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Autistic spectrum disorders
Published in Michael Horvat, Ronald V. Croce, Caterina Pesce, Ashley Fallaize, Developmental and Adapted Physical Education, 2019
Michael Horvat, Ronald V. Croce, Caterina Pesce, Ashley Fallaize
Consequently, criteria and definitions changed in the DSM–5 to address these issues. However, even though the criteria and definitions have changed, many professionals still refer to the “older” classification system in discussing and addressing the needs of these children. Therefore, before discussing the new criteria, it would be favorable to first summarize criteria and definitions used in the DSM–IV–TR. This will facilitate the reader’s understanding of the new criteria and how they have evolved from previous versions. In addition, much of the earlier research into the psychomotor domain of individuals with ASD were conducted on them under the older classification system of DSM–IV–TR. Therefore, it is essential to understand this previous classification system to understand implications of previous research on teaching methodologies used with these individuals.
ENTRIES A–Z
Published in Philip Winn, Dictionary of Biological Psychology, 2003
Older classification systems used the terms HEBEPHRENIA, PARANOIA and CATATONIA to describe different types of schizophrenia. Contemporary classification systems have devel oped from these and use a number of subtypes of schizophrenia: DSM-IV recognizes paranoid, catatonic, undifferentiated and residual types. Alternatively, the signs and symptoms were differentiated by Tim Crow into TYPE I SCHIZOPHRENIA and TYPE II SCHIZOPHRENIA. Characteristic of type I were the so-called 'positive' symptoms (signs and symptoms abnormal by their presence) including DELUSION, HALLUCINATION, disorganized speech and thinking, and disorganized or catatonic behaviour. Type II included the so-called 'negative' symptoms of schizophrenia (features abnormal by their absence) include WITHDRAWAL, APATHY, and flat or inappropriate MOOD.
Leukaemias
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2014
The leukaemias are classified in accordance with salient pathological features of the abnormal excessive haemopoietic cells. The principal purpose is an attempt to group together conditions that share molecular features and so reduce the overall heterogeneity of the leukaemias. In the current (2008) World Health Organization (WHO) classification system for haematologic cancers, three major categories of acute leukaemia are considered: acute myeloid leukaemia (AML) and related precursor neoplasms, precursor lymphoid neoplasms (encompassing the entities previously known as acute lymphoblastic leukaemia [ALL]) and acute leukaemias of ambiguous lineage.1,2 The classification comprises five major categories of myeloid neoplasms: AML and related neoplasms, myeloproliferative neoplasms (MPN; encompassing BCR-ABL1-positive chronic myeloid leukaemia [CML] and BCR-ABL1-negative), myelodysplastic syndromes (MDS), myelodysplastic (MDS)-MPN, and molecularly characterized myeloid or lymphoid neoplasms associated with eosinophilia. The lymphoid neoplasms classification includes chronic lymphocytic leukaemia (CLL) as well as other subtypes of indolent lymphoid leukaemias. This WHO classification accommodates some, but not all, of the molecular information accrued in recent years and a new classification is due to be published in early 2015. Pari passu, the older classification for acute leukaemias, proposed by the French–American–British (FAB) group, based entirely on morphology and cell surface membrane markers has been revised and modified and remains valuable in clinical practice.3,4
Vitreomacular disorders: a review of the classification, pathogenesis and treatment paradigms including new surgical techniques
Published in Clinical and Experimental Optometry, 2021
Mali Okada, Daniel Chiu, Jonathan Yeoh
Prior to the development and widespread use of OCT, VMD were classified based on clinical observations using biomicroscopy. The original description by Gass et al. in 1988 and updated in 1995 described stages of idiopathic macular hole formation: Stage 1 to 4 (Table 1).16–18 An additional precursor or risk factor stage (Stage 0) was later added to represent vitreofoveal traction without retinal deformation, as observed in fellow eyes of those with confirmed FTMH.19 Vitreomacular traction was not viewed as a distinct entity in this older classification system.
Clinical features of large vessel vasculitis (LVV): Elderly-onset versus young-onset
Published in Modern Rheumatology, 2021
Satoshi Morinaka, Hiroto Tsuboi, Shinya Hagiwara, Toshiki Sugita, Daiki Tabuchi, Ryota Sato, Taihei Nishiyama, Shota Okamoto, Toshihiko Terasaki, Mizuki Yagishita, Hiroyuki Takahashi, Yuya Kondo, Isao Matsumoto, Takayuki Sumida
Third, many older patients did not meet the criteria for either TAK or GCA and tended to be treated with PSL alone. In our study, of 29 patients in the elderly group, 12 were clinically diagnosed with GCA, 7 of whom met the criteria for GCA. Six were clinically diagnosed with TAK, 3 of whom met the TAK classification criteria except ‘age at disease onset ≤ 40 years’, and 11 were diagnosed as unclassifiable (includes an older classification known as ‘aortitis syndrome’). The 6 patients clinically diagnosed as TAK had common features: absence of temporal artery symptoms, absence of PMR symptoms, and upper extremity symptoms consistent with vascular lesions in the left subclavian and left carotid arteries. Other features included female gender (5 patients), absence of pathologic findings on temporal artery biopsy (1 patient), and HLA-B*52 positivity (2 patients). As the classification of LVV is still immature, an elderly onset LVV would tend to be diagnosed as GCA. GCA without temporal artery involvement can be classified as either LV-GCA or TAK but it may be classified as LV-GCA based on age alone. In one previous study, all elderly LVVs were classified as GCA by age [11]; however, elderly onset TAK has also been reported [3]. Since there is little evidence to classify elderly patients with LVV as GCA (or LV-GCA) by age alone, we suggest that elderly patients with LVV who meet the clinical features of TAK should be classified as TAK. On the other hand, early-onset GCA is quite rare [8] and this study found no cases of GCA in the younger group. It is reasonable to exclude young people in the GCA criteria but the classification criteria for TAK are unreasonable because they do not consider the presence of elderly-onset TAK. As cases at the borderline age of 40–50 years are inadequately studied, new LVV classification criteria are needed to accurately classify cases between 40 and 50 years of age based on clinical, laboratory, and imaging findings.
Low intra-operative diagnostic accuracy does not affect postoperative treatment of acute appendicitis
Published in Acta Chirurgica Belgica, 2020
Eric E. Vinck, Ricardo A. Villarreal, Carlos Luna-Jaspe, Luis F. Cabrera, Tim F. Peterson, Felipe Bernal, Carmen L. Roa
The most common causes of acute appendicitis are fecaliths and follicular hyperplasia. Fecaliths are found in 18% of appendicitis and 29% of normal appendices [11–13]. The presence of fecaliths in the appendix lumen may cause distension and pain without signs of inflammation. This same event happens in neurological hyperplasic appendices. Another condition that generates appendicular pain is appendicular serosal inflammation (serositis) caused by neighboring pelvic inflammatory disease; in these cases, the appendix itself is normal. Macroscopically, visible changes are a glistening serosa and serosal vessel injection [9–14]. Some authors believe that mucosal and submucosal inflammation is not sufficient to cause pain or symptoms. The histopathological diagnosis of acute appendicitis requires the involvement of the muscularis to be considered as ‘endo-appendicitis’ since true appendicitis is a transmural process. Another histological component significant to pathologists is ‘peri-appendicitis.’ This refers to the secondary inflammation of neighboring tissues [12–16]. When the appendicular inflammatory process initiates, it usually compromises the tip of the appendix and makes its way down the lumen. Although the newer classification of acute appendicitis, complicated (perforated) and noncomplicated (nonperforated), helps guide the surgeon in the postoperative management and antibiotic use, the older classification helps to better understand the pathophysiological process of acute appendicitis. When folicular hyperplasia or fecaliths obstruct mucosal outflow, intraluminal pressure increases. When this obstruction compromises lymphatic outflow, edema occurs. This edematous stage is macroscopicaally characterized by a congested and distended tube which eventually affects the meso-appendix. Histologically, vessel dilation, thickening of the appendicular wall and narrowing of the lumen are seen [13–18]. As intraluminal obstruction persists, pressure rises over the normal venous outflow threshold normally 65 mmHg, bacteria overgrow, and an infectious response results. This phlegmonous stage is macroscopically evident by the presence of fibrin and purulent exudates on the surface, and microscopically by neutrophilic infiltration with inflamed and ulcerated mucosa with crypt abscess. Further vascular obstruction compromises arterial irrigation and continuing intra-luminal pressure exceeding 85 mmHg, lead to necrosis and perforation [15–19]. Bacterial overgrowth is more prominent in this gangrenous stage. An intra-operative gangrenous appendix appears with greenish purple discoloration as a result of necrosis. Histologically, gangrenous appendicitis show vascular thrombosis, ischemia and necrosis of the appendicular wall [16–20] (Table 1).