loss of this excitation reduces the inhibition of the thalamus and the initiated cortical movements are facilitated without normal feedback control. The pathogenesis of hemibalism is similar, but less complicated, a direct lesion of glutamatergic neurons in the subthalamic nucleus leads to disinhibition of thalacortical projections.
Some movement dysfunctions, such as parkinsonism and Korea, may result from changes in discrete populations of neurons that use a specific neurotransmitter. Such selective vulnerability is commonly present in degenerative neurological diseases, both hereditary and sporadic, and under toxic, nutritional and inflammatory conditions.
Structural disease, which affects more than one cell type, is common only in hemibalism, in which it is almost always found a lesion of the subtalamic nucleus, usually a stroke.
Diagnostic approach and differential diagnosis for frequent clinical presentations of movement dysfunctions are based on different algorithms but, most begin with determining whether movement dysfunction is due to an excess or lack of movement (e.g. hyperkinetic or hypokinetic dysfunction of movement).
From the point of view of hyperkinetic dysfunctions of movement, abnormal involuntary movements are divided into those that are rhythmic and those that are irregular. Those that are rhythmic are called tremors. Tremor is divided into three types: rest tremor, postural tremor and intentional tremor. The resting tremor is maximal at rest and becomes less pronounced with movement.
It is characteristic of parkinsonism, a hypokinetic dysfunction of movement, and is therefore commonly associated with bradykinesis and stiffness in the toothed wheel. A rest tremor that develops acutely is usually due to toxins or dopamine-blocking drugs (such as phenothiazines). If the onset is insidious, the diagnostic approach is the same as for Parkinson's disease.
Postural tremor is maximum when the position of the limbs is actively maintained against gravity, it is reduced by rest and does not increase marked during voluntary movement towards a target. Postural tremor is maximum when the position of the limbs is actively maintained against gravity, it is reduced by rest and does not increase marked during voluntary movement towards a target.
Postural tremor that develops acutely is usually due to toxic or metabolic factors (e.g. hyperthyroidism) or stress. The insidious onset of a postural tremor suggests an essential benign or familial tremor. An intentional tremor is more pronounced during the voluntary movement towards a target and is not present during fasting or at rest. It's a sign of cerebellar disease.
The asterixis, which may at first glance resemble tremor, is an intermittent inhibition of muscle contraction that occurs in metabolic encephalopathy. This leads, for example, to a momentary and repetitive partial flexion of the wrist while attempting the sustained extension of the wrist.
Abnormal involuntary movements that are irregular are further characterized by their speed and place of occurrence and by the possibility of being suppressed voluntarily. The slowest are athetosis and dystonia. Athetosis is a slow contortion, a synuous movement that occurs almost continuously in the distal muscles.
Distonia is a deviation of posture varying slowly, but almost continuously, involving one or more joints (may occur in proximal or distal limbs or in axial structures). Distonia is a more sustained deviation of posture than athetosis, although these two phenomena overlap considerably. Among the rapid irregular movements, nerve tics are controlled with voluntary effort, while the others do not.
Nerve tics frequently appear repetitive in one place, but are sometimes multifocal. Korea, hemibalism and myoclonia are rapid, irregular seizures that cannot therefore be suppressed. Hemibalism is the most distinctive of them. It manifests itself as a sudden and often violent throwing movement of the proximal limb, usually an arm.
Hemibalism usually occurs acutely, due to the infarction of the contralateral subtalamic nucleus, but occasionally occurs subacutely or chronically, due to other lesions of this nucleus. Korea is a rapid, spastic, irregular movement that tends to occur in the distal limbs or in the face, but can also occur in the proximal limbs and axial structures. Acute onset is usually toxic due to excessive therapy with levodopa and dopamine agonists.
In children it can be associated with acute articular rheumatism and in such cases it is designated as Sydenham Korea. The progressive onset in Korea is typical of degenerative neurological diseases, such as Huntington's Korea.
Myoclonia is a fast, short, irregular movement that is usually multifocal. Myoclonia can occur spontaneously at rest, in response to sensory stimuli, or with voluntary movements. It is a symptom that occurs in a wide variety of metabolic and neurological diseases. Posthypoxic intentional myoclonia is a special type of myoclonic syndrome that occurs as a sechele of transient cerebral anoxia.
Myoclonia can result from diseases with lipid storage, encephalitis, Creutzfeldt-Jakob disease or metabolic encephalopathy due to respiratory failure, chronic renal failure, liver failure or electrolyte imbalance. Myoclonia is also a feature of certain types of epilepsy.
There's more to say about hypokinetic movement disorders. These syndromes manifest themselves as bradykinesis, with a mask appearance but facial inexpressivity, loss of associated limb movements during walking and rigid "block" return.
If bradykinesis is associated only with a rest tremor, stiffness in the toothed wheel or impaired postural reflexes (especially with a tendency to fall on the back), Parkinson's disease is considered. If cognitive, language, upper motor neuron, sensory or autonomic signs are also present, there is a degenerative multisystemic neurological disease.
We'll continue tomorrow with everything related to imbalance and walking disorders.
Pleasant,
soothing or party-filled weekend and good will... Each
according to the possibilities...
Dorin, Merticaru