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The endopelvic fascia is the extraperitoneal cellular tissue of the uterus (the parametrium) pulse pressure 75 generic coreg 12.5mg with mastercard, vagina arrhythmia jaw pain buy coreg 25 mg low price, bladder and rectum blood pressure medication causes nightmares purchase coreg 12.5 mg with mastercard. Within this endopelvic fascia are three important condensations of connective tissue which sling the pelvic viscera from the pelvic walls blood pressure 200110 buy 25mg coreg otc. These three ligaments act as supports to the cervix of the uterus and the vault of the vagina, in conjunction with the important elastic muscular foundation provided by levator ani. The uterus and its broad ligaments, therefore, form a partition across the pelvic floor dividing off an anterior compartment, containing the bladder (the uterovesical pouch), from a posterior compartment, containing the rectum (the pouch of Douglas or recto-uterine pouch). The ureter passes forwards to the bladder deep to this ligament and lateral to and immediately above the lateral fornix of the vagina. Taken together with the ovarian ligament, it is equivalent to the male gubernaculum testis and can be thought of as the pathway along which the female gonad might have descended, but in fact did not, to the labium majus (the female homologue of the scrotum). Vaginal examination the relations of the vagina to the other pelvic organs must be constantly borne in mind when carrying out a vaginal examination. Inspection (by means of a speculum) enables the vaginal walls and cervix to be examined and a biopsy or cytological smear to be taken. Inspection of the introitus while straining detects prolapse and the presence of stress incontinence. Collections of fluid, malignant deposits, prolapsed uterine tubes and ovaries or coils of distended bowel may be felt in the pouch of Douglas. The strength of the perineal muscles can be assessed by asking the patient to tighten up her perineum. In the normal anteverted uterus the anterior lip of the cervix presents; in retroversion, either the cervical os or the posterior lip are first to be felt. Bimanual examination assesses the pelvic size and position of the uterus, enlargements of ovary or uterine tubes and the presence of other pelvic masses. The obstetrician can assess the pelvic size in both the transverse and anteroposterior diameter. Particularly important is the distance from the lower border of the symphysis pubis to the sacral promontory, which is termed the diagonal conjugate. All these four tubes lie close together caudally, projecting into the anterior (urogenital) compartment of the cloaca. One system disappears in the male, the other in the female, each leaving behind congenital remnants of some interest to the clinician. In the male, the paramesonephric duct disappears, apart from the appendix testis and the prostatic utricle. More caudally, they come together and fuse in the midline (dragging, as they do so, a peritoneal fold from the side wall of the pelvis which becomes the broad ligament). The median structure so formed differentiates into the epithelium of the uterine body (endometrium), cervical canal and upper one-third of the vagina, which are first solid and later become canalized. The rest of the vaginal epithelium develops by canalization of the solid sinuvaginal node at the back of the urogenital sinus. This accounts for the differences in lymphatic drainage of the upper and lower vagina. The muscle of the Fallopian tubes, uterine body, cervix and vagina develops from surrounding mesoderm, so that remnants of the 160 the abdomen and pelvis Paramesonephric ducts Parietal peritoneum (i) Broad ligament (ii) (d). Genital tract mesonephric duct system of the female are found in the myometrium, cervix and vaginal wall. All stages of division of the original double tube may persist from a bicornuate uterus to a complete reduplication of the uterus and vagina. Alternatively, there may be absence, hypoplasia or atresia of the duct system on one or both sides. Failure of canalization of the originally solid caudal end of the duct results, after puberty, in the accumulation of menstrual blood above the the posterior abdominal wall 161 obstruction. First the vagina may distend with blood, then the uterus and then the tubes (haematocolpos, haematometra and haematosalpinx, respectively). The posterior abdominal wall the bed of the posterior abdominal wall is made up of three bony and four muscular structures. The psoas must be dealt with in more detail because of the involvement of its sheath in the formation of a psoas abscess. The psoas major arises from the transverse processes of all the lumbar vertebrae and from the sides of the bodies and the intervening discs of the T12 to L5 vertebrae. It passes downwards and laterally at the margin of the brim of the pelvis, narrowing down to a tendon which crosses the front of the hip joint beneath the inguinal ligament to be inserted, with iliacus, into the lesser trochanter of the femur. The psoas major, together with iliacus, flexes the hip on the trunk, or, alternatively, the trunk on the hips. Psoas minor, absent in 40% of subjects, lies on psoas major and attaches to the iliopubic eminence. On the right side is a normal psoas sheath; on the left side it is shown distended with pus, which tracks under the inguinal ligament to present in the groin. Pus from a tuberculous infection of the lumbar vertebrae is limited in its anterior spread by the anterior longitudinal vertebral ligament, and therefore passes laterally into its sheath (psoas abscess), which may also be entered by pus tracking down from the posterior mediastinum in disease of the thoracic vertebrae.

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Sirolimus is associated with venoocclusive disease of the liver after myeloablative allogeneic stem cell transplantation halou arrhythmia coreg 25 mg line. Sirolimus and tacrolimus without methotrexate as graft-versus-host disease prophylaxis after matched related donor peripheral blood stem cell transplantation heart attack xbox order 6.25 mg coreg fast delivery. Matched and mismatched allogeneic stem-cell transplantation from unrelated donors using combined graft-versus-host disease prophylaxis including rabbit anti-T lymphocyte globulin blood pressure levels cheap coreg generic. Clinical outcomes of human herpesvirus 6 reactivation after hematopoietic stem cell transplantation hypertension va rating buy online coreg. High-dose cyclophosphamide as single-agent, short-course prophylaxis of graft-versus-host disease. Endpoints for clinical trials testing treatment of acute graft-versus-host disease: a joint statement. Response of 443 patients to steroids as primary therapy for acute graft-versus-host disease: comparison of grading systems. Etanercept, mycophenolate, denileukin, or pentostatin plus corticosteroids for acute graft-versus-host disease: a randomized phase 2 trial from the blood and marrow transplant clinical trials network. Comparison of chronic graftversus-host disease after transplantation of peripheral blood stem cells versus bone marrow in allogeneic recipients: long-term follow-up of a randomized trial. Administration of cyclosporine for 24 months compared with 6 months for prevention of chronic graft-versus-host disease: a prospective randomized clinical trial. Prophylactic rituximab after allogeneic stem cell transplantation prevents steroid-requiring chronic graft-vs-host disease [abstract]. Therapy for chronic graft-versus-host disease: a randomized trial comparing cyclosporine plus prednisone versus prednisone alone. Prednisone and azathioprine compared with prednisone and placebo for treatment of chronic graft-v-host disease: prognostic influence of prolonged thrombocytopenia after allogeneic marrow transplantation. Randomized clinical trial of thalidomide, cyclosporine, and prednisone versus cyclosporine and prednisone as initial therapy for chronic graft-versus-host disease. Comparison of short-term response and long-term outcomes after initial systemic treatment of chronic graftversus-host disease. Effectiveness of donor natural killer cell alloreactivity in mismatched hematopoietic transplants. Donor selection for natural killer cell receptor genes leads to superior survival after unrelated transplantation for acute myelogenous leukemia. Poor agreement between clinician response ratings and calculated response measures in patients with chronic graftversus-host disease. Antileukemic effect of graftversus-host disease in human recipients of allogeneic-marrow grafts. Donor leukocyte transfusions for treatment of recurrent chronic myelogenous leukemia in marrow transplant patients. Therapy of relapsed leukemia after allogeneic hematopoietic cell transplantation with T cells specific for minor histocompatibility antigens. Many patients who recover from immediate posttransplant problems eventually regain health and return to normal activities of life. It is characterized by immune dysregulation, decreased organ function, significant morbidity, and impaired survival. With survivorship, a shift in survivorship care occurs from large transplant centers to community health care providers. Preventive measures as well as early detection and treatment are important aspects to reducing morbidity and mortality. Susceptible patients need to be identified early, and screened for modifiable risk factors with early intervention where possible. Premature cardiovascular disease after allogeneic hematopoietic stem cell transplantation. Growth hormone deficiency in adults leads to insulin resistance and is characterized by dyslipidemias and hypertension. Hyperleptinemia has been implicated as the pathobiologic link between transplant and metabolic syndrome. Radiation has a dose-dependent impact on vasculature and endothelium in animal models. Chronic hypomagnesemia is common early after transplantation33 and is known to induce insulin resistance, diabetes, and metabolic syndrome. In addition, transplant survivors have unique risk factors such as exposure to ionizing radiation, immunosuppressant use (including steroids), and endocrinopathies. Residual effects from radiation, endocrine dysfunction (including steroid exposure, hypogonadism, hypothyroidism, and growth hormone deficiency), and endothelial damage have been implicated. Gonadal dysfunction will occur in the majority of transplant survivors and is linked to conditioning intensity and recipient age. Endocrinopathy and metabolic syndrome are strongly associated with gonadal dysfunction. As the age and life expectancy of survivors continue to rise, second malignancies are expected to become an increasingly common complication. The oral cavity, salivary glands, liver (prior hepatitis C exposure), skin, brain, breast, thyroid, and bone/connective tissue were the sites with a significant increase in secondary malignancy. When chemotherapy alone is used for conditioning, the rates of solid tumors are still increased, as evidenced by a report examining solid tumor incidence in survivors who underwent high-dose busulfan-cyclophosphamide conditioning.

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Nevertheless low vs diamond heart attack order coreg with american express, the mechanisms underlying such modulation have been difficult to explore in animal studies arteria sacralis mediana 6.25 mg coreg overnight delivery. The advent of human brain imaging provided an important new avenue for deciphering the neural basis of psychological modulation of pain arteria 2000 order 6.25 mg coreg overnight delivery. In recent years blood pressure normal newborn discount coreg 6.25 mg amex, brain imaging experiments have explored the mechanisms underlying attentional and emotional modulation of pain, as well as activity related to the expectation of pain and placebo analgesia. Effect of Attention and Distraction on Pain-Evoked Activity in the Brain Before brain imaging allowed the exploration of psychological variables in humans, a few studies were performed in which attentional state was manipulated in non-human primates and action potentials from single neurons were recorded. These studies revealed that for some neurons in the dorsal horn and the thalamus, the activity evoked by a noxious stimulus was enhanced when the monkey was performing a task that required attention to the noxious stimulus rather than when performing a task that required attention to be diverted to a visual stimulus (Bushnell et al 1984, Bushnell and Duncan 1989). A, Attention preferentially modulates pain intensity ratings, whereas emotional state preferentially modulates pain unpleasantness. B, Cortical pain areas that showed the largest modulations in attentional and emotional conditions. Several studies in patients with chronic pain and/or depression show enhanced responses during anticipation of pain, which may be one factor contributing to the enhanced pain perception in these patients (Song et al 2006, Strigo et al 2008, Burgmer et al 2010). Anticipation and Placebo Analgesia Anticipation of a reduction in pain is a main factor contributing to the placebo effect (Benedetti et al 2005). Therefore, increased prefrontal activation could also reflect increased engagement of pain facilitatory or inhibitory circuits, depending on the exact area. Chronic pain conditions are often accompanied by reduced spontaneous activity in the thalamus and an associated abnormal burst discharge (Gucer et al 1978, Hirayama et al 1989, Lenz et al 1989). Reversal of thalamic hypoperfusion with successful pain relief has been described in patients with cancer pain (Di Piero et al 1991) and various neuropathic pain conditions (Hsieh et al 1995, Iadarola et al 1995, Peyron et al 1995, Duncan et al 1998). In the case of neuropathic pain, decreased spontaneous activity in the thalamus is consistent with deafferentation of the somatosensory system, and it is therefore not straightforward to establish any pain-relevant pathophysiology of decreased thalamic activity. In addition, it is intriguing to note that thalamic hypoperfusion has been observed in patients with fibromyalgia (reviewed by Williams and Gracely 2006), which is not linked to deafferentation. Functional imaging studies also provide evidence that nociceptive afferent drive at the level of the spinal cord, thalamus, and cortex is reduced during placebo analgesia (Wager et al 2004, Eippert et al 2009b, Watson et al 2009). Although significant progress has been made, the study of chronic pain has been considerably more difficult than the study of acute experimental pain for a variety of reasons, including the lack of controllability and heterogeneity of patient groups. In particular, it is often difficult to determine whether brain alterations are a cause or a consequence of chronic pain because of a distinct lack of longitudinal studies. Nevertheless, it is clear that although clinical pain states fundamentally activate similar brain regions as do acute pain stimuli, differences exist that seem to reflect changes in the psychological state related to chronic pain states, as well as alterations in pain modulatory systems. In addition to changes in processing, evidence is accumulating that prolonged pain is associated with structural brain alterations. Finally, two clinical pain states, cluster headache and migraine, will be discussed in more detail because ample evidence suggests that the primary pathophysiology of these conditions is located in the brain. Cerebral Processing of Clinical Pain Several methods have been used to examine the processing of clinical pain. All these different approaches have shown that brain activation associated with clinical pain states overlaps with areas that process acute pain stimuli. Nevertheless, differences are observed for clinical pain and can be grouped broadly into three categories. Baliki and colleagues (2006) used an interesting approach in analyzing patients with chronic low back pain that helped in understanding the engagement of additional forebrain areas in clinical pain: when activations present during periods of rapidly increasing pain were statistically separated from periods of sustained high-level pain, activations associated with the rapid increases in pain were similar to those observed in healthy people during acute pain. Cerebral Processing of Experimental Pain in Chronic Pain States Instead of imaging brain activation associated with clinical pain, it would be more practical in many instances to use acute experimental stimuli to probe the pain-processing circuitry in patients with chronic pain. In line with the generalized hyperalgesia that is observed in many of these patients, activation of pain-processing regions is typically increased when stimuli are used that are of the same intensity as in the healthy control group. When the perceived intensity is equated between patients and controls rather than stimulus intensity, brain activation is not generally different in patients (Giesecke et al 2004). In the next section, studies are presented that provide more specific information on how altered cerebral pain modulation might amplify the processing and experience of pain. Evidence for Altered Supraspinal Pain Modulation in Clinical Pain the idea that faulty supraspinal pain modulatory circuitry contributes to clinical pain has become increasingly popular in recent years, perhaps also because in many instances a mismatch between perceived pain intensity and objectifiable (peripheral) disease cannot be resolved with current diagnostic tools. Although animal data provide strong evidence for an altered balance between endogenous pain inhibition and facilitation, data in humans are still relatively scarce. It is well known from the animal literature that pathways that modulate ascending nociceptive signals descend from the brain stem to the spinal cord (Fields and Heinricher 1985, Porreca et al 2002). Consequently, the brain stem has received much attention in human pain imaging studies in recent years. A study in healthy volunteers in whom sensitization to punctuate stimuli was achieved by capsaicin injection provided evidence that the brain stem is also involved in pain facilitation in humans (Lee et al 2008). Evidence in patients comes from a study of individuals with painful hip osteoarthritis (Gwilym et al 2009). Patients rated punctuate stimuli as "sharper" when applied to the lateral aspect of the thigh. Thus, this study provides evidence that brain stem mechanisms might play a role in neuropathic symptoms in a disorder that has traditionally been considered a nociceptive condition. Animal studies have largely concentrated on the brain stem as the site of endogenous pain modulation, but many studies in healthy volunteers have shown that the higher brain centers are important pain modulators, at least in humans, that mediate the effects of cognition, emotion, and other highorder processes on pain processing. The degree of activation in this region correlated with the severity of depressive symptoms in this largely not clinically depressed sample. Animal experiments had demonstrated that the receptive fields of neurons in S1 that respond to innocuous stimuli move to adjacent skin areas when nerve lesions or amputations interrupt their original input. This reorganization of receptive fields of deafferentiated neurons was initially thought to be a protective mechanism against the development of phantom sensations. When this prediction was tested in human amputees, however, the opposite relationship was observed: the amount of phantom limb pain was positively correlated with the amount of cortical reorganization, as determined by using innocuous somatosensory stimuli (Flor et al 1995, Montoya et al 1998, Grusser et al 2001, Karl et al 2001). This observation parallels findings that greater damage to the somatosensory pathways is associated with greater pain, such as with syringomyelia and post-herpetic neuralgia (Fields et al 1998, Hatem et al 2010, Petersen and Rowbotham 2010).

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Ratio scaling methods have been used to assess pain magnitude pulse pressure under 30 purchase coreg 12.5mg with amex, including variations in which the response is another adjustable stimulus modality (Gracely et al 1978a) blood pressure graph best buy coreg, the response is made to both painful and non-painful stimulus modalities (Duncan et al 1988) arterial insufficiency discount 6.25 mg coreg free shipping, or various responses are used to quantify the magnitude implied by the labels in a pain category scale pulse jet pressure proven 25 mg coreg. These values are used in analysis of the scale when it is applied to pain measurement (Gracely et al 1979). One important, but rarely used feature of quantified verbal categories is the presentation of response choices in random order, which requires a unique cognitive task that avoids a common problem with other methods. Though possibly difficult for the subject, this method avoids the rating biases. Forcing choices based on meaning may facilitate discrimination of different pain dimensions, as discussed later. In addition to randomization, quantified category values permit the use of hybrid scales that combine verbal and graphic ratings by placing descriptors in appropriate locations on an analog or category continuum as shown in Figure 20-3 (Naliboff et al 1997, Sternberg et al 2001). In addition, the response is easily remembered, which confounds measures of repeat reliability or studies of pain memory. Subjects indicate their pain magnitude by marking the line at the appropriate point. The ease of administration and scoring has contributed to the widespread use of this method. The lack of a distinct response category avoids the confounding factor of remembering discrete responses. When using these scales to describe a range of painful stimuli, subjects typically spread their responses out to cover the entire range of possible responses. In the extreme case, this tendency results in the same scale for any stimulus set. The most widely used scale is the visual analog scale, which is commonly displayed as a horizontal 10-cm line labeled at the extremes, although it can be presented in several possible orientations and label formats. Subjects are instructed to use the semantic space on the right to form a response and then report the appropriate number on the left. This type of scale is especially useful for situations such as telephone surveys or neuroimaging studies in which a manual response is to be avoided or is impossible. Such measures can indicate pathological states, such as abnormally prolonged sensations, that are not evaluated by ordinary scaling methods (Gracely 1991, Graven-Nielsen et al 1997). Scaling methods that require greater cognitive demands have been applied to pain assessment. Two similar methods, functional measurement and conjoint measurement, require a single response to not one stimulus but rather to an integrated impression of two or more stimuli. These stimuli can both be painful, or subjects can respond to a combination of pain evoked by somatosensory stimulation and pain implied A 100 289 by either a verbal descriptor (Gracely and Wolskee 1983) or the discomfort of an aversive tone (Algom et al 1986). These stimulus integration methods provide more information than that available from single-stimulus, single-response designs. The method may also be used to assess physiological interaction or additivity (Lautenbacher et al 2007). Scaling Suprathreshold Pain Sensation: Stimulus-Dependent Methods Similar to measures of pain threshold and tolerance, these procedures use a physical measure of stimulus intensity as the dependent measure. These "staircase" or "adaptive" methods, which are commonly used to measure pain threshold, have been adapted to assess suprathreshold pain sensation. In these methods, an interactive computer program continuously adjusts the intensity of stimuli so that some fall within specific response categories. Figure 20-5 shows an example in which staircases are titrated between "no pain" and "mild," "mild" and "moderate," or "moderate" and "intense. In each case the magnitude of responses to specific stimulus intensities are used to adjust future stimulus intensities to maintain response magnitudes at specific levels. These stimulus-dependent scaling procedures are useful in clinical populations because they automatically equalize the psychological range of stimulus-evoked sensations, thereby ensuring that subjects with widely varying pain sensitivity receive similar sensory experiences. Multiple random staircase evaluation of pain intensity evoked by a 1-cm2 contact thermode. Fifty-six subjects received 5-second heat stimuli applied to the volar side of the forearm. On each trial, one of six independent staircases is chosen at random and a stimulus temperature associated with that staircase is delivered. A response from the 4-point response scale shown at the right, a criterion between a pair of categories, and the response history determine the next stimulus to be delivered by that staircase the next time that it is randomly chosen. In this example a pair of staircases is associated with each of the three intervals between the response categories. Subjects used either scale to measure an actual sensation, the heaviness of weights, or sensations implied by verbal descriptors ranging from "faint" to "extremely intense. This report further differentiated these groups: Italians were supposedly more present centered, whereas Jews were concerned about the future. Irish were influenced by negative social connotations of pain expression, whereas Americans were thought to genuinely be stoical. Within 2 decades these differences were partly confirmed in the experimental pain laboratory.

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Air conduction (the fork being held beside the ear) is normally louder than bone conduction (the fork being held against the mastoid process) heart attack zippo lighter purchase 12.5mg coreg with mastercard. It also supplies the carotid sinus (baroreceptor) and carotid body (chemoreceptor) heart attack or gas discount coreg 12.5 mg otc. It is attached to the upper part of the medulla by four or five rootlets along the groove between the olive and the inferior cerebellar peduncle arteria rectalis media order coreg 25 mg with amex. Below the jugular foramen the nerve courses downwards and forwards between the internal carotid artery and the internal jugular vein to reach the styloid process prehypertension prevention buy online coreg. From here it passes along the stylopharyngeus muscle to enter the pharnyx between the superior and middle constrictors. Here, it breaks up into its terminal branches, which supply the posterior onethird of the tongue and the mucous membrane of the pharynx (including the tonsil). The tympanic branch, which is continued as the lesser superficial petrosal nerve, conveys the preganglionic parasympathetic fibres to the otic ganglion (parotid secretomotor fibres). The only other branch of significance is the carotid nerve, which arises just below the skull and runs down on the internal carotid artery to supply both the carotid body and carotid sinus. This small twig serves as the afferent limb of the baroreceptor and chemoreceptor reflexes from the carotid sinus and body, respectively. However, such lesions are frequently difficult to detect and rarely occur as isolated phenomena since there is so often associated involvement of the vagus or its nuclei. The vagus nerve (X) the vagus has the most extensive distribution of all the cranial nerves, innervating the heart and the major part of the respiratory and alimentary tracts. Central connections the dorsal nucleus of the vagus in the medulla is a mixed visceral afferent and efferent nucleus. It receives sensory fibres from the heart, the lower respiratory tract and the alimentary tract as far as the distal 414 the nervous system transverse colon; in addition, it gives rise to preganglionic parasympathetic motor fibres to the heart and to the smooth muscles of the bronchi and gut. From the nucleus ambiguus efferent fibres pass to the striped muscles of the pharynx and larynx. Distribution the nerve is connected to the side of the medulla by about ten filaments that lie in series with the glossopharyngeal nerve along the groove between the olive and the inferior cerebellar peduncle. These filaments unite to form a single bundle that passes beneath the cerebellum to the jugular foramen. Two sensory ganglia are associated with this part of the nerve: a superior, within the jugular foramen, and an inferior, immediately beneath the skull. The vagus then passes vertically downwards to the root of the neck, lying in the posterior part of the carotid sheath between the internal jugular vein and the internal and then common carotid arteries. There are a number of important branches in the neck: pharyngeal to the pharyngeal and palatal musculature by way of the pharyngeal plexus; superior laryngeal, supplying the interior of the larynx above the vocal folds and the cricothyroid and inferior constrictor muscles; and the superior and inferior cardiac branches which are inhibitory to the heart. Below the level of the subclavian arteries the course and relations of the nerve on the two sides differ. On the right side the recurrent laryngeal branch is given off as the vagus crosses the subclavian artery; beyond this, the vagus descends through the superior mediastinum in close association with the great veins. Behind the root of the lung it takes part in the formation of the pulmonary plexus and then passes on to the oesophagus to form, with its fellow, the oesophageal plexus. The left vagus enters the thorax in close association with the great arteries, lying at first lateral to the common carotid and then crossing the arch of the aorta. The left recurrent laryngeal branch, which is given off as the vagus crosses the aortic arch, passes below the ligamentum arteriosum, behind the arch and then ascends in the groove between the trachea and the oesophagus. The vagus then passes behind the root of the lung, enters into the formation of the pulmonary plexus and passes on to the oesophagus to form a plexus from which emerge two trunks, named anterior and posterior vagal trunks, each comprising fibres from both the left and right vagus. The two vagi then enter the abdomen through the oesophageal opening in the diaphragm, the anterior vagus passing on to the anterior surface and the posterior passing to the posterior aspect of the stomach. Beyond this it is difficult to trace the course of the nerves, but branches are given to the coeliac, hepatic and renal plexuses and, by way of these plexuses, are distributed to the fore- and midgut and to the kidneys. According to standard descriptions, the cranial root is formed by a series of rootlets that emerge from the medulla between the olive and the inferior cerebellar peduncle. These rootlets are considered to join the spinal root, travel with it briefly, then separate within the jugular foramen and are distributed with the vagus nerve to supply the musculature of the palate, pharynx and larynx. All the rootlets that form the accessory nerve arise caudal to the olive and no connections can be demonstrated between the accessory nerve and the vagus in the jugular foramen. Thus, according to this study the accessory nerve has no cranial component and consists only of the structure hitherto referred to as the spinal root of the accessory nerve. This spinal root is formed by the union of fibres from an elongated nucleus in the anterior horn of the upper five cervical segments, which leave the cord midway between the anterior and posterior roots, join, then pass upwards through the foramen magnum. The accessory nerve and the converging rootlets of the vagus nerve then enter the jugular foramen in a shared sheath of dura. The glossopharyngeal nerve enters the jugular foramen anterior to the vagus through a separate dural sheath. The accessory nerve passes backwards over the internal jugular vein to the sternocleidomastoid muscle, which it pierces (and supplies), and then crosses the posterior triangle of the neck to enter and supply the deep surface of the trapezius. Surface marking of the spinal accessory nerve the extracranial course of the spinal accessory nerve can be marked out by a line which runs from the tragus of the ear to a point at the junction of the middle and lower thirds of the anterior border of the trapezius. This line will be seen to cross the palpable transverse process of the atlas (which 416 the nervous system lies immediately inferior to the mastoid process) and also the junction of the upper and middle thirds of the posterior border of the sternocleidomastoid muscle. There is, however, a good deal of variation in the precise position of the nerve as it crosses the posterior triangle of the neck. This follows, for example, most block dissections of the lymph nodes of the neck, the nerve being sacrificed in clearing the posterior triangle. The accessory nerve may also be damaged inadvertently during a supraclavicular lymph node biopsy.

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