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Clinical presentation

The most frequent clinical presentations of brain AVMs are hemorrhage, seizure, chronic headache, and focal deficits not related to hemorrhage (Mast et al. 1995). [Pg.56]

Brain AVMs are lesions that are not affected by important anatomic modifications over time. However, as was outlined by Berenstein and Lasjaunias (1992), AVMs are dynamic, i.e., they undergo continuous subtle anatomic and hemodynamic changes. A cerebral AVM becomes clinically evident i dien the host s capacity to compensate effectively has reached its threshold. Cerebral AVMs are often symptomatic in young adults, typically before the age of 40 (Hofmeister et al. 2000). [Pg.56]

From an anatomic point of view, the natural history of brain AVMs may rarely include enlargement, decrease, or regression (Minakawa et al. 1989 Chen et al. 1991 Krapf et al. 2001). Surprisingly, in a small series of 20 patients followed up by an- [Pg.56]

Intracranial hemorrhage is the most common clinical presentation of brain AVM, with a frequency of between 30% and 82% (Mast et al. 1995). Identification of factors increasing the risk of bleeding of a brain AVM is very important with regard to the treatment strategy. However, two difficulties are encountered in an analysis of the literature  [Pg.57]

Several factors may increase the risk of a first hemorrhage in case of brain AVM. [Pg.57]


Heriditary lysosomal storage disorder with an heterer-ogeneous clinical presentation including mental retardation and skeletal changes. The disease is caused by... [Pg.622]

Short-chain acyl-CoA dehydrogenase (SCAD) deficiency has been recorded in only a few patients and these show wide variation in clinical presentation. The defect has been seen in infants with a syndrome of psychomotor retardation and failure to thrive. These infants showed abnormal organic aciduria, and drastically decreased SCAD activity was demonstrable in cultured fibroblasts. Muscle symptoms were only part of a wider syndrome in all infants and children so far reported to have SCAD deficiency, but were the sole presenting feature in two adult patients, in whom lipid storage was demonstrable in skeletal muscle. The gene encoding for human SCAD has been mapped to chromosome 12. [Pg.306]

This complex contains 11 polypeptide subunits of which only one is encoded by mtDNA. Defects of complex III are relatively uncommon and clinical presentations vary. Fatal infantile encephalomyopathies have been described in which severe neonatal lactic acidosis and hypotonia are present along with generalized amino aciduria, a Fanconi syndrome of renal insufficiency and eventual coma and death. Muscle biopsy findings may be uninformative since abnormal mitochondrial distribution is not seen, i.e., there are no ragged-red fibers. Other patients present with pure myopathy in later life and the existence of tissue-specific subunits in complex III has been suggested since one of these patients was shown to have normal complex 111 activity in lymphocytes and fibroblasts. [Pg.311]

Complex V catalyzes the phosphorylation of ADP to ATP. Deficiencies of complex V are rare and clinical presentation is usually nonprogressive muscle weakness. One subject included growth retardation, sensorineural deafness, and involvement of basal ganglia, which are occasional features of various other respiratory chain abnormalities. [Pg.312]

Various syndromes associated with hypereosinophilia involve skeletal muscle. There is a rare form of polymyositis which is characterized by this feature (defined as exceeding 1,500 eosinophils/mm for at least six months). Clinical presentation includes skin changes, heart and lung involvement, and peripheral neuropathy as well as proximal myopathy. The condition must be distinguished from trichinosis and other parasitic infections associated with hypereosinophilia. Muscle biopsy findings are interstitial and perivascular infiltrates in which eosinophils predominate but are accompanied by lymphocytes and plasma cells, and occasional muscle fiber necrosis. Fascitis may also be associated with hypereosinophilia (Shulman s syndrome). This condition is characterized by painful swelling of skin and soft tissues of trunk and extremities and weakness of limb muscles. Biopsy of muscle... [Pg.336]

Actinic keratosis treated with imiquimod 5% cream. Clinical presentation after 15 days of treatment vesicles on an erythematous base... [Pg.137]

The diagnosis of PIH is often made by history and clinical presentation. It is characterized by macules and patches of varying shades of hyperpigmentation limited to the sites of inflamed skin lesions. Lesions of the preceding inflammatory process may be present at vari-... [Pg.178]

The phenotype and clinical presentation of antiretroviral toxic neuropathy (ATN) are similar to those of HIV-associated DSP. However, ATN is more likely to be painful, and has an abrupt onset and rapid progression. The main diagnostic clue is the temporal relationship of peripheral neuropathy to the start of NRTI therapy and stabilization, or at least the partial resolution when therapy is interrupted (Moyle and Sadler 1998). ATN most often develops after a mean of 16 to 20 weeks of treatment, unless there are other conditions that lower the threshold. Symptomatic improvement over weeks to months has been reported in two thirds of patients after discontinuation of the offending drug, but may be preceded by an initial period of worsening symptoms, also known as coasting (Berger et al. 1993). Despite the improvement, most patients do not return to a completely asymptomatic state (Hoke and Comblath 2004). [Pg.57]

The clinical presentation of MM in HIV-infected patients is similar to that in other patients with vasculitic neuropathy (Hoke and Comblath 2004). It is characterized by symptoms and signs of sensory involvement, with numbness and tingling in the distribution of one peripheral nerve trunk. Sequential involvement of other noncontiguous peripheral or cranial nerves progresses over days to weeks. The initial multifocal and random neurologic features may evolve to symmetrical neuropathy (Ferrari et al. 2006). [Pg.60]

Abromson-Leeman S, Bronson R, Luo Y, Berman M, Leeman R, Leeman J, Dorf M (2004) T-ceU properties determine disease site, clinical presentation, and cellular pathology of experimental autoimmune encephalomyelitis. Am J Pathol 165 1519-1533 Adamson DC, Wildemann B, Sasaki M, Glass JD, McArthur JC, Christov VI, Dawson TM, Dawson VL (1996) Immunologic NO synthase elevation in severe AIDS dementia and induction by HIV-1 gp41. Science 274 1917-1921... [Pg.136]

Treatment duration may vary based on clinical presentation... [Pg.94]

CLINICAL PRESENTATION AND DIAGNOSIS OF CHRONIC HEART FAILURE... [Pg.39]

Clinical Presentation and Diagnosis of Acute Heart Failure... [Pg.52]

Classified as the most complicated clinical presentation of AHF with the worst prognosis... [Pg.53]


See other pages where Clinical presentation is mentioned: [Pg.2179]    [Pg.1080]    [Pg.1251]    [Pg.284]    [Pg.191]    [Pg.192]    [Pg.244]    [Pg.255]    [Pg.258]    [Pg.279]    [Pg.291]    [Pg.294]    [Pg.113]    [Pg.112]    [Pg.148]    [Pg.159]    [Pg.173]    [Pg.237]    [Pg.238]    [Pg.26]    [Pg.14]    [Pg.39]    [Pg.51]    [Pg.52]    [Pg.53]    [Pg.68]    [Pg.69]   
See also in sourсe #XX -- [ Pg.647 , Pg.648 ]

See also in sourсe #XX -- [ Pg.190 , Pg.340 , Pg.1469 , Pg.1508 , Pg.1989 ]




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