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African apes and orangutans experience temporal and spatial fluctuations in fruit availability with similar behavioral consequences. Relying on the African apes as a comparative ecogeographic model, this chapter examines jaw form among Pongo pygmaeus morio, P.p. wurmbii, and P. abelii to determine if these populations differ predictably in ways that reflect their ecological profiles. Pongo p. morio is characterized by the longest lean fruiting periods and relies to the greatest extent on resistant and hard foods. These orangutans are found to exhibit the relatively most robust mandible, and thus display the relatively greatest capacity to counter large and repetitive jaw loads. Pongo abelii, which maintains a fruit-dominated diet even in times of fruit scarcity, displays the relatively least robust mandible. Orangutans are further shown to display a relationship between variance in energy intake, feeding efficacy, and relative brain size, suggesting a link among morphological divergence, behavioral ecology, and life history.

The phylum Micrognathozoa consists of only one species, the microscopic Limnognathia maerski, which was discovered in a cold spring at Disko Island in Greenland. Limnognathia is a cylindrical worm with a rounded head and abdomen, and a mid-body characterised by transverse wrinkles. The species has cellular tissues, with paired ovaries that probably consist of naked oocytes. The presence of the unusual internal skeletal lamina suggests that it is a sister group of the rotifers, while the complicated jaws are very similar to those of both gnathostomulids and the free-living rotifers. These observations strongly support Limnognathia’s position within the Gnathifera.

Huge disaster movies became popular, and the need for “more bodies” meant more work for stuntwomen. Movies celebrating stuntmen were released: Stunts (1977), Hooper (1978), and The Stunt Man (1980). New stunts sometimes led to accidents and injuries caused by inexperienced crews, rushing the shot, and a lack of safety regulations. Trust eroded between stunt people and crews, and stuntwomen learned to rely on their instincts.

The jaw jerk (or masseter reflex) is a monosynaptic reflex that presents an opportunity to study the peripheral and central function of the trigeminal nerve. It is elicited by tapping the midpoint of the chin with a special reflex hammer containing a microswitch to simultaneously trigger the sweep of the oscilloscope. Surface recordings are made bilaterally from the masseter muscles. Stimulation of the spinal cord can be accomplished with specialized stimulators, capable of delivering high voltages or high-density magnetic fields. The cervical spinal cord can be stimulated, however, with equipment normally present in the electromyography laboratory. The latency obtained is a combination of conduction time through the spinal cord, plus peripheral conduction through the sciatic nerve. The peripheral component can be determined by eliciting the corresponding M and minimal F waves on peroneal stimulation at the fibular head.

When bob wright awoke on Sunday March 1, 1970, he didn’t feel like getting in a boat. He had attended a wedding reception late into the previous night, and the morning in Victoria had broken cold and blustery. But he had promised to show his whale-catching operation to Don White, Paul Spong’s former research assistant. Wright already had an orca at his new oceanarium, Sealand of the Pacific, but he was keen to try his hand at capture, and he especially hoped to trap an albino killer whale often seen in local waters. When White and a friend arrived for the excursion, however, Wright wasn’t feeling very eager. “Bob is totally hung over, but he is feeling responsible,” White recalled. “He has told me to come, so he feels like we’ve got to do it.” Along with trainer Graeme Ellis, the three men piled onto Wright’s twenty-foot Bertram runabout and started for Pedder Bay. As the boat rounded Trial Island and cruised west past Victoria, the sea became choppy and Wright grew queasier. But minutes later, as they approached Race Rocks, he forgot all about his hangover. “Fuck!” he yelled. “It’s the white whale!” Sure enough, a group of orcas with what appeared to be an albino member was passing Bentinck Island and heading straight for Pedder Bay. The sighting was lucky, but the timing awful. Wright wasn’t set for a capture that day. His seine nets were in storage, and at first he couldn’t hail any of his Sealand staff. Determined not to let this opportunity pass, he gunned the Bertram into the bay and made straight for the Lakewood—a charter fishing boat he had rigged for orca catching. As Wright gathered his crew on the vessel, the excitement was palpable. “We were playing macho whale hunters,” White reflected, “and Bob Wright was our Captain Ahab.” With only one light net on board, the operation would have to be perfect, and everyone watched anxiously as the whales lingered near the mouth of Pedder Bay. Finally, as the sun began to set, the orcas entered.

Ted griffin awoke with a start, but he wasn’t sure why. It was a warm night in August 1970, and all seemed calm and quiet. Water lapped against the boat’s hull as the lights of Coupeville flickered a mile and a half away. Yet something wasn’t right. The breathing of the whales behind the capture nets sounded clipped and nervous. “How long have they been blowing that way?” he asked the two men on watch. “Blowing? What way?” they answered. “All night I guess.” Straining his eyes in the dark, Griffin scanned the enormous pen, anchored just off the old Standard Oil dock. Everything seemed to be in order—except on the north side. The marker lights there were too far apart. He roused Goldsberry, and the partners jumped into a skiff to investigate. When they reached the floating lights, Griffin stared down at a loose cork line, puzzled. The net looked split. “Not split—cut!” yelled Goldsberry. “And in more than one place.” Griffin couldn’t believe it. Suddenly the orcas’ anxious breathing made sense. During the night, someone had slashed a section of the net. Large portions of loose mesh now drifted in the current, threatening to drown any whales nearby. Griffin and Goldsberry shouted for their crew, and in the following hours everyone worked feverishly in the dark—reattaching lines, mending mesh, anchoring nets. Had they reacted in time? Had the animals managed to avoid danger? Griffin needed to find out. Donning his wetsuit, he slipped over the cork line and into Penn Cove’s murky waters. At first, he was hopeful. All the whales seemed to be swimming near the surface. But a moment later, his eye caught a shimmer of white—perhaps a shark caught in the net? No, it was a tiny orca calf, no more than eight feet long. Ensnared in a floating portion of mesh, the little whale hung lifeless, head down. Other divers found two more, also calves. Initially, Griffin felt only nausea, but that soon gave way to rage. He wanted to lash out at those responsible.

The appearance of the tool constitutes, for the palaeontologist, a decisive step in the process of ‘hominization’. This step raises an intriguing problem for the neurobiologist: what, on a biological level and, more specifically, in terms of the organization of nervous structures, permitted the crossing of the ‘cerebral Rubicon’ which separates man from other primates? The study of fossil man has clearly established the presence of manufactured tools beside skeletons that had the fundamental characteristics of the human species, i.e. upright posture, prehensile hands, a reduction of jaw size, and a significant enlargement of the skull. These findings highlight three major fields of enquiry for the neurobiologist.

Towards the end of July 1953 a congress of palaeontologists was held in London under the auspices of the Wenner-Gren Foundation. The problems of fossil man were the subject of its deliberations. Java man, Neanderthal man, Rhodesian man, the South African prehumans—all these were given close attention. But Piltdown man was not discussed. Not surprisingly. He had lost his place in polite society. What more could one usefully say about him? Yet, unofficially, the Dawn Man did manage an appearance. Most of those present had not seen the original fossil specimens, so on a tour of the Natural History Museum these were shown along with others housed there. The sight of the actual fragments provoked the familiar tail-chasing discussion. As always there were those who could not feel that the famous jaw really harmonized with the rest, but there were others who took the opposite view. The enigma remained. At the dinner that night Dr. Oakley remarked casually to Dr. Washburn of Chicago and myself that owing to Dawson’s early death in 1916 the Museum had no record of the exact spot where the remains of the second Piltdown had been found. They knew the place—Sheffield Park—but the actual spot or even the field had never been marked on a map. ‘The fact is’, said Oakley, ‘that all we know about site II is on a postcard sent in July 1915 by Dawson to Woodward, and an earlier letter in that year, from neither of which can one identify the position of Piltdown II.’ This was surprising. The second group of finds had done so much to convince many people that the first Piltdown man was by no means an isolated phenomenon. One had imagined that if it were ever thought worthwhile it would be possible to go and excavate the second site. Now it appeared that this had never been done because the second site could not be located, though Woodward had apparently visited it before the second find. This curious piece of information greatly puzzled me.

Almost any single one of the techniques employed in the investigations suffices to reveal the elaborateness of the deception which was perpetrated at Piltdown. The anatomical examination, the tests for fluorine and nitrogen bear particularly good witness to this; even the radio-activity results taken alone, led the physicists to remark on the ‘great range of activity shown by specimens from this one little site’; ‘it is difficult to avoid the conclusion that the different bones in the Piltdown assemblage have had very different geological and chemical histories’. We have merely to take account of the stained condition of the whole assemblage, to realize the thoroughness of the fraud. From the Vandyke brown colour of the unnaturally abraded canine we infer with certainty that it was deliberately ‘planted’. The superficiality of the iron impregnation, combined with the chromium, tells as much as regards the orang jaw. And it is this iron-staining which finally shows that the rest, human and animal, was without doubt, all ‘planted’. The iron-staining has two peculiar features. It seems probable that ferric ammonium sulphate (iron alum) was the salt employed. This salt is slightly acid. The peculiarity of this salt (and, indeed, of any acid sulphate) is that in bone which contains little organic matter such as the cranium of Piltdown I, or Piltdown II, the beaver bones and hippo teeth, it brings about a detectable change in the crystal structure of the bone. In the apatite in which the calcium of the bone is held, the phosphate is replaced by sulphate to form gypsum. This change is quite unnatural, for neither gypsum nor sufficient sulphate occur in the gravels at Piltdown to bring it about. So the iron-sulphate-staining is an integral part of the forger’s necessary technique. He also used chromium compounds to aid the iron-staining probably because he thought it would assist the production of iron oxide. Chromium compounds are oxidizing. The basic strategy underlying the Piltdown series of forgeries now seems reasonably clear. Two main elements in the plan taken together explain nearly all the features of the affair quite satisfactorily.

This chapter considers how the tongue, neck, and jaw cause tension in singers, along with some pedagogical ways of controlling them. The tongue occupies much of the vocal tract and can alter the spatial arrangements of the buccopharyngeal (mouth-pharynx) cavity, which is the chief resonance chamber of the voice. The neck, in which the chief instrument of phonation is housed, is a complex of muscular systems attaching to the head and to the torso. What one does with the nuchal muscles (back of the neck) and muscles of the submandibular area (below the jaw) influences laryngeal function. The jaw is capable of both lateral and perpendicular movements, and hence can affect the entire phonatory operation.

This chapter focuses on the “incorrupt jaw and tongue” of St. Anthony of Padua, known for his legendary ability to use vocal timbres and histrionics in preaching. Thousands of devout pilgrims come to visit the ornate shrine of St. Anthony in the Italian city of Padua. Several parts of his vocal mechanism, which functioned so mellifluously 750 years ago, have become objects of religious veneration in the cathedral at Padua. The saint's “incorrupt” tongue has endured not only physically but spiritually, and the thoughts expressed by that ancient vocal instrument continue to speak to us today, in part because of the “golden delivery” that came from efficient physiologic and acoustic use of his vocal tract. One doesn't have to be a believer to recognize that ideas conveyed through specific vocal timbres evoke strong emotional and spiritual responses.

This chapter showcases Howard Skempton’s miniature, The Maldive Shark. It is dedicated to his friend, the composer and singer Brian Dennis (1941–98). The captivating text ruminates on the relationship between the shark and the smaller fish that encircle it, as it makes its ponderous progress. The poem’s imagery is often lurid (‘sawpit of mouth’, ‘charnel of maw’) and is laden with alliteration (‘white triple tiers of glittering gates’), giving the singer the opportunity to relish the sounds as they roll off the tongue. Despite all this verbal detail, a seamless overall legato has to be preserved, with notes given their full value. The piece lies comfortably within the baritone’s natural compass, and the vocal dynamic is mezzo piano throughout, so a good degree of tonal control will prove advantageous.

Now you have an understanding of the anatomy of the maxilla and mandible, the TMJs, and jaw musculature, we can examine how these structures work together to produce the complex actions involved in the biting and chewing of food. Technically, incision is biting a piece from a larger chunk of food and mastication is the grinding down of that piece into smaller components and mixing them with saliva. Mastication is often used to cover both actions. Box 26.1 briefly compares the anatomy of the human dentition to that of other mammals. As well as knowledge of the TMJ, muscles of mastication, and other muscles used in jaw movements, it is necessary to appreciate some aspects of the static and dynamic relationships of the teeth to understand chewing movements. The first thing to notice is the bigger width of the upper dental arch compared to the lower arch, a condition known as anisognathy. In Figure 26.1A , you can see that the maxillary molars overhang the mandibular teeth by half a cusp width so the buccal cusps of the lower molars and premolars occlude between the buccal and palatal cusps of the maxillary teeth. Observe also that the long axis of the maxillary molars and premolars incline buccally while the corresponding axis of the mandibular teeth incline lingually; the occlusal plane of the posterior teeth is thus curved transversely as illustrated in Figure 26.1A . It would be possible to chew food simply by moving the teeth up and down without any side-to-side movement, but this would be inefficient and not make full use of the cusps on the occlusal surfaces of posterior teeth. However, we can only chew on one side at a time because of the anisognathy of the upper and lower teeth. Due to anisognathic jaw positions, the maxillary anterior teeth are also going to protrude in front of the mandibular anterior teeth. Figure 26.1B illustrates the normal relationships of the anterior teeth. The maxillary incisors overhang the mandibular incisors by about 2–3 mm in the horizontal plane; this is called the overjet. The upper incisors usually have a vertical overhang, the overbite, of about the same amount. As mentioned in Chapter 24 , the mouth at rest is closed by tonic contraction of the muscles of mastication and facial expression.

This chapter will focus on preparing you to undertake an OSCE in the skill of basic life support (BLS), in a cardiac arrest situation, following the Resuscitation Council (UK) Guidelines (2010). Basic life support guidance is aimed especially at adults who in their professions have a duty to respond to a cardiac arrest. Basic life support refers to maintaining the airway, breathing and circulation without the use of any equipment, other than protective devices (Resuscitation Council (UK) 2010). A number of studies (Ahmet and Sarac 2009; Berdowski et al. 2009; Oermann et al. 2011) recognize that effective implementation of guidance is likely to be enhanced by comprehensive and timely education. Soar et al. (2010) suggest that survival from cardiac arrest is dependent on a number of factors—particularly that respondents are well equipped and practiced in the skill and that quality educational packages are readily available to those responders. This chapter will endeavour to provide you with the relevant information to revise the components required to complete an OSCE in the skill. Emphasis is placed on the importance of providing effective, good quality chest compressions whilst minimizing any pauses and so maximizing blood flow and oxygenation. Note: The first aspect of the BLS skill you will be expected to carry out during your OSCE is a full risk assessment of the situation including safety and infection control issues. A respondent to any medical emergency should not put themselves or those around them at any risk. If this is impossible, however, measures should be taken to minimize that risk whilst ensuring no further harm comes to the casualty. In your OSCE, you will be expected to review the surrounding area for hazards, e.g. deep water, electricity, oncoming vehicles, fire and smoke, falling debris, biological threats, etc., to ensure your own and the patient’s safety. Note: This will depend on the way in which your OSCE station has been set up and if there are no threats to yourself or the patient you will need to verbalize to the examiner that you have checked the surrounding area and that it is safe for you to continue.

The neurology section of the PACES examination is often the major cause of (unnecessary!) anxiety for MRCP candidates. The key is to approach the patient in a logical fashion. Some neurology cases are simply an exercise in pattern recognition – noticing the frontal balding and ptosis of myotonic dystrophy, the distal wasting and pes cavus of Charcot–Marie–Tooth disease, for example. However, in those cases without obvious clues to the underlying diagnosis, a clear systematic approach will usually pay dividends. When faced with a neurological problem, the first question that should be posed is the site of the lesion. During the course of the examination, identify signs that might help in localization: • Cortex: signs of dysfunction of higher cognitive function. • Subcortical: upper motor neuron (UMN) signs (hypertonia, pyramidal pattern of weakness, hyper-reflexia, extensor plantars), slowness of thought. • Basal ganglia: cogwheel rigidity, resting tremor, bradykinesia, postural instability, dyskinesias, dystonias. • Brainstem: cranial nerve abnormalities with contralateral UMN signs. • Cerebellum: gait ataxia, nystagmus, finger-nose ataxia, past-pointing. • Spinal cord: bilateral UMN signs, presence of a sensory level. • Nerve root: lower motor neuron (LMN) signs (wasting, weakness, hyporeflexia, sensory loss) in a myotomal or dermatomal distribution. • Single or multiple nerve/plexus: LMN signs that are focal, and are not consistent with a nerve root lesion. • Polyneuropathy: LMN signs, more pronounced distally, affecting the legs more than the hands, diminished reflexes, sensory signs. • Neuromuscular junction: weakness without sensory involvement or significant wasting, usually but not invariably proximal, which fluctuates (either with time of day or during the course of the examination). • Muscle: wasting and weakness with normal reflexes and sensation. Once the lesion has been localized, consider the disease processes that commonly affect that site. Clues may be obtained from the history, if you are permitted to ask questions. The most helpful aspect of the history is usually the speed of onset: • Seconds: electrical disturbance (i.e. epilepsy), trauma. • <5 minutes: infarction. • > 5 minutes: migraine, haemorrhage. • Minutes–hours: infection, inflammation, drugs. • Hours–days: infection, inflammation, nutritional, drugs.

The definition of fibromyalgia includes widespread pain in all four quadrants (areas) of the body. What happens when you have fibromyalgia-like pain located in only one or two quadrants of the body? Limited forms of the syndrome have distinct features and terms used to describe them. Myofascial pain syndrome encompasses many regional pain conditions ranging from temporomandibular joint dysfunction in the jaw to a low back pain syndrome. The diagnosis of myofascial pain syndrome requires that at least one trigger point be present and that, when it is pressed, pain is referred to another site. This chapter will review regional myofascial pain, relate it to fibromyalgia pain pathways, and discuss its management and prognosis. Our current concepts of tender points, trigger points, and regional pain amplification were developed by two of the best-known physical medicine thinkers, Janet Travell and David Simons. Beginning in the early 1940s, Dr. Travell became well known as John F. Kennedy’s physician, who nursed him back to health in the 1950s when back pain restricted his ability to walk. Later, she became Lyndon Johnson’s White House physician. Travell and Simon’s textbook on myofascial pain remains a classic and was updated by them as recently as 1992. Dr. Travell (who died in 1997 at the age of 95) and Dr. Simons formed close working relationships with rheumatologists, and their influence permeates every fibromyalgia study relating to tender points and regional pain. Neurologists, neurosurgeons, and orthopedists diagnosed and treated localized muscle and nerve pain long before there were rheumatologists. At about the same time that rheumatologists were becoming recognized and organized into a certifiable subspecialty, an equally small group of doctors were organizing themselves into a specialty known as physical medicine and rehabilitation. These doctors (who call themselves physiatrists) do not perform surgery, are not internists or family physicians, and do not manage autoimmune diseases. They concern themselves with areas not addressed by rheumatologists such as stroke, cardiac, and spinal cord injury rehabilitation. Physical medicine doctors usually practice in a hospital or hospital-like environment and work closely on a daily basis with physical therapists, occupational therapists, speech therapists, social workers, psychologists, and other allied health professionals.

Odontogenic cysts and tumours arise from inclusion of tooth-forming epithelium and mesenchyme in the jaw bones during development. Cysts also arise from non-odontogenic epithelium trapped during fusions or from vestigial structures. In addition, bone cysts that can arise at other skeletal sites may also occur in the jaws. Odontogenic cysts and tumours may be classified according to their putative developmental origins and biology. The classification of jaw cysts is shown in Fig. 6.1. Odontomes are hamartomatous develop­mental lesions of the tooth-forming tissues. Odontogenic tumours are uncommon and are usually benign. Ameloblastoma is the most com­mon odontogenic tumour and is described in detail. The other odon­togenic tumours are rare and only the principal features are presented. Very rare congenital lesions of possible odontogenic origin are men­tioned in the final section. A cyst may be defined as pathological cavity lined by epithelium with fluid or semi-fluid contents. However, clinically, the term encompasses a broader range of benign fluid-filled lesions, some of which do not possess an epithelial lining. The preferred definition is, therefore, ‘a pathological cavity having fluid or semi-fluid contents that has not been created by the accumulation of pus’. Cysts are commonly encountered in clinical dentistry and are generally detected on radiographs or as expansions of the jaws. Most cysts have a radiolucent appearance and are well circumscribed, often with a corticated outline. At least 90% of jaw cysts are of odontogenic origin. The clinico-pathological features of jaw cysts are summarized in Table 6.1. The incidence of the four most common jaw cysts are provided in Table 6.2. The epithelial lining of odontogenic cysts originates from residues of the tooth-forming organ. • Epithelial rests of Serres are remnants of the dental lamina and are thought to give rise to the odontogenic keratocyst, lateral periodon­tal, and gingival cysts. • Reduced enamel epithelium is derived from the enamel organ and covers the fully formed crown of the unerupted tooth. The dentiger­ous (follicular) and eruption cysts originate from this tissue, as do the mandibular buccal and paradental cysts. • Epithelial rests of Malassez form by fragmentation of Hertwig’s epi­thelial root sheath that maps out the developing tooth root. Radicular cysts originate from these residues.

Cranial nerve examination is one of the commonly assessed areas of the nervous system in the MRCPCH clinical examination. The examiner may ask you to examine some of the cranial nerves or just the eye. This guide will take you through a systematic nerve examination, which is followed by most practitioners. You may need to individualize the examination sequence to suit your style. The key competence skills required in the cranial nerve examination are given in table 9.1. Cranial nerves cases commonly encountered in the MRCPCH Clinical Exam are listed in table 9.2. Causes of the different cranial nerve lesions are given in table 9.3. These steps are repeated in every system to reiterate their importance and to help you recollect the initial approach of any clinical exam. Also refer to chapter 4. • On entering the examination room, demonstrate strict adherence to infection control measures by washing your hands or by decontaminating them with alcohol rub. • Introduce yourself both to the parents and the child. • Talk slowly and clearly with a smile on your face. • Establish rapport with the child and parents. • Ensure privacy. • Positioning: examine the older child while they sit on the edge of the bed or on a chair. It is preferable to examine the younger child on a parent’s lap rather than on a couch, as this can cause much anxiety. The aim of the visual survey is to capture every available clue, which may help you to reach the correct diagnosis. • Look at the child and try to estimate their approximate age. • Always consider whether the findings combine to form a recognizable clinical syndrome. Common syndromes with cranial nerve involvement include Aicardi’s syndrome, Angelman’s syndrome, Arnold–Chiari malformation, Crouzon’s syndrome, Lesch–Nyhan syndrome, Sturge–Weber syndrome, and Werdnig–Hoff man disease.

This chapter discusses the role of the jaw in singing. Jaw tension is often a problem for singers. When there is tension in the mandible (jaw) there generally is a corresponding rigidity in the tongue muscles, which subsequently is transferred to the level of the larynx. Exercises to reduce jaw tension are a part of most vocal pedagogies. Many jaw problems result directly from concepts the singer has about arranging ideal resonator “space.” The resonator tube (the vocal tract) extends from the larynx to the lips, and alters its position in reaction to postures of the jaw and tongue. A singer must know how the jaw actually works in phonation if satisfactory solutions to mandibular tension are to be found. Many singers suffering from temporomandibular joint syndrome find that this condition can go away by not hanging the jaw in the hope of “opening” the throat.