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If the knee is lax discount cialis 10mg with visa, as can be measured by clinical examination or with the KT-1000 arthrometer generic 5mg cialis visa, the ACL is not functioning to protect the knee against pivotal motions generic cialis 10 mg. The MRI can determine if the ligament is com- pletely torn, but cannot differentiate the degree of laxity. After the initial injury, there is a 50% chance of damage to the menis- cus. In the chronic situation, the incidence of meniscal tear is 75%, and the torn portion of the meniscus usually has to be removed. In the long term, the removal of all, or part of the meniscus, is associ- ated with an increased incidence of osteoarthritis. What Is the Average Time Needed Before the Patient Can Return to Sports After the Surgery? The answer is four to six months, but sometimes, it may take as long as one year to fully return to a pivotal sport. Treatment Options for ACL Injuries How Long Will the Patient Be Out of Work? If the work involves physical activity, it will take three to four months or until your legs are strong enough. Physical therapy is necessary for approximately one to six weeks postoperatively. The therapy goal is to reduce the pain and swelling, regain range of motion, and increase the strength of the muscles. Therapy may have to be modified based on the individual’s progress through the weeks of rehabilitation. The outcome of the ACL reconstruction depends not so much on the type of graft, but on the technique of placing the graft in the correct position, the fixation of the graft, and the postoperative rehabilitation. Because of the minimum harvest site morbidity, the most common graft used in our sports clinic is the hamstring graft. The patellar tendon graft is used for the athlete who wants to return to sports quickly, for example, at three months. The earlier return to activities is based on the faster healing of the bone-to- bone healing of the patellar tendon graft when compared to the tendon- to-bone healing with the hamstring graft. In a recent metaanalysis of the literature com- paring the hamstring and patellar tendon grafts, no significant difference in outcome was found. However, the patellar tendon grafts were a little more stable, and the patient was able to return to the same level of sports 18% more often than those who received the hamstring graft. Synthetic materials are not routinely used to substitute for the ACL because of the higher incidence of failure. These materials are indicated in special situations, such as multiple ligament injuries or some reoperations. The allograft is obtained from a cadaver, so a minimal risk of disease transmission exists. In addition, the graft takes longer to incorporate and often has tunnel enlargement as a result. Long-term results have shown more failures with the use of the allograft than with other options. After the surgery, the patient will have to use a Zimmer extension splint, or a functional brace for four to six weeks to protect the graft until it heals to the bone. The patient can return to sports four to six months after surgery, but with the brace on. Because the screws now used are made of a special sugar-type compound, they will dissolve within a couple of years after the surgery. The patient will spend just a few hours in the hospi- tal day care recovery room after the surgery. It also can cause more damage to the articular surface and the meniscus, thereby leading to later osteoarthritis. There is some weakness of the hamstrings after removal of the semitendinosus and the gracilis tendons. There is usually no weakness after patellar tendon harvest, but pain around the kneecap is common postoperatively. More damage, or “wearing out,” of the articular surface will occur if the knee continues to give way.

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Thirty-one of the 44 entered academic neurology and most went on to run their own training programs—wonderful legacy! His philosophy was to attract the best and the brightest and instill in than the joys of academia purchase cialis 10mg on line. As one of his pupils generic cialis 2.5 mg, I can personally attest to his strong character order 5mg cialis fast delivery, teaching and motiva- tional skills, academic achievements, but most importantly to his ability to be a friend and long-term counselor. This book is a testimony to the quality and quantity of an impressive group of residents trained over the years at Johns Hopkins. Haller Professor of Pediatric Neurology Director, Child Neurology Johns Hopkins University School of Medicine Contributors Anthony M. Avellino Division of Pediatric Neurosurgery, Children’s Hospital and Regional Medical Center, University of Washington School of Medicine, Seattle, Washington, U. Bale Division of Neurology, Department of Pediatrics, The University of Utah School of Medicine, Salt Lake City, U. Shannon Barnett Department of Psychiatry, The Johns Hopkins Hospital, Baltimore, Maryland, U. Belman Department of Neurology, School of Medicine, State University of New York (SUNY) at Stony Brook, Stony Brook, New York, U. Bergin Childrens Hospital, Department of Neurology, Boston, Massachusetts, U. Bibat Neurogenetics Unit, Kennedy Krieger Institute, Johns Hopkins Medical Institutions, Baltimore, Maryland, U. Ian Butler The University of Texas Medical School at Houston, Houston, Texas, U. Department of Neurological Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland, U. Cohn Johns Hopkins Hospital, Children’s Center, McKusick-Nathans Institute of Genetic Medicine, Baltimore, Maryland, U. Conry George Washington University School of Medicine, Children’s National Medical Center, Washington, D. Courvoisie Division of Child and Adolescent Psychiatry, Department of Psychiatry and Behavioral Sciences, The Johns Hopkins Medical Institutions, Baltimore, Maryland, U. Martha Bridge Denckla Johns Hopkins University School of Medicine, Kennedy Krieger Institute, Baltimore, Maryland, U. Dure, IV Division of Pediatric Neurology, Department of Pediatrics, The University of Alabama at Birmingham, Birmingham, Alabama, U. Paul Grahan Fisher The Beirne Family Director of Neuro-Oncology at Packard Children’s Hospital, Stanford University, Stanford, California, U. Freeman Pediatrics and Neurology, Johns Hopkins Hospital, Baltimore, Maryland, U. Natan Gadoth Department of Neurology, Meir General Hospital, Kfar Saba, Israel William Davis Gaillard Department of Neurology, Children’s National Medical Center, Washington, D. Gailloud Division of Interventional Neuroradiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, U. Gilbert Cincinnati Children’s Hospital Medical Center, Movement Disorders Clinics, Cincinnati, Ohio, U. Fiona Goodwin Department of Pediatric Neurology, Child Health, University of Southampton and Southampton University Hospitals, Southampton, U. Grados The Johns Hopkins Hospital, Department of Psychiatry, Division of Child and Adolescent Psychiatry, Baltimore, Maryland, U. Gray Kennedy Krieger Institute, Department of Neuropsychology, Baltimore, Maryland, U. Carolyn Elizabeth Hart Mecklenburg Neurological Associates, Charlotte, North Carolina, U. Hayflick Molecular and Medical Genetics, Pediatrics and Neurology, Oregon Health & Science University, Portland, Oregon, U. Michael Hemphill Department of Neurology, Medical College of Georgia, Savannah Neurology, Savannah, Georgia, U. Alec Hoon Johns Hopkins University School of Medicine, Kennedy Krieger Institute, Baltimore, Maryland, U. Judy Huang Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, U.

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This dissociation may be seen in a variety of clinical circumstances: ● Argyll Robertson pupil: small irregular pupils with reduced reac- tion to light discount cialis 20 mg amex, typically seen in neurosyphilis; the absence of miosis and/or pupillary irregularity has been referred to as pseudo-Argyll Robertson pupil buy 10mg cialis overnight delivery, which may occur with sarcoidosis cialis 5 mg amex, diabetes, and aberrant regeneration of the oculomotor (III) nerve ● Holmes-Adie pupil: dilated pupil showing strong but slow reaction to accommodation but minimal reaction to light (tonic > phasic) ● Parinaud’s syndrome (dorsal rostral midbrain syndrome): due to a lesion at the level of the posterior commissure, and character- ized by vertical gaze palsy, lid retraction (Collier’s sign) or ptosis, and large regular pupils responding to accommodation but not light. Philadelphia: Lippincott Williams & Wilkins, 2002: 135-146 Cross References Argyll Robertson pupil; Collier’s sign; Holmes-adie pupil, Holmes-adie syndrome; Lid retraction; Parinaud’s syndrome; Pseudo-argyll Robertson pupil; Pupillary reflexes Light Reflex - see PUPILLARY REFLEXES Locked-in Syndrome The locked-in syndrome results from de-efferentation, such that a patient is awake, self-ventilating and alert, but unable to speak or move; vertical eye movements and blinking are usually preserved, affording a channel for simple (yes/no) communication. The most common cause of the locked-in syndrome is basilar artery thrombosis causing ventral pontine infarction (both pathologi- cal laughter and pathological crying have on occasion been reported to herald this event). Other pathologies include pontine hemorrhage and central pontine myelinolysis. Bilateral ventral midbrain and internal capsule infarcts can produce a similar picture. The locked-in syndrome may be mistaken for abulia, akinetic mutism, coma, and catatonia. Neurology 1971; 21: 459-478 Cross References Abulia; Akinetic mutism; Blinking; Catatonia; Coma; Pathological crying, Pathological laughter Lockjaw - see TRISMUS Logoclonia Logoclonia is the tendency for a patient to repeat the final syllable of a word when speaking; hence it is one of the reiterative speech disor- ders (cf. It may be described as the festinating rep- etition of individual phonemes. Logoclonia is an indicator of bilateral brain injury, usually involv- ing subcortical structures, and may be seen in the late stages of demen- tia of Alzheimer type (but not in semantic dementia). Cross References Echolalia; Festination, Festinant gait; Palilalia; Perseveration - 187 - L Logopenia Logopenia Logopenia is a reduced rate of language production, due especially to word finding pauses, but with relatively preserved phrase length and syntactically complete language, seen in aphasic syndromes, such as primary progressive aphasia. Cross References Aphasia Logorrhea Logorrhea is literally a flow of speech, or pressure of speech, denoting an excessive verbal output, an abnormal number of words produced during each utterance. The term may be used of the output in the Wernicke/posterior type of aphasia, or of an output which superficially resembles Wernicke aphasia but in which syntax and morphology are intact, rhythm and articulation are usually normal, and paraphasias and neologisms are few. Moreover comprehension is better than antic- ipated in the Wernicke type of aphasia. Patients may be unaware of their impaired output (anosognosia) due to a failure of self-monitoring. Logorrhea may be observed in subcortical (thalamic) aphasia, usually following recovery from lesions (usually hemorrhage) to the anterolateral nuclei. Similar speech output may be observed in psychi- atric disorders, such as mania and schizophrenia. New England Journal of Medicine 1992; 326: 531-539 Cross References Aphasia; Delirium; Echolalia; Jargon aphasia; Wernicke’s aphasia Long Tract Signs - see UPPER MOTOR NEURONE (UMN) SYNDROME “Looking Glass Syndrome” - see MIRROR AGNOSIA Lower Motor Neurone (LMN) Syndrome A lower motor neurone (LMN) syndrome constitutes a constellation of motor signs resulting from damage to lower motor neurone path- ways, i. Following the standard order of neurological examination of the motor system, the signs include: ● Appearance: muscle wasting; fasciculations (or “fibrillations”) may be observed or induced, particularly if the pathology is at the level of the anterior horn cell - 188 - Lower Motor Neurone (LMN) Syndrome L ● Tone: reduced tone (flaccidity, hypotonus), although this may simply reflect weakness ● Power: weakness, often marked; depending on the precise patholog- ical process, weakness often affects both flexor and extensor muscles equally (although this is not always the case) ● Coordination: depending on the degree of weakness, it may not be possible to comment on the integrity or otherwise of coordination in LMN syndromes; in a pure LMN syndrome coordination will be normal ● Reflexes: depressed (hyporeflexia) or absent (areflexia); plantar responses are flexor. It is often possible to draw a clinical distinction between motor symptoms resulting from lower or upper motor neurone pathology and hence to formulate a differential diagnosis and direct investiga- tions accordingly. Sensory features may also be present in LMN syn- dromes if the pathology affects sensory as well as motor roots, or both motor and sensory fibers in peripheral nerves. Cross References Areflexia; Fasciculation; Fibrillation; Flaccidity; Hyporeflexia; Hypotonia, Hypotonus; Neuropathy; Reflexes; Upper motor neurone (UMN) syndrome; Weakness - 189 - M Macrographia Macrographia is abnormally large handwriting. It may be seen in cere- bellar disease, possibly as a reflection of the kinetic tremor and/or the impaired checking response seen therein (cf. Cross References Micrographia; Tremor Macropsia - see METAMORPHOPSIA Macrosomatognosia - see “ALICE IN WONDERLAND” SYNDROME Macro-Square-Wave Jerks - see SQUARE-WAVE JERKS Macula Sparing, Macula Splitting Macula sparing is a feature of an homonymous hemianopia in which central vision is intact, due to damage confined to the occipital cortex without involving the occipital pole. This may occur because anasto- moses between the middle and posterior cerebral arteries maintain that part of area 17 necessary for central vision after occlusion of the pos- terior cerebral artery. Cortical blindness due to bilateral (sequential or simultaneous) posterior cerebral artery occlusion may leave a small central field around the fixation point intact, also known as macula sparing. Macula splitting, an homonymous hemianopia which cuts through the vertical meridian of the macula, occurs with lesions of the optic radiation. Cross References Cortical blindness; Hemianopia; Visual field defects Maculopathy Maculopathy is any process affecting the macula, with changes observ- able on ophthalmoscopy. These processes may produce a central or ring scotoma and visual failure. Common causes include: ● Diabetes mellitus: edema and hard exudates at the macula are a common cause of visual impairment, especially in noninsulin dependent diabetes mellitus. Cross References Cherry red spot at the macula; Retinopathy; Scotoma; Visual field defects Magnetic Movements Movements may be described as magnetic in varying contexts: ● the following or tracking movements of an alien hand in corti- cobasal degeneration, reaching out to touch or grasp the exam- iner’s hand or clothing, as in forced groping; ● in a hesitant gait (ignition failure), with seeming inability to lift the feet (“stuck to the floor”) in gait apraxia. Cross References Alien hand, Alien limb; Forced groping; Gait apraxia; Grasp reflex Main d’Accoucheur Main d’accoucheur, or carpopedal spasm, is a posture of the hand with wrist flexion in which the muscles are rigid and painful. Main d’ac- coucheur is so called because of its resemblance to the posture of the hand adopted for the manual delivery of a baby (“obstetrical hand”). This tetanic posture may develop in acute hypocalcemia (induced by hyperventilation, for instance) or hypomagnesemia, and reflects muscle hyperexcitability.

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Only a commitment to the somewhat boring task of observing the student take the history cheap 10mg cialis amex, perform the physical examination and explain things to the patient will allow you to identify and correct any deficiencies generic 2.5mg cialis with mastercard. This type of activity is particularly essential with junior students and must be conducted in a sympathetic and supportive way generic cialis 2.5 mg overnight delivery. Provide a good teaching environment: the more senior and prestigious you are, the more intimidating you are likely to appear to the students. It is vital that you adopt a friendly and helpful manner and reduce the natural and inevitable apprehension felt by your students. Not only may they be apprehensive about you, but they will also be apprehen- sive about their impending contact with patients. You can assist this by preparing the patients and by showing to the students you understand their fears. IMPROVING THE CLINICAL TUTORIAL Clinical tutorials are all too oftendidactic with the emphasis being on a disease rather than on the solving of patient problems. We firmly believe the clinical teacher should concentrate on the latter. The students will inevitably have many other opportunities to acquire factual information but relatively little time to grapple with the more difficulttask of learning to apply their knowledge to patient problems. It is sad, but true, that in traditional medical schools the students are often as much to blame as their teachers by encouraging didactic presentations, particularly when examinations are imminent. Surprisingly, clinical teaching 75 in problem-based schools often exhibits the same char- acteristics. Plan the teaching: once again it is important to establish the aims of the sessions you have been allocated. In either case you must be sure in your own mind what you intend to achieve in each session. Involve the student: make it clear from the beginning that you expect most of the talking to be done by the students and that all of them are to participate, not just the vocal minority. At the first session, explain what tasks you expect them to perform in preparation for each tutorial. You may, for example, expect them to prepare cases for discussion or to read up aspects of the literature on a particular subject. Provide a good teaching environment: the way in which you set up the session is vital for its success, particularly when you wish to encourage active participation. Your role as a facilitator, not the fount of all knowledge, must be emphasised and you must resist the temptation to intervene with extra information all the time. This is very hard to avoid but if it happens too frequently you will soon find all conversation is channelled in your direction and there will be no interaction between the students. As the clinical tutorial is another form of small group teaching you should read Chapter 4 for further advice. Concentrate on clinical problem solving: in the last thirty years there has been a substantial research effort into how doctors and students go about solving clinical problems. The findings have major implications for the clinical teacher, though as yet there is little evidence that this has been widely recognised. The traditional way of teaching students is to require them to take a full history, perform a comprehensive examination and only then come up with a differential diagnosis. The implication has been that clinical examination is a routine and sequential process with serious thinking about diagnosis and management being deferred until the student is away from the bedside. This is not the way doctors or students actually operate even though they may appear to do so on superficial observation. The bulk of time spent interviewing and examining the patient will then be used to confirm or refute these hypotheses. This approach to problem solving is a natural ability and does not have to be taught in its own right. These findings provide one of the arguments for why increasing numbers of medical schools are using problem-based learning as the keystone of the curriculum. Patient problems are used to trigger the search for factual information rather than teaching factual information before exposing students to patient problems (see Chapter 7).

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