To see the other types of publications on this topic, follow the link: Focal lesion.
Books on the topic 'Focal lesion'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 42 books for your research on the topic 'Focal lesion.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse books on a wide variety of disciplines and organise your bibliography correctly.
1
Lencioni, Riccardo, Dania Cioni, and Carlo Bartolozzi, eds. Focal Liver Lesions. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/b137465.
Full text
2
Old, Sally Louise. Focal lesions in toxicity studies: Methods and models. Leicester: De Montfort University, 1996.
Find full text
3
Bartolotta, Tommaso Vincenzo, Adele Taibbi, and Massimo Midiri. Atlas of Contrast-enhanced Sonography of Focal Liver Lesions. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17539-3.
Full text
4
Shamsi, Kohkan. Medical imaging of focal liver lesions: A clinico-radiologic approach. Amsterdam: Elsevier, 1994.
Find full text
5
Vigaray, Rafael Alvarez. La rescisión por lesión en el derecho civil espaǹol común y foral. Granada, España: Editorial COMARES, 1989.
Find full text
6
Meyrier, Alain, and Patrick Niaudet. Primary focal segmental glomerulosclerosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0057_update_001.
Full textAbstract:
Primary focal segmental glomerulosclerosis (FSGS) causes nephrotic syndrome and by definition is not caused by any of the known causes of podocyte toxicity or focal segmental sclerosis such as viral infections or toxins. A number of genetic causes of FSGS are commonly diagnosed in early childhood. Other causes of segmental scarring need to be distinguished. Genotypes in APOL1 of African origin are associated with higher incidence of FSGS and poorer responses to treatment. Cellular and collapsing FSGS are variants of FSGS in which there is overt acute podocytopathy and they have a relatively poor prognosis. A glomerular tip lesion is thought to have a slightly better prognosis than other types. Some cases of primary FSGS respond to high-dose corticosteroids, sometimes only after prolonged therapy. Response to steroids is a good prognostic sign, and without a response, progressive loss of renal function is likely. A circulating factor is implicated by the observation that proteinuria can recur in a donor kidney within hours of transplant. Plasma exchange appears to remove this factor but it is not conclusively identified.
7
Freer, Phoebe E. Skin Lesions. Edited by Christoph I. Lee, Constance D. Lehman, and Lawrence W. Bassett. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190270261.003.0050.
Full textAbstract:
Skin lesions are commonly seen on breast imaging. Often, a raised skin lesion is encountered incidentally during screening mammography and can be mistaken for a mass within the breast parenchyma. In most cases, lesions confined within the dermis are benign. Occasionally, focal skin involvement may be the presenting sign of a breast cancer that is either locally extensive to the skin or has an inflammatory component. This chapter reviews the key imaging and clinical features of skin lesions that may be encountered either incidentally on breast imaging or on diagnostic imaging as an area of patient concern. Imaging features of skin lesions, the differential diagnoses, and further management will be reviewed. Topics discussed include benign epithelial cysts (i.e., sebaceous cyst and epidermal inclusion cysts), seborrheic keratosis, keloid and dermal nevi, cellulitis, and inflammatory and locally advanced breast cancers.
8
Anderson, Mark D., and Karl E. Misulis. Neuro-Oncology. Edited by Karl E. Misulis and E. Lee Murray. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190259419.003.0025.
Full textAbstract:
Cancers require neurologic care for multiple facets of evaluation and diagnosis. Among the most common are diagnosis of a CNS mass lesion, localization and diagnosis of new focal deficits, seizures or encephalopathy in cancer patients, suspected paraneoplastic disorders, and neurologic complications of cancer treatment. This chapter discusses common and important disorders likely to be encountered in a hospital neurology practice.
9
Carton, James. Renal pathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0010.
Full textAbstract:
This chapter discusses renal pathology, including acute kidney injury (AKI), chronic kidney disease (CKD), nephrotic syndrome, hereditary renal diseases, Alport’s syndrome and thin basement membrane lesion, hypertensive nephropathy, diabetic nephropathy, minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous glomerulopathy, glomerulonephritis, IgA nephropathy, post-infectious glomerulonephritis, C3 glomerulopathy, anti-glomerular basement membrane disease, monoclonal gammopathy-associated kidney disease, acute tubular injury, acute tubulointerstitial nephritis, reflux nephropathy, and obstructive nephropathy.
10
Katirji, Bashar. Case 15. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0019.
Full textAbstract:
Ulnar nerve lesions are the second most common mononeuropathies encountered in clinical practice. The majority of ulnar neuropathies are across the elbow, more specifically due to entrapment or compression of the ulnar nerve at the cubital tunnel or ulnar groove. This case highlights the clinical and electrodiagnostic findings of ulnar neuropathies across the elbow and discusses the challenges in making an accurate diagnosis. Focal slowing of conduction velocities and/or conduction block are the main findings that pinpoint the site of the lesion, while the needle electromyography is poor in accurate localization, mostly due to the limited number of ulnar innervated muscles in the forearm. Important additional testing that often is recommended to aid in the accurate diagnosis of ulnar nerve lesions across the elbow includes the dorsal ulnar sensory nerve action potential, ulnar motor conduction study recording the first dorsal interosseous, and inching studies across the elbow.
11
Wee, Aileen, Pichet Sampatanukul, and Nirag Jhala. Cytohistology of Focal Liver Lesions. Cambridge University Press, 2014.
Find full text
12
Salkowski, Lonie R. Mass with Indistinct Margins. Edited by Christoph I. Lee, Constance D. Lehman, and Lawrence W. Bassett. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190270261.003.0024.
Full textAbstract:
Masses described as having indistinct margins lack a clear demarcation of a portion or the entire margin from the surrounding tissues. The indistinctness of the margin raises the possibility of infiltration; therefore, this descriptor implies suspicion for malignancy. “Indistinct” differs from “obscured.” A mass with obscured margins insinuates that the surrounding tissues masks or covers the presence of the lesion. This chapter, appearing in the section on asymmetry, mass, and distortion, reviews the key imaging and clinical features, imaging protocols and pitfalls, differential diagnoses, and management recommendations for masses with indistinct margins. Topics discussed include differentiation of the mass with indistinct margins from an obscured mass and focal asymmetry, and how the presence of adjacent features can increase the suspicion of the mass with indistinct margins.
13
Lencioni, Riccardo, Dania Cioni, Carlo Bartolozzi, A. L. Baert, and various. Focal Liver Lesions: Detection, Characterization, Ablation. Springer, 2010.
Find full text
14
Bland, Jeremy D. P. Focal neuropathies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0019.
Full textAbstract:
Focal neuropathies discusses the clinical, neurophysiological, and imaging assessment of the group of localized nerve lesions which are often referred to as ‘tunnel syndromes’. It first sets out general principles about how to define these syndromes and for their clinical, neurophysiological, and imaging assessment. Secondly, it discusses the relative importance of neurophysiological testing in diagnosis, prognosis, and the detection of coincident pathology when assessing these disorders. Finally, it then applies these principles to the example conditions of carpal tunnel syndrome, ulnar neuropathy at the elbow, peroneal neuropathy at the knee, and tarsal tunnel syndrome, and illustrates the use of neurophysiological tests as part of a comprehensive assessment intended to guide patient management.
15
Mahta, Ali, and Peter B. Crino. Focal Cortical Dysplasias. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0039.
Full textAbstract:
Focal cortical dysplasias (FCDs) are common malformations of cerebral cortical development that are highly associated with medically intractable epilepsy. FCDs have been classified according to neuropathological subtypes (type Ia, Ib, IIA, IIb, and III) based on the severity of cytoarchitectural disruption, and the presence of unique cell types (e.g., balloon cells). Most FCDs can be detected by neuroimaging studies and will require respective epilepsy surgery to cure refractory seizures. The pathogenesis of FCDs remains to be defined, although current belief is that these lesions result from sporadic somatic mutations occurring in brain development. A link to the mammalian target of rapamycin cascade has been defined for some FCD subtypes.
16
Focal Liver Lesions: Detection, Characterization, Ablation (Medical Radiology). Springer, 2006.
Find full text
17
(Editor), Julien Bogousslavsky, and Jeffrey L. Cummings (Editor), eds. Behavior and Mood Disorders in Focal Brain Lesions. Cambridge University Press, 2000.
Find full text
18
Bogousslavsky, Julien, and Jeffrey L. Cummings, eds. Behavior and Mood Disorders in Focal Brain Lesions. Cambridge University Press, 2000. http://dx.doi.org/10.1017/cbo9780511722110.
Full text
19
Julien, Bogousslavsky, and Cummings Jeffrey L. 1948-, eds. Behavior and mood disorders in focal brain lesions. Cambridge, UK: Cambridge University Press, 2000.
Find full text
20
Midiri, Massimo, Adele Taibbi, and Tommaso Vincenzo Vincenzo Bartolotta. Atlas of Contrast-enhanced Sonography of Focal Liver Lesions. Springer, 2016.
Find full text
21
Midiri, Massimo, Tommaso Vincenzo Bartolotta, and Adele Taibbi. Atlas of Contrast-enhanced Sonography of Focal Liver Lesions. Springer, 2015.
Find full text
22
(Foreword), A. L. Baert, R. Lencioni (Editor), D. Cioni (Editor), and C. Bartolozzi (Editor), eds. Focal Liver Lesions: Detection, Characterization, Ablation (Medical Radiology / Diagnostic Imaging). Springer, 2005.
Find full text
23
Muche, Marion, and Seema Baid-Agrawal. Hepatitis B. Edited by Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0185_update_001.
Full textAbstract:
Hepatitis B virus (HBV) has been causally linked to a variety of renal diseases, the most common being glomerular diseases and systemic autoimmune disease. Membranous nephropathy (MN) is the commonest HBV-associated glomerulonephritis (HBV-GN), followed by membranoproliferative glomerulonephritis (MPGN), mesangial proliferative glomerulonephritis, immunoglobulin (Ig)-A nephropathy, and focal segmental glomerulosclerosis (FSGS). Polyarteritis nodosa is a rare manifestation. The incidence of HBV-associated renal diseases seems to be decreasing with the introduction of vaccination programmes.HBV-MN is the most frequent cause of nephrotic syndrome in children in countries with high endemicity of HBV infection. The clinical course is usually benign in children with high rates of spontaneous remission rates and low risk of progression to renal failure. The prognosis is worse in adults. Of the systemic autoimmune disorders associated with HBV infection that involve the kidneys, the strongest link has been found with polyarteritis nodosa (PAN), a lesion that causes arteritis of medium-sized renal vessels. HBV-associated PAN (HBV-PAN) usually manifests in the first year after infection, and is clinically indistinguishable from classic PAN.Diagnosis of HBV-GN or -PAN is based on the clinical picture, histological findings, evidence of viral replication in serum and/or liver and detection of HBV antigens or DNA in the tissue. Besides deposition of immune complexes, other mechanisms such as virus-induced cytopathic damage have been proposed to explain the pathogenesis.HBV-GN and HBV-PAN appear to respond to antiviral treatment. Both show remission after HBeAg seroconversion. The available studies predominantly employed first-generation agents like interferon alpha and lamivudine, which showed suppression of viral replication and clinical remission of HBV-associated renal disease. Immunosuppressive therapy appears to be inevitable for the control of severe HBV-PAN and could be helpful in addition to antiviral treatment for cases of HBV-GN not responding clinically to antiviral treatment.
24
Katirji, Bashar. Electrodiagnostic Findings in Neuromuscular Disorders. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0004.
Full textAbstract:
Neuromuscular disorders are often classified into four major categories: anterior horn cell disorders, peripheral neuropathies, neuromuscular junction disorders and myopathies. This chapter discusses the electrodiagnostic and clinical EMG findings in these various neuromuscular disorders. Peripheral neuropathies are subdivided into focal mononeuropathies, radiculopathies, plexopathies and generalized peripheral polyneuropathies. Focal peripheral nerve lesions and generalized peripheral polyneuropathies may be axonal or demyelinating, and manifest quite distinctly on nerve conduction studies. Neuromuscular junction disorders may be presynaptic, as seen with the Lambert-Eaton myasthenic syndrome, or postsynaptic, as seen with myasthenia gravis.
25
Manohar, Sanjay, Valerie Bonnelle, and Masud Husain. Neurological Disorders of Attention. Edited by Anna C. (Kia) Nobre and Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.027.
Full textAbstract:
Attention deficits are a frequent and particularly disabling consequence of many neurological disorders, from patients with focal brain lesions through to individuals with traumatic brain injury or neurodegenerative conditions, such as Parkinson’s disease. They are often associated with apparent confusion, fatigue, irritability, and increased time and effort to perform even simple everyday tasks, and constitute a real challenge for rehabilitation. In many cases, attention deficits may be crucial factors underlying failures of memory and higher cognitive functions, contributing to difficulties in resuming previous activities and independent daily living. Here the authors first consider four aspects of attention—selective, sustained, executive, and divided—together with brain regions and networks considered to underpin normal attention and disorders of attention. The authors focus on focal brain lesions, traumatic brain injury and Parkinson’s disease as important examples illustrating the effects of different brain pathologies on attention function.
26
Popescu, Bogdan Florin Gh, Yong Guo, and Claudia Francesca Lucchinetti. Multiple Sclerosis: Pathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0081.
Full textAbstract:
The pathology of MS consists of areas of focal demyelination, known as plaques or lesions, characterized by inflammation, gliosis, and relative axonal preservation. Recent neuropathological studies have established that white matter lesions are heterogenous with respect to the targets of injury and mechanisms of demyelination, highlighting the need for the identification of surrogate clinical and/or paraclinical markers that would correlate with immunopatterns in the general MS population and for the design of novel therapeutic strategies specifically tailored to each immunopattern. Recent neuropathological studies have also shown the cortex is an early target of the MS disease process, and that inflammatory cortical demyelination may be driven by meningeal inflammation.
27
Mills, Kerry R., ed. Oxford Textbook of Clinical Neurophysiology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.001.0001.
Full textAbstract:
The Oxford Textbook of Clinical Neurophysiology provides a comprehensive account from world experts of the modern practice of the specialty. It deals with the full range of techniques giving the underpinning basic science and clinical use. The importance of clinical skills, as well as technical expertise are emphasized. Section I reviews the physiology of nerve, muscle, and cortex, and the digital techniques used to study them. Section II discusses the techniques for nerve conduction, electromyography (EMG), electroencephalography (EEG), magnetoencephalography, evoked potentials, and transcranial magnetic stimulation, including axonal excitability measurement, reflex studies, sleep studies pelvic floor neurophysiology and intracranial EEG. Section III reviews focal and generalized neuropathy, nerve, root, and plexus lesions, neuromuscular junction disorders, muscle disease, paediatric conditions, neurodegenerations, such as amyotrophic lateral sclerosis and EMG-guided botulinum toxin therapy. Section IV reviews generalized and focal epilepsy, status epilepticus, coma, presurgical evaluation for epilepsy, syncope, paediatric conditions, sleep disorders and intraoperative monitoring. This title incudes video content and is written for trainees and trainers in clinical neurophysiology.
28
Carr, Lucinda J. An overview of cerebral palsy. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.013003.
Full textAbstract:
♦ Cerebral palsy is a permanent disorder of movement or posture due to non-progressive lesions of the immature brain♦ Magnetic resonance imaging is generally recommended and can provide important prognostic information♦ Only a minority of cases are due to birth trauma♦ Modern classification systems incorporate function as well as anatomical involvement♦ Management aims to maximize a child’s potential both as an individual and within society. Other associated conditions may impact on quality of life and participation♦ Multidisciplinary involvement is essential with use of physiotherapy, orthotics, and tone management (focal and systemic) as necessary.
29
Barsoum, Rashad S. Schistosomiasis. Edited by Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0194_update_001.
Full textAbstract:
The urinary system is the primary target of Schistosoma haematobium infection, which leads to granuloma formation in the lower urinary tract that heals with fibrosis and calcification. While the early lesions may be associated with distressing acute or subacute symptoms, it is the late lesions that constitute the main clinical impact of schistosomiasis. The latter include chronic cystitis, ureteric fibrosis, ureterovesical obstruction or reflux which may lead to chronic pyelonephritis. Secondary bacterial infection and bladder cancer are the main secondary sequelae of urinary schistosomiasis.The kidneys are also a secondary target of S. mansoni infection, attributed to the systemic immune response to the parasite. Specific immune complexes are responsible for early, often asymptomatic, possibly reversible, mesangioproliferative lesions which are categorized as ‘class I’. Subsequent classes (II–VI) display different histopathology, more serious clinical disease, and confounding pathogenic factors. Class II lesions are encountered in patients with concomitant salmonellosis; they are typically exudative and associated with acute-onset nephrotic syndrome. Classes III (mesangiocapillary glomerulonephritis) and IV (focal segmental sclerosis) are progressive forms of glomerular disease associated with significant hepatic pathology. They are usually associated with immunoglobulin A deposits which seem to have a significant pathogenic role. Class V (amyloidosis) occurs with long-standing active infection with either S. haematobium or S. mansoni. Class VI is seen in patients with concomitant HCV infection, where the pathology is a mix of schistosomal and cryoglobulinaemic lesions, as well as amyloidosis which seems to be accelerated by the confounded pathogenesis.Early schistosomal lesions, particularly those of the lower urinary tract, respond to antiparasitic treatment. Late urological lesions may need surgery or endoscopic interventions. As a rule, glomerular lesions do not respond to treatment with the exception of class II where dual antiparasitic and antibiotic therapy is usually curative. Patients with end-stage kidney disease may constitute specific, yet not insurmountable technical and logistic problems in dialysis or transplantation. Recurrence after transplantation is rare.
30
Niaudet, Patrick, and Alain Meyrier. Idiopathic nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0054_update_001.
Full textAbstract:
Idiopathic nephrotic syndrome is defined by the combination of massive proteinuria, hypoalbuminaemia, hyperlipidaemia, and oedema, and of non-specific histological abnormalities of the glomeruli. Light microscopy may disclose minimal change disease, diffuse mesangial proliferation, or focal segmental glomerular sclerosis (FSGS). The two main causes of idiopathic nephrotic syndrome are characterized histologically. On electron microscopy the glomerular capillaries show a fusion of visceral epithelial cell (podocyte) foot processes and with the exception of some variants no significant deposits of immunoglobulins or complement by immunofluorescence. In a majority of children only minimal changes are seen on light microscopy. These children are referred to as having ‘minimal change disease’. In adults with idiopathic nephrotic syndrome, lesions of FSGS are more frequent.
31
Kettler, Mark D. Circumscribed Mass: Invasive Cancer. Edited by Christoph I. Lee, Constance D. Lehman, and Lawrence W. Bassett. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190270261.003.0018.
Full textAbstract:
Most invasive breast cancers present as focal asymmetries, areas of architectural distortion, or irregular masses with indistinct or spiculated margins. Some present as round or oval masses with circumscribed margins; however, most round or oval masses have microlobulated, indistinct, or spiculated margins and may be associated with characteristic malignant calcifications. This chapter, appearing in the section on circumscribed mass, reviews the key clinical and imaging features, differential diagnosis, and management recommendations for invasive breast cancers, which can present as circumscribed masses on mammography and sonography. Examples include medullary carcinoma, mucinous carcinoma, invasive papillary carcinoma, and high-grade invasive ductal carcinoma. These lesions may present as solid or complex masses with circumscribed margins and may be confused with several benign breast conditions.
32
Shaibani, Aziz. Muscle Stiffness and Cramps. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0020.
Full textAbstract:
Muscle stiffness is a nonspecific term meaning limited muscle mobility that is not due to weakness. It is opposite to flexibility. Muscle and joint pain may be described as stiffness. Painful sustained muscle cramps are usually associated with muscle stiffness. A careful history is paramount. Exercise-induced muscle cramps are usually myopathic (metabolic or mitochondrial myopathy), while resting and nocturnal cramps are neurogenic (neuropathy, motor neuron disease, etc). Metabolic cramps are electrically silent. Focal or generalized stiffness is typically seen in stiff person syndrome. Upper motor neuron lesions are associated with spasticity and stiffness (HSP, PLS, myelopathies, etc.). Painful cramps and fasciculations are important clues to peripheral nerve hyperexcitability disorder, which may also present with neuromyotonia. Not unusually, no cause is found for muscle cramps and stiffness. Symptomatic treatment frequently helps.
33
Shaibani, Aziz. Muscle Stiffness and Cramps. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0020.
Full textAbstract:
Muscle stiffness as a nonspecific term means limited muscle mobility. Muscle and joint pain may be described as stiffness. Painful, sustained muscle cramps are usually associated with muscle stiffness. A careful history is paramount. Exercise-induced muscle cramps are usually myopathic (metabolic or mitochondrial myopathy) while resting, and nocturnal cramps are neurogenic [neuropathy, motor neuron disease (MND), etc.]. Metabolic cramps are electrically silent. Focal or generalized stiffness is typically seen in stiff person syndrome (SPS). Upper motor neuron (UMN) lesions are associated with spasticity and stiffness [hereditary spastic paraplegia (HSP), primary lateral sclerosis (PLS), myelopathies, etc.]. Painful cramps and fasciculation are important clues to peripheral nerve hyperexcitability disorder, which may also present with neuromyotonia. Not unusually, no cause is found for muscle cramps and stiffness. Symptomatic treatment frequently helps.
34
Papanicolaou, Andrew C. In Search of the Mnemonic Traces of Concepts. Edited by Andrew C. Papanicolaou. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199764228.013.20.
Full textAbstract:
This chapter focuses on the search for mnemonic traces of concepts that are thought to exist in the form of neuronal circuits in the brain. It begins with a review of the evidence derived from observations of the effects of focal brain lesions suggesting that there are several brain regions specialized for recognizing objects belonging to different categories. It then considers brain areas that have been identified through functional neuroimaging, including the fusiform face area, the parahippocampal place area, and the extra-striate body area. It also examines the specialization of the anterior part of the temporal lobes, especially the left, for naming, and whether these and other brain areas contain mnemonic traces of concepts or traces of cardinal concept features. Finally, it discusses the “top-down” activation of category-specific areas and the idea of distributed storage of concept features.
35
Kimura, Jun. Nerve conduction studies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0006.
Full textAbstract:
This chapter examines the principles and practice of nerve conduction studies, which constitute an extension of the clinical history-taking and physical examination, rather than a separate laboratory test. Therefore, in order to take best advantage of the physiological assessment, we need to formulate a reasonable differential diagnosis based on their clinical examination. Nerve conduction studies will help clinicians by confirming the clinical diagnosis, characterizing the neuropathic process by documenting demyelination or axonal degeneration, which dictates the speed and manner of nerve impulse propagation, localizing the site of lesions, differentiating a focal versus diffuse process, and quantitating the abnormalities by the size of the elicited response, which approximately corresponds to the number of functional nerve and muscle fibres. The chapter will appeal to those interested in a broad review of electrodiagnostic medicine and to those wanting a current update on the state-of-the art information of nerve conduction techniques.
36
Holt, Fabian. Introduction. Edited by Fabian Holt and Antti-Ville Kärjä. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190603908.013.1.
Full textAbstract:
This chapter introduces new analytical framings of popular music in the Nordic countries and the implications therefore for broader discussions of the region’s uniqueness and global presence. The introduction first develops a broad interpretative narrative a broad interpretative narrative grounded in social science and considers its implications for existing cultural and disciplinary narratives. The second part closes in on more detailed issues of musical knowledge, drawing from the intellectual history of music, particularly musicology, while also integrating lessons from other disciplines such as geography. The specific focal points of the second part are the three thematic dimensions of the handbook—geography, history, and identity. Moreover, the literatures on Nordic popular music are discussed in detail. The final section introduces the individual chapter contributions.
37
Stirling-Zanda, Simonetta. The Privileges and Immunities of the Family of the Diplomatic Agent. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198795940.003.0007.
Full textAbstract:
The focal point of this chapter is Article 37(1) of the VCDR which grants, under certain conditions, immunities to family members of diplomats. Significant questions in this regard remain unresolved—not least the concept of the ‘diplomatic family’ itself. State practice shows that a certain discretion has been exercised against a backdrop of existing and evolving customary law. The result has been a generally balanced approach. Nevertheless, obiter dicta and calls for exceptions to the rules are beginning to appear with increasing frequency; concerns are expressed regarding the consequences of immunities for other treaties and for fundamental human rights. This chapter provides a comparative survey of the interpretation of Article 37(1), but also reflects on the codification history and on lessons drawn from the preparatory work.
38
Farfan, Penny. “[W]ithout the assistance of any girls”. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190679699.003.0004.
Full textAbstract:
This chapter focuses on Vaslav Nijinsky’s Afternoon of a Faun (1912) to consider how modernist performance could queer sex without representing same-sex relations and in the process become a focal point for sexually dissident spectatorship. In the ballet, the Faun bypasses a group of nymphs in favor of a solitary sexual experience. In doing so, he thwarts narrative expectations, foregrounding an autonomous male sexuality that was thrown into relief by the two-dimensionality of Nijinsky’s choreography. This relationship between modernist form and queer content produced a representation of male sexuality that was neither conventionally masculine nor effeminate. Afternoon of a Faun’s significance as a key work of queer modernism is underscored by its role in the historical emergence of an identifiably gay and lesbian audience, as well as by the mythologization of Nijinsky as the Faun as both an enabling and cautionary figure of queer sexuality.
39
Grant, Robert. Neurocutaneous syndromes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0235.
Full textAbstract:
This chapter describes several neurocutaneous syndromes, including tuberous sclerosis, neurofibromatosis, Sturge–Weber syndrome, Von-Hippel–Lindau disease and ataxia telangiectasia amongst others.Tuberous sclerosis, also known as Epiloia or Bournville’s Disease, is an autosomal dominant multisystem disease it usually presents in childhood with a characteristic facial rash, adenoma sebaceum, seizures, and sometimes learning difficulties. Central nervous system lesions in tuberous sclerosis are due to a developmental disorder of neurogenesis and neuronal migration. Other organs such as the heart and kidney are less commonly involved. The condition has very variable clinical expression and two-thirds of cases are thought to be new mutations, therefore it is important to examine and screen relatives. Management may involve many specialists and close co-operation between specialists is essential.The neurofibromatoses are autosomal-dominant neurocutaneous disorders that can be divided into ‘peripheral’ and ‘central’ types, although there is significant overlap. The characteristic features of neurofibromatosis type 1 are café au lait spots, neurofibromas, Lisch nodules, osseous lesions, macrocephaly, short stature and mental retardation, axillary freckling, and associations with several different types of tumours.Sturge–Weber syndrome involves a characteristic ‘port-wine’ facial naevus or angioma associated with an underlying leptomeningeal angioma or other vascular anomaly. It affects approximately 1/20 000 people. There can be seizures, low IQ, and underlying cerebral hemisphere atrophy as a result of chronic state of reduced perfusion and increased oxygen extraction. Patients may present with focal seizures which are generally resistant to anticonvulsant medication and can develop glaucoma.Von-Hippel– Lindau disease is one of the most common autosomal-dominant inherited genetic diseases that are associated with familial cancers. Von-Hippel–Lindau disease is characterized by certain types of central nervous system tumours, cerebellar and spinal haemangioblastomas, and retinal angiomas, in conjunction with bilateral renal cysts carcinomas or phaechromocytoma, or pancreatic cysts/islet cell tumours (Neumann and Wiestler 1991).Other neurocutaneous syndromes discussed include Hypomelanosis of Ito, Gorlin syndrome, Sjogren–Larsson syndrome, Proteus syndrome, Hemiatrophy and hemihypertrophy, Menke’s syndrome, Xeroderma pigmentosum and Cockayne’s syndrome.
40
Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0144_update_001.
Full textAbstract:
Paget’s disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.
41
Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0144.
Full textAbstract:
Paget's disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.
42
Alchi, Bassam, and David Jayne. The patient with antiphospholipid syndrome with or without lupus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.
Full textAbstract:
Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent arterial or venous thrombosis and/or pregnancy loss, accompanied by laboratory evidence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and antibodies directed against beta-2 glycoprotein 1 (β2GP1). APS may occur as a ‘primary’ form, ‘antiphospholipid syndrome,’ without any known systemic disease or may occur in the context of systemic lupus erythematosus (SLE), ‘SLE-related APS’. APS may affect any organ system and displays a broad spectrum of thrombotic manifestations, ranging from isolated lower extremity deep vein thrombosis to the ‘thrombotic storm’ observed in catastrophic antiphospholipid syndrome. Less frequently, patients present with non-thrombotic manifestations (e.g. thrombocytopaenia, livedo reticularis, pulmonary hypertension, valvular heart disease, chorea, and recurrent fetal loss).The kidney is a major target organ in both primary and SLE-related APS. Renal involvement is typically caused by thrombosis occurring at any location within the renal vasculature, leading to diverse effects, depending on the size, type, and site of vessel involved. The renal manifestations of APS include renal artery stenosis and/or renovascular hypertension, renal infarction, APS nephropathy (APSN), renal vein thrombosis, allograft vasculopathy and vascular thrombosis, and thrombosis of dialysis access.Typical vascular lesions of APSN may be acute, the so-called thrombotic microangiopathy, and/or chronic, such as arteriosclerosis, fibrous intimal hyperplasia, tubular thyroidization, and focal cortical atrophy. The spectrum of renal lesions includes non-thrombotic conditions, such as glomerulonephritis. Furthermore, renal manifestations of APS may coexist with other pathologies, especially proliferative lupus nephritis.Early diagnosis of APS requires a high degree of clinical suspicion. The diagnosis requires one clinical (vascular thrombosis or pregnancy morbidity) and at least one laboratory (LA, aCL, and/or anti-β2GP1) criterion, positive on repeated testing.The aetiology of APS is not known. Although aPL are diagnostic of, and pathogenic in, APS, a ‘second hit’ (usually an inflammatory event) may trigger thrombosis in APS. The pathogenesis of the thrombotic tendency in APS remains to be elucidated, but may involve a combination of autoantibody-mediated dysregulation of coagulation, platelet activation, and endothelial injury.Treatment of APS remains centred on anticoagulation; however, it has also included the use of corticosteroids and other immunosuppressive therapy. The prognosis of patients with primary APS is variable and unpredictable. The presence of APS increases morbidity (renal and cerebral) and mortality of SLE patients.