STUDY - Technical - New Dacian's Medicine
Nervous
system disorders
(1)
Translation Draft
The main disorders of the nervous system, which are constituted as signs of the disease, are represented by lypotimia, syncope, dizziness and vertigo.
Syncopa is defined as a transient loss of consciousness with postural collapse, caused by a decrease in cerebral blood flow. Although it is often preceded by fainting and dizziness (presincope), it may not present as a cause cardiac asistola or ventricular tachycardia.
Symptoms of presincope can manifest as "dizziness", always without true vertigo, or can be simulated by a previous warning (aura) of attack. The sequence of symptoms is stereotypical and includes amplification of dizziness, blurred vision that precedes blindness, diaphoresis and feeling of weight in the lower limbs progressing towards postural rocking.
These symptoms increase in severity until consciousness is lost or ischemia is frequently corrected by settlement in clinostatism. An important, sometimes difficult, diagnostic problem is the differentiation of syncope from convulsion. During the following posts, syncope and dizziness will be taken into account from the particular point of view of clinical manifestations and differential evaluation (as a sign of the disease).
I'll start with the syncope. At the beginning of a syncopal attack, the patient is almost always seated upright, either orthostatic or sitting. A cardiac etiology, such as the Adam-Stokes crisis, is special from this point of view.
The patient is prevented by the imminent lypothymia by a feeling of "bad state", dizziness and the movement or swing ingating of the floor or surrounding objects. The patient becomes confused and may fall, visual spots may appear, vision will become blurred and ringing in the ears.
Nausea and sometimes vomiting accompany these symptoms. An obvious pallor or grayish-grey color of the face appears and generalized sweating occurs. In some patients, a onset with presincopal symptoms may allow the time needed to protect against injury but, in others, the appearance of syncope is sudden and without premonitoring symptoms. The onset ranges from instantaneous to 10 to 30 seconds, rarely longer.
The depth and duration of unconsciousness is variable. Sometimes the patient is not completely broken from the environment, other times a deep coma is present. The patient may remain in this state for a few seconds or minutes and even up to half an hour.
Usually, the patient is stretched, motionless, with relaxed skeletal muscles, but sometimes a few clonic contractions of the limbs and face can occur, immediately after the onset of unconsciousness, in some situations short tonic-clonic seizures occur. Sphincterian control is usually maintained. Pulse is weak or apparently absent, blood pressure is low to undetectable, and breathing can be imperceptible.
Once the patient is in a horizontal position, gravity no longer prevents blood flow to the brain. The amplitude of the pulse can increase, the color returns to the face, the breath becomes faster and deeper and the patient regains consciousness (there is usually an immediate return of consciousness).
However, some patients may not realize the state of physical weakness and lifting too quickly may precipitate another lipotimia. In some patients, especially those with transient tachyarrhythmias, there may be no residual symptoms after the initial syncope. Headache and drowsiness which, along with mental confusion, are the usual sequelae of seizures, does not follow a syncopal attack.
The "list" of causes of syncope is based on established or presumed physiological mechanisms, but the most common types of lipotimia can be reduced to a few simple mechanisms. Syncopa results from a sudden impairment of brain metabolism, usually caused by hypotension, with a reduction in cerebral blood flow.
Several mechanisms make circulatory adaptations in the vertical position. Approximately three-quarters of the systemic blood volume is contained in the venous bed and any interference with the venous return may cause reductions in cardiac output. Cerebral blood flow can still be maintained as long as systemic arterial vasoconstriction is performed, but when this adaptive mechanism ceases, severe hypotension with cerebral hypoperfusion leads to syncope in less than half of normal patients.
Normally, the accumulation of blood in the lower half of the body is prevented by: 1. pressure reflexes that induce constriction of peripheral arterioles and venulations, 2. reflex acceleration of heart rate by aortic and carotid reflexes and 3. improvement of venous return to the heart through the activity of limb muscles.
Placing a normal person on a table in a horizontal position to achieve muscle relaxation and then slowly tilting up the table leads to decreased heart rate and allows a slight accumulation of blood in the lower limbs. This may subsequently be followed by a slight transient decrease in systolic blood pressure and, in patients with deficient vasomotor reflexes, may produce lipotimia.
There are several types of syncope. Vasopressor syncope (vaso-vagal) or neurocardiogenic is the usual fainting that can be found in normal people and is responsible for about 50% of all cases of syncope.
It is often recurrent and can be frequently triggered by emotional stress (especially in a crowded, high-temperature room), fear (e.g. at the dentist), extreme fatigue, trauma or pain. However, many episodes occur without obvious historical causes.
In its classical form, vasopressor syncope comprises a number of symptoms including hypotension, bradycardia, nausea, pallor and diaphoresis. Syncopa occurs characteristically in states of diminished venous return, which lead to a reduced beating volume (cardiovascular) and a reflex increase in sympathetic activity.
In individuals with sensitivity, this increase in sympathetic activity leads to cardiac hypercontractility and excessive stimulation of ventricular mechanoreceptors (vagal fibers) which in turn lead to a decrease in sympathetic status and activation of the parasympathetic nervous system through a centrally mediated vasomotor reflex.
The overall result is a vicious circle of inadequate peripheral vasodilation and relative bradycardia, which causes progressive and syncope hypotension, which can be remitted by lying down and lifting the lower limbs. Orthostatic stress induced by the prolonged 60-80-degree tilted meal test is a sensitive technique for the reproduction of syncope in many patients with this syndrome.
Using a low-dose infusion of isoproteinerol increases the sensitivity of the tilted mass test and can lead to false positive tests when higher doses are used. Vasopressor syncope can occur with severe sudden pain, especially if it originates in the viscera, and can also rarely accompany a severe migraine.
Postural (orthostatic) hypotension with syncope affects people who have a chronic defect or variable instability of vasomotor reflexes. The decrease in blood pressure at the time of taking the orthostatic position is due to a loss of vasoconstrictor reflexes in the vessels of resistance and capacity of the lower limbs.
Although the syncopal crisis differs slightly from the vasopressor syncope, the effect of the position is essential. Sudden lifting from a lying position or a prolonged orthostatic position are precipitating factors. Postural syncope can occur in the following situations: 1. in otherwise normal people who have deficient postural reflexes (In such individuals, loss of consciousness can occur when tilting the table on which they are placed. In these circumstances, a slight initial decrease in blood pressure and then a stabilisation at a lower level was observed. Later, shortly after, the compensatory reflexes suddenly fail and blood pressure collapses rapidly. This situation is frequently familial) and 2. in primary vegetative autonomic insufficiency and in dysautonomias.
In the second case, three syndromes were delineated: 1. acute and subacute dysautonomia (In this rare condition, an otherwise healthy adult or child develops over a period of several days or weeks a complete or partial paralysis of sympathetic and parasympathetic nerve systems. Pupil reflexes are abolished and tear, salivation and sweating are absent or diminished. Impotence, paresis of the bladder and intestinal muscles and orthostatic hypotension are present. Proteins in cerebrospinal fluid - CRL - are frequently increased. Motor and sensory nerve fibers are integral, but nonmyelinized autonomic fibers exhibit degeneration.),
2. chronic post-ganglionary autonomic insufficiency (affection of middle-aged and old people, who progressively develop chronic orthostatic hypotension, sometimes in association with impotence and sphincter disorders. Typically, after maintaining the orthostatic position for 5 to 10 minutes, blood pressure drops by at least 35 mmHg, pulse pressure decreases and there is no compensatory tachycardia, pallor or nausea. Men are affected more frequently than women),
3. Chronic preganglionary autonomic insufficiency (In this condition, orthostatic hypotension together with anhydrosis, impotence and sphincter disorders, is associated with a disorder of the central nervous system - CNS. These conditions, designated as multisystemic atrophies include syndromes that manifest themselves through tremor, extrapyramidal stiffness and akinesis - Shy-Drager syndrome - progressive cerebellar degeneration, in several cases of a familial character and a much more variable extrapyramidal and cerebellar disorder - striatonim degeneration. These syndromes lead to severe and frequent lyexistence in a few years.)
Differential diagnosis between postganglionary peripheral chronic insufficiency and preganglionary central insufficiency is based on anatomological and pharmacological data. In the postganglionary type, the degeneration of neurons in the sympathetic ganglia occurs, while in the central type the degeneration of preganglionary cells in the lateral intermediate horn of the thoracic marrow occurs.
In the postganglionary peripheral type, the resting levels of norepinephrine are below normal due to the insufficiency of release of norepinephrine from the postganglionary endings and there is a hypersensitivity to injected norepinephrine. In the central type, the rest levels of norepinephrine are normal. When standing up, as opposed to the reaction of the normal individual, in both types there is a minimal or absent increase in levels of norepinephrine.
And in both types, plasma levels of dopamine betahydroxylase (the enzyme that converts dopamine to norepinephrine) are subnormal.
In the end of this post we will discuss other causes of postural syncope. 1. After loss of physical training, e.g. after a prolonged illness with bed rest, especially in elderly people with reduced muscle tone or after prolonged weightlessness, as in flights in outer space. 2. After sympatectomy that abolished vasopressor reflexes. 3. In diabetic, alcoholic or other neuropathies.
The most common form of neurogenic orthostatic hypotension is that which accompanies diseases of the peripheral nervous system. Examples consist of diabetic polyneuropathy, beri-beri, polyneuropathy in amyloidosis and Adie syndrome. Usually, orthostatic hypotension with sweating disorders, impotence and sphincter damage.
The lesions probably involve the unmyelinated postganglionary fibers in the peripheral nerves. In patients receiving antihypertensive and vasodilating drugs, as well as in those who may have hypovolemia due to diuretics, excessive sweating or adrenal insufficiency.
There is also the small syncope, a disorder commonly found in older men that occurs during or after urination, especially after waking from sleep, is probably a special type of vasopressor syncope. Decrease in intravescal pressure can trigger sudden vasodilation and vagal mediated bradycardia.
The main disorders of the nervous system, which are constituted as signs of the disease, are represented by lypotimia, syncope, dizziness and vertigo.
Syncopa is defined as a transient loss of consciousness with postural collapse, caused by a decrease in cerebral blood flow. Although it is often preceded by fainting and dizziness (presincope), it may not present as a cause cardiac asistola or ventricular tachycardia.
Symptoms of presincope can manifest as "dizziness", always without true vertigo, or can be simulated by a previous warning (aura) of attack. The sequence of symptoms is stereotypical and includes amplification of dizziness, blurred vision that precedes blindness, diaphoresis and feeling of weight in the lower limbs progressing towards postural rocking.
These symptoms increase in severity until consciousness is lost or ischemia is frequently corrected by settlement in clinostatism. An important, sometimes difficult, diagnostic problem is the differentiation of syncope from convulsion. During the following posts, syncope and dizziness will be taken into account from the particular point of view of clinical manifestations and differential evaluation (as a sign of the disease).
I'll start with the syncope. At the beginning of a syncopal attack, the patient is almost always seated upright, either orthostatic or sitting. A cardiac etiology, such as the Adam-Stokes crisis, is special from this point of view.
The patient is prevented by the imminent lypothymia by a feeling of "bad state", dizziness and the movement or swing ingating of the floor or surrounding objects. The patient becomes confused and may fall, visual spots may appear, vision will become blurred and ringing in the ears.
Nausea and sometimes vomiting accompany these symptoms. An obvious pallor or grayish-grey color of the face appears and generalized sweating occurs. In some patients, a onset with presincopal symptoms may allow the time needed to protect against injury but, in others, the appearance of syncope is sudden and without premonitoring symptoms. The onset ranges from instantaneous to 10 to 30 seconds, rarely longer.
The depth and duration of unconsciousness is variable. Sometimes the patient is not completely broken from the environment, other times a deep coma is present. The patient may remain in this state for a few seconds or minutes and even up to half an hour.
Usually, the patient is stretched, motionless, with relaxed skeletal muscles, but sometimes a few clonic contractions of the limbs and face can occur, immediately after the onset of unconsciousness, in some situations short tonic-clonic seizures occur. Sphincterian control is usually maintained. Pulse is weak or apparently absent, blood pressure is low to undetectable, and breathing can be imperceptible.
Once the patient is in a horizontal position, gravity no longer prevents blood flow to the brain. The amplitude of the pulse can increase, the color returns to the face, the breath becomes faster and deeper and the patient regains consciousness (there is usually an immediate return of consciousness).
However, some patients may not realize the state of physical weakness and lifting too quickly may precipitate another lipotimia. In some patients, especially those with transient tachyarrhythmias, there may be no residual symptoms after the initial syncope. Headache and drowsiness which, along with mental confusion, are the usual sequelae of seizures, does not follow a syncopal attack.
The "list" of causes of syncope is based on established or presumed physiological mechanisms, but the most common types of lipotimia can be reduced to a few simple mechanisms. Syncopa results from a sudden impairment of brain metabolism, usually caused by hypotension, with a reduction in cerebral blood flow.
Several mechanisms make circulatory adaptations in the vertical position. Approximately three-quarters of the systemic blood volume is contained in the venous bed and any interference with the venous return may cause reductions in cardiac output. Cerebral blood flow can still be maintained as long as systemic arterial vasoconstriction is performed, but when this adaptive mechanism ceases, severe hypotension with cerebral hypoperfusion leads to syncope in less than half of normal patients.
Normally, the accumulation of blood in the lower half of the body is prevented by: 1. pressure reflexes that induce constriction of peripheral arterioles and venulations, 2. reflex acceleration of heart rate by aortic and carotid reflexes and 3. improvement of venous return to the heart through the activity of limb muscles.
Placing a normal person on a table in a horizontal position to achieve muscle relaxation and then slowly tilting up the table leads to decreased heart rate and allows a slight accumulation of blood in the lower limbs. This may subsequently be followed by a slight transient decrease in systolic blood pressure and, in patients with deficient vasomotor reflexes, may produce lipotimia.
There are several types of syncope. Vasopressor syncope (vaso-vagal) or neurocardiogenic is the usual fainting that can be found in normal people and is responsible for about 50% of all cases of syncope.
It is often recurrent and can be frequently triggered by emotional stress (especially in a crowded, high-temperature room), fear (e.g. at the dentist), extreme fatigue, trauma or pain. However, many episodes occur without obvious historical causes.
In its classical form, vasopressor syncope comprises a number of symptoms including hypotension, bradycardia, nausea, pallor and diaphoresis. Syncopa occurs characteristically in states of diminished venous return, which lead to a reduced beating volume (cardiovascular) and a reflex increase in sympathetic activity.
In individuals with sensitivity, this increase in sympathetic activity leads to cardiac hypercontractility and excessive stimulation of ventricular mechanoreceptors (vagal fibers) which in turn lead to a decrease in sympathetic status and activation of the parasympathetic nervous system through a centrally mediated vasomotor reflex.
The overall result is a vicious circle of inadequate peripheral vasodilation and relative bradycardia, which causes progressive and syncope hypotension, which can be remitted by lying down and lifting the lower limbs. Orthostatic stress induced by the prolonged 60-80-degree tilted meal test is a sensitive technique for the reproduction of syncope in many patients with this syndrome.
Using a low-dose infusion of isoproteinerol increases the sensitivity of the tilted mass test and can lead to false positive tests when higher doses are used. Vasopressor syncope can occur with severe sudden pain, especially if it originates in the viscera, and can also rarely accompany a severe migraine.
Postural (orthostatic) hypotension with syncope affects people who have a chronic defect or variable instability of vasomotor reflexes. The decrease in blood pressure at the time of taking the orthostatic position is due to a loss of vasoconstrictor reflexes in the vessels of resistance and capacity of the lower limbs.
Although the syncopal crisis differs slightly from the vasopressor syncope, the effect of the position is essential. Sudden lifting from a lying position or a prolonged orthostatic position are precipitating factors. Postural syncope can occur in the following situations: 1. in otherwise normal people who have deficient postural reflexes (In such individuals, loss of consciousness can occur when tilting the table on which they are placed. In these circumstances, a slight initial decrease in blood pressure and then a stabilisation at a lower level was observed. Later, shortly after, the compensatory reflexes suddenly fail and blood pressure collapses rapidly. This situation is frequently familial) and 2. in primary vegetative autonomic insufficiency and in dysautonomias.
In the second case, three syndromes were delineated: 1. acute and subacute dysautonomia (In this rare condition, an otherwise healthy adult or child develops over a period of several days or weeks a complete or partial paralysis of sympathetic and parasympathetic nerve systems. Pupil reflexes are abolished and tear, salivation and sweating are absent or diminished. Impotence, paresis of the bladder and intestinal muscles and orthostatic hypotension are present. Proteins in cerebrospinal fluid - CRL - are frequently increased. Motor and sensory nerve fibers are integral, but nonmyelinized autonomic fibers exhibit degeneration.),
2. chronic post-ganglionary autonomic insufficiency (affection of middle-aged and old people, who progressively develop chronic orthostatic hypotension, sometimes in association with impotence and sphincter disorders. Typically, after maintaining the orthostatic position for 5 to 10 minutes, blood pressure drops by at least 35 mmHg, pulse pressure decreases and there is no compensatory tachycardia, pallor or nausea. Men are affected more frequently than women),
3. Chronic preganglionary autonomic insufficiency (In this condition, orthostatic hypotension together with anhydrosis, impotence and sphincter disorders, is associated with a disorder of the central nervous system - CNS. These conditions, designated as multisystemic atrophies include syndromes that manifest themselves through tremor, extrapyramidal stiffness and akinesis - Shy-Drager syndrome - progressive cerebellar degeneration, in several cases of a familial character and a much more variable extrapyramidal and cerebellar disorder - striatonim degeneration. These syndromes lead to severe and frequent lyexistence in a few years.)
Differential diagnosis between postganglionary peripheral chronic insufficiency and preganglionary central insufficiency is based on anatomological and pharmacological data. In the postganglionary type, the degeneration of neurons in the sympathetic ganglia occurs, while in the central type the degeneration of preganglionary cells in the lateral intermediate horn of the thoracic marrow occurs.
In the postganglionary peripheral type, the resting levels of norepinephrine are below normal due to the insufficiency of release of norepinephrine from the postganglionary endings and there is a hypersensitivity to injected norepinephrine. In the central type, the rest levels of norepinephrine are normal. When standing up, as opposed to the reaction of the normal individual, in both types there is a minimal or absent increase in levels of norepinephrine.
And in both types, plasma levels of dopamine betahydroxylase (the enzyme that converts dopamine to norepinephrine) are subnormal.
In the end of this post we will discuss other causes of postural syncope. 1. After loss of physical training, e.g. after a prolonged illness with bed rest, especially in elderly people with reduced muscle tone or after prolonged weightlessness, as in flights in outer space. 2. After sympatectomy that abolished vasopressor reflexes. 3. In diabetic, alcoholic or other neuropathies.
The most common form of neurogenic orthostatic hypotension is that which accompanies diseases of the peripheral nervous system. Examples consist of diabetic polyneuropathy, beri-beri, polyneuropathy in amyloidosis and Adie syndrome. Usually, orthostatic hypotension with sweating disorders, impotence and sphincter damage.
The lesions probably involve the unmyelinated postganglionary fibers in the peripheral nerves. In patients receiving antihypertensive and vasodilating drugs, as well as in those who may have hypovolemia due to diuretics, excessive sweating or adrenal insufficiency.
There is also the small syncope, a disorder commonly found in older men that occurs during or after urination, especially after waking from sleep, is probably a special type of vasopressor syncope. Decrease in intravescal pressure can trigger sudden vasodilation and vagal mediated bradycardia.
I
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Dorin, Merticaru