Low purity Mexican black tar heroin is most common on the West coast blood pressure bottom number high discount hydrochlorothiazide 12.5mg line, while high purity Columbian heroin dominates in the East and most mid-western states pulse pressure 49 discount hydrochlorothiazide 12.5 mg on line. Medical and Recreational Uses: Morphine is used medicinally for the relief of moderate to severe pain in both acute and chronic management pulse pressure gap discount hydrochlorothiazide 12.5 mg line. It can also be used to sedate a patient pre-operatively and to facilitate the induction of anesthesia arrhythmia echocardiogram cheap 25mg hydrochlorothiazide amex. A usual adult oral dose of morphine is 60-120 mg daily in divided doses hypertension etiology buy generic hydrochlorothiazide 25 mg, or up to 400 mg daily in opioid tolerant patients heart attack risk assessment order 25 mg hydrochlorothiazide with mastercard. Recreationally, daily heroin doses of 5-1500 mg have been reported, with an average daily dose of 300-500 mg. Depending on the demographic region, the street purity of heroin can range from 11-72% (average U. Heroin may be cut with inert or toxic adulterants such as sugars, starch, powdered milk, quinine, and ketamine. Route of Administration: Morphine: oral, intramuscular, intravenous, rectal, epidural, and intrathecal administration. Heroin: smoked, snorted, intravenous ("mainlining"), and - 73 - subcutaneous ("skin popping") administration. Black tar heroin is typically dissolved, diluted and injected, while higher purity heroin is often snorted or smoked. Heroin has little affinity for opiate receptors and most of its pharmacology resides in its metabolism to active metabolites, namely 6-acetylmorphine, morphine, and morphine-6-glucuronide. Pharmacokinetics: the oral bioavailability of morphine is 20-40%, and 35% is bound in plasma. M6G is an active metabolite with a higher potency than morphine, and can accumulate following chronic administration or in renally impaired individuals. Close to 90% of a single morphine dose is eliminated in the 72 hours urine, with 75% present as M3G and less than 10% as unchanged morphine. Heroin has an extremely rapid half-life of 2-6 minutes, and is metabolized to 6-acetylmorphine and morphine. Both heroin and 6-acetylmorphine are more lipid soluble than morphine and enter the brain more readily. Peak plasma morphine concentrations occur within an hour of oral administration, and within 5 minutes following intravenous injection. Following oral doses of 1080 mg, corresponding peak morphine concentrations in serum were 0. In 10 intravenous drug fatalities, where morphine was the only drug detected, postmortem whole blood morphine concentrations averaged 0. Following a single 12 mg intravenous mg dose of heroin, a peak heroin concentration of 0. A single 5 mg intravenous dose of heroin produced a peak plasma morphine concentration of 0. Intranasal administration of 12 mg heroin in 6 subjects produced average peak concentrations of 0. Interpretation of Urine Test Results: Positive morphine urine results generally indicate use within the last two to three days, or longer after prolonged use. It is important to hydrolyze urine specimens to assess a urine morphine concentration. Effects: Depends heavily on the dose of morphine or heroin, the route of administration, and previous exposure. Following an intravenous dose of heroin, the user generally feels an intense surge of euphoria ("rush") accompanied by a warm flushing of the skin, dry mouth, and heavy extremities. Psychological: Euphoria, feeling of well-being, relaxation, drowsiness, sedation, lethargy, disconnectedness, self-absorption, mental clouding, and delirium. Side Effect Profile: Drowsiness, inability to concentrate, apathy, lessened physical activity, constipation, urinary retention, nausea, vomiting, tremors, itching, bradycardia, severe respiratory depression, and pulmonary complications such as pneumonia. Overdose can include slow, shallow breathing, clammy skin, convulsions, extreme somnolence, severe respiratory depression, apnea, circulatory collapse, cardiac arrest, coma, and death. Duration of Effects: Depending on the morphine dose and the route of administration, onset of effects is within 15-60 minutes and effects may last 4-6 hours. The duration of analgesia increases progressively with age although the degree of analgesia remains unchanged. Following heroin use, the intense euphoria lasts from 45 seconds to several minutes, peak effects last 1-2 hours, and the overall effects wear off in 3-5 hours, depending on dose. Tolerance, Dependence and Withdrawal Effects: Both morphine and heroin have high physical and psychological dependence. With regular use, tolerance develops early to the duration and intensity of euphoria and analgesia. Withdrawal can begin within 6-12 hours after the last - 75 - dose and may last 5-10 days. Major withdrawal symptoms peak between 48-72 hours after the last dose and include drug craving, restlessness, irritability, dysphoria, loss of appetite, tremors, severe sneezing, diarrhea, nausea and vomiting, elevated heart rate and blood pressure, chills alternating with flushing and excessive sweating, goose-flesh, abdominal cramps, body aches, muscle and bone pain, muscle spasms, insomnia, and severe depression. Morphine may enhance the neuromuscular blocking action of skeletal muscle relaxants and produce an increased degree of respiratory depression. Small doses of amphetamine substantially increase the analgesia and euphoriant effects of morphine and may decrease its sedative effects. Partial agonists such as buprenorphine, nalbuphine, butorphanol, and pentazocine will precipitate morphine withdrawal. Performance Effects: Laboratory studies have shown that morphine may cause sedation and significant psychomotor impairment for up to 4 hours following a single dose in normal individuals. Early effects may include slowed reaction time, depressed consciousness, sleepiness, and poor performance on divided attention and psychomotor tasks. Late effects may include inattentiveness, slowed reaction time, greater error rate in tests, poor concentration, distractibility, fatigue, and poor performance in psychomotor tests. Subjective feelings of sedation, sluggishness, fatigue, intoxication, and body sway have also been reported. Significant tolerance may develop making effects less pronounced in long-term users for the same dose. In a laboratory setting, heroin produced subjective feelings of sedation for up to 5-6 hours and slowed reaction times up to 4 hours, in former narcotic addicts. Euphoria and elation could also play a role on perception of risks and alteration of behaviors. Effects on Driving: the drug manufacturer states that morphine may impair the mental and/or physical abilities needed to perform potentially hazardous activities such as driving a car, and patients must be cautioned accordingly. Driving ability in cancer patients receiving long-term morphine analgesia (mean 209 mg daily) was considered not to be impaired by the sedative effects of morphine to an extent that accidents might occur. There were no significant differences between the morphine treated cancer patients and a control group in vigilance, concentration, motor reactions, or divided attention. In several driving under the influence case reports, where the subjects tested positive for morphine and/or 6acetylmorphine, observations included slow driving, weaving, poor vehicle control, poor coordination, slow response to stimuli, delayed reactions, difficultly in following instructions, and falling asleep at the wheel. Other characteristic indicators may include presence of fresh injection marks, track marks, flaccid muscle tone, droopy eyelids, drowsiness or "on-the-nod", and low raspy slow speech. Mild to moderately impairing if morphine is used as medication on a regular basis for chronic pain. Severely impairing in acute situations if used orally, or as an intravenous medication, or if either drug is taken illicitly. A case of high opiate tolerance: implications for drug analyses and interpretations. A randomized controlled trial of single doses of morphine, lorazepam and placebo in healthy subjects. Concentration-related effects of morphine on cognition and motor control in human subjects. Pharmacokinetics and pharmacodynamics of sedatives and analgesics in the treatment of agitated critically ill patients. Subjective, psychomotor, and analgesic effects of oral codeine and morphine in healthy volunteers. Subjective, psychomotor, and physiological effects of cumulative doses of opioid mu agonists in healthy volunteers. Comparing the subjective, psychomotor and physiological effects of intravenous nalbuphine and morphine in healthy volunteers. Comparing the subjective, psychomotor and physiological effects of intravenous pentazocine and morphine in normal volunteers. Comparing the subjective, psychomotor and physiological effects of intravenous butorphanol and morphine in healthy volunteers. A dose-response analysis of the subjective, psychomotor and physiological effects of intravenous morphine in healthy volunteers. Synonyms: 1-phenylcyclohexylpiperidine; amp, angel dust, animal tranquilizer, dips, dust, elephant, embalming fluid, formaldehyde, fry, hog, ozone, peace pill, rocket fuel, Sernyl, Sernylan, super kools, TicTac, tranq, water, wet. Source: Synthetic chemical made in clandestine laboratories, or diverted from veterinary sources. Drug Class: Hallucinogen, dissociative anesthetic, psychotomimetic, sedative-hypnotic. Medical and Recreational Uses: Formerly used as a surgical anesthetic, however, there is no current legitimate medical use in humans. Potency, Purity and Dose: A light dose typically consists of 3-5 mg; a common dose is 5-10 mg; while a strong dose is greater than 10 mg. Lighter doses are usually smoked, intravenously or intranasally administered, while heavier doses are commonly ingested orally. Route of Administration: Smoked, intravenous injection, snorted, added as eye drops, oral ingestion, and transdermal absorption. All these patients had at least one manifestation of toxic psychosis and/or acute delirium, in addition to other symptoms. The most common physical findings were combativeness-agitation (64%), depressed level of consciousness (50%), hypertension (43%), miosis (43%) and tachycardia (43%). Effects: Psychological: Effects are usually dose dependent, and include euphoria, calmness, feelings of strength and invulnerability, lethargy, disorientation, loss of coordination, distinct changes in body awareness, distorted sensory perceptions, impaired concentration, disordered thinking, illusions and hallucinations, agitation, combativeness or violence, memory loss, bizarre behavior, sedation, and stupor. Physiological: Rise in blood pressure and heart rate, flushing, profuse sweating, generalized numbness of extremities, blurred vision, grimacing facial expression, speech difficulties, ataxia, muscular incoordination, marked analgesia, nystagmus, and anesthesia. In the anesthetized state, the patient remains conscious with a staring gaze and rigid muscles. Side Effect Profile: Excessive salivation, nausea, vomiting, amnesia, combativeness, severe anxiety, paranoia, flashbacks, seizures, coma, and death. Long periods of use may lead to memory loss, difficulties with speech and thinking, depression, weight loss, liver function abnormalities, and rhabdomyolysis. Duration of Effects: Onset of effects is very rapid when smoked or injected (1-5 minutes) and are delayed when snorted or orally ingested (30 minutes), with a gradual decline of major effects over 4-6 hours. Consciousness is regained within 10-60 minutes following intravenous administration, with a prolonged recovery period of 3-18 hours. Upon abrupt discontinuation, physical distress, lack of energy, and depression are reported. Long periods of use may lead to memory loss, difficulties with speech and thinking, depression, and weight loss. Subjective sensation of intoxication has been reported up to 8 hours and slowed reaction time up to 14 hours. Effects on Driving: Fifty-six (56) subjects were arrested for erratic driving and were evaluated by a drug recognition examiner. Other characteristic indicators may include rigid muscles, cyclic behavior, sudden turn to violence, lack of response to - 81 - painful stimuli, trance-like state or blank stare, sweating, incomplete or delayed verbal responses. Severe impairment of mental and physical abilities can occur following single doses. Corticolimbic dopamine neurotransmission is temporally dissociated from the cognitive and locomotor effects of phencyclidine. Clinical findings and concentrations in biological fluids after nonfatal intoxication. Phencyclidine intoxication: Clinical experience in 27 cases confirmed by urine assay. Pharmacokinetic and pharmacodynamic evaluation of phencyclidine and its decadeutero variant. Pyrolytic characteristics, pharmacokinetics, and bioavailability of smoked heroin, cocaine, phencyclidine and methamphetamine. Phencyclidine disrupts long- but not short-term memory within a spatial learning task. Behavioral symptomatology indicative of cannabinoids or phencyclidine intoxication in man. Source: Toluene is an aromatic hydrocarbon, occurring naturally in crude oil and in the tolu tree. It is produced during the process of making gasoline and other fuels from crude oil, in making coke from coal, and as a by-product in the manufacture of styrene. Toluene has numerous commercial and industrial applications and is a solvent in paints, lacquers, thinners, glues, correction fluid and nail polish remover, and is used in the printing and leather tanning processes. Recreational use is most common among younger adolescents primarily because it is readily available, inexpensive and legal. Potency, Purity and Dose: Solvents in many commercial and industrial products are often mixed and the solvent "sniffer" is often exposed to other solvents in addition to toluene. Acute and chronic accidental exposure to toluene can also occur, particularly in work environments. May be sniffed directly from on open container, or "huffed" from a rag soaked in the substance and held to the face.
Additional pathways extend to the corpus striatum blood pressure 160100 order 25mg hydrochlorothiazide fast delivery, the cerebellum prehypertension eyes cheap 25 mg hydrochlorothiazide with mastercard, the red nucleus high blood pressure medication list new zealand order 25mg hydrochlorothiazide with visa, the substantia nigra blood pressure medication uk discount hydrochlorothiazide 12.5 mg without a prescription,the tectum blood pressure value chart buy 12.5 mg hydrochlorothiazide amex,and the nuclei of the thalamus heart attack telugu purchase hydrochlorothiazide 25mg on-line,subthalamus, and hypothalamus. General Arrangement the reticular formation consists of a deeply placed continuous network of nerve cells and fibers that extend from the spinal cord through the medulla,the pons,the midbrain,the subthalamus, the hypothalamus, and the thalamus. The diffuse network may be divided into three longitudinal columns: the first occupying the median plane, called the median column, and consisting of intermediate-size neurons; the second, called the medial column, containing large neurons; and the third, or lateral column, containing mainly small neurons. With the classic neuronal staining techniques,the groups of neurons are poorly defined, and it is difficult to trace an anatomical pathway through the network. However,with the new techniques of neurochemistry and cytochemical localization, the reticular formation is shown to contain highly organized groups of transmitter-specific cells that can influence functions in specific areas of the central nervous system. The monoaminergic groups of cells, for example, are Functions of the Reticular Formation From the previous description of the vast number of connections of the reticular formation to all parts of the nervous system,it is not surprising to find that the functions are many. It can also bring about reciprocal inhibition; for example, when the flexor muscles contract, the antagonistic extensors relax. The reticular formation, assisted by the vestibular apparatus of the inner ear and the vestibular spinal tract, plays an important role in maintaining the tone of the antigravity muscles when standing. The so-called respiratory centers of the brainstem, described by neurophysiologists as being in the control of the respiratory muscles, are now considered part of the reticular formation. The reticular formation is important in controlling the muscles of facial expression when associated with emotion. For example, when a person smiles or laughs in response to a joke, the motor control is provided by the reticular formation on both sides of the brain. This means that a person who has suffered a stroke that involves the corticobulbar fibers and exhibits facial paralysis on the lower part of the face is still able to smile symmetrically (see p. By virtue of its central location in the cerebrospinal axis, the reticular formation can influence all ascending pathways that pass to supraspinal levels. In particular, the reticular formation may have a key role in the "gating mechanism" for the control of pain perception (see p. Higher control of the autonomic nervous system, from the cerebral cortex, hypothalamus, and other subcortical nuclei, can be exerted by the reticulobulbar and reticulospinal tracts,which descend to the sympathetic outflow and the parasympathetic craniosacral outflow. Either directly or indirectly through the hypothalamic nuclei, the reticular formation can influence the synthesis or release of releasing or release-inhibiting factors and thereby control the activity of the hypophysis cerebri. By means of its multiple afferent and efferent pathways to the hypothalamus, the reticular formation probably influences the biologic rhythms. Multiple ascending pathways carrying sensory information to higher centers are channeled through the reticular formation, which, in turn, projects this information to different parts of the cerebral cortex, causing a sleeping person to awaken. In fact, it is now believed that the state of consciousness is dependent on the continuous projection of sensory information to the cortex. Different degrees of wakefulness seem to depend on the degree of activity of the reticular formation. Incoming pain sensations strongly increase the activity of the reticular formation, which, in turn, greatly excites the cerebral cortex. From the above description, it must be apparent that the reticular formation,almost totally ignored in the past,is now being shown to influence practically all activities of the body. Now it is recognized, as the result of research, that the limbic system is involved with many other structures beyond the border zone in the control of emotion, behavior, and drive; it also appears to be important to memory. Anatomically, the limbic structures include the subcallosal, the cingulate, and the parahippocampal gyri, the hippocampal formation, the amygdaloid nucleus, the mammillary bodies, and the anterior thalamic nucleus. The alveus, the fimbria, the fornix, the mammillothalamic tract, and the stria terminalis constitute the connecting pathways of this system. Hippocampal Formation the hippocampal formation consists of the hippocampus, the dentate gyrus, and the parahippocampal gyrus. The hippocampus is a curved elevation of gray matter that extends throughout the entire length of the floor of the inferior horn of the lateral ventricle. The convex ventricular surface is covered with ependyma, beneath which lies a thin layer of white matter called the alveus. The alveus consists of nerve fibers that have originated in the hippocampus, and these converge medially to form a bundle called the fimbria. The hippocampus terminates posteriorly beneath the splenium of the corpus callosum. The dentate gyrus is a narrow, notched band of gray matter that lies between the fimbria of the hippocampus and the parahippocampal gyrus. Posteriorly, the gyrus accompanies the fimbria almost to the splenium of the corpus callosum and becomes continuous with the indusium griseum. The indusium griseum is a thin, vestigial layer of gray matter that covers the superior surface of the corpus callosum. Embedded in the superior surface of the indusium griseum are two slender bundles of white fibers on each side called the medial and lateral longitudinal striae. The parahippocampal gyrus lies between the hippocampal fissure and the collateral sulcus and is continuous with the hippocampus along the medial edge of the temporal lobe. Anterior nucleus of thalamus Indusium griseum with medial and lateral longitudinal striae Body of fornix Stria terminalis Stria medullaris thalami Region of habenular commissure and habenular nuclei Occipital lobe Crus of fornix Mammillothalamic tract Stria terminalis Fimbria Hippocampus Frontal lobe Anterior commissure Column of fornix Mammillary body Olfactory bulb Olfactory tract Amygdaloid body Temporal lobe Uncus Dentate gyrus Parahippocampal gyrus Figure 9-3 Medial aspect of the right cerebral hemisphere showing structures that form the limbic system. Pes hippocampi Uncus Hippocampus Fornix Collateral eminence due to collateral sulcus Parahippocampal gyrus Lateral sulcus Dentate gyrus Splenium of corpus callosum Fimbria Crus of fornix Cavity of lateral ventricle Posterior horn of lateral ventricle Figure 9-4 Dissection of the right cerebral hemisphere exposing the cavity of the lateral ventricle, showing the hippocampus, the dentate gyrus, and the fornix. Indusium griseum covering genu of corpus callosum Medial longitudinal striae Lateral longitudinal stria Indusium griseum covering superior surface of body of corpus callosum Indusium griseum covering splenium of corpus callosum Figure 9-6 Dissection of both cerebral hemispheres showing the superior surface of the corpus callosum. It is situated partly anterior and partly superior to the tip of the inferior horn of the lateral ventricle. It is fused with the tip of the tail of the caudate nucleus, which has passed anteriorly in the roof of the inferior horn of the lateral ventricle. The amygdaloid nucleus consists of a complex of nuclei that can be grouped into a larger basolateral group and smaller corticomedial group. The mammillary bodies and the anterior nucleus of the thalamus are considered elsewhere in this text. These three layers are the superficial molecular layer, consisting of nerve fibers and scattered small neurons; the pyramidal layer, consisting of many large pyramid-shaped neurons; and the inner polymorphic layer, which is similar in structure to the polymorphic layer of the cortex seen elsewhere. The dentate gyrus also has three layers,but the pyramidal layer is replaced by the granular layer. The granular layer is composed of densely arranged rounded or oval neurons that give rise to axons that terminate on the dendrites of the pyramidal cells in the hippocampus. Connecting Pathways of the Limbic System the connecting pathways of the limbic system are the alveus, the fimbria, the fornix, the mammillothalamic tract, and the stria terminalis. The alveus consists of a thin layer of white matter that lies on the superior or ventricular surface of the hippocampus. The fibers converge on the medial border of the hippocampus to form a bundle called the fimbria. The fimbria now leaves the posterior end of the hippocampus as the crus of the fornix. The crus from each side curves posteriorly and superiorly beneath the splenium of the corpus callosum and around the posterior surface of the thalamus. The two crura now converge to form the body of the fornix, which is applied closely to the undersurface of the corpus callosum. As the two crura come together,they are connected by transverse fibers called the commissure of the fornix. Anteriorly, the body of the fornix is connected to the undersurface of the corpus callosum by the septum pellucidum. Inferiorly, the body of the fornix is related to the tela choroidea and the ependymal roof of the third ventricle. The body of the fornix splits anteriorly into two anterior columns of the fornix, each of which curves anteriorly and inferiorly over the interventricular foramen (foramen of Monro). Then, each column disappears into the lateral wall of the third ventricle to reach the mammillary body. The mammillothalamic tract provides important connections between the mammillary body and the anterior nuclear group of the thalamus. The stria terminalis emerges from the posterior aspect of the amygdaloid nucleus and runs as a bundle of nerve fibers posteriorly in the roof of the inferior horn of the lateral ventricle on the medial side of the tail of the caudate nucleus. It follows the curve of the caudate nucleus and comes to lie in the floor of the body of the lateral ventricle. Afferent Connections of the Hippocampus Afferent connections of the hippocampus may be divided into six groups. Fibers arising from the septal nuclei (nuclei lying within the midline close to the anterior commissure) pass posterior in the fornix to the hippocampus. Fibers arising from one hippocampus pass across the midline to the opposite hippocampus in the commissure of the fornix. Fibers from the indusium griseum pass posteriorly in the longitudinal striae to the hippocampus. Fibers from the entorhinal area or olfactory-associated cortex pass to the hippocampus. Fibers arising from the dentate and parahippocampal gyri travel to the hippocampus. Efferent Connections of the Hippocampus Axons of the large pyramidal cells of the hippocampus emerge to form the alveus and the fimbria. The body of the fornix splits into the two columns of the fornix, which curve downward and forward in front of the interventricular foramina. Fibers pass posterior to the anterior commissure to enter the mammillary body, where they end in the medial nucleus. Fibers pass posterior to the anterior commissure to end in the anterior nuclei of the thalamus. Fibers pass posterior to the anterior commissure to enter the tegmentum of the midbrain. Fibers pass anterior to the anterior commissure to end in the septal nuclei, the lateral preoptic area, and the anterior part of the hypothalamus. Consideration of the above complex anatomical pathways indicates that the structures comprising the limbic Structure of the Hippocampus and the Dentate Gyrus the cortical structure of the parahippocampal gyrus is six layered. As the cortex is traced into the hippocam- Limbic System 311 Anterior nucleus of thalamus Frontal lobe Indusium griseum Body of fornix Reticular formation Hypothalamus Uncus Temporal lobe Mammillary body Parahippocampus Figure 9-7 Diagram showing some important afferent and efferent connections of the limbic system. Physiologists now recognize the importance of the hypothalamus as being the major output pathway of the limbic system. Functions of the Limbic System the limbic system, via the hypothalamus and its connections with the outflow of the autonomic nervous system and its control of the endocrine system, is able to influence many aspects of emotional behavior. These include particularly the reactions of fear and anger and the emotions associated with sexual behavior. There is also evidence that the hippocampus is concerned with converting recent memory to long-term memory. A lesion of the hippocampus results in the individual being unable to store long-term memory. It is interesting to note that injury to the amygdaloid nucleus and the hippocampus produces a greater memory loss than injury to either one of these structures alone. The various afferent and efferent connections of the limbic system provide pathways for the integration and effective homeostatic responses to a wide variety of environmental stimuli. The reticular formation not only modulates the control of motor systems but also influences sensory systems. By means of its multiple ascending pathways, which project to different parts of the cerebral cortex, it is believed to influence the state of consciousness. Loss of Consciousness In experimental animals, damage to the reticular formation, which spares the ascending sensory pathways,causes persistent unconsciousness. Pathologic lesions of the reticular formation in humans can result in loss of consciousness and even coma. It has been suggested that the loss of consciousness that occurs in epilepsy may be due to inhibition of the activity of the reticular formation in the upper part of the diencephalon. Unfortunately, this drug, as well as most other antipsychotic drugs, has major motor side effects on the dopaminergic receptors within the extrapyramidal system, producing abnormal involuntary movements. Research is now concentrating on finding a drug that will block the limbic dopamine receptors but without effect on the receptors of the extrapyramidal system (substantia nigracorpus striatum). It is clear, however, that there is still no direct evidence that excessive production of dopamine by certain neurons actually contributes to schizophrenia. Destruction of the Amygdaloid Complex Unilateral or bilateral destruction of the amygdaloid nucleus and the para-amygdaloid area in patients suffering from aggressive behavior in many cases results in a decrease in aggressiveness,emotional instability,and restlessness; increased interest in food; and hypersexuality. Monkeys that have been subjected to bilateral removal of the temporal lobes demonstrate what is known as the Klьver-Bucy syndrome. They become docile and show no evidence of fear or anger and are unable to appreciate objects visually. Moreover, the animals indiscriminately seek partnerships with male and female animals. Precise stereotactic lesions in the amygdaloid complex in humans reduce emotional excitability and bring about normalization of behavior in patients with severe disturbances. Limbic System the anatomical connections of the limbic system are extremely complex, and since their significance is not fully understood, it is unnecessary for a student of medicine to commit all of them to memory. The results of neurophysiologic experiments, which have included stimulation and ablation of different parts of the limbic system in animals, are not entirely clear. Nevertheless, certain important roles have been inferred: (1) the limbic structures are involved in the development of sensations of emotion and with the visceral responses accompanying those emotions, and (2) the hippocampus is concerned with recent memory. Schizophrenia the symptoms of schizophrenia include chronically disordered thinking, blunted affect, and emotional withdrawal. Clinical research has shown that if the limbic receptors to dopamine are blocked by a pharmacologic agent, the worst symptoms of schizophrenia are lessened. Phenothiazine admin- Temporal Lobe Dysfunction Temporal lobe epilepsy may be preceded by an aura of acoustic or olfactory experience.
Purchase 25mg hydrochlorothiazide fast delivery. Renal Clearance Renal Plasma Flow and Glomerular Filtration Rate.
Classification Panels are responsible for and to manage any video recording necessary for classification purposes associated with the competition pulse pressure 90 discount hydrochlorothiazide 25 mg with amex. Sufficient Insufficient Player submits additional documents Protest Panel Assessment (when available pulse pressure 64 discount hydrochlorothiazide 25mg on-line. Short Stature Upper Limb Impairment Lower Limb Impairment No Do you meet the minimum impairment criteria? Clear evidence must include spasticity grade 3 on the legs usually rendering them non-functional for ambulation over a long distance without the use of assistive devices pulse pressure fitness cheap hydrochlorothiazide 12.5mg with mastercard. Bilateral amputation: one amputation through or above the knee and the other below the knee (ankle completely missing) blood pressure 6050 discount hydrochlorothiazide 12.5 mg on-line. Criterion #5 Knee extension loss of 3 muscle grade points (muscle grade of two) blood pressure medication upset stomach discount hydrochlorothiazide 12.5 mg line. Criterion #6 Knee flexion loss of 3 muscle grade points (muscle grade 2) Criterion #7 Ankle plantar flexion loss of 3 muscle grade points (muscle grade of two) blood pressure vitamins buy discount hydrochlorothiazide 25 mg line. Note: the minimal impairment criteria must be accompanied by the trunk balance assessment and the technical assessment on the court. Clear evidence must include spasticity grade 1-2 in the affected limbs (at least one leg must be affected). Upper motor neuron reflex pattern must be demonstrated (one of these signs): · Positive unilateral babinski · Clear unilateral clonus 4 beats or more · Noticeably brisk reflexes or clear difference in reflexes left vs. Demonstrate a limitation in function based on spasticity, ataxia, athetosis or dystonic movements while performing during match or training. For ataxia and athetosis the Player must have clear signs of cerebellar dysfunction with incoordination of the lower limb. Dysmetria and/or dyssynergia For ataxia and athetosis the Player must have clear signs of cerebellar dysfunction with incoordination of the lower limb. Shows marked difficulty in stopping, starting, turning, balance and explosive movements 1. Limb Deficiency Amputation resulting from trauma or congenital limb deficiency (dysmelia). Unilateral amputation of half of the foot, measured on the non-amputated foot from the tip of the great toe to the posterior aspect of calcaneus. Criterion #3 Knee Flexion deficit of >60 degree Criterion #4 Knee Extension deficit of >30 degree. Criterion #5 Knee flexion loss of 3 muscle grade points (muscle grade of two) Criterion #6 Knee extension loss of 3 muscle grade points (muscle grade of two). Measurements to be taken from the inferior aspect of the anterior superior iliac spine to the most medial tip of medial malleolus on same side. Plus Upper motor neuron reflex patter must be demonstrated: Clear unilateral clonus 4 beats or more Playing arm If only playing arm impairment then same criteria as for non-playing arm. Unilateral dysmelia in which the length of the affected arm measured from acromion to fingertip is equal in length or shorter than the combined length of the humerus and the radius of the unaffected arm. The player must meet the same criteria below and classification measurements will be completed at each competition until the age of 18 (achondroplasia or other) For males: o o o Maximum standing height </=145cm and Arm length </=66 cm and Sum of standing height plus arm length </=200cm For females: o o o o o Maximum standing height </=137cm and Arm length </= 63 cm and Sum of standing height plus arm length </=190cm Maximum standing height: measured in standing position bare foot against the wall. The programme defines the requirements needed for different levels of certification and the conditions to maintain certification and to advance to a higher level. Information recorded shall include but not limited to , the tournaments worked on, the role performed (International Classifier or Chief Classifier), the number of Player Evaluations undertaken (national and international), participation in protests and role (national and international), training courses completed, mentoring undertaken, training conducted / courses assisted on. International Classifier certification means that an individual has met the required competencies and is proficient to be an International Para-Badminton Classifier. An Evaluation Report and a recommendation from the Course Facilitator is sent to the Head of Classification. International Classifiers and Senior International Classifiers must meet the minimum requirements to revalidate their qualifications or to meet the minimum criteria to advance a level as described in Table 1 over. The Head of Classification shall review the status of each International Classifier in relation to the minimum criteria to maintain the credential or minimal eligibility criteria to advance from International Level to Senior International Level. This includes advancing from International Level Classifier to Senior International Classifier. These are: National Level 2 Classifier National Level 1 Classifier National Level 1 Classifier Workshop this is a non-assessed workshop, open to anyone with an interest in Para badminton classification. The duties of a National Level 1 Classifier may include, but are not limited to: o o o o being part of a Classification Panel at national para-badminton tournaments; being part of a Protest Panel at national para-badminton tournaments; attending and as required, running classification meetings at tournaments; and assisting in and supporting trainee national classifiers. The duties of a National Level 2 Classifier may include, but are not limited to: o o o o being part of a Classification Panel at national para-badminton tournaments; being part of a Protest Panel at national para-badminton tournaments; attending and as required, running classification meetings at tournaments; and assisting in and supporting trainee national classifiers. Please provide copies of any medical diagnosis for example medical imaging, X-rays etc. Limitations due to pain are not taken into account for the purposes of classification if that is the only condition. For submission: - Please type on this form and when completed print out and sign. If I do not agree with the results of the Classification Panel I agree to abide by the Protest and Appeals process as defined in the Classification Regulations; Be videotaped and photographed during the Player Evaluation process (where such is appropriate, necessary and respects at all times my right to privacy) to include my activity on and off the field of play during the competition. The Player Evaluation process will require me to participate in sport-like exercises and activities, and that there is a risk of injury in participating in these exercises and activities. Policy scope this policy applies to players submitting their data to the Classification Panel for the purpose of being classified. This can include: name, contact information, date of birth, medical file and treatments, etc. Some of this data may constitute protected personal information under national data protection laws where you reside. Any medical information underpinning this classification will remain confidential. International transfers Your data will be made available via electronic means to members of the Classification Panel who may be located outside the country where you reside. The data protection and privacy laws of these countries may not be equivalent to those in your own country. In any case, these persons are subject to strict deontological and contractual controls. Rights You may have certain rights under applicable laws, including rights to access and/or correct any inaccurate data and remedies with respect to any unlawful processing of your data. Data retention It may be necessary to retain your data for a period corresponding to the length of your participation in Para-Badminton. An appeal is a formal objection to the manner in which Classification Procedures are followed or the way a Protest was conducted at a Para-Badminton Tournament. The Regulation of Reproduction and the Attraction of (and Problem with) Best Interests Reasoning. The Prominence of Best Interests Reasoning in Family Law and Its Attraction as a Justificatory Move. The companion Article, Beyond Best Interests, can be found in a latter Issue in this Volume of Minnesota Law Review. Co-Director, Petrie-Flom Center for Health Law Policy, Biotechnology, and Bioethics. Thanks to Adrienne Asch, Gaia Bernstein, Rachel Brewster, Dan Brock, John Bronsteen, Gabriella Blum, June Carbone, Carter Dillard, Hal Edgar, Einer Elhauge, Elizabeth Emens, Nita Farahany, Marsha Garrison, Axel Gosseries, Abby Gluck, Jim Greiner, Allison Hoffman, Trudo Lemmens, Lewis Kaplow, Duncan Kennedy, Adam Kolber, Adriaan Lanni, Dan Markel, Melissa Murray, Gerry Neuman, Bill Rubenstein, Christopher Robertson, Ben Roin, Ben Sachs, Nadia Sawicki, Elizabeth (Buffy) Scott, Ganesh Sitaraman, Michael Stein, Mark Tushnet, and David Wasserman for helpful comments on earlier drafts. Boris Babic, Peter Chang, Teel Lidow, Justin McAdam, and Russell Kornblith provided excellent research assistance. The Persistence of Best Interests: Some Examples from Legislatures, Courts, and Scholars. Criminal Prohibition of Adult Brother-Sister and First Cousin-First Cousin Incest. Reproductive Technology Access Restrictions, Parental Fitness Screening, and the Adoption Analogy. The Soundness of the Non-Person-Affecting Principle Approach as a Moral Criterion. Can Criminal Law Restrictions on Reproduction be Justified by Non-PersonAffecting Principles? This is but one among a series of pressing questions about reproduction: Should the State permit anonymous sperm donation? Should brother-sister or first cousin-first cousin incest between adults be made criminal? What underlies all of these seemingly disparate questions (and many others) is whether the State can permissibly attempt to influence our decisions about whether, when, and with whom to reproduce. This turns out to be a question with far-reaching implications because such interventions take many forms, including criminal sanctions. One prominent type of justification given for these (and a myriad of other) attempts to regulate reproduction is concern for the best interests of the children that will result from reproduction (sometimes also referred to as child welfare analysis). For example, in the debate over whether the State or physicians should restrict access to reproductive technology for unmarried individuals,3 both sides cite to copious empirical literature on whether and to what extent children born into single-parent families suffer compared to those born into twoparent families. In authorizing adoption, in determining which parent should have custody upon divorce, in determining when a child should be removed from its family of origin and put into child protective services, and in countless other areas of family law, the protection of the best interests of existing children serves as a powerful organizing principle that justifies state intervention. While courts, legislatures, physicians, and commentators frequently speak in a parallel idiom to justify state regulation of reproduction, in this Article I show that such justifications are problematic. Drawing on insights from bioethics and the philosophy of identity relating to the so-called Non-Identity Problem, I show why this form of justification, at least as typically stated, is fallacious. Unless the State`s failure to intervene would foist upon the child a life not worth living, any attempt to alter whether, when, or with whom an individual reproduces cannot be justified on the basis that harm will come to the resulting child, since but for that intervention the child would not exist. To put the point in the language of distinctions I have developed in earlier work,5 legislatures, judges, and scholars problematically treat the reasons justifying state interference with an individual`s right to remain the legal parent of an existing child as fully overlapping with the reasons justifying state interference with an individual`s (potential) right to become a genetic parent and bring a child into existence. The best interests argument acts as a smoke screen that prevents us from excavating the true justification for these two-parent households have nothing to do with biology, but instead are related to increased income, supervision, and parental attention); Marsha Garrison, Is Consent Necessary? Harlow, Paternalism Without Paternity: Discrimination Against Single Women Seeking Artificial Insemination by Donor, 6 S. My larger project is to show a secret ambition of best interests reasoning, whose significance lies not in what it says but in what it stops us from saying. While I am not claiming that there is an intentional misrepresentation on the part of scholars, legislatures, etc. I begin in Part I by offering a framework that describes the dimensions of the regulation of reproduction. I show why best interests reasoning-a justificatory idiom prominent in family law-seems from a political theory perspective to be a very appealing method of justifying government intervention in the reproductive area. I then show the subtle error made when transposing these arguments from the context of protecting already-existing children to the question of government programs that affect who will come into existence. Here I explain the Non-Identity Problem and show its implicit acceptance in the jurisprudence rejecting the wrongful life tort. More precisely, Kahan`s claim is that the rhetoric of deterrence displaces an alternative expressive idiom that produces incessant illiberal conflict over status such that [c]itizens of diverse commitments converge on the deterrence idiom to satisfy social norms against contentious public moralizing; public officials likewise converge on it to minimize opposition to their preferred policy outcomes. In this respect my approach differs from Kahan`s, whose attitude toward the secret ambition of deterrence is more mixed. I review examples of the (mis)use of this reasoning to support policies such as abstinence education, the prohibition on brother-sister incest, the barring of anonymity in sperm and egg donation, the preventing of reproductive technology access for single individuals, and others. The first attempts to expand the category of lives not worth living for which no Non-Identity Problem occurs. In the conclusion, I briefly plot four very different ways of justifying the regulation of reproduction on substitute theories relating to legal moralism, virtue ethics, reproductive externalities, and wronging-while-overallbenefiting. Developing these theories and their problems is a task I undertake in a companion paper that will come out in a different issue of this Journal. My aim is nothing short of re-writing our way of thinking about the regulation of reproduction. I show that it is an attractive kind of justificatory move, in political philosophical terms, because it marshals a particular kind of third-party effect as a ground for limiting autonomous action: harm to a vulnerable third party to whom parents stand in a fiduciary relationship-their child. I then demonstrate why reasoning associated with the Non-Identity Problem makes this transposition problematic. I should make clear up front that my starting point about human reproduction is a modestly libertarian view; the State has to offer some justification for limiting individuals` reproductive choices, although I am open to such justifications taking many different forms. While I think this is an intuitive and logical starting point that matches the preconceived notions most of us have about our reproductive lives, it is not the only possible one. We could instead hypothetically begin with a view that individuals have no freedom to reproduce except in the cases where the State grants them that privilege and start by asking whether a particular instance of reproduction is one that the State should justifiably permit. The first dimension is the target reproductive decision (or simply target for short) the State seeks to influence. For our purposes we can crudely distinguish three such targets: whether, when, and with whom individuals reproduce. Abstinence education aims to delay reproduction by teenagers or other unmarried individuals and thus influences when individuals reproduce. Prohibitions on brother-sister incest, programs aimed at carrier screening for Tay-Sachs or other heritable genetic disorders, and statutes barring sperm donor anonymity attempt to influence with whom individuals reproduce. The second dimension goes to the means by which the State seeks to influence the target decisions (means for short). These interventions can roughly be ordered from strongest to weakest in terms of their level of intrusion. Physical alteration is the most intrusive, for example, sterilization of the severely mentally retarded. Criminal prohibition is also extremely intrusive, for example, making it a crime to engage in brother-sister incest or to purchase surrogacy services. Less intrusively, the State may make certain status determinations immutable (particularly as to parentage) and/or make contracts surrounding reproduction unenforceable; for example, California treats gestational surrogacy contracts (where the surrogate carries the fetus to term but does not contribute the egg for fertilization) as enforceable but not traditional surrogacy contracts (where the surrogate is both the genetic mother and carries the fetus to term).
Instead 2014 buy hydrochlorothiazide 12.5mg with visa, urgent treatment of the underlying cause of the acidosis is probably the best approach heart attack grill arizona buy hydrochlorothiazide 25 mg amex. Relieve hypoxia immediately by ensuring an adequate airway and delivering sufficient oxygen to keep the blood fully oxygenated arteria axilar 25 mg hydrochlorothiazide fast delivery. Such patients should be given 100% oxygen and hyperventilated to increase blood oxygenation blood pressure categories generic hydrochlorothiazide 12.5mg overnight delivery. Hyperbaric oxygenation may improve the situation arteria3d mayan city pack hydrochlorothiazide 25 mg for sale, and if a hyperbaric chamber is available heart attack would feel like a heart attack discount hydrochlorothiazide 25mg overnight delivery, it should probably be utilized for patients with life-threatening exposure. Severe anemia (hematocrit less than 25) in a comatose patient should be treated with transfusion of whole blood or packed red cells. The absence of cells in the spinal fluid does not rule out acute bacterial meningitis; if there is a high index of suspicion, the lumbar puncture can be repeated in 6 to 12 hours. The centrifuged sediment should also be examined by Gram stain, as occasionally organisms may be seen even before there is pleocytosis. It usually is advisable to adjust both electrolyte and acid-base imbalances slowly, since too rapid correction often leads to overshoot or intracellular-extracellular imbalances and worsens the clinical situation. Many emergency departments can provide a rapid assessment of toxic drugs (Table 76). Therefore, no stuporous or comatose patient suspected of having ingested sedative drugs should ever be left alone. This is particularly true in the minutes immediately following the initial examination; the stimulation delivered by the examining physician may arouse the patient to a state in which he or she appears relatively alert or his or her respiratory function appears normal, only to lapse into coma with depressed breathing when external stimulation ceases. The management of specific drug poisonings is beyond the scope of this chapter,88,94 but certain general principles apply to all patients suspected of having ingested sedative drugs. Both respiratory and cardiovascular failure may occur with massive sedative drug overdose. Anticipation and early treatment of these complications often smooth the clinical course. Insert an endotracheal tube in any stuporous or comatose patient suspected of drug overdose and be certain that an apparatus for respiratory support is available in case of acute respiratory failure. The placement of a central venous line allows one to maintain an adequate blood volume without overloading the patient. Give generous amounts of fluid to maintain blood volume and blood pressure, but avoid overhydrating oliguric patients. Place a pulse oximeter on the finger, but also measure arterial blood gases; a difference between the two (oxygen saturation gap) may indicate poisoning. Carbon monoxide, methemoglobin, cyanide, and hydrogen sulfide cause an increased oxygen saturation gap. Once the vital signs have been stabilized, one should attempt to remove, neutralize, or reverse the effects of the drug. Attempts to remove poi- son from the gastrointestinal tract and thus prevent absorption have included inducing vomiting with syrup of ipecac,95 gastric lavage,96 cathartics,97 activated charcoal ingestion,98 and whole bowel irrigation. Multiple doses of charcoal administered at an initial dose of 50 to 100 g, and then at a rate of not less than 12. In addition to eliminating drugs from the small bowel, the agents may interrupt the enteroenteric and, in some cases, the enterohepatic circulation of drugs. Doses above 5 g in adults may cause acute hepatic injury, especially if combined with other hepatotoxins such as ethanol, and when acetaminophen overdose is suspected, the patient should be treated with N-acetylcysteine as well. Once one has considered the possibilityofpsychogenicunresponsivenessandperformed the appropriate neurologic examination, little difficulty arises in making the definitive diagnosis. If the patient meets the clinical criteria for psychogenic unresponsiveness, no further laboratory tests are required. In emergency evaluation of the unresponsive patient, the Amytal interview may establish the diagnosis and ``wake the patient up,' so that one may begin more definitive treatment. However, it also breaks down a major psychologic defense, and should only be done in conjunction with definitive psychiatric treatment. Hence, it is necessary to secure emergency psychiatric consultation, and often the patient must be admitted to the psychiatric service. If there is any suspicion of a mass lesion, immediate imaging is mandatory despite the absence of focal signs. Conversely, the presence of hemiplegia or other focal signs does not rule out metabolic disease, especially hypoglycemia. At all times during the diagnostic evaluation and treatment of a patient who is stuporous or comatose, the physician must ask him- or herself whether the diagnosis could possibly be wrong and whether he or she needs to seek consultation or undertake other diagnostic or therapeutic measures. Fortunately, with constant attention to the changing state of consciousness and a willingness to reconsider the situation minute by minute, few mistakes should be made. Intubation without premedication may worsen outcome for unconsciousness patients with intracranial hemorrhage. Intubating laryngeal mask airway allows tracheal intubation when the cervical spine is immobilized by a rigid collar. Emergency department intubation of trauma patients with undiagnosed cervical spine injury. Spinal cord injury as a result of endotracheal intubation in patients with undiagnosed cervical spine fractures. The approach is based on the belief that after a history and a general physical and neurologic examination, the informed physician can, with reasonable confidence, place the patient into one of four major groups of illnesses that cause coma. The specific group into which the patient is placed directs the rest of the diagnostic evaluation and treatment. Flumazenil in drug overdose: randomized, placebo-controlled study to assess cost effectiveness. A riskbenefit assessment of flumazenil in the management of benzodiazepine overdose. Adjunctive valproic acid for delirium and/or agitation on a consultation-liaison service: a report of six cases. Sedation patterns in pediatric and general community hospital emergency departments. Eye care for patients receiving neuromuscular blocking agents or propofol during mechanical ventilation. A randomised controlled study of the efficacy of hypromellose and Lacri-Lube combination versus polyethylene/Cling wrap to prevent corneal epithelial breakdown in the semiconscious intensive care patient. Detected and overlooked cervical spine injury in comatose victims of trauma: report from the Pennsylvania Trauma Outcomes Study. A comparison of different grading scales for predicting outcome after subarachnoid haemorrhage. Does modification of the Innsbruck and the Glasgow coma scales improve their ability to predict functional outcome? The cuff-leak test is a simple tool to verify severe laryngeal edema in patients undergoing long-term mechanical ventilation. Middle ear effusion in intensive care unit patients with prolonged endotracheal intubation. Peripheral arterial blood pressure monitoring adequately tracks central arterial blood pressure in critically ill patients: an observational study. Beta lactam antibiotic monotherapy versus beta lactam-aminoglycoside antibiotic combination therapy for sepsis. No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury. Effects of head posture on cerebral hemodynamics: its influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation. Influence of body position on jugular venous oxygen saturation, intracranial pressure and cerebral perfusion pressure. Mannitol bolus preferentially shrinks non-infarcted brain in patients with ischemic stroke. Efficacy and safety of hypertonic saline solutions in the treatment of severe head injury. Isovolume hypertonic solutes (sodium chloride or mannitol) in the treatment of refractory posttraumatic intracranial hypertension: 2 mL/kg 7. The effect of large doses of dexamethasone on the cerebrospinal fluid pressure in patients with supratentorial tumors. Refractory increased intracranial pressure in severe traumatic brain injury: barbiturate coma and bispectral index monitoring. Clinical outcome and cognitive impairment in patients with severe head injuries treated with barbiturate coma. Effect of intracranial pressure monitoring and targeted intensive care on functional outcome after severe head injury. Decompressive craniectomy for severe traumatic brain injury: evaluation of the effects at one year. Clinical and radiological predictors of recanalisation and outcome of 40 patients with acute basilar artery occlusion treated with intra-arterial thrombolysis. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Acid-base and electrolyte analysis in critically ill patients: are we ready for the new millennium? National academy of clinical biochemistry laboratory medicine practice guidelines: recommendations for the use of laboratory tests to support poisoned patients who present to the emergency department. Critical Care Toxicology: Diagnosis and Management of the Critically Poisoned Patient, 2005, 11690. Since that time, several committees and reviewers have sought to establish appropriate clinical and laboratory criteria for brain death based on retrospective analyses. The earliest widely known definition is that of the 1968 Ad Hoc Committee of the Harvard Medical School to examine the criteria of brain death (called, at the time, ``irreversible coma'2) (Table 81). At present, in the United States the principle that brain death is equivalent to the death of the person is established under the Uniform Determination of Death Act. If all the organs, save the brain, were artificial, that individual would still be alive. Conversely, when the brain is dead, sustaining the other organs by artificial means is simply preserving a dead body and not keeping the individual alive. Thus, although this chapter uses the term brain death, the term as we use it carries the same import as death. Three medical considerations emphasize the importance of the concept of brain death: (1) transplant programs require the donation of healthy peripheral organs for success. The early diagnosis of brain death before the systemic circulation fails allows the salvage of such organs. However, ethical and legal considerations demand that if one is to declare the brain dead, the criteria must be clear and unassailable. Unresponsive coma Apnea Absence of cephalic reflexes Absence of spinal reflexes Isoelectric electroencephalogram Persistence of conditions for at least 24 hours Absence of drug intoxication or hypothermia Table 82 Clinical Criteria for Brain Death in Adults and Children in the United States A. No potentially anesthetizing amounts of either toxins or therapeutic drugs can be present; hypothermia below 308C or other physiologic abnormalities must be corrected to the extent medically possible. Irreversible structural disease or a known and irreversible endogenous metabolic cause due to organ failure must be present. Absence of pupillary responses to light and pupils at midposition with respect to dilation (46 mm) 2. It is even more important to know when to fight for life than to be willing to diagnose death. Their best use demands that one identify and select patients who are most likely to benefit from intensive techniques, so that these units are not overloaded with individuals who can never recover cerebral function. The cornerstone of the diagnosis of brain death remains a careful and sure clinical neurologic examination (Table 82). In addition, a thorough evaluation of clinical history, neuroradiologic studies, and laboratory tests must be done to rule out potential confounding variables. The second indispensable tenet is that the vital structures of the brain necessary to maintain consciousness and independent vegetative survival are damaged beyond all possible recovery. The cause of brain damage must be known irreversible structural or metabolic disease. This first criterion is crucial, and the diagnosis of brain death cannot be considered until it is fulfilled. The reason for stressing this point is that both in the United States and abroad often ``coma of unknown origin' arising outside of a hospital is due to depressant drug poisoning. Witnesses cannot be relied upon for accurate histories under such circumstances because efforts at suicide or homicide can readily induce false testimony by companions or family. Even in patients already in the hospital for the treatment of other illnesses, drug poisoning administered by self or others sometimes occurs and at least temporarily can deceive the medical staff. Accordingly, the diagnosis of an irreversible lesion by clinical and laboratory means must be fully documented and unequivocally accurate before considering a diagnosis of brain death. The ease of being mistaken in such a diagnosis is illustrated by some of the results of a collaborative study sponsored several years ago by the National Institutes of Brain Death 333 Table 83 Most Common Etiologies of Brain Death 1. Traumatic brain injury Aneurysmal subarachnoid hemorrhage Intracerebral hemorrhage Ischemic stroke with cerebral edema and herniation 5. Fulminant hepatic necrosis with cerebral edema and increased intracranial pressure From Wijdicks,6 with permission. If scans are normal and clinical history is equivocal for the origin of cerebral demise, an examination of the cerebral spinal fluid is indicated. A prospective study7 evaluated 310 patients with cardiac arrest or other forms of acute medical coma who met the clinical criteria of brain death for 6 hours; none improved despite maximal treatment. Jorgenson and Malchow-Moller8 systematically examined the time required for recovery of neurologic functions in 54 patients following cardiopulmonary arrest, and plotted these times against eventual outcomes.
