STUDY - Technical - New Dacian's Medicine
Acute
Confusion and Coma (1)
Translation Draft
Confusional states and coma are among the most common problems of general medicine. It is estimated that more than 5% of presentations to the emergency rooms of large municipal hospitals are due to conditions that cause impaired consciousness.
Because minor impairment of consciousness (confusion) cannot be easily separated from decreased levels of consciousness (sleepiness, stupor and coma) and these two are caused by many similar medical conditions.
Although the interpretation of consciousness is a psychological and philosophical problem, the distinction between the level of consciousness or waking state and the content of consciousness or consciousness has a neurological significance. The wake/alert state is maintained by a system of neurons located at the level of the brain stem and at the level of the thalamus, the upper reticulated activator system (SRA) and by its extensive connections with the cerebral hemispheres.
Therefore, the reduction in wakefulness results from depression of neuronal activity either in the cerebral hemispheres or at the level of the SRA. Consciousness and thinking are dependent on integrated and organized ideas, subjective experience, emotions and mental processes, each of which is to some extent located in anatomically defined regions of the brain.
Self-consciousness requires the body to feel this personal current of emotional thoughts and experiences. The inability to maintain the coherent sequence of ideas, frequently accompanied by inattention or disorientation, is the best definition for confusion, and this is a condition of the content of consciousness.
I'll start with the states of reduced alertness. The non-physiological situation of reduced alertness and diminished reactivity is a continuum that in extreme form characterizes the state similar to deep sleep from which the patient cannot be awakened, called a coma.
Drowsiness is a condition that simulates shallow sleep, from which the patient can be easily awakened by touch or noise and can maintain his alertness for some time. The stupor defines a condition from which the patient can be awakened only by vigorous stimuli and makes an effort to avoid uncomfortable or aggravating stimulation.
As already mentioned, both drowsiness and stupor are expected with the installation of some degree of mental confusion. Therefore, in these states the verbal response is incorrect, slowed, or absent during the wake-up period.
Coma indicates a condition from which the patient cannot be awakened by stimulation and there is no gesture to avoid painful stimuli. In clinical practice, these terms should be supplemented by a narrative description of the patient's state of behaviour and responsiveness evoked by various specific stimuli, as observed in the patient's bed. Such descriptions are preferable to ambiguous, summary terms such as semicoma or obnubilation, the definitions of which differ depending on the clinician.
Confusion, confusion, is a behavioral state of reduced mental stability, coherence, comprehension and motivation. Inattention and disorientation are the main early signs. However, with the aggravation of the acute confusional state there is a deterioration of memory, perception, understanding, problem-solving ability, language, praxis, spatial visual function and various aspects of emotional behavior, each of which is identified in a specific region of the brain.
During early impairment, it is difficult to determine whether these complex mental functions are reduced only as a result of a predominant defect of attention, but overall cortical dysfunction is expected in the case of metabolic diseases and pharmacological agents, which are the most common sources of acute confusion. The patient is said to have encephalopathy when, in addition to confusion, he also has elements of drowsiness.
Confusion can be a characteristic of dementia, in which case the chronicization of the process and sometimes the disproportionate effect on memory distinguish it from acute confusion. Confusional state can also result from a deficiency of a single superior mental cortical function, such as impaired language comprehension, memory loss or loss of spatial appreciation, in which case each state is defined by dominant behavioral change (i.e. aphasia, dementia, agnosia) rather than characterizing the condition as confusion.
Drowsiness caused by systemic metabolic changes or brain damage is characteristically accompanied by confusion (encephalopathy). In these situations, the main problem that causes the level of consciousness to decrease must be established. A difficult circumstance occurs when the process that ultimately leads to drowsiness or stupor begins with confusion or delirium in the patient in full wakefulness. The confused patient is usually quiet, does not lean towards dialogue and is mentally inactive.
In some cases confusion is accompanied by delusions (misperceptions of vision, sound or sense of touch) or hallucinations (spontaneous endogenous perceptions). While psychiatrists use the term delirium interchangeably with confusion, neurologists prefer to reserve it as a description for hallucinatory hypersympatotonic agitation, most often due to alcohol or stopping drugs or hallucinatory drugs.
Now let's move on to come-like syndromes and associated states. Coma is characterized by a total impossibility of awakening. Many other syndromes describe patients as seemingly insensitive or unresponsive, but are considered separately because of their special significance. The vegetative state, a totally unfortunate term, describes patients who were previously comatose but whose eyelids were opened, leaving the impression that they are in a state of alertness.
In these we can observe the presence of yawning, grunting and disordered movements of the limbs and head, but also a total inability to respond to commands or communicate, essentially being a "vigil coma". There are associated signs of extensive damage to both cerebral hemispheres, for example, Babinski signs, positioning of limbs in the state of shelling or decerebration, and absence of response to visual stimuli.
The functions of the autonomic nervous system, such as cardiovascular control, thermoregulator and neuroendocrine, are preserved and may exhibit periods of hyperactivity. The vegetative state results from the overall damage of the cerebral cortex, most often by cardiac arrest or craniocerebral injury. Akinetic mutism refers to a fully or partially awake patient who remains immobile and silent when unstimulated.
The condition can be determined by hydrocephalus, tumor masses in the region of the third ventricle or by large bilateral lesions in the cingulate gyrus or other areas of both frontal lobes. Periductal or lower diencephalic lesions may cause a similar condition. Abulia can be seen as a mild form of akinetic mutism with the same anatomical origins. the abulic patient is hypokinetic and slow in responses but generally gives correct answers. It typically stops while reciting numbers or sequential calculations and, late, resumes the correct string.
The state of inner blockage describes a pseudocoma in which patients are awake but disaffected, respectively, do not have the desire to speak or perform movements of the limbs, face or pharyngeal. Common causes are infarction or hemorrhage of the anterior bridge that severs all corticospinal and corticobulbar descending pathways.
Activation of the SRA, vertical movements of the eye and lifting of the eyelids remain unaffected. Such eye movements can be used by the patient to signal the examiner. A similar state of awakening simulating non-responsiveness may occur as a result of total paralysis of the limb muscles, eye and oropharyngeal muscles in severe cases of acute Guillain-Barre syndrome (a disease of the peripheral nerve).
Unlike the brain stem, the vertical movements of the eye are not selectively spared. Certain psychiatric conditions mimic coma, causing apparent op to lack of response. Catatonia is a term for a specific hypomobile syndrome, associated with major psychosis. In the typical form, the liket patients appear conscious, have their eyes open, but do not make voluntary or responsive movements, although they blink spontaneously and do not seem disturbed.
"Demandy flexibility" may also be associated, in which the limbs remain in their position when raised by the examiner. Once you've recovered, these patients remind you of something that happened to them during catatonic stupor. Patients in a pseudocomatous or hysteric state show signs of trying to appear co-comatose, although some ingenuity on the part of the examiner is required to demonstrate this. They can resist lifting the eyelids, blink to virtual hazards when the eyelids are kept open, all these signs denying the head injury.
There's something to be said for the anatomical correlations of consciousness. A normal level of consciousness (wakefulness) depends on the activation of the cerebral hemispheres by groups of neurons located in the SRA of the brain stem. All these components and the links between them must be retained to maintain normal consciousness.
Therefore, the main causes of the comet are 1. bilateral hemispheric damage (injury) by ischemia, trauma or other rarer brain disorders, 2. suppression of brain function by drugs, toxins or hypoxia or by internal metabolic disorders such as hypoglycaemia, nitrogenemia, liver failure or hypercalcemia and 3. lesions of the brain stem that cause proximal damage to the SRA.
SRA is a physiological system contained in the rosral part of the reticulated formation and consists of neurons located bilaterally, in the tegmental gray matter of the brain stem and stretching from bulb to diencephalus. Animal experiments and clinical and anatomological observations have established that the region of the reticular formation which is of paramount importance in maintaining the state of wakefulness extends from the rosral bridge to the caudal diencephalus. It is inferred practical importance, namely that destructive lesions that cause coma also affect the structures adjacent to the brain stem of the upper deck, the mesencephalus and the diencephalus, which are involved in pupillary function and eye movements.
The abnormalities found in these systems provide adequate, albeit indirect, indications of direct damage to the brain stem as a source of comet. Injuries to the cerebral hemispheres do not directly affect the SRA of the brain stem, although a secondary dysfunction of the upper brain stem often results from compression caused by a mass in a cerebral hemisphere (such as the case of transtentorial hernia).
The SRA neurons of the brain stem are projected rostalononly onto the cortex, primarily through the talamic relay shells that exert a tonic influence on the cerebral cortex. Experiments on primates suggest that the sRA of the trunk affects the level of consciousness by suppressing the activity of nonspecific nuclei which, in turn, exhibit a predominantly inhibitory effect on the cortex, but this is an oversimplification.
It is believed that high-frequency rhythms (30-40 Hz) synchronize cortical and talamic neurons during wakefulness. The basis of the behavioral response to environmental stimuli (somesthetic, auditory and visual) depends on the rich innervation that SAR receives from these sensory systems. Retransmission between SRA and thalamic and cortical areas is performed through neurotransmitters. Of these, the influences of acetylcholine and biogenic amines on awakening were studied most.
Cholinergic fibers link the mesencephalus to other areas of the upper brain stem, thalamus and cortex. And serotonin and norepinephrine have important functions in regulating the sleep-wake cycle. Their role in awakening and coma has not been clearly established, although the alarm effects of amphetamines may be mediated by the release of catecholamines.
I'll continue in tomorrow's post!
Confusional states and coma are among the most common problems of general medicine. It is estimated that more than 5% of presentations to the emergency rooms of large municipal hospitals are due to conditions that cause impaired consciousness.
Because minor impairment of consciousness (confusion) cannot be easily separated from decreased levels of consciousness (sleepiness, stupor and coma) and these two are caused by many similar medical conditions.
Although the interpretation of consciousness is a psychological and philosophical problem, the distinction between the level of consciousness or waking state and the content of consciousness or consciousness has a neurological significance. The wake/alert state is maintained by a system of neurons located at the level of the brain stem and at the level of the thalamus, the upper reticulated activator system (SRA) and by its extensive connections with the cerebral hemispheres.
Therefore, the reduction in wakefulness results from depression of neuronal activity either in the cerebral hemispheres or at the level of the SRA. Consciousness and thinking are dependent on integrated and organized ideas, subjective experience, emotions and mental processes, each of which is to some extent located in anatomically defined regions of the brain.
Self-consciousness requires the body to feel this personal current of emotional thoughts and experiences. The inability to maintain the coherent sequence of ideas, frequently accompanied by inattention or disorientation, is the best definition for confusion, and this is a condition of the content of consciousness.
I'll start with the states of reduced alertness. The non-physiological situation of reduced alertness and diminished reactivity is a continuum that in extreme form characterizes the state similar to deep sleep from which the patient cannot be awakened, called a coma.
Drowsiness is a condition that simulates shallow sleep, from which the patient can be easily awakened by touch or noise and can maintain his alertness for some time. The stupor defines a condition from which the patient can be awakened only by vigorous stimuli and makes an effort to avoid uncomfortable or aggravating stimulation.
As already mentioned, both drowsiness and stupor are expected with the installation of some degree of mental confusion. Therefore, in these states the verbal response is incorrect, slowed, or absent during the wake-up period.
Coma indicates a condition from which the patient cannot be awakened by stimulation and there is no gesture to avoid painful stimuli. In clinical practice, these terms should be supplemented by a narrative description of the patient's state of behaviour and responsiveness evoked by various specific stimuli, as observed in the patient's bed. Such descriptions are preferable to ambiguous, summary terms such as semicoma or obnubilation, the definitions of which differ depending on the clinician.
Confusion, confusion, is a behavioral state of reduced mental stability, coherence, comprehension and motivation. Inattention and disorientation are the main early signs. However, with the aggravation of the acute confusional state there is a deterioration of memory, perception, understanding, problem-solving ability, language, praxis, spatial visual function and various aspects of emotional behavior, each of which is identified in a specific region of the brain.
During early impairment, it is difficult to determine whether these complex mental functions are reduced only as a result of a predominant defect of attention, but overall cortical dysfunction is expected in the case of metabolic diseases and pharmacological agents, which are the most common sources of acute confusion. The patient is said to have encephalopathy when, in addition to confusion, he also has elements of drowsiness.
Confusion can be a characteristic of dementia, in which case the chronicization of the process and sometimes the disproportionate effect on memory distinguish it from acute confusion. Confusional state can also result from a deficiency of a single superior mental cortical function, such as impaired language comprehension, memory loss or loss of spatial appreciation, in which case each state is defined by dominant behavioral change (i.e. aphasia, dementia, agnosia) rather than characterizing the condition as confusion.
Drowsiness caused by systemic metabolic changes or brain damage is characteristically accompanied by confusion (encephalopathy). In these situations, the main problem that causes the level of consciousness to decrease must be established. A difficult circumstance occurs when the process that ultimately leads to drowsiness or stupor begins with confusion or delirium in the patient in full wakefulness. The confused patient is usually quiet, does not lean towards dialogue and is mentally inactive.
In some cases confusion is accompanied by delusions (misperceptions of vision, sound or sense of touch) or hallucinations (spontaneous endogenous perceptions). While psychiatrists use the term delirium interchangeably with confusion, neurologists prefer to reserve it as a description for hallucinatory hypersympatotonic agitation, most often due to alcohol or stopping drugs or hallucinatory drugs.
Now let's move on to come-like syndromes and associated states. Coma is characterized by a total impossibility of awakening. Many other syndromes describe patients as seemingly insensitive or unresponsive, but are considered separately because of their special significance. The vegetative state, a totally unfortunate term, describes patients who were previously comatose but whose eyelids were opened, leaving the impression that they are in a state of alertness.
In these we can observe the presence of yawning, grunting and disordered movements of the limbs and head, but also a total inability to respond to commands or communicate, essentially being a "vigil coma". There are associated signs of extensive damage to both cerebral hemispheres, for example, Babinski signs, positioning of limbs in the state of shelling or decerebration, and absence of response to visual stimuli.
The functions of the autonomic nervous system, such as cardiovascular control, thermoregulator and neuroendocrine, are preserved and may exhibit periods of hyperactivity. The vegetative state results from the overall damage of the cerebral cortex, most often by cardiac arrest or craniocerebral injury. Akinetic mutism refers to a fully or partially awake patient who remains immobile and silent when unstimulated.
The condition can be determined by hydrocephalus, tumor masses in the region of the third ventricle or by large bilateral lesions in the cingulate gyrus or other areas of both frontal lobes. Periductal or lower diencephalic lesions may cause a similar condition. Abulia can be seen as a mild form of akinetic mutism with the same anatomical origins. the abulic patient is hypokinetic and slow in responses but generally gives correct answers. It typically stops while reciting numbers or sequential calculations and, late, resumes the correct string.
The state of inner blockage describes a pseudocoma in which patients are awake but disaffected, respectively, do not have the desire to speak or perform movements of the limbs, face or pharyngeal. Common causes are infarction or hemorrhage of the anterior bridge that severs all corticospinal and corticobulbar descending pathways.
Activation of the SRA, vertical movements of the eye and lifting of the eyelids remain unaffected. Such eye movements can be used by the patient to signal the examiner. A similar state of awakening simulating non-responsiveness may occur as a result of total paralysis of the limb muscles, eye and oropharyngeal muscles in severe cases of acute Guillain-Barre syndrome (a disease of the peripheral nerve).
Unlike the brain stem, the vertical movements of the eye are not selectively spared. Certain psychiatric conditions mimic coma, causing apparent op to lack of response. Catatonia is a term for a specific hypomobile syndrome, associated with major psychosis. In the typical form, the liket patients appear conscious, have their eyes open, but do not make voluntary or responsive movements, although they blink spontaneously and do not seem disturbed.
"Demandy flexibility" may also be associated, in which the limbs remain in their position when raised by the examiner. Once you've recovered, these patients remind you of something that happened to them during catatonic stupor. Patients in a pseudocomatous or hysteric state show signs of trying to appear co-comatose, although some ingenuity on the part of the examiner is required to demonstrate this. They can resist lifting the eyelids, blink to virtual hazards when the eyelids are kept open, all these signs denying the head injury.
There's something to be said for the anatomical correlations of consciousness. A normal level of consciousness (wakefulness) depends on the activation of the cerebral hemispheres by groups of neurons located in the SRA of the brain stem. All these components and the links between them must be retained to maintain normal consciousness.
Therefore, the main causes of the comet are 1. bilateral hemispheric damage (injury) by ischemia, trauma or other rarer brain disorders, 2. suppression of brain function by drugs, toxins or hypoxia or by internal metabolic disorders such as hypoglycaemia, nitrogenemia, liver failure or hypercalcemia and 3. lesions of the brain stem that cause proximal damage to the SRA.
SRA is a physiological system contained in the rosral part of the reticulated formation and consists of neurons located bilaterally, in the tegmental gray matter of the brain stem and stretching from bulb to diencephalus. Animal experiments and clinical and anatomological observations have established that the region of the reticular formation which is of paramount importance in maintaining the state of wakefulness extends from the rosral bridge to the caudal diencephalus. It is inferred practical importance, namely that destructive lesions that cause coma also affect the structures adjacent to the brain stem of the upper deck, the mesencephalus and the diencephalus, which are involved in pupillary function and eye movements.
The abnormalities found in these systems provide adequate, albeit indirect, indications of direct damage to the brain stem as a source of comet. Injuries to the cerebral hemispheres do not directly affect the SRA of the brain stem, although a secondary dysfunction of the upper brain stem often results from compression caused by a mass in a cerebral hemisphere (such as the case of transtentorial hernia).
The SRA neurons of the brain stem are projected rostalononly onto the cortex, primarily through the talamic relay shells that exert a tonic influence on the cerebral cortex. Experiments on primates suggest that the sRA of the trunk affects the level of consciousness by suppressing the activity of nonspecific nuclei which, in turn, exhibit a predominantly inhibitory effect on the cortex, but this is an oversimplification.
It is believed that high-frequency rhythms (30-40 Hz) synchronize cortical and talamic neurons during wakefulness. The basis of the behavioral response to environmental stimuli (somesthetic, auditory and visual) depends on the rich innervation that SAR receives from these sensory systems. Retransmission between SRA and thalamic and cortical areas is performed through neurotransmitters. Of these, the influences of acetylcholine and biogenic amines on awakening were studied most.
Cholinergic fibers link the mesencephalus to other areas of the upper brain stem, thalamus and cortex. And serotonin and norepinephrine have important functions in regulating the sleep-wake cycle. Their role in awakening and coma has not been clearly established, although the alarm effects of amphetamines may be mediated by the release of catecholamines.
I'll continue in tomorrow's post!
Have
a nice weekend!
Dorin, Merticaru