The current health reports do not provide an accurate estimate of the frequency of people who are in a persistent vegetative state (PVS), worldwide. Ten years ago Japan was estimated for a ratio of 2 to 3 per 100,000. It is likely that the absolute number of such cases has increased significantly as a result of current practices in critical care medicine, cardiorespiratory support, intravenous feeding and control of infections in patients with severe brain damage. A large and growing problem facing this result is as emotionally painful, expensive and usually unwanted modern medical treatment.
VEGETATIVE NERVOUS SYSTEM
The vegetative life consists of sympathetic and parasympathetic systems.
DESCRIPTION sympathetic system
It is formed by a double chain of ganglia or extends from the 1st. last cervical vertebra to the sacrum.
Just two or three nodes merging 7 this segment:
* Superior cervical ganglion. – Get 4 or 5 ramicomunicantes and gives off branches to vessels and organs of the head neck and heart.
* Middle cervical ganglion. – Receives ramicomunicaciones V and Vi and emits cervical nerves to the thyroid and heart.
* Lower cervical ganglion. – Arriving at the seventh and eighth cervical ramicomunicaciones. It also gives branches to the heart and the vessels of the arm.
Comprised of eleven or twelve each receiving node or two ramicomunicantes.
* The first 4 nodes emit branches to the heart, aorta, esophagus and lungs.
* The 4 or 5 nodes that follow, are the greater splanchnic nerve, its branches and that interrupt efferent lymph of Lobstein and after passing through the diaphragm ends in the semilunar ganglion, whose connectedness forming fillets out the solar plexus, which in turn, gives rise to many side plexuses.
* The following are the splanchnic lymph lower nerve that follows similar route as the greater splanchnic and also ends in semilunar ganglion, thereby contributing to form the solar plexus.
Consisting of three to five nodes. Their efferent branches, mainly confluent inferior mesenteric ganglion, then form plexuses, to vessels and organs of the region.
Formed by 4 or 5 nodes. At the bottom simpa’tica chain, side joins the other by the coccygeal ganglion, and odd half cromofn oxygen.
The autonomic or parasympathetic sistma consists of 3 parts:
* The cranial parasympathetic
* The neumagstrico
* The pelvic parasympathetic
Or parasympathetic cranial
The sympathetic fibers are the cranial nerves: oculomotor, facial, and glossopharyngeal trignimo.
Sympathetic portion of the oculomotor. Born in the papillary core is interrupted in the ciliary ganglion and then becomes part of the short ciliary nerves. It is related to the optical life.
The facial nerve nucleus born and accompanying tear throughout your journey to this nerve. Are interrupted in the geniculate ganglion and the sphenopalatine. Trigeminal relate. Go to the lacrimal glands, pharynx and palate.
There are also other fibers (that go with the broker Wrisberg) for the submandibular and sublingual glands.
When accompanying fiber Glossopharyngeal born in salivary nucleus, to the ganglion Anderson, having previously crossed Ehrenritter ganglion. Anderson goes ganglion to form the nerve of Jacobson, etc., Interrupting the optical node to go to the parotid. They are related to the sympathetic and trignimo.
When accompanying trigeminal fibers that apparently are not their own, but depend on other nerves, and cranial or thoracolumbar.
Being born at the bulb, crossing plexiform and jugular ganglia, gives off branches to all thoracic organs (esophagus, trachea, lung and heart); crosses later in diaphragm and ends at the semilunar ganglion, in the manner of the splanchnic and thereby forming call them so memorable Wrisberg handle. In the abdomen innervates the stomach, small intestine, etc..
Formed by three roots that unite to form a single nerve, pelvic nerve, also called erector. It then divides into two branches which are to form: a visceral plexus and other colorectal.
SCHEME excitation functions of the sympathetic
Asialia or dry mouth or thick saliva (mucous glands)
Dilates the muscles of the esophagus
Constrains the cardia
Dilates the coronary
Accelerates the heart
Decreases oculocardio reflection (no decrease pulsations by compressing the eyeballs).
Increases blood pressure
Dilates the muscles of the esophagus
Action splanchnic and solar plexus
Lumbar and straight:
Collapses the ureter.
* The vessels of bladder
* The sphincter
* The urethra
SCHEME excitation functions of the parasympathetic
Mucisas secretion and salivary glands.
Salivary (parotid, saliva fluid).
Vago itself (vagus):
Contract your bronchial (asthma)
Inhibitor heart (bradycardia)
Vasoconstriction of the coronary arteries.
Increases oculocardiac reflex
Gastric and gastric hypermotility Hiperseccin
Constricts the hepatic artery
Dilates the portal
Idem of the external genitalia
It relaxes the sphincter of the bladder
Idem of the musculature of the urethra
Collapses the bladder detrusor
Dilates the vessels of the colon, rectum and anus.
Contract the muscles of the colon and rectum (colic spasm).
Exploration methods of the vegetative system
Course of functional antagonism of sympathetic and parasympathetic systems, the imbalance of both systems will be manifested by increased tone or dominance of one over the other, and as the sympathetic or parasympathetic dominant are called, respectively sympathicotonia or vagotonia the syndromes that originate it.
Action of the sympathetic and parasympathetic systems
The a-receptor receptor of smooth muscles are excited by the sympathetic mimetics, while the b-receptors are inhibited.
PERSISTENT VEGETATIVE STATE
Pathologic loss of consciousness may result a variety of brain damage including without limitation, nutritional insufficiency, poisoning, stroke, infections, direct physical injury or degenerative disease. The abrupt loss of consciousness is usually an acute state of sleep, as if asleep, called a coma, which can have varying degrees of recovery or a serious chronic neurological impairment. People with severe damage to the cerebral hemispheres often go into a state of unconsciousness called chronic vegetative state, in which the body cyclically wakes and sleeps, but does not express or cerebral metabolic evidence indicating behavior or cognitive function is able to respond in a learned manner to events or external stimuli. This condition can cause total loss of cognitive damage that lead to coma or may develop more slowly as a final result of progressive structural changes, such as Alzheimer’s disease, which in its final stages can destroy the psychological functions of the brain. When such cognitive loss lasts more than a few weeks, the condition is called a persistent vegetative state (PVS) because the body maintains the functions necessary to continue vegetative survival. Recovery of vegetative state is possible, especially during the first days or weeks after the start, but the tragedy is that many people in PVS live for many months or years if provided with food and other artificial means.
After the medical authorities have determined that a person is awake but unconscious, vegetative state duration depends on the nature of the brain damage, the duration of unconsciousness and estimated prognosis.
Some people under 35 with coma after a head injury, as well as an occasional patient with coma after intracranial hemorrhage, can recover very slowly. So, what seems to be an EVP from one to three months after an accident, resulting coma, in rare cases may evolve into a wastage in less than six months. Moreover, the chances of regaining independence after being vegetative for three months, are very slim. There has been a few exceptions, but some of these may represent patients who entered a closed state, undetected, moments after waking from a coma caused by injuries. Finally, all are severely disabled.
Despite these rare cases, the information indicates that the unconscious state for six months predicted with a high degree of precision and recovery will not be a big failure, despite the nature of the brain damage. Consequently, a conservative approach to the diagnosis of a PVS would observe the unconscious for at least 12 months, although cognitive recovery after six months is extremely rare in patients older than 50 years.
The risk of a forecast error from the widespread use of the above criteria, is so small that it will implement the decision as a conclusion seems entirely justifiable forecast. The determination of a physician that a person is unlikely to regain consciousness, is the usual introduction to the discussion on maintaining or discontinue life support. Although the family can be the first to raise the issue, until the doctor has ventured an opinion on the prognosis, not considered, generally, the issue of maintaining treatment. Once you are facing the issue of maintaining or discontinue life support, consider its ethical and legal.
Ten Theses on the persistent vegetative state
Paolo Cattorini The subject in a persistent vegetative state is a living human being, which prevents disease perform the functions of consciousness typically personal, and therefore should be treated as a person, providing him care that are proportional to their pathological condition. To defend this thesis, the author begins with a conception of the person who stresses the unity between body and consciousness: human life evolves continuously from birth to death because it is the same body which gradually develops its superior capabilities and which is affected by the disease.
It criticizes the thesis cortical death, to be consistent, should qualify to that found in an irreversible coma, not only as a person but also as not-man. We argue, however, in light of current scientific data, the notion of brain death or total brain death.
The author examines other issues discussed frequently in bioethics on the notion of death: vicariabilidad of brain functions, replace the hypothesis of the brain, and the man’s identity consists entirely prosthesis.
Doctors Nancy Childs, the Healthcare Rehabilitation Center of Austin, and Walt Mercer, Henry Ford Hospital in Detroit, announced the surprising recovery case of a woman who spent 15 months in a vegetative state “permanent” and suddenly awoke to greet his mother. “This forces us, say doctors in a written report, to resign, for ethical reasons, the notion of persistent vegetative state.” This coma was being used as an excuse by various pressure groups anti-life to achieve the legalization of euthanasia. What is cerebral palsy Cerebral palsy is a disorder in the development caused by damage to the developing brain, either before or after birth. Brain injury can not be repaired. However, cerebral palsy is not progressive.
This alteration can affect vision, hearing, language, coordination and mental abilities. Damage to the brain can also result in mental retardation, seizures or learning difficulty, breathing, feeding and digestion.
The degree of disability depends on the severity and location of damage in the brain. Because other disorders have symptoms similar to cerebral palsy, a proper assessment is important for accurate diagnosis. Early detection can also reduce the development of problems. The Gillette Children’s is dedicated to the diagnosis and treatment of cerebral palsy at an early stage, to ensure the best outcome.
As a result of brain damage, children may have problems with movement (motor control), abnormal muscle tone (rigidity) or poor balance. Untreated, or early intervention, abnormal motor control and abnormal tone may result in deformities of muscles and bones.
For more information on cerebral palsy, move the cursor and press here: Understanding cerebral palsy (comprising cerebral palsy). For additional material about cerebral palsy, contact our Family Resource Center (Family Resource Center) at (612) 229-3938.
Treatment of a child with Cerebral Palsy Cerebral Palsy Although not curable, specialized treatment can help reduce the symptoms associated with cerebral palsy.
Spasticity that interferes with optimum function, can be reduced with some drugs. These drugs can be administered orally or by injection or through an implanted pump. Surgery as selective dorsal rhizotomy can reduce spasticity and allow better control of the muscles are not affected. Orthopedic surgery is another treatment option.
Rehabilitation can help the child to acquire skills to be more self-sufficient. Adaptive equipment such as braces, walkers and devices to communicate, help children and their families manage the daily challenges presented by cerebral palsy.
Diagnosis of brain death
“A person is dead when he has come though the irreversible cessation of circulatory and respiratory functions or irreversible cessation of all brain functions, including the brain stem. Determination of death must be in accordance with accepted medical standards. ‘
The concept of death as brain death is accepted both from a medical standpoint as legal, ethical and religious (by most religions), since the function of the entire brain more accurately represents “life” that the persistence of the functions cardiorespiratory no brain activity.
Diagnostic Criteria for Brain Death
Checking the ME will be signed by three doctors, one of which must be a neurosurgeon or neurologist and the department head of the unit in question or his substitute, may not participate in any of these organ removal process. The Royal Decree 426/80 establishes enforceable legal safeguards in order to ensure the correctness of diagnosis described in the Annexes to respect, and treated in this course in subsequent lectures deeper.
The diagnosis of brain death is based on three premises:
* Existence of some prerequisites diagnosis, among which include the presence of a lesion of the brain structures and known because of state or situaciun finding of irreversibility and the absence of other diseases that may mimic brain death.
* The demonstration by clinical examination of the complete cessation of brain function and brainstem. *
* Investigations that evaluate neuronal function.
* The use of instrumental explorations confirming the cessation of the functions of the central nervous system:
Investigations that evaluate intracerebral blood flow
COMA AND RELATED DISORDERS AWARENESS
It is often called the doctor to treat patients whose primary abnormality is the disturbance of consciousness, ranging from simple confusion to coma. In large municipal hospitals is estimated that about 3 percent of total admissions corresponds to diseases caused coma and although this figure seems high, serves to emphasize the importance of this class of diseases, and the need to acquire theoretical and practical knowledge of them.
DESCRIPTION OF STATES OF CONSCIOUSNESS normal and impaired
It is the individual’s normal, wide awake, which responds to stimuli and psychological states for his behavior and his language has the same perception of himself and his environment than ourselves. This state can fluctuate in During the day, the more acute alertness to deep concentration, with reduced net care field, or even get to sleepiness.
It is a state of physical and mental inactivity which the patient can be awakened to acquire normal consciousness. The sleeping person shows little sign of being aware of himself or his environment. However, it differs in that the comatose patient can still respond to stimuli not used to, and sometimes it is capable of some mental activity in the form of dreams, which leave some trace in memory. Of course, you can usually recover consciousness when despieta.
It is a state in which the physical and mental activity is minimized. Although inaccessible to many stimuli, the patient opens his eyes, looks at the examiner and there appears to be unconscious. It responds to spoken commands or the response is slow and inadequate. As a rule, no alteration or plantar tendon reflexes, and often the patient presents shaky movements, sudden muscle twitching, restlessness or stereotyped motor activity and reflection of pressure or suction. In psychiatry, the term stupor has special meaning: a state in which the impressions of the outside world are received normally, but the activity is characterized by negativism, for example, catatonic schizophrenia.
Pathology and physiological COMA
Recently been clarified and extended the old neuropathological observations which indicated that the smaller lesions accompanied by lasting eat always located in the midbrain and communications tlamo.En Bremer, Morison and Dempsey, and Moruzzi and Magoun, is the essence of recent neurophysiological studies or consistent in the fact that an ascending series of destructive lesions in the spinal cord, medulla, pons and cerebellum, afectanel no consciousness until it reaches the level of the midbrain and the diencephalon (thalamus .) Cross sections in the upper brainstem invariably produce prolonged states that there is no response, whereas stimulation of the reticular formation in the rostral brain stem results in an animal gets drowsy or asleep alert and electroencephalographic acmbios appear relevant. It has been found that as anesthetics are abolishing consciousness will also suppress the activity of the reticular activating upper portion, without any interference at least at certain levels, transmission of specific sensory impulses.
Displayed on the anatomical studies reticular activating system of the upper side of the brainstem receives the specific sensory pathways, which projects not only to the sensory cortex of the parietal lobe, as do the relay nuclei sensitivity somatic, but the entire cerebral cortex. In turn, the cerebral cortex has connections which feed corticofugas nerve impulses reticular.Por training therefore appears that sensory stimulation has a dual effect: brain lead to information from the outside world and provide the energy that activates parts of the system that which depends nervous consciousness.
The study of a group of human cases in which coma preceded death for several days, you will find two main types of injury. In the first group may be demonstrated macroscopically visible injury, such as a tumor, an abscess, intracerebral hemorrhage, subarachnoid, subdural or epidural, extensive infarction or meningitis. Generally the injury affects only a portion of the cortex and bloanca, and gives much of the brain intact. Rarely is located in the thalamus or the midbrain, which would explain the coma. But in other cases the coma is accompanied by a temporal lobe tentorial herniation with compression, isquem and secondary hemorrhage in the midbrain and thalamus bottom, or a brainstem desplazamienrodel. The detailed clinical records show the coincidence of these shifts and eat with secondary hernias. Will find exceptional bilateral lesion extending into the cortex and subcortical white matter, as a result of bilateral infarcts or hemorrhages, viral encephalitis, hypoxia or ischemia, and thalamic or mesencephalic uninjured. In a second group (larger than the first) no injuries visible to the eye, and often not found any abnormalities with the pathologic techniques. In these cases the injury is due to toxic or metabolic states, and subcellular or molecular level. Sometimes the brain with normal macroscopic appearance present cellular alterations ordinary visible under the microscope and can sr characteristics, for example, the hepatic coma. Generally microscopic lesions are too diffuse to correlate anatoclnica. Thus we have pathological changes that are compatible with respect Physiology deductions that a prolonged coma injury relates everywhere corticodiencfalos neuronal systems, but that only the upper portion lesions in the brainstem can be small and inconspicuous.
Mechanisms by which upsets DISEASE AWARENESS
Our conocimientode nervous system diseases is so limited that it is not possible to identify all the different mechanisms through which consciousness is altered. Several mechanisms are already known disorder mesenceflodiencfalo-cortical systems and probably others.
In a number of pathological processes with direct hayinterferencia metabolic activities nerviosasen cells in the cerebral cortex and brain nuclear masses. Hypoxia, hypoglycemia, hyperosmolar states and hypoosmolar, acidosis, alkalosis, the hipercalemiay the hipoliemia, hyperammonemia and deficienciasde thiamine, nicotinic acid, vitamin B12, pantothenic acid and pyridoxine, are well known examples.
The intimate details of these underlying biochemical changes have not yet fully clarified, but now there are appropriate methods for study. At present, the cerebral blood flow volume in humans and is determined quite accurately (Schmidt method – Kety) measuring the rate of diffusion of inert gases such as N2O or krypton, inside the brain, that is , the time required for the gas to reach the same degree of concentration in the jugular venous and arterial blood, after 10 minutes of inhalation. The normal value for cerebral blood flow (CBF) is 700 to 800 ml per minute. The cerebral metabolic index (BMI = oxygen consumption per minute) while determinaal oxygen measuring the difference between the blood pressure and the jugular vain, and multiplying this difference by the cerebral blood flow volume. The glucose and other nutrients and metabolites can be measured as they enter and leave the brain. Can be carried out microchemical testing on brain tissue and cerebrospinal fluid (CSF). Normally the brain consumes 3.3 ml of O2 by 100 g. Brain per minute. The important point for our study is that brain metabolism or blood flow is reduced in metabolic disorders leading to coma. Oxygen values below 2.0ml per 100g. are incompatible with a state alerta.En hypoglycemia, cerebral blood flow is normal or higher than normal, while the IMC is decreased because of the deficiency of the substrate. In thiamine deficiency and vitamin B12, cerebral blood flow is normal or slightly decreased, and BMI is probably decreased because of the deficiency of the coenzyme. The extremes of the body, either hyperthermia (temperature below 36 C, 97F), probably exert cause coma without specific effect on the metabolism of neurons.
BEFORE THE CONDUCT CLINICAL comatose patient
The comma is not a separate disease entity, but is always a symptomatic expression of disease. Sometimes the key condition is perfectly obvious, as in the case of the individual who receives any trauma to the head and knocked unconscious, but often the patient arrives at the hospital in a coma and has little or no immediate information about him. The doctor, then, is forced to hold the clinical problem to careful scrutiny in many ways. To do this efficiently must have extensive knowledge of pathology and study the problem in a methodical way so as not to leave unexplored any common and treatable causes of coma.
It should be noted that when the comatose patient is first seen, certain simple therapeutic measures should precede diagnostic procedures. They should do a quick review in order to ensure that the comatose patient has free breathing, which is not in shock or, if there has been any trauma, it is not bleeding from the wound. In patients who have suffered head injuries may have fractured cervical vertebrae therefore care should be taken when moving the head and cueelo, because sometimes inadvertently injured spinal cord. It should be an immediate investigation into the patient’s previous health, if traumtismo suffered some head or seizures, and the circumstances in which it was found. Persons who accompany the patient to the hospital comatose not be allowed to leave until they have been interrogated.
Measuring temperature, pulse, breathing rate, and blood pressure is useful in the diagnosis. Fever suggests severe general infection, such as pneumonia, bacterial meningitis or brain injury that has disrupted the temperature regulating centers. Excessively high fever 41.6 to 43.3 C accompanied by dry skin, heat stroke suggests. The hypothermia is frequently observed in barbiturate intoxication or in the extracellular fluid deficiency or peripheral circulatory failure or slow breathing indicates mixedema.La morphine or barbiturate intoxication or hypothyroidism, while breathing and rapid frofunda suggests pneumonia, but may prsentarse in diabetic or uremic acidosis, and also in some diseases such as hyperpnoea intracranial central neurogenic nature .. Rapid breathing that is accompanied by fever estertorespiratorios and is a frequent sign in lobar.Las pneumonia diseases that increase intracranial pressure or damage the brain, especially the brain stem. Severe hypertension occurs in patients with cerebral haemorrhage and hypertensive encephalopathy and, occasionally, in patients with increased intracranial pressure, while sidno hypotension is common in diabetic coma in alcohol and barbiturate intoxication and internal bleeding, myocardial infarction, dissecting aneurysm of the aorta, the gram-negative septicemia and Addison’s disease.
Inspection of the skin also has great clinical value. The sianosis of the lips and nail beds indicate inadequate oxygenation. The multiple abrasions, particularly a wound or area of softening in the skull may indicate the possibility of a head injury. The cherry-red color indicates carbon monoxide poisoning. Ear Bleeding from the nose or in the orbits also favor the possibility of trauma. The swelling and hyperemia of the face and conjunctiva and the telangiectasias are common stigma of alcoholism, while marked pallor suggests internal bleeding. The presence of a rash maculohemorrgica indicates the possibility of meningococcal infection, staphylococcal endocarditis, typhus or spotted fever of the Rocky Mountains. Pellagra can be diagnosed by typical skin lesions on the hands and face. The face may have myxedema. The skin is sallow hipodrenalismo pituitary. Excessive sweating suggests hypoglycemia or shock while dry skin, suggests diabetic acidosis and uremia. The skin turgor is reduced to dehydration. If the patient has been immobile for some time will have blood blisters formed on the pressure points.
The smell of the breath can also orient toward the nature of disorder that causes coma. The smell of alcohol is easily recognized. The fruity fermetadas of diabetic coma, urinous smell of uremia, the stench of hepatic coma, also are distinctive enough to be identified by all physicians who possess a keen sense of smell.
You can determine whether or not you eat accompanied by meningeal irritation or focal diseases of the brain or brain stem.
Circular movements are altered in various ways. In superficial coma metabolic eyes move from side to side in a disorderly manner, as the slow eye movements during sleep surface, and disappears as brainstem function is depressed. Oculocephalic reflections caused by the sudden turn or tilt of the head that causes the eyes to move in conjugated form in the opposite direction are exaggerated. These reflections are not normal people and whether any, manifest integrity segmental structures of the midbrain and the pons with integrity of eye movements, and cranial third, fourth and fifth.
As to the meaning of the postures and movements prevailing in the comatose patient, it can be said that the concern, pressure movements, and the presence of certain purposive movements of an arm and a leg or all four limbs mean that the beam or corticospinal bundles are intact.
ANECDOTES OF RESEARCH
1. – For research of this paper attended the Universidad San Ignacio de Loyola, and I had access to the Internet, where I collect various information.
2. – Then I attended with fellow Neoplastic Hospital and we did the following: We noticed with surprise that the Library of this hospital is exclusively for college students, however, to insist that they provided books, but unfortunately they were in English.
For obvious reasons we had to pull out of this place, to try to talk to a doctor, but these were denied assistance in more than one occasion, as they were busy.
This hospital visit served me well, as I had never attended a library and did not know it works.