Given that participants were carefully selected by the Wessely School themselves (the Trial literature states that people would be selected only if they were deemed ”suitable” by the Wessely School) diabetes diet exchange program buy cheapest glycomet, it seems that the trial is not “randomised” as claimed by the Investigators – it is only randomised within the trial diabetes definition in hindi purchase glycomet pills in toronto. Furthermore treatment of diabetes discount glycomet generic, how can the results of an intervention in any trial be “evidence‐based” for efficacy in a disorder when those most severely affected by that disorder are excluded from the outset? A further 28 local support teams were set up to provide “training resources for health professionals” and to provide “specialist assessment” and advice on how to overcome “too much focus on normal bodily sensations diabetes prevention first nations buy 500 mg glycomet mastercard, personality traits diabetes zentrum düsseldorf quality 500 mg glycomet, avoidance behaviour and learned helplessness” (Environmental Issues Forum: Spring /Summer 2004:14‐17) blood sugar glucose order glycomet 500mg online. It is now supporting the Wessely ‘management’ programme and is diabetes test nyc quality glycomet 500mg, I see diabetes in dogs symptoms buy generic glycomet on line, to be actively involved in the development of the new treatment centres” (Hansard: Lords: 22nd January 2004:656:27:1180). If it were already known that a drug made 50% of patients worse, would a clinical trial of that drug be permitted to continue, and would people be willing to take part in such a trial? Although the therapist had said the purpose of the meeting was to wish me well for my future, he was very angry and defensive at the meeting due to me disengaging; he obviously had pressure on him to keep his numbers up ‐ but that was no reason to treat me in such a way e) It was quite apparent during the 6 sessions I had with the therapist that he was more interested in his research findings than genuinely helping me. The same person repeated her concerns in a comment posted to the New Statesman website: “it was quite obvious to me that the ‘therapist’ was trying to manipulate the results and had immense pressure put on him to secure specific findings. Due to having studied psychology for 4 years and myself being a psychiatric nurse (as was the therapist), his ‘tactics’ were very transparent. Although I was extremely ill following a relapsehis concern was only for his research and his behaviour resembled that of a bad car salesman who realised the sale he thought he had secured was slipping from his grasp. There is no way any research which relies on self reporting by vulnerable patients that are influenced by unscrupulous ‘therapists’ with a vested interest in obtaining specific outcomes can be classed as scientific or reliable”. When recruitment to the trial proved to be such a problem, an additional amount of £702,975. Wessely School psychiatrists are disparaging about pacing as a method of self‐management. A recent systematic review concluded that there was insufficient evidence to recommend adaptive pacing at present”. The Trial Identifier also states that the Trial will “indicate which patient characteristics predict which response to which treatment” and that it will “define the essential aspects of effective treatment as a step towards the development of more efficient therapies” (a possible forecast of the provision of even more psychosocial “Fatigue” Clinics throughout the nation, as both White and Pinching have publicly envisaged in their respective submissions to various Parliamentary committees and inquiries). In the opinion of many, not a single reason put forward by the Trial Investigators has merit. It is already known that “perpetuating factors” do not, as believed by the Wessely School, include being in receipt of State benefits, having “aberrant illness beliefs”, being “deconditioned” or belonging to a self‐help organisation. Sub‐grouping, however, is contrary to the Wessely’s School’s intention of lumping together all states of “medically unexplained” fatigue, an approach that does not enhance scientific understanding in any way but intentionally obfuscates it. This is in direct contrast to the Wessely School’s seemingly non‐scientific modus operandi for which they have received many millions of pounds sterling. It is generally accepted that when people are aware of being recorded/filmed, there is an additional area of subtle pressure being applied to which they will react and which might influence their responses. Not to inform participants of the precise nature of these “other research purposes” does not accord with the research requirement for transparency and would seem to be in breach of the Declaration of Helsinki (see below). This seems implausible: video recordings of nurses administering potent chemotherapy are not made just so that the nurses delivering the therapy can be supervised. It is known from Peter White himself that there were serious difficulties in procuring enough therapists (see Section 2 above). Therefore the procedure for notifying everyone of severe adverse reactions did not apply to all severe adverse events. This statement is curious, because of the 21 people who experienced a severe adverse event, it appears that at least 13 chose to continue with the trial. If the 8 withdrawals were from the 80 participants who had completed the trial, that is a 10% withdrawal rate up to February 2007. No mention is made of the severity of physical illness or of serious and demonstrable organic pathology as predictors of a negative outcome to the Wessely School’s own brand of cognitive restructuring. Outcome measures were discussed at the First Meeting of the Trial Steering Committee held on 22nd April 2004 at St Bartholomew’s Hospital, London. It was noted that there may need to be an adjustment of the threshold needed for entry to ensure improvements were more than trivial” (emphasis added). This appears to indicate concern that any improvement might be minor and not statistically significant, a result that might be unacceptable to the Investigators. The Minutes do not record an answer being given to the question that was asked, ie. The Chalder Fatigue Scale has been much used by the Wessely School but its validity has been legitimately questioned. There are different instruments for scoring symptoms, one being the Likert Scale which has gradations in measurement, for example, patients can rate themselves on a scale of 1 – 5, and can identify if they feel fine (score 1), or quite fatigued (score 3), or if they are exhausted (score 5). The Chalder Fatigue Scale is different; it is a bimodal scale, which essentially means that it has a two‐way answer only ‐‐ patients must answer simply “yes” or “no” (ie. This has been suggested to be because it does not just have a low ceiling for each individual question, but also for the total score. In other words, people cannot be shown to “get worse” on the Chalder Fatigue Scale even if they feel ‐‐ and are ‐‐ worse. Since it cannot be used to measure the effect of an intervention, Tom Kindlon from Ireland has correctly and repeatedly asked why the 11‐item bimodal Chalder Fatigue Scale is being used as a primary outcome measure in these trials. The Chalder Fatigue Scale has been described by an Oxford mathematical physicist as “a parody of modern scientific measurement” (personal communication). Christine Hunter of the Alison Hunter Memorial Foundation raised vital questions about outcome measures that the Trial Investigators have not mentioned: “What precise measures will be used to assess benefit from these trials? For instance, improved swallowing, less abdominal pain and distension, less vomiting, improved gastric emptying, reduced diarrhoea, weight gain, able to cease nasogastric tube feeding, or headache eased, rolling over in bed unaided? There is no consensus about them; they are used only in Britain and only by the Wessely School. As noted above, they lack diagnostic specificity, have been shown to have no predictive validity, and to select a widely heterogeneous patient population. It is virtually unheard of for studies to use criteria that have been superseded (as mentioned above, Michael Sharpe himself – who was lead author of the Oxford criteria ‐‐ stated in 1997 that the Oxford criteria “have been superseded by international consensus”. The Oxford criteria stipulate that people with “organic brain diseases” are to be excluded. There can be no credible doubt that the Oxford case definition excludes those with neurological disorders and as noted above, this was confirmed in 1991 by psychiatrist Anthony David (colleague of Simon Wessely and co‐author of the Oxford criteria): “British investigators have put forward an alternative, less strict, operational definition which is essentially chronic fatigue in the absence of neurological signs (but) with psychiatric symptoms as common associated features” (Postviral syndrome and psychiatry. If there is no strict adherence to the entry criteria, then the results will be flawed from the outset ‐‐ either the criteria are adhered to , or the results will be flawed: there is no other scientifically credible interpretation. I should emphasise that the London criteria will not be used as an inclusion criteria (sic) but will be used as predictors of response to treatment”. It is a straightforward fact that if those with a classified neurological disorder are excluded from the outset by virtue of the Oxford entry criteria, no amount of “secondary analysis” will reveal those with a classified neurological disorder. Professor Peter White informed the Joint Trial Steering Committee and Data Monitoring and Ethics Committee on 27th September 2004 that the London criteria have not previously been used in research. White was incorrect, because Jason et al used one of the several versions of the proposed (but unpublished) “London criteria” in the paper “Variability in Diagnostic Criteria for Chronic Fatigue Syndrome May Result in Substantial Differences in Patterns of Symptoms and Disability” (Eval Health Prof 2003:26(1):3‐22). However, the Dowsett and Ramsay paper in question does not mention the term “London criteria” (Myalgic encephalomyelitis – a persistent enteroviral infection? Dowsett and Ramsay simply said they “adopted the following clinical criteria” for the selection of patients for that one study, which does not constitute “existing diagnostic criteria”. There is no methods paper which specifically describes them as a “case definition”; they have never been approved nor have they even been finally defined (there are various versions); they have never been operationalised or validated and despite there being much internet traffic about the alleged authorship, it remains uncertain who the authors are. Notwithstanding, claims were made on the internet by one of the purported authors of the proposed “London criteria” that they had been operationalised, and that five published studies had used them. When contacted, he expressed surprise because he had been led to believe that the “London criteria” had been published and validated. Exercise‐induced fatigue precipitated by trivially small exertion (physical or mental) 2. Fluctuation of symptoms usually precipitated by either physical or mental exercise. These symptoms should have been present for at least 6 months and should be ongoing 5. A Written Answer to a Parliamentary Question tabled by the Countess of Mar states: “The National Institute for Health and Clinical Excellence will consider in August 2010 whether there is a need to review its clinical guideline on Chronic fatigue syndrome / myalgic encephalomyelitis” (Hansard: Lords: 5th May 2009). One reason why a research team might include participants’ newsletters in their study design is to encourage participants to remain within the project. Newsletters aimed at offering general information to trial participants are not unknown (Blanton S et al. The same issue says: “We have already received some informal feedback on the experience of participating in the study. Comments so far received have included: ‘I really think it is good to be part of something that will make a difference to so many people’. It also says: “Our website is intended to keep all our participants up to date on the trial. The second Participants’ Newsletter (March 2007) says: “In our last newsletter we asked for feedback and for contributions from participants and we can happily report that we have received both. Any similar contribution from participants who are receiving any of the trial treatments will be gratefully received”. Providing participants with adequate information is obligatory, but exposing participants or potential participants to selected opinions of other participants (and of a doctor) is uncalled for in an on‐going trial. Inviting and publishing letters of praise for a clinical trial that is not yet complete might be deemed unethical and might even invalidate the whole trial. If, for example, those people who had written in such glowing terms at the start of the interventions subsequently knew they had not in fact improved at the end of the trial, they would be unlikely to admit so in the subjective questionnaire which is intended to inform the outcome, as the published letters would surely influence those participants’ subsequent answers to their outcome questionnaires. For trial participants to be praising the trial during a research project ought to invalidate their own data. Giving participants information that could influence the data they themselves provide – by exposing them to the selected opinion of other participants – might be viewed as publishing selective data from the trial 252 before it was completed. When participants are recruited from a patient population known to have suffered stigma and marginalisation, such tactics are not something that responsible researchers would want to risk without ethical approval. It was also agreed that there needed to be a specific working group to plan the public relation strategy and that this would have the following elements: Positive public education and information about the trial (and) the correction of disinformation being circulated about the trial. Rhiannon Powell’s letter also refers to the Government’s Pathways to Work programme; a “1200% increase back to work” is mentioned in her letter (“one delegate was keen to know the number of people a 1200% increase back to work equates to”). It is perhaps noteworthy that Sir Hugh Sykes (brother of Richard Sykes PhD whose work on “Conceptual Issues in Somatoform and Similar Disorders” is referred to in Section 1 above) is a non‐ executive Director of A4e (Action for Employment), the largest European provider of Welfare to Work programmes and author of “Welfare to Work – the New Deal: Maximising the Benefits” (with grateful acknowledgement to meagenda. Rhiannon Powell’s letter goes on to say that among Chandler Chicco’s forthcoming actions was “the possibility of us contacting someone involved in raising awareness for the issue for people with chronic fatigue (sic)”. The same Minutes record: “The question was asked as to how to deal with any emails or hateful correspondence received. It was agreed that these should not be directly responded to , but should be retained as evidence for the future should it be needed. The retaining as “evidence”of any “lobbyist mail” as “evidence for the future” seems sinister, especially when such “lobbyist” mail may be the desperate pleadings of sick people seeking appropriate investigations and care. I am pleased to say that I understand that the Independent will publish all three letters this Thursday”. The same applies to other records gathered for our study, including your medical notes and the database holding the collected data from the trial. This will be held securely at St Bartholomew’s Hospital, in London, and it will be used only to monitor recruitment. However, the leaflet also said: “occasionally, other researchers will need to see your notes so that they can audit the quality of our work. An audit might be run by one of the universities helping with our study or hospital regulatory authorities, or by one of the organisations funding our study”. As already noted, funders are the Medical Research Council; the Scottish Chief Scientist’s Office; the Department of Health and the Department for Work and Pensions. Concerning confidentiality, participants who asked: “Will you keep my details confidential? Most of the named patients, some of whom live in sheltered accommodation, can be – and have been ‐‐ identified. It concluded that “nearly a third of patients attending Scottish Neurology clinics have medically unexplained symptoms” which, given the well‐published beliefs of Professor Sharpe, is an unsurprising conclusion. This serious breach of confidentiality by Professor Sharpe was reported by Ian Johnston in the Scotsman on 19th August 2005. The University of Edinburgh promised to launch an investigation; a spokeswoman said at the time that Professor Sharpe had been made aware of the situation but was on holiday. This confidential information was stolen from an unlocked drawer in the therapists’ office. His letter continued: “The burglary was reported to Southwark police on the day that it happened, which was Wednesday 22nd March 2006. It was only after the theft that Professor Trudie Chalder sought advice on how to secure the data properly. The letter also said: “The Principal Investigator for this centre, Professor Trudie Chalder, is awaiting advice from the Trust R&D as to whether the affected participants should be made aware of the theft”. It seems that the patients involved were not warned that confidential information about them had been stolen. Maj noted the possible conflict of interest between a psychiatrist’s allegiance to a given school of thought and the primary interest represented by the progress of science. He said: “Along with the fact that the proponents of some specific psychotherapies may be less interested in the scientific validation of their techniques, this allegiance effect may bias the evidence concerning the relative efficacy of the various psychotherapies” and he noted the possible conflict between the secondary interest “represented by a psychiatrist’s political commitment and the primary interest represented by the patients’ welfare”. Maj continued: “It has been rightly pointed out that there are now in our field ‘special interest groups’, consisting of prominent opinion leaders with significant financial conflicts of interest who exercise a powerful impact on the field in their various capacities. They may exercise an equally powerful impact on our field acting, for instance, as contributors to mental health policy guidelines or consultants to governments. Moreover, when acting as referees for scientific journals or evaluating research projects submitted to public agencies, they mayunfairly favour colleagues who share their political credo”. The Association of Medical Research Charities “Guidelines on Good Research Practice” states: “Researchers should declare and manage any real or potential conflicts of interest, both financial and professional. These might include: Where researchers have an existing or potential financial interest in the outcome of the research: Where the researcher’s personal or professional gain arising from the research may be more than might be usual for research”. This means exhibiting impeccable scientific integrity and following the principles of good research practice”. How one is perceived to act influences the attitudes and actions of others, and the credibility of scientific research overall”. The Research Governance Framework for Health and Social Care, Second Edition, 2005, warns at section 9. Such connections could have a significant influence on a participant’s decision to join a research project, and therefore ought to have been declared. The Principal Investigators’ “circumstances that might lead to conflicts of interest” include information about their association, consultation, hospitality and employment with insurance companies and the Department for Work and Pensions, every one of which might be considered to “affect the independent judgement of the researcher(s)”, yet initially the Investigators declared no financial or other conflicts of interest (see below). However, on 28th July 2007 Simon Darnley, General Manager for Prisma Health (sdarnley@prismahealth. The previous year, the same Simon Darnley from King’s (who has responsibility for supervising the Prisma assessment and treatment programmes for all clients referred by insurance companies) gave Workshop 9 at the British Association for Behavioural and Cognitive Psychotherapies Congress in Warwick, in which he said: “There is increasing focus on Return to Work with the success of programmes such asthe privately funded Prisma Programme. However, with clients who are not currently working, clinical progress may be limited because therapists have insufficient influence on the non‐clinical maintaining factors. We will explore the therapeutic implications of working within a politically generated environment, asking ‘What happens when you mix politics with therapy’, (and) ‘How ethical is it to use motivational techniques when the result is cessation of benefit? This should be borne in mind when reading the section below on “Data‐gathering for non‐clinical purposes”. At the Trial Steering Committee meeting on 22nd April 2004, all members present were asked to declare any conflict of interest. Amongst those present were Professors Peter White, Michael Sharpe and Trudie Chalder. Professor Aylward seems to have an unfortunate track record in relation to accuracy – see Appendix V. This is a serious issue, because there is written evidence that Professors Peter White, Michael Sharpe and Trudie Chalder may have been less transparent than was required of them. Since it was believed that Professors White, Sharpe and Chalder all did have obvious and serious conflicts of interest and since any such conflicts had been denied by them, representations were made questioning why their known conflicts of interest had been denied. I can confirm that I was aware of the potential for competing interests that you have stated. The roles that Professor White, Professor Sharpe and Professor Chalder have undertaken for the agencies and companies that you stipulate. I am content, as the Director of that guideline, these potential competing interests did not in any way influence the synthesis of the evidence or the guideline recommendations”. There is thus written confirmatory evidence from Dr Ira Madan that Professors White, Sharpe and Chalder all did have what she referred to as “competing interests”, but that she was “content” about the situation. Furthermore, they were not required to make conflict‐of‐interest declarations, even though their conflicts were known about by Dr Madan. A search of PubMed for Professor White’s own declarations of interest just for the years 2004 to 2009 reveals that in many of the papers, he did not declare any competing interests at all, despite clear warnings from the journals that “Authors are responsible for recognising and disclosing financial and other conflicts of interest that might bias their workauthors must disclose any commercial associations that might impose a conflict of interest in connection with the study” (Journal of Rehabilitation Medicine, in which Peter White published an article on Chronic Fatigue Syndrome in 2008:40(10):882‐885). The Gibson Report of 2006 expressed concern about these competing financial interests at page 31, section 6. Those parliamentarians who expressed this concern included the former Chairman of a House of Commons Science and Technology Select Committee and former Dean of Biology; a member of the Home Affairs Select Committee; a Minister of State for the Environment; a former President of the Royal College of Physicians; the Deputy Speaker of the House of Lords, and a former Health Minister and Honorary Fellow of the Royal College of Physicians. To date, nothing whatever has been instituted to remedy this unacceptable situation. Cargo cult science is a term used to describe work that has the semblance of being scientific, but whilst such studies follow all the apparent precepts of scientific investigation, they are missing something essential: they lack scientific integrity. Cargo cult scientists conduct flawed research that fails to produce useful results. Physicist and Nobel Laureate Richard Feynman summarised it thus: “We really ought to look into theories that don’t work, and science that isn’t science. And it’s this type of integrity, this care not to fool yourself, that is missing to a large extent in much of the research in Cargo Cult Science. The Times Online reports disconcerting findings about scientific studies: “Faking scientific data and failing to report commercial conflicts of interest are far more common than previously thought, a study suggests”. Dr Daniele Fanelli of the University of Edinburgh, who carried out the investigation, says: “Increasing evidence suggests that known frauds are just the tip of the iceberg”.
Acoustic recordings—if possible video folds) that are located in the larynx blood glucose while fasting order glycomet 500mg on line, commonly referred recordings—should encompass content (vocal-text) rele to as the voice box diabetes diet fruit buy glycomet 500 mg. Therefore diabetes symptoms poly buy generic glycomet 500mg line, abnormal voice is a con vant to the work needs and work conditions of the sequence of the underlying phonatory pathophysiology mody diabetes definition cheap glycomet 500mg visa, patient type 1 diabetes symptoms yahoo buy genuine glycomet on-line. Keep in mind that a mismatch may and aerodynamic forces; the vibration is generated as be present between the acoustic and visual data (ie diabetes prevention of complications discount glycomet 500mg on line, the air expelled under pressure from the lungs passes large lesion but a relatively good voice diabetes medications that start with l order glycomet 500 mg on-line, or a small lesion between the vocal cords and sets the cords into an oscil and a very poor voice) diabetes mellitus youtube buy glycomet paypal, that not all glottic lesions latory motion. The intrinsic laryngeal have at your disposal a comprehensive documentation muscles include the thyroarytenoid muscles, the pairs of the phonatory mechanism. Documentation that of lateral cricoarytenoid muscles, the posterior cri shows objectively the location of the lesion or the coarytenoid muscles, and the interarytenoid muscle, mechanism of dysphonia is a necessity when postopera which consists of both transverse and oblique portions. When operating on a patient, one the intrinsic laryngeal muscles are innervated by the must have preoperative stroboscopic mapping and voice recurrent laryngeal nerves and all muscles, with the recordings. These include delayed auditory feedback, voice load tests, muscles are principally responsible for pitch elevation. The challenge of determin of the glottis are affected, including the subglottic and ing work-related voice/speech disabilities in California. The and voice may not be a product only of the true vocal Hague: Kugler Publishing, 2001:149–154. This specific vagus nerve motions produced by the action of the paired extrinsic branching explains why combined recurrent and superior laryngeal musculature. These vertical laryngeal motions laryngeal nerve injuries (eg, paralysis) are rare. The action of are crucial in phonation (singing), swallowing, respira the cricothyroid musculature is also responsible for the tion, and yawning, and in speech articulation. A review of compensatory mechanism for al wider posterior gap will be present, and the arytenoids will ternative phonation sources in humans. Current evidence for the or ceed via the brainstem nuclei and the left and right ganic etiology of spastic dysphonia. Signals terminate in the motor end plates ments of the recurrent laryngeal nerve removed from pa of the intrinsic laryngeal muscles via the left and right tients with adductor spasmodic dysphoria revealed myelin abnormalities in 30% of the nerves examined, while neuro recurrent laryngeal nerves, resulting in vocal cord con logic examination indicated brain stem or basal ganglia dis tractions. The body of the vocal cords is formed by the two thy the recurrent laryngeal nerve is a mixed nerve con roarytenoid muscles, which contain fast (adductive) and taining an average of 1200 myelinated axons and thou slow (eg, phonatory) fibers that determine the length, sands of unmyelinated axons, including some special contour, and glottic closure shape of the vocal cords ized endoneural organs. With regard to phonation, the vocal cords are divided into the upper vibratory lips (dotted line) and the lower vibratory lips (dashed lines). If the lesion is located on the superior surface of scopic illumination or super-fast filming, where it is the vocal cord away from the vibratory edge, the voice seen to undulate, proceeding from the inferior (ie, may not be affected at all, even if the lesion is large. A common sense real estate rule the area between the upper and lower lips adjusts as of “location, location, location” should prevail. In other pitch and loudness change; therefore, when a phona words, it is often the location and not the size of the tory lesion is located within this space, its location and lesion that determines its value to the voice quality. Typically, more severe symptoms are caused by also subdivided into the vibratory (membranous) small but anteriorly located lesions than by larger and nonvibratory (cartilaginous) portions. At rest, lesions located toward the upper lip or on the superior they outline a V-shaped space called the glottis (see phonatory surfaces. The front of this V forms the anterior lesion located ± 3 mm above the lower lip profoundly glottic commissure, and the back of the V forms the affects the voice, whereas even a large inferiorly located posterior glottic commissure. The posterior end of web (< 3 mm below the lower lip) does not affect the each vocal cord (the thyroarytenoid muscle) inserts voice. The maximum width of the posterior the cover is subdivided into the outer and the inner commissure occurs during inspiration or cough and layers and the lamina propria; the latter consists of three measures approximately 9–12 mm, or three times layers: superficial (the Reinke space), intermediate, and the most posterior width of the muscular portion of deep. Obliteration of the Reinke space the vocal cords at rest is approximately 13 mm for retards or prevents the mucosal vibratory wave, result women and 16 mm for men. However, if one approximate for phonation, the entire glottis is closed vocal cord is stiff but straight (nonvibratory) and the in a male, whereas a small posterior chink is often other vibrates and approximates well against the nonvi present in a female, giving the female voice quality a brating vocal cord, the voice may be remarkably good slightly softer and airy tone. Therefore, it is tic phonatory closure allow variations in normal voice important at times not to “repair” the stiff vocal cord, qualities. Vocal Pathologies: Diagnosis, Treatment and phonation produced higher spectral levels and a less steep fall. They also determine the shape of the mucosal vibra speech, singing, or other forms of communication are tory wave, which in turn determines the pitch, loudness, formed. The amplitude of the mucosal vibra the voices of opera singers, specific sound regions are tory wave is wider at the lower pitches, whereas reduced amplified; these areas are referred to as formants (F1– mucosal vibratory wave amplitude predominates at high F5), and their combination determines the characteris pitches or at any pitch level when the cover is stiff. Opera singers form unique vocal tract the duration and shape of the mucosal vibratory shapes to allow noninjurious and efficient singing, and wave cycle form specific opening and closing phases they show a unique clustering of powerful spectral that determine specific vibratory modes or vocal quali peaks (the so-called singing formants) at about 3 kHz. This clustering results in an acoustic boost that helps a the time interval between cycles is called the funda singer to compete with the sound of an orchestra. The pro mental period (F0), whereas in perceptual terms it is duction of singers’ formants is possible when the entire referred to as a pitch period. Orna pressure (P), the intraoral pressure (Ps io), and the glottal mentation in voice can result from specific vocal tract resistance, all of which are responsible for the Bernoulli configurations and specific time-locked acoustic events, effect, which separates the approximated vocal cords with rate approximating 5–6 Hz for vibrato or vocal during phonation. It is interesting to note that tremor-like vocal To generate sound, P must reach at least 5 cm Hs 2O, oscillations having similar rate may be present in decep but P can exceed 50 cm Hs 2O in loud or overly pres tion. Typically, a normal conversational voice is produced between 6–10 cm Shipp, T, Izdebski K. Letter: Vocal frequency and vertical larynx H2O P at approximately 65–70 dB, whereas a loud voices positioning by singers and nonsingers. Current evidence for the existence of laryn tance cannot be measured directly, but is estimated to geal macrotremor and microtremor. Acta Otolaryngol 10442747] (The study describes acoustic differences in voice Scand. Any voice con vocal fatigue, voice breaks, cough, globus syndrome, and, dition, but specifically when hoarseness is present and the occasionally, dysphagia. Common Speech Disorders in Otolaryn in medical complications (including potential legal conse gologic Practice. Rochester, Minnesota: American Academy of quences), as well as delays in treatment and a potential loss Otolaryngology Press, 1979. San many patients with dysphonia, especially patients who use Diego: Plural Publishing, 2007. Voice and vocal patients may be accused of “wrong” singing or poor train cord findings in asthma inhaler (Advair) users. Western Sec ing because no visible pathology was noted at the initial tion: Triological Society. Symptoms, laryngeal findings, and cord lesions that affect the mucosal vibratory wave, result 24-hour pH monitoring in patients with suspected gastroesoph ing in air loss, noise, vocal cord stiffness, and pitch restric ageal-pharyngeal reflux. The psychoacoustic and psy unintentional injury to the recurrent laryngeal nerve), (b) chometric analyses require a trained ear and longstanding the planned treatment (eg, an overinjection of polytef [ie, expertise, not unlike what is needed to assess auscultatory Teflon] during attempts to correct breathy paralytic dys noises. However, the problems with these analyses result phonia or irradiation), or (c) a change to the underlying from the potential for loose terminology and a non-uni nature of the primary dysphonia as a function of treatment form interpretation. A subjective description of one type of (eg, denervation of the vocal cord to combat vocal spastic dysphonia used over 350 different clinical terms. There ity, Botox, and vagal stimulation); (10) functional dyspho fore, using numerical perceptual rating scales is preferred nia (eg, persistent prepubertal voice in a postpubertal male, when subjectively assessing voice problems. Attempts to elective aphonia, ventricular dysphonia, and inhalational use acoustic objective analysis to detect voice quality corre dysphonia); (11) gender euphoria; (12) emotional causes; lations with underlying pathology continue, but solutions and (13) environmental-occupational causes. Speech Evaluation in A harsh, rough, and stiff voice quality with a Medicine and Psychiatry, Vol. The subjective assessment often uses a mixture of per Sudden pitch or loudness breaks in the absence of ceptual and musical terms to describe the patient’s clearly visible phonatory mucosal lesions may be voice quality, pitch, loudness, the duration and rate of an indicator of functional problems, postpubertal phonation, prosody, registration, tessitura, and respira dysphonia, or virilization of the female voice. A limited upper pitch range with soft breathy phonation, no mucosal lesions, and rotation of Common Assessment Findings the posterior larynx can indicate superior laryn Below is a review of terms used to clinically describe the geal nerve involvement. These semantic descriptors Rapid pitch (at about 5–6 Hz) and intensity oscil can be quite accurate, but when the voice is abnormal lations reflect vocal tremor, whereas pitch-depen the term hoarseness is a generic word used by most clini dent oscillations or vocal arrests reflect specific cians (and lay people) when referring to or describing movement disorders, while in muscular tension many kinds of dysphonia. Hoarseness is frequently used dysphonia, or functional (psychosomatic) dys as a wastebasket term and leads to a wrong impression phonia oscillations my be random. It is especially used in error when one is Odynophonia describes a sensation rather than attempting to define a rough or harsh voice quality, voice quality and is associated with pain or dis since this is typically associated with vocal cord stiffness comfort when speaking or vocalizing. Total aphonia, or lack of voice in the absence of a Breathy or soft voice is used to describe a voice that phonatory cough, can indicate severe separation is generated by incomplete glottic closure (eg, in of the glottis either caused by organic and func unilateral vocal cord paralysis, vocal cord bowing, tional origins or following total laryngectomy. Asthma A diplophonic or multiphonic voice is present like wheezing happens only on exhalation when when the vibratory pattern between the vocal the vocal cords are open. This inhale asthma medications, vocal cord mucosa can condition can be caused by a myriad of benign be affected and severe dysphonia can occur. Typ and malignant mucosal lesions, neurologic com ically, stopping medication is enough to reverse plications, laryngeal fractures, or psychosomatic the condition. A wet, gargling voice, also referred to as hydro No matter how the voice sounds, the sound of the phonia, describes phonation that is produced by pathologic voice may evoke negative emotions that are excessive mucus within the glottic space. This incongruence can be very frustrating and tion that is mixed with a ventricular vibration. An under standing of these factors by the examining clinician goes a long way toward enhancing bedside manners. The purpose is to map out phonatory characteristics, demonstrate phonatory deficits, and correlate findings with visual (ie, physiologic) data. Bar ring minor technical problems, either dedicated instru mentation or a computerized approach can be used for a fast, reliable, and reproducible acoustic analysis. Acoustic analysis provides information on sound dura tion, loudness, pitch, and spectral context, including Figure 28–2. Intonation pattern of a sentence spoken static and dynamic pitch changes of the voice during by a male speaker showing pitch (lower tracing) and in speech. Current evidence for the existence of laryngeal distance from D1 to A6 on a piano. This distinction icap Index and laboratory measurements and shows that these two methods give independent information and essentially is of import when examining patients with gender reas correlate poorly. However, in objective When assessing patients who sing professionally, acoustic terms, pitch refers to the fundamental frequency their vocal registration should be included in the evalu of the voice or the speaking fundamental frequency, both ation. Using a musical scale notation is a preferred of which are recorded in vocal cycles per second or hertz method of communicating clinical findings to these (Hz). San Diego: that is obtained by subtracting the duration of the pitch College Hill Press, 1997. Fundamental frequency is age and gender depen Loudness represents acoustic intensity that is measured in dent. The average level of fundamental frequency for a decibels and is dependent on both the subglottic air pres child is approximately 250 Hz; it is 200 Hz for an adult sure and the airflow exiting the glottis. Obtaining the abso female, and for an adult male, it is approximately 120 lute phonatory intensity is difficult; therefore, it is typically Hz. The maximum fundamental frequency range for reported in relative rather than in absolute decibels. Wide mid-frequency ranges and lowest at both the low and high filter spectrography shows vocal tract resonation, repre levels of fundamental frequency. The typical loudness level of speaking mental frequency; (6) the size and speed of amplitude fluc is approximately 65–75 dB. Values below or above this tuations; (7) the richness of harmonics; (8) the relative measure are considered pathologic. These features are critical when analyzing vocal cord stiffness, vibratory irregularity due to lesions that are To make a more orderly representation of pitch and benign, mucosal, iatrogenic (eg, with the use of Teflon or loudness, a profile of the fundamental frequency, mea thyroplasty), or that cause adynamic vibration. These fea sured in decibels and referred to as a phonetogram, has tures are also significant when evaluating patients who use been developed. The phonetogram, which is a voice their voices professionally, have neurologic or functional range profile, represents the minimums and the maxi dysphonias, have carcinoma, or experience stridor, noise, mums of vocal loudness at selected levels of fundamen wheezing, or obstructive airway problems (eg, snoring). Clinically, a phonetogram is a Long-Time Average Spectrum reflection of the vocal capacities rather than the mea surement of the glottic function. Vocal intensity pro the long-time average spectrum technique is used to files are used to assess vocal cord paralysis, vocal cord plot compressed speech spectrum levels over time. This bowing, presbyphonia, odynophonia, functional disor technique relates the acoustic parameters to perceptual ders, and patients who use their voices professionally. Overpressure and breathiness in spastic dysphonia: an Spectrography acoustic and perceptual study. Correlation with perceptual as sessment of weak and strangled voice was shown to be valid. The use of the multidimensional voice profile is advantageous in comparing pretreatment and post-treat ment results. It also provides an overall description of dysphonia, because single acoustic parameters alone are insufficient in delineating the complexity of phonatory pathologies. The multidimensional voice profile can compare individual clinical data with a built-in database adjusted to age and gender. A Rate Analysis thin line outside the “map” corresponds to previous mea surements. Fundamental frequency values can be derived from the position of the tenth harmonic. The fuzzy dark por tions of the spectrograph represent the noise present in voiceless consonants. Pathologic vocal rates are between 5 Hz and 6 Hz, a rate similar to the vibrato rate. San Diego: Sin A normal voice is produced when the glottic approxi gular Publishing Group, 1995. Current evidence for the existence of laryn centage of vocal cord contact area loss can be derived geal macrotremor and microtremor. Therefore, substantial difficulties in maintaining vowels on target are encountered when singers must sing loudly. Therefore, vowel production should be examined when studying patients who sing professionally. Maximum Phonation Time the maximum phonation time corresponds to the time an individual can phonate per each inhalation. Phonoscopic transoral rigid procedure mum phonation time values are between 17 and 35 sec onds for adult males and between 12 and 26 seconds for showing the on-line visualization of the vibratory process adult females. The glottographic signal and longing this time is characteristic for an overapproximated pitch and intensity values are displayed for analysis. Although the maximum phonation time lacks diag nostic capabilities, it is useful in the preoperative and post operative assessments of unilateral vocal cord paralysis and over many vibratory cycles while newly introduced high bowing, in monitoring medialization (eg, thyroplasty or speed stroboscopy shows consective cycles and not aver various intracordal injections), and in lateralization proce ages it can only show short sign duration. The most dures (eg, Botox injections, as well as nerve resections, detailed images are obtained either via a 90° or a 70° blocks, or stimulation). San Diego: for either immediate or subsequent viewing and analy College Hill Press, 1997. New York: Springer Phonoscopy provides the clinician with a wealth of Verlag, 1981. Baltimore: Williams on the principle of illuminating a vibrating object with & Wilkins, 1996. Vocal Pathologies: Diagnosis, Treatment and it vibrates, therefore making the vibrating object appear Case Studies. High-speed imaging: ap Laryngovideostroboscopy or digital stroboscopy pro plications and development. Logopedics Phoniactrics Vo vides an image of the vocal cord vibrations averaged cology 2003;28:3,133–139. New York: Springer-Ver expired during the first second (the forced expiratory lag, 1981. The individual values can be fitted against expected age and gender val Electroglottography is another method of evaluating ues, with critical values for a normal population ranging vocal cord vibration. The interpretation of aerody of electrical impedance across tissue and open space. Other forms of glottographic technology include Granqvist S, Hertegard S, Larsson H, Sundberg J. A new tech analysis of vocal fold vibration and transglottal airflow: ex ploring a new experimental setup. The article points that relationships be however, its clinical value remains questionable at this tween these two entities is complex specifically with respect to time. These dis vibrations: high-speed imaging, kymography, and acoustic analysis: a preliminary report. Surface electrodes can only be used to 15907431] (This article assesses potential use of this tool for sample muscles that are close to the skin’s surface (ie, voice pathology analysis. Electroglottographic measurements of glot tal function in vocal fold paralysis in women. Electrodes in laryngeal electromyography: cord paralysis, stenosis, webs, or patients who use their reliability comparison. They are also useful when the volume of gas ment of vocal cord mobility problems in children. These tests are useful when determining the differential diagnoses of psychogenic dysphonias. The voice load test: an objective acoustic test to assess left cricothyroid muscle, the right cricothyroid muscle, voice quality as a factor of voice usage over time. In Proceed ings of the 2nd World Voice Congress and 5th International and the right thyroarytenoid muscle. An upper esophageal insufflation test is used ficacy and usefulness of electromyography, with a specific to test failures in acquiring voice after tracheal punc focus on the pediatric patient as well as in determining the ture procedures. Because sudden change in aerodynam differential diagnosis of vocal cord paralysis versus vocal cord fixation. Intrinsic laryngeal gases of other density than air (eg, helium), such tests muscle activity in a spastic dysphonia patient. Similarly, the head-position Prognostic value of laryngeal electromyography in vocal ing test, which can cause changes in vocal cord approxi fold paralysis.
Factors that contribute to cataract formation include oxidative damage (from free radical reactions) diabetes in dogs last stages buy glycomet with a mastercard, ultraviolet light damage diabetes medications weight gain buy cheap glycomet 500 mg, and malnutrition diabetes mellitus 2 medications purchase 500mg glycomet overnight delivery. No medical treatment has been established to retard or reverse the underlying chemical changes diabetes mellitus quotes buy glycomet 500 mg low price. At present non sugar diabetes in dogs buy glycomet 500 mg line, evidence for a protective effect from B vitamins diabetic a1c buy discount glycomet 500mg online, multivitamins diabetes high blood pressure buy 500mg glycomet free shipping, or carotenoids is inconclusive diabetes type 2 ppt buy generic glycomet online. Most cataracts are not visible to the casual observer until they become dense enough to cause severe vision loss. On ophthalmoscopy, the ocular fundus becomes increasingly more difficult to visualize as the lens opacity becomes denser until the fundus reflection is completely absent. A mature cataract is one in which all of the lens substance is opaque; the immature cataract has some transparent regions. This liquid may escape through the intact capsule, leaving a shrunken lens with a wrinkled capsule. A hypermature cataract in which the lens nucleus floats freely in the capsular bag is called a morgagnian cataract (Figure 8–1). A and B: “Coronary” type cortical cataract (frontal and cross-sectional views): club-shaped peripheral opacities with clear central lens; slowly progressive. C: “Cuneiform” type cortical cataract: peripheral spicules and central clear lens; slowly progressive. D: Nuclear sclerotic cataract: diffuse opacity principally affecting nucleus; slowly progressive. E: Posterior subcapsular cataract: plaque of granular opacity on posterior capsule; may be rapidly progressive. F: “Morgagnian” type (hypermature lens): the entire lens is opaque, and the lens nucleus has fallen inferiorly. Generally speaking, the decrease in visual acuity is directly proportionate to the density of the cataract. However, some individuals who have clinically significant cataracts when examined with the ophthalmoscope or slitlamp see well enough to carry on with normal activities. Others have a decrease in visual acuity out of proportion to the observed degree of lens opacification. This is due to distortion of the image by the partially opaque lens or the cataract being located in the posterior visual axis. The Cataract Management Guideline Panel recommends reliance on clinical judgment combined with visual acuity as the best guide to the appropriateness of surgery but recognizes the need for flexibility, with due regard to a patient’s particular functional and visual needs, the environment, and other risks, all of which may vary widely. The earliest symptom may be improved near vision without glasses (“second sight”) due to increased refractive power of the central lens, creating a myopic (nearsighted) shift in refraction. Other symptoms may include poor hue discrimination, a need for increased light, and monocular diplopia. Cortical cataracts are caused by changes in hydration of lens fibers creating clefts in a radial pattern around the equatorial region. Visual function is variably affected, depending on how near the opacities are to the visual axis. They tend to cause visual symptoms earlier in their development owing to involvement of the visual axis. Common symptoms include glare and reduced vision under bright lighting conditions. This lens opacity can also result from trauma, corticosteroid use (topical or systemic), inflammation, or exposure to ionizing radiation. If surgery is indicated, lens extraction improves visual acuity in over 90% of cases. The remainder of patients either has preexisting retinal damage or, in rare cases, develops complications that prevent significant visual improvement, for example, intraocular hemorrhage perioperatively, or infection, retinal detachment, or glaucoma postoperatively. Childhood cataracts are divided into two groups: congenital (infantile) cataracts, which are present at birth or appear shortly thereafter, and acquired cataracts, which occur later and are usually related to a specific cause. About one-third of childhood cataracts are hereditary, while another third are secondary to metabolic or infectious diseases or associated with a variety of syndromes. Congenital Cataract Congenital lens opacities are common and often visually insignificant (see also Chapter 17). Opacity that is out of the visual axis or not dense enough to interfere significantly with light transmission requires no treatment other than observation. Congenital cataracts that cause significant visual loss must be detected early, preferably in the newborn nursery by the pediatrician or family physician. Large, dense, white cataracts may present as leukocoria (white pupil), noticeable by the parents, but many dense cataracts cannot be seen by the parents. Unilateral infantile cataracts that are dense, central, and larger than 2 mm in diameter will cause permanent deprivation amblyopia if not treated within the first 2 months of life and thus require surgical management on an urgent basis. Even then, there must be careful attention to avoidance of amblyopia (see also Chapter 17) related to postoperative anisometropia (difference in focus power between the two eyes). Equally dense bilateral cataracts may require less-urgent management, although bilateral deprivation amblyopia can result. When surgery is undertaken, there must be as short an interval as is reasonably possible between treatment of the two eyes. Acquired Cataract Acquired cataracts often do not require the same urgent care (aimed at 403 preventing amblyopia) as infantile cataracts because the children are usually older and the visual system more mature. Surgical assessment is based on the location, size, and density of the cataract, but a period of observation along with subjective visual acuity testing is helpful. Because unilateral cataract in children will not produce any symptoms or signs that parents would routinely notice, screening programs are important for case finding. Air rifle pellets and fireworks are a frequent cause; less-frequent causes include arrows, rocks, contusions, and ionizing radiation. This is usually due to ocular contusion and is only detectable through a well-dilated pupil. The lens usually becomes white soon after the entry of a foreign body, since interruption of the lens capsule allows fluid to penetrate into the lens structure. For example, a minute fragment of a steel hammer may pass through the cornea and lens and lodge in the vitreous or retina. The cataract usually begins in the posterior subcapsular area and may eventually involve the entire lens 405 structure. Intraocular diseases commonly associated with the development of cataracts are chronic or recurrent uveitis, glaucoma, retinitis pigmentosa, and retinal detachment. The visual prognosis is not as good as in ordinary age-related cataract due to the underlying ocular disease. This type of cataract is sometimes seen as an ocular complication of diabetes mellitus. Other drugs associated with cataract include phenothiazines and amiodarone (see Chapter 22). The generally preferred method in adults and older children preserves the posterior portion of the lens capsule and thus is known as extracapsular cataract extraction. An incision is made at the limbus or in the peripheral cornea, either superiorly or temporally. An opening is created in the anterior capsule (anterior capsulorhexis), and the nucleus and cortex of the lens are removed. The technique of phacoemulsification is now the most common form of extracapsular cataract extraction in developed countries. It uses a handheld ultrasonic vibrator to disintegrate the hard nucleus such that the nuclear material and cortex can be aspirated through a small incision of approximately 2. This same incision size is then adequate for insertion of foldable intraocular lenses. If a rigid intraocular lens is used, the wound needs to be extended to approximately 5 mm. In developing countries, particularly rural areas, the instruments for phacoemulsification are often not available. The main intraoperative complication of extracapsular surgery is posterior capsular tear, for which the main predisposing factors include previous trauma, dense cataract, unstable lens, and small pupil, possibly leading to displacement of nuclear material into the vitreous (“dropped nucleus”) that generally necessitates complex vitreoretinal surgery. Intraocular Lenses There are many styles of intraocular lenses, but most designs consist of a central 407 optic and two legs (or haptics) to maintain the optic in position. The optimal intraocular lens position is within the capsular bag following an extracapsular procedure. This is associated with the lowest incidence of postoperative complications, such as pseudophakic bullous keratopathy, glaucoma, iris damage, hyphema, and lens decentration. The newest posterior chamber lenses are made of flexible materials such as silicone and acrylic polymers, allowing the lens implant to be folded and thus decreasing the required incision size. Lenses with multifocal optics can provide good vision for both near and distance without glasses. If there is inadvertent damage to the posterior capsule during extracapsular surgery, an intraocular lens can be placed in the anterior chamber or sutured to lie in the ciliary sulcus. Methods of calculating the correct dioptric power of an intraocular lens are discussed in Chapter 21. If an intraocular lens cannot be safely placed or is contraindicated, postoperative refractive correction generally requires a contact lens or aphakic spectacles. Postoperative Care the patient is usually ambulatory on the day of surgery but is advised to move cautiously and avoid straining or heavy lifting for about a month. Protection at night by a metal shield is often suggested for several days after surgery. Topical postoperative antibiotics and anti-inflammatory drops are used for 4–6 weeks after surgery. Complications of Adult Cataract Surgery Cataract surgery in adults has a very low rate (2–5%) of complications that result in permanent impairment of vision. The most serious but rare complications are perioperative intraocular hemorrhage (< 0. Suspicion of endophthalmitis requires vitreous tap for microscopy and culture and intravitreal injection of antibiotics (see Table 22–1). Other complications include retinal detachment, cystoid macular edema, glaucoma, corneal edema, and ptosis. Posterior Capsule Opacification About 10% of eyes require treatment for posterior capsule opacification 408 following uncomplicated phacoemulsification surgery (Figure 8–9). Persistent lens epithelium on the capsule favors regeneration of lens fibers, giving the posterior capsule a “fish egg” appearance (Elschnig’s pearls). The proliferating epithelium may produce multiple layers, leading to opacification. Their contraction produces numerous tiny wrinkles in the posterior capsule, resulting in visual distortion. Complications include a transient rise in intraocular pressure, damage to the intraocular lens, and rupture of the anterior hyaloid face with forward displacement of vitreous into the anterior chamber, potentially leading to rhegmatogenous retinal detachment or cystoid macular edema. The rise in intraocular pressure is usually detectable within 3 hours after treatment and resolves within a few days with treatment. Small pits or cracks may occur on the intraocular lens but usually have no effect on visual acuity. Childhood Cataract Surgery Cataract surgery in young children is often hindered by more difficult anterior capsulorhexis, as well as the frequent need to make an opening in the posterior capsule (posterior capsulorhexis) and to remove part of the vitreous (anterior vitrectomy) to reduce the incidence of posterior capsule opacification, which is much higher than after adult cataract surgery. The cataracts are less dense than in adults and can usually be removed by an irrigation–aspiration technique, without 409 the need for phacoemulsification. Optical correction can consist of spectacles in older bilaterally aphakic children, but most childhood cataract operations are followed by contact lens correction, with adjustment of power as the refractive status of the eye changes with growth. They 184avoid the difficulties associated with contact lens wear, but there are difficulties calculating the appropriate power. Prognosis the visual prognosis for childhood cataract patients requiring surgery is not as good as that for patients with age-related cataract. The associated amblyopia and occasional anomalies of the optic nerve or retina limit the degree of useful vision that can be achieved in this group of patients. The prognosis for improvement of visual acuity is worst following surgery for unilateral congenital cataracts and best for incomplete bilateral congenital cataracts that are slowly progressive. Hereditary Lens Dislocation Hereditary lens dislocation is usually bilateral and may be an isolated familial anomaly or due to inherited connective tissue disorder such as homocystinuria, 410 Marfan syndrome, or Weill-Marchesani syndrome (see Chapter 15). The vision is blurred, particularly if the lens is dislocated out of the line of vision. If dislocation is partial, the edge of the lens and the zonular fibers holding it in place can be seen in the pupil. If the lens is completely dislocated into the vitreous, it may be visible with an ophthalmoscope. If that is the case, the cataract may have to be removed, but there is a significant risk of vitreous loss, predisposing to retinal detachment. If the lens is free in the vitreous, it may lead in later life to the development of glaucoma of a type that responds poorly to treatment. Traumatic Lens Dislocation Partial or complete traumatic lens dislocation may occur following a contusion injury such as a blow to the eye with a fist. If the dislocation is partial, there may be no visual symptoms; but if the lens is floating in the vitreous, the patient will have significantly blurred vision. Iridodonesis, a quivering of the iris when the patient moves the eye, is a common sign of lens dislocation and is due to the lack of lens support. This is present both in partially and in completely dislocated lenses but is more marked in the latter. Uveitis and glaucoma are common complications of dislocated lens, particularly if dislocation is complete. If uveitis or uncontrollable glaucoma occurs, lens extraction may need to be done despite the poor results possible from this operation. For completely dislocated lenses, the technique of choice is pars plana lensectomy or phacofragmentation, depending on the density of cataract. Some partially dislocated (subluxed) lenses are amenable to phacoemulsification with various adaptations, such as capsular tension rings or support hooks. Topical bromfenac for prevention and treatment of cystoid macular edema following cataract surgery: A review. Long-term results of pediatric cataract surgery and primary intraocular lens implantation from 7 to 22 months of life. One goal of this chapter is to help the medical student, intern, resident, general ophthalmologist, and optometrist become aware of the indications for vitreoretinal surgery, many of which are time sensitive. Many vitreoretinal conditions have implications for the family medical practitioner, internist, and emergency physician. The outer surface of the vitreous, known as the cortex, is in contact with the lens (anterior vitreous cortex) and adherent in varying degrees to the surface of the retina (posterior vitreous cortex) (Figure 9–2). The vitreous consists of a three-dimensional matrix of collagen fibers and a hyaluronan gel. The vitreous cortex is adherent to the lens and especially to the retinal surface to varying degrees. Aging, hemorrhage, inflammation, trauma, myopia, and other processes often cause hypocellular contraction of the vitreous collagen matrix. The posterior vitreous cortex then separates from areas of low adherence to the retina and may produce traction on areas of greater adherence. The vitreous base extends from the equator anteriorly and is a zone of permanent and strong adherence. The vitreous is also more adherent to the optic nerve and, to a lesser extent, the macula and retinal vessels. Adherence to the macular region is a significant factor in the pathogenesis of epimacular membrane, macular hole, vitreomacular schisis, and vitreomacular traction syndrome. Previously it was taught that the vitreous developed cavities from a process known as syneresis, ultimately resulting in “collapse” of the vitreous. It is now believed that collagen cross-linking and selective loss of retinal adherence rather 417 than cavity formation are the primary events. Even though the vitreous may migrate inferiorly when separated from the retina, this process causes less force at the zones of vitreoretinal adherence than the traction caused by saccadic eye motion. Saccadically induced, dynamic forces play a significant role in the development of retinal breaks (tears), damage to the retinal surface, and bleeding from torn vessels (Figure 9–3). Further contraction of the vitreous caused by invasion of retinal pigment epithelial, glial, or inflammatory cells may result in sufficient static traction to detach the retina without retinal tears. Motion of partially detached vitreous (white arrow), induced by saccades (black arrow) and resulting in a retinal break (arrowhead). Prior to vitreoretinal surgery, vitreous “bands” were thought to cause traction on the retina, and largely unsuccessful attempts were made to cut them with scissors. The visualization provided by vitreoretinal endoillumination systems has contributed to our knowledge of anatomy and demonstrated that these bands are contiguous with the transparent posterior vitreous cortex, which is also responsible for substantial traction. Traction bands virtually only exist when penetrating trauma creates a path through the vitreous or from severe necrosis, usually from Toxocara canis infection. Vitreoretinal traction can often be inferred by the 418 configuration of the retinal surface (Figure 9–4). Transparent vitreous is best seen with a narrow, off-axis slitbeam using a three-mirror contact lens and stereo biomicroscopy (Figure 9–5). A biomicroscope with a broad, on-axis slitbeam or a direct ophthalmoscope is not suitable for observing the vitreous. Abnormal retinal configuration (white arrows) indicating vitreoretinal traction (black arrows). Narrow, off-axis slitbeam, contact lens, and biomicroscope offer the best view of transparent vitreous. Indirect ophthalmoscopes provide a large field of view, are capable of looking “around” some lenticular and vitreous opacities, and provide a stereoscopic view. Many observers only attempt to look “through” the vitreous, ignoring the opportunity to look “at” the vitreous, especially if it is abnormal.
While this is a tolerable problem for most adults diabetes prevention funding glycomet 500mg overnight delivery, it is a potential cause of amblyopia in young children blood glucose level after eating order glycomet 500mg online. Therefore diabetes symptoms neuropathy 500mg glycomet overnight delivery, sustained raised intraocular pressure in a child with hyphema should be treated aggressively diabetes treatment vitamins discount glycomet 500 mg visa, possibly including anterior chamber washout diabetes specialist buy glycomet without prescription. Iron released from a retained foreign body is absorbed by many intraocular tissues including the cornea metabolic disease dairy cattle order glycomet with a mastercard, lens diabetic promotions discount generic glycomet uk, and retina diabetes in dogs for dummies cheap glycomet 500 mg amex, leading to greenish discoloration (siderosis oculi). Copper (chalcosis oculi) is deposited particularly in the Descemet’s membrane, lens capsule, and retina. Thus intraocular foreign bodies containing iron or copper should be removed whenever possible. After external exposure of uveal tissue, an autoimmune granulomatous inflammation may develop in both the injured and uninjured eye (sympathetic ophthalmia) (see Chapter 7). Symptoms may begin as early as 1–2 weeks after the trauma but may not develop for several years. Local and systemic immunosuppression with steroids and other agents is required to preserve vision. Removal of a severely traumatized eye within 7–10 days of the injury reduces the likelihood of sympathetic ophthalmia. Monocular double vision persists with closure of the fellow eye, whereas binocular double vision resolves when either eye is closed. Significant injury to the cornea will frequently cause 851 substantial corneal warping (irregular astigmatism) leading to monocular diplopia. Binocular diplopia can be caused by injury to the third, fourth, or sixth cranial nerves or to the extraocular muscles. After surgical repair and release of extraocular muscle entrapment, diplopia may persist because of neuromuscular damage, and extraocular muscle surgery may be required. Injuries to the nasolacrimal system can occur anywhere from the punctum to the nasolacrimal duct. Obstruction of any component of the nasolacrimal system leads to chronic overflow of tears (epiphora). Isolated obstruction of the nasolacrimal duct can also lead to infection of the lacrimal sac (dacryocystitis). Obstruction of the canaliculus or nasolacrimal duct may require dacryocystorhinostomy or a Jones tube. Mechanisms of injury capable of causing ocular and periorbital injury are often sufficient to cause severe facial and brain injury (Figure 19–15). A team-based approach, often with maxillofacial surgeons, plastic surgeons, and neurosurgeons, is necessary to provide the best possible cosmetic and functional outcome for the patient. Three-dimensional reconstructed computed tomography scan of unhelmeted motorcycle accident victim with bilateral panorbital fractures, frontal sinus fractures, and mandibular fracture. All of the disorders that may cause vision loss are discussed more fully in other chapters. Differentiating between different degrees of reduction of vision is important because the demands for medical, social, and rehabilitative interventions vary. Reduction of vision has been defined in many different ways, resulting in multiple terms that may not be consistent with one another. Whereas to the lay person it implies complete loss of vision, the term “blindness” is often used for individuals who have significant and useful residual vision, an extreme example being the use of the term “color blindness” for individuals with mild color vision deficiency. The differences between the various categorizations and the variable terminology emphasize the importance of knowing which definitions are used whenever statistics about reduction of vision are compared. Categorizations of Reduction of Vision 858 Presenting visual acuity, rather than best-corrected visual acuity, acknowledges the importance of uncorrected (or undercorrected) refractive error as a cause of vision loss worldwide and almost doubles its overall prevalence. For legal blindness in the United States and eligibility for certification as severely sight impaired (blind registration) or sight impaired (partially sighted registration) across Europe, which are relevant to eligibility for financial and other support, best-corrected visual acuity is still used. Driving Privileges In the United States, the visual requirements for driving vary from state to state 859 for both private and commercial drivers. For private drivers, 20/40 best-corrected visual acuity with both eyes is the most common requirement, but some accept less. These requirements set a safety margin between letter chart performance in the office and on-the-road performance under adverse conditions. The requirements for commercial drivers are often more stringent, not because they drive in a different visual environment, but because a wider safety margin is deemed desirable. In Canada, the legal limit for driving for private drivers is best-corrected visual acuity with both eyes of 20/50 (6/15) or better and a continuous field of vision horizontally no less than 120° and vertically 15° above and below central fixation, and with no evidence of diplopia within the central 40° of fixation. Other countries have similar but varying requirement for visual acuity, visual field, and absence of diplopia. Health professionals, particularly ophthalmologists, are obligated to ensure that patients failing the relevant requirements do not drive, if necessary by informing the licensing body. Population-based studies indicate that the global prevalence of vision loss has been declining since the early 1990s, with less vision loss from infectious diseases such as trachoma but increasing vision loss from conditions related to aging, such as cataract and age-related macular degeneration. Accordingly, the majority of individuals with vision loss are older (82% over the age of 50) but also poor, with close to 90% living in low and middle-income countries. Vision loss is additionally clustered in disadvantaged communities in rural areas and urban slums, where the risk of blindness is 10–40 times higher than in the industrially developed regions of Europe and America. Women are at much 860 higher risk of vision loss, with population-based surveys estimating that 64% of those with vision loss worldwide are women. It is estimated that over 12 million children (between the ages of 5 and 15) with impaired vision could have normal vision with correction of refractive error alone. The leading causes of blindness are cataract, glaucoma, age-related macular degeneration, and corneal opacities. Vision loss caused by infectious diseases such as trachoma is decreasing due to improvements in public health. Causes of Worldwide Vision Loss and Blindness Causes of vision loss around the world are influenced by the level of social development and local geography. In developing countries, besides refractive error, cataract is the leading cause, with glaucoma, trachoma, leprosy, onchocerciasis, and xerophthalmia also being important. Corneal scarring is a significant cause of monocular vision loss in the developing world, accounting for 850,000 cases of blindness per year in India alone. In more developed countries, vision loss is to a great extent related to the aging process. Although cataract is still an important cause of vision loss, the leading causes of blindness in North America and other developed countries are age-related macular degeneration, diabetic retinopathy, and glaucoma. Other causes are herpes 861 simplex keratitis, retinal detachment, retinal vascular disorders, and inherited retinal degenerative disorders. Differences again exist when comparing the relative causes in developed and developing countries. The major causes in developing countries are corneal scarring, trachoma, genetic diseases, and cataract. In many parts of the developing world, the facilities available for treating cataract are grossly inadequate, being hardly sufficient to cope with new cases and completely inadequate for dealing with the backlog of existing cases, currently estimated to be 10 million. It is not fully understood why the frequency of cataract varies so greatly in different geographic areas, although exposure to ultraviolet radiation and recurrent episodes of dehydration, often occurring in severe diarrheal diseases, are thought to be important. With decreasing mortality rates and changing demographics, age-related causes of vision loss, including cataract, are expected to continue to rise. Although no current medical treatments exist to delay the development of cataract, it is estimated that a 10-year delay in cataract formation would reduce the number of individuals requiring surgery by 45%. Until an effective treatment that can prevent or delay cataract formation is devised, it will remain a leading cause of vision loss and will become an increasingly important global public health concern. Uncorrected Refractive Error Uncorrected refractive error is clearly avoidable through the provision of 862 corrective lenses; however, this remains a major cause of vision loss throughout the world, even in developed countries such as the United States, but particularly in developing countries where limited access to eye care professionals, low prevalence of eye health-seeking behavior, and low affordability of corrective lenses remain major problems. Glaucoma the incidence of vision loss due to glaucoma has decreased in recent years as a result of earlier detection, improved medical and surgical treatment, and a greater awareness and understanding of the disorder. However, in many developing countries, glaucoma remains a common cause of vision loss. This is especially the case in West Africa, where untreated open-angle glaucoma is extremely common. In China and Southeast Asia, there appears to be a preponderance of narrow-angle glaucoma. Approximately 3 million individuals worldwide are blind due to glaucoma, and a simple easy method of detecting patients at risk still does not exist. Treatment is also a major problem because of the poor compliance of most patients for taking daily eye drops. A simple but safe surgical procedure may ultimately be the only solution for reducing the needless burden of vision loss from this disease. Trachoma Trachoma causes bilateral keratoconjunctivitis, generally in childhood, which leads in adulthood to corneal scarring that, when severe, causes vision loss. About 40 million people have trachoma, most of them in Africa, the Middle East, and Asia. It can be treated with various antibiotics, including tetracyclines and erythromycin, but azithromycin is proving to be the drug of choice. The number of individuals who are blind from trachoma has dropped from 6 million to 1. Prevention of spread of infection will require provision of proper sanitary facilities, including clean water for drinking and washing, waste disposal, fly control, and behavioral change in hygiene. Onchocerciasis 863 Onchocerciasis is transmitted by bites of the blackfly, which breeds in clear running streams. It is endemic in the greater part of tropical Africa and Central and South America. The most heavily infested zone is the Volta River basin, which extends over parts of Dahomey, Ghana, Ivory Coast, Mali, Niger, Togo, and Upper Volta. Worldwide, 15–20 million people are affected by onchocerciasis, with half a million individuals in hyperendemic areas blinded by the disease. The major ophthalmic manifestations of onchocerciasis are keratitis, uveitis, retinochoroiditis, and optic atrophy. The disease is prevented by insect eradication and personal protection by screening. Treatment with ivermectin is extremely effective in killing the microfilaria and sterilizing the adult females residing in nodules in the body. The effect of the mass distribution of ivermectin in areas where onchocerciasis is endemic is a public health success story. Like leprosy, onchocerciasis is definitely decreasing in its importance as a worldwide cause of vision loss because of successful treatment programs. Other Causes Age-related macular degeneration, diabetic retinopathy, and corneal disorders are discussed elsewhere (see Chapters 6, 10, and 15). Leprosy, Xerophthalmia, and Hereditary Disease Prevention of Vision Loss 864 Preventive medicine is increasingly important in attempts to fulfill society’s expectations of modern medicine with the resources available. Although prevention is a logical approach to the solution of many problems in all branches of medicine, in practice, there are a number of hurdles to overcome. For any particular condition, it is essential that individuals at risk be easily identified. If their identification requires population screening, the process should be easy to perform, accurate, and reliable. Preventive measures must be both effective and acceptable to the target population. Unwarranted interference with the at-risk individual’s lifestyle only leads to poor compliance. Legislation may be required for certain measures but may engender resentment when it is felt to infringe on personal liberty. For preventive medicine to be successful, there must be cooperation among all segments of society—not just the medical community—in identifying problem areas, establishing workable solutions, and disseminating information. The successes that have been achieved in occupational health are an example of what can be accomplished if a consensus of opinion is established. In ophthalmology, the major avenues for preventive medicine are ocular injuries and infections, genetic and systemic diseases with ocular involvement, and ocular diseases in which the early treatable stages are often unrecognized or ignored. Injuries can vary from closed globe (blunt trauma or chemical injuries) to open globe injuries including rupture, perforation, and penetration (see Chapter 19). Occupational Injuries Eye injuries remain a significant risk to worker health, especially among individuals in jobs requiring intensive manual labor. Grinding or drilling commonly propels small fragments of metal into the environment at high velocity, and these projectiles can easily lodge on the cornea or penetrate the globe through the cornea or sclera. Tools with sharp ends are also commonly involved in producing penetrating ocular injuries. Welding arcs produce ultraviolet radiation that may cause epithelial keratitis (“arc eye”). Industrial chemicals—particularly those containing high concentrations of alkali or acid—can rapidly produce severe ocular damage that is often bilateral and associated with a poor visual outcome. New legislation, increased worker training, particularly targeting groups most at risk, provision of effective eye protection equipment, and development of a culture of safety in the workplace have led to a decline in eye injuries. Safety guards must be fitted to all machinery, and safety goggles must be worn whenever the worker is doing hazardous work or is in the workplace area where such hazards exist. It is surprising how many workers assume that they are no longer at risk of injury when they are not themselves performing hazardous tasks even though they are in the vicinity of work being performed by others. The growing interest in “do-it-yourself” projects in the home exposes many more individuals to the risks of ocular injury from machinery, tools, and chemicals. Education of the public to recognize and minimize such risks, which may not be obvious to the ordinary householder or hobbyist, is particularly important. Early recognition and urgent expert ophthalmologic assessment of any injuries sustained are essential. In the case of chemical injuries, immediate copious lavage of the eyes with sterile water, saline if available, or tap water for at least 5 minutes is the most important method of limiting the damage incurred. Neglect of penetrating injuries or corneal foreign bodies markedly increases the potential for long-term morbidity. Obtaining an accurate history is crucial in identifying the possibility of a penetrating injury. This is particularly true when medical help is sought some time after the injury and the patient may not realize the importance of a seemingly minor episode of trauma. Any worker who presents with unexplained visual loss or intraocular inflammation must be carefully questioned about the possibility of recent ocular injuries, and the possibility of an occult intraocular foreign body must be borne in mind. Chronic exposure to ultraviolet light or ionizing radiation, such as from improperly screened nuclear materials or in radiology departments, can lead to 866 early and rapid cataract, and care must be taken to monitor and decrease exposure. In one study, the prevalence of cataract was 64% in radiology technicians, 16% in radiologists, 10% in respiratory physicians, and 2% in nuclear medicine department staff, with an overall relative risk of 5 compared to unexposed health care workers. Nonoccupational Injuries the marked reduction in the incidence of severe ocular and facial damage associated with car windshield injuries as a result of legislation requiring the wearing of seatbelts demonstrates the effectiveness of such regulations. Similar attempts to reduce the incidence of injuries from fireworks by limiting their availability have not yet been as successful. Various sports and other activities are notorious for the high incidence of severe injuries to the eye (Table 20–4). Protective, toughened plastic glasses with refractive correction are available to lower risk in certain situations. Sports and Other Activities Predisposing to Ocular Injuries and the Types of Such Injuries Acute keratitis from ultraviolet irradiation, such as seen after exposure to a welding arc, may also occur during skiing if protective goggles are not worn. People wearing contact lenses and with previous history of eye diseases are more vulnerable. Prevention of the keratitis is best achieved with sunglasses with sidepieces and goggles with polarized or photochromic lenses. The role of long term exposure to ultraviolet light in the etiology of age-related macular degeneration is still debated. There is substantial evidence linking ultraviolet 867 exposure to the development of cataract. However, since ultraviolet exposure occurs from the time of birth, the benefit of regular use of ultraviolet filters in spectacle lenses or sunglasses as a preventive measure has not been demonstrated. The role of ultraviolet light exposure in the etiology of certain corneal disorders—particularly pterygium—and of basal cell carcinoma and melanoma of the eyelids is widely accepted. Education of the public about the dangers of skin cancer following prolonged sun exposure is very important. Ultraviolet-blocking skin creams should not be used around the eyes, and for that reason, reliance must be placed on avoiding unnecessary exposure to the sun or the use of sunglasses. In patients with xeroderma pigmentosum, the eyelids and bulbar conjunctiva frequently develop carcinomas and melanomas, and their development can be minimized, if not prevented entirely, by protective lenses. Solar retinitis (eclipse retinopathy) is a specific type of radiation injury that usually occurs after solar eclipses as a result of direct observation of the sun without an adequate filter. Under normal circumstances, sun-gazing is difficult because of the glare, but cases have been reported in young people who have suffered self-inflicted macular damage by deliberate sun-gazing, perhaps while under the influence of drugs. The optical system of the eye behaves as a strong magnifying lens, focusing the light onto a small spot on the macula, usually in one eye only, and producing a thermal burn. The resulting edema of the retinal tissue may clear with minimal loss of function, or it may cause significant atrophy of the tissue and produce a defect that is visible ophthalmoscopically. Eclipse retinopathy can easily be prevented by the use of adequate filters when observing eclipses. Similar to eclipse retinopathy is the iatrogenic retinal damage that may occur from use of the operating microscope, indirect ophthalmoscope (photic retinopathy), and misdirected recreational laser. The risk of damage from the operating microscope can be reduced by the use of filters to block both ultraviolet light and the blue portion of the visible spectrum, light barriers such as an opaque disk placed on the cornea, or air injected into the anterior chamber. Preventive measures are based on maintenance of the integrity of the normal barriers to infection and avoidance of inoculation with pathogenic organisms. The 868 pathogenicity of various organisms and the size of the inoculum required to establish infection vary enormously according to the state of the eye. Most organisms enter the eye through a defect in the ocular surface or via the bloodstream, but some organisms are able to penetrate intact corneal epithelium (Table 20–5). Organisms Able to Penetrate Intact Corneal Epithelium the major barrier to exogenous ocular infection is the epithelium of the cornea and conjunctiva. This can be damaged directly by trauma, including surgical trauma and contact lens wear, or by the secondary effects of other abnormalities of the outer eye, such as lid abnormalities or tear deficiency.
Discount glycomet 500 mg with amex. Diabetes leicht erklärt. Diabetea einfach und kurz erklärt. Typ-1 Diabetes.
