By C. Pyran. Gannon University. 2018.

Lesser responses include medial movement cheap 10 mg alavert amex allergy wheat, tensing alavert 10mg online allergy testing on 6 year old, or corrugation of the pharyngeal wall. In addition there may be head withdrawal, eye water- ing, coughing, and retching. Some studies claim the reflex is absent in many normal individuals, especially with increasing age, without evident functional impairment; whereas others find it in all healthy individuals, although variable stimulus intensity is required to elicit it. The afferent limb of the reflex arc is the glossopharyngeal (IX) nerve, the efferent limb in the glossopharyngeal and vagus (X) nerves. Hence individual or combined lesions of the glossopharyngeal and vagus nerves depress the gag reflex, as in neurogenic bulbar palsy. Dysphagia is common after a stroke, and the gag reflex is often performed to assess the integrity of swallowing. Some argue that absence of the reflex does not predict aspiration and is of little diagnos- tic value, since this may be a normal finding in elderly individuals, whereas pharyngeal sensation (feeling the stimulus at the back of the pharynx) is rarely absent in normals and is a better predictor of the absence of aspiration. Others find that even a brisk pharyngeal response in motor neurone disease may be associated with impaired swallowing. A video swallow may be a better technique to assess the integrity of swallowing. Journal of Neurology, Neurosurgery and Psychiatry 1996; 61: 96-98 Cross References Bulbar palsy; Dysphagia Gait Apraxia Gait apraxia is a name given to an inability to walk despite intact motor systems and sensorium. Patients with gait apraxia are often - 133 - G Ganglionopathy hesitant, seemingly unable to lift their feet from the floor (“magnetic gait”) or put one foot in front of the other. Arms may be held out at the sides to balance for fear of falling; fear may be so great that the patient sits in a chair gripping its sides. These phenomena may be observed with lesions of the frontal lobe and white matter connections, with or without basal ganglia involvement, for example in diffuse cere- brovascular disease and normal pressure hydrocephalus. A syndrome of isolated gait apraxia has been described with focal degeneration of the medial frontal lobes. In modern classifications of gait disorders, gait apraxia is subsumed into the categories of frontal gait disorder, frontal disequilibrium, and isolated gait ignition failure. Gait apraxia is an important diagnosis to establish since those afflicted generally respond poorly, if at all, to physiotherapy; moreover, because both patient and therapist often become frustrated because of lack of progress, this form of treatment is often best avoided. Human walking and higher- level gait disorders, particularly in the elderly. Neurology 1993; 43: 268-279 Rossor MN, Tyrrell PJ, Warrington EK, Thompson PD, Marsden CD, Lantos P. Progressive frontal gait disturbance with atypical Alzheimer’s disease and corticobasal degeneration. Journal of Neurology, Neurosurgery and Psychiatry 1999; 67: 345-352 Cross References Apraxia Ganglionopathy - see NEUROPATHY Ganser Phenomenon The Ganser phenomenon consists of giving approximate answers to questions which can at times verge on the absurd (Q: “How many legs does a cow have? This may occur in psychiatric disease, such as depression, schizophrenia, and malingering, and sometimes in neurological disease (head injury, epilepsy). A Ganser syndrome of hallucinations, conver- sion disorder, cognitive disorientation and approximate answers is also described but of uncertain nosology. London: Arnold, 2001: 74-94 Gaping Gaping, or involuntary opening of the mouth, may occur as a focal dystonia of the motor trigeminal nerve, also known as Brueghel syn- drome after that artist’s painting De Gaper (“Yawning man,” ca. Afflicted individuals may also - 134 - Gegenhalten G demonstrate paroxysmal hyperpnea and upbeating nystagmus, sug- gesting a brainstem (possibly pontine) localization of pathology. The condition should be distinguished from other cranial dystonias with blepharospasm (Meige syndrome). Neurology 1996; 46: 1767-1769 Cross References Blepharospasm; Dystonia; Nystagmus Gaze-Evoked Phenomena A variety of symptoms have been reported to be evoked, on occasion, by alteration of the direction of gaze: ● Amaurosis: lesion, usually intraorbital, compressing central retinal artery ● Laughter ● Nystagmus: usually indicative of cerebellar lesion; may occur as a side-effect of medications; also convergence-retraction nystagmus on upgaze in dorsal midbrain (Parinaud’s) syndrome ● Phosphenes: increased mechanosensitivity in demyelinated optic nerve ● Segmental constriction of the pupil (Czarnecki’s sign) following aberrant regeneration of the oculomotor (III) nerve to the iris sphincter ● Tinnitus: may develop after resection of cerebellopontine angle tumors, may be due to abnormal interaction between vestibular and cochlear nuclei ● Vertigo Cross References Leopold NA. Journal of Neurology, Neurosurgery and Psychiatry 1977; 40: 815-817 Gaze Palsy Gaze palsy is a general term for any impairment or limitation in conjugate (yoked) eye movements. Preservation of the vestibulo-ocular reflexes may help dif- ferentiate supranuclear gaze palsies from nuclear/ infranuclear causes. Cross References Locked-in syndrome; Supranuclear gaze palsy; Vestibulo-ocular reflexes Gegenhalten Gegenhalten, or paratonia, or paratonic rigidity, is a resistance to pas- sive movement of a limb when changing its posture or position, which is evident in both flexor and extensor muscles (as in rigidity, but not spasticity), which seems to increase further with attempts to get the patient to relax, such that there is a resistance to any applied movement - 135 - G Gerstmann Syndrome (German: to counter, stand ones ground).

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Videos and films for this purpose are commercially available in some disciplines order alavert 10 mg line allergy medicine nose bleeds. WHEN THINGS GO WRONG Throughout this book we present the view that things are less likely to go ‘wrong’ if you have carefully prepared yourself for the teaching task best 10mg alavert allergy cure. However, unexpected difficulties can and do arise, so strategies to deal with these need to be part of your teaching skills. In our experience problems in teaching large groups are likely to fall into one of the following categories. An equipment failure can be a potential disaster if you have prepared a computer presentation or a series of slides or transparencies for projection. Preventive measures in- clude having a thorough understanding of your equip- ment, back-up equipment on hand, and learning to change blown bulbs or remove jammed slides. If these measures are of no avail, you will have to continue on without the materials and may do so successfully provided that you have taken care to have a clear record in your notes of the content of your material. You may then be able to present some of the information verbally, on a blackboard or whiteboard, or on an overhead transparency if the original problem was with the slide projector. You will not, of course, be able to use this approach with illustrations and you may have to substitute careful description and perhaps blackboard sketches to cover essential material. Whatever you do, do not pass around your materials, which may be damaged and, of course, by the time most of the audience receive them, they are no longer directly relevant to what you are saying! Do not start apologising or communicate your sense of ‘panic’ if this should happen. Instead, pause, calmly evaluate your situation, decide on a course of action, and continue. One lecturer we know invites students to check their notes while she simply cleans the board as she thinks through what to do next! We have deliberately avoided the use of the word ‘problem’ in relation to your interaction with students because the ‘problem’ may be with you (that is, your manner, your preparation or presentation, for example) or it could be more in the form of a genuinely motivated intellectual challenge to what you have been doing or saying. It is essential to be clear as to exactly what the challenge is and why it has occurred before you act. We cannot go into all aspects of classroom management and discipline here, but we can identify a number of principles and refer you to more detailed discussions elsewhere (McKeachie’s Teaching Tips is a useful reference). Disruptive behaviour and talking in class are common challenges and must not be ignored, both for the sake of your own concentration and for the majority of students who are there to learn. Simply stopping talking and waiting patiently for quiet usually overcomes minor disturbances. If this happens more than once the other students will usually make their displeasure known to the offenders. If the disruption is more serious, you will have to speak directly to the students concerned and indicate that you are aware of the offence. But do try initially to treat it with humour or you may alienate the rest of the class. If the problem persists, indicate that you will be unable to tolerate the situation again and that you will have to ask them to leave. Make sure you do just this if the problem re- emerges, Do so firmly and calmly. If the situation leads to confrontation, it is probably best if you leave the room. Make every attempt to meet the offenders afterwards to deal with the problem. There is no need for this and the majority of students will look for firm but fair disciplinary measures. An added measure is to arrange arriving and leaving classes so that you have time to get to know at least some of the students in the class – especially potentially trouble- some ones. The active learning strategies we have suggested in this chapter are also ways of addressing these challenges – both by engaging students in their own learning (and using up some of their energy in this way!

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He was one of the founding members and presi- dent of the Chicago Orthopedic Society buy alavert 10mg free shipping allergy symptoms sleepy. When the American Board of Orthopedic Surgery was Edwin Warner RYERSON founded in 1934 buy alavert 10mg amex allergy forecast nj, he became a member, was 1872–1961 vice president in 1935, and served on the board until 1940. Ryerson was one of the Edwin Warner Ryerson was born on March 14, organizers of the Clinical Orthopedic Society; and 1872, in New York City, where he attended in 1914 he was president of that association, school; he was graduated from Harvard Medical which was to become the force behind the cre- School in 1897. He was the house surgeon at ation of the American Academy of Orthopedic Boston Children’s Hospital from 1897 to 1898 Surgeons. In 1899, he migrated west and began the geons was formed in 1933 by a small group of practice of orthopedic surgery in Chicago. He was always interested in teaching; his first Ryerson was a leader among the Founders Group appointment was that of instructor in the princi- and was elected first president of the Academy in ples of surgery at Rush Medical College, a posi- 1933. From that date until presidents and a welcome guest at meetings of the 1935, his teaching career was quite active. He executive committee after his term of office had became professor of orthopedic surgery at the expired. Ryerson lived to see the Academy 293 Who’s Who in Orthopedics become the largest, most powerful, and most still present as he spoke of his appreciation of this useful orthopedic organization in the world. Ryerson died on February 3, 1961, at his a member of the International Society of Ortho- home in Fort Lauderdale. His teachings and con- pedic Surgery and Traumatology, the Institute of tributions to orthopedic surgery in Chicago and Medicine of Chicago, and the American College throughout the world will be long remembered. He served on the board of governors of the American College of Surgeons in 1947. He wrote many articles on orthopedic subjects and is, perhaps, best remembered for the Ryerson triple arthrodesis of the ankle. For several years he edited the Yearbook of Orthopedic Surgery and Traumatology. Ryerson’s professional life is best epitomized by what a former associate said of him: “He was a good teacher and surgeon; he always gave his best to his patients. Ryerson in his later life through his attendance at local meetings, including those of the Chicago Committee on Trauma, where his discussions of papers were always to the point. He was meticulous in his choice of words and insisted that others be equally meticulous. Luke’s Hospital, his operating room was always open to the younger men, and he would take time to explain the operative procedure. Although his Amulya Kumar SAHA primary interest was orthopedics, he would often observe other types of surgery being done. Fre- 1913– quently he came into my operating room to observe the procedure and give helpful sugges- Amulya Kumar Saha was born in 1913 in Pabna tions. Unbeknown to him, he was frequently in undivided India (now in Bangladesh). After referred to by the younger men as Uncle Ned, graduating with degrees in both science and medi- which indeed was a term of endearment. Ryerson belonged to several clubs in a surgical specialist and quickly rose to the rank Chicago and was an ardent and enthusiastic of major. In his later years his interest changed United Kingdom for additional training and study from golf to daily visits to the docks, seeing the in surgery. He received the titles of FRCS (Eng), many ships in port and conversing with their FRCS (Edin), and MChOrth (L’Pool) in 1948. Basu at the Indian Academy of Orthopedic Surgeons in January Museum in 1940. He delivered his first disserta- 1961, a lapel pin was given to each of the past tion to the Liverpool orthopedic group in 1948. It was my privilege Thereafter, the shoulder was one of his abiding and pleasure after this meeting to present this pin interests. On his return to India, Saha was first appointed Although he had some difficulty walking at that to the post of reader in surgery in Gwalior time, the spark in his eyes and kindly smile were Medical College. Subsequently, he joined the 294 Who’s Who in Orthopedics Nilratan Sircar Medical College and the Univer- ble. He was of the opinion that the Bankart lesion sity of Calcutta as associate professor of surgery, possibly was not the cause of recurrent anterior where he served from 1949 to 1955. From 1955 dislocation and occurred from lack of the stabi- to 1963, he served as professor director in the lizing factors and superimposed trauma.

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Brain 1981; 104: 701-709 Cross References Facilitation; Reflexes Jitteriness Jitteriness implies an exaggerated startle response buy alavert 10mg low cost allergy treatment xerosis, reflecting CNS overactivity purchase 10mg alavert free shipping allergy-x for dogs reviews. This may be confused in neonates with clonic seizures, but in the former there is stimulus sensitivity and an absence of associated ocular movements. However, both may occur in hypoxic-ischemic or metabolic encephalopathies or with drug withdrawal. Cross References Seizures Joint Position Sense - see PROPRIOCEPTION Jugular Foramen Syndrome The glossopharyngeal (IX), vagus (X), and accessory (XI) cranial nerves may be damaged by lesions at or around the jugular foramen, producing a jugular foramen (or Vernet’s) syndrome. This produces: ● Dysphagia, dysphonia, palatal droop, impaired gag reflex; ipsilat- eral reduced taste sensation on the posterior one third of the tongue, and anesthesia of the posterior one third of the tongue, soft palate, pharynx, larynx and uvula, due to glossopharyngeal and vagus nerve involvement. The differential diagnosis includes retropharyngeal or retroparotid space occupying lesions, which may in addition involve the hypoglos- sal nerve (XII; Collet-Sicard syndrome) and the sympathetic chain with or without the facial nerve (VII; Villaret’s syndrome). Cross References Dysphagia; Dysphonia; Gag reflex Junctional Scotoma, Junctional Scotoma of Traquair Despite the similarity of these terms, they are used to refer to different types of scotoma: ● Junctional scotoma: Unilateral central scotoma with contralateral superior tem- poral defect, seen with lesions at the anterior angle of the chi- asm; this is said to damage the ipsilateral optic nerve plus the crossing loop of fibers (Wilbrand’s knee) originating from the inferonasal portion of the contralateral eye (it may be noted that some authors have questioned whether such a loop in fact exists). Postgraduate Medical Journal 2002; 78: 106, 112-113 Cross References Scotoma; Visual field defects - 177 - K Kayser-Fleischer Rings Kayser-Fleischer rings are deposits of copper, seen as a brownish dis- coloration, in Descemet’s membrane. Although often visible to the naked eye (difficult in people with a brown iris), they are best seen with slit-lamp examination. Since they are a highly reliable sign of intra- cerebral copper deposition in Wilson’s disease (hepatolenticular degen- eration), any patient suspected of this diagnosis (i. Very occasionally cases of neuro- logical Wilson’s disease without Kayser-Fleischer rings have been reported. Kayser-Fleischer ring: Hepatolenticular degeneration (Wilson’s disease). Neurology 1995; 45: 1261-1262 Cross References Dystonia; Parkinsonism Kernig’s Sign Kernig’s sign is pain in the lower back (and also sometimes the neck) and resistance to movement with passive extension of the knee on the flexed thigh in a recumbent patient. It is indicative of meningeal mechanosensitivity due to inflammation, either infective (meningitis) or chemical (subarachnoid hemorrhage), in which case it may coexist with nuchal rigidity and Brudzinski’s (neck) sign. If unilateral it may indicate irritation of the lumbosacral nerve roots from a ruptured intervertebral disc (in which case Lasègue’s sign may also be present). London: Imperial College Press, 2003: 365-366 Cross References Brudzinski’s (neck) sign; Lasègue’s sign; Nuchal rigidity Kernohan’s Notch Syndrome Raised intracranial pressure as a result of an expanding supratentorial lesion (e. If the midbrain is shifted against the contralateral margin (free edge) of the tentorium, the cerebral peduncle on that side may be compressed, resulting in a hemiparesis which is ipsilateral to the supratentorial lesion (and hence may be considered “false-localizing”). There may also be an oculomotor nerve palsy ipsilateral to the lesion, which may be partial (unilateral pupil dilatation). Neurology 2000; 55: 1751 Cross References “False-localizing signs”; Hemiparesis; Hutchinson’s pupil Kinesis Paradoxica Kinesis paradoxica is the brief but remarkably rapid and effective movement sometimes observed in patients with Parkinson’s disease or post-encephalitic parkinsonism, despite the poverty and slowness of spontaneous movement (akinesia, hypokinesia; bradykinesia) seen in these conditions. Cross References Akinesia; Bradykinesia; Hypokinesia; Parkinsonism Klazomania Klazomania was the term applied to the motor and vocal tics seen as a sequel to encephalitis lethargica (von Economo’s disease), along with parkinsonism and oculogyric crises. This observation helped to pro- mote the idea that tics were due to neurological disease rather than being psychogenic, for example in Gilles de la Tourette syndrome. Compulsory shouting (Benedek’s “klazomania”) associated with oculogyric spasm in chronic epidemic encephalitis. Acta Psychiatrica Scandinavica 1961; 36: 369-377 Cross References Coprolalia; Echolalia; Parakinesia, Parakinesis; Tic Kleptomania Kleptomania, a morbid impulse to steal, has been related to the obses- sive-compulsive spectrum of behaviors in patients with frontal lobe dysfunction. Journal of Neurology, Neurosurgery and Psychiatry 2001; 70: 279 (abstract) Cross References Frontal lobe syndromes Klüver-Bucy Syndrome The Klüver-Bucy syndrome consists of a variety of neurobehavioral changes, originally observed following bilateral temporal lobectomy (especially anterior tip) in monkeys, but subsequently described - 179 - K Knee Tremor in man. The characteristic features, some or all of which may be present, are: Visual agnosia (e. Journal of Neurology, Neurosurgery and Psychiatry 1993; 56: 311-313 Klüver H, Bucy P. Cross References Apathy; Hypermetamorphosis; Hyperorality; Hyperphagia; Hyper- sexuality; Visual agnosia Knee Tremor A characteristic tremor of the patellae, sometimes known as knee bob- bing, juddering, or quivering, may be seen in primary orthostatic tremor (POT; “shaky legs syndrome”). It is due to rapid rhythmic con- tractions of the leg muscles on standing, which dampen or subside on walking, leaning against a wall, or being lifted off the ground, with dis- appearance of the knee tremor; hence this is a task-specific tremor. Auscultation with the diaphragm of a stethoscope over the lower limb muscles reveals a regular thumping sound, likened to the sound of a distant helicopter. EMG studies show pathognomonic synchronous activity in the leg muscles with a frequency of 14-18Hz, thought to be generated by a central oscillator (peripheral loading does not alter tremor frequency). A number of drugs may be helpful in POT, including phenobarbi- tone, primidone, clonazepam, and levodopa, but not propranolol (cf.

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