Download e-book for iPad: Central Pain Syndrome: Pathophysiology, diagnosis and by Sergio Canavero

By Sergio Canavero

ISBN-10: 0521866928

ISBN-13: 9780521866927

Critical ache Syndrome is a neurological situation as a result of harm particularly to the significant fearful approach - mind, brainstem, or spinal wire. this is often the single updated e-book to be had at the scientific elements (including prognosis and treatment) of CPS administration. The authors have built a truly entire reference resource on principal discomfort, which include historical past fabric, pathophysiology, and diagnostic and healing details. A scientific secret for a hundred years with out potent medication, this ebook turns the concept that of incurability of primary soreness on its head offering a rational method of treatment according to a rational thought.

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Sample text

1994) 73 Tasker et al. 2 (19À81, median 66) Stroke group Age of pts (years, mean) Andersen et al (1995) 40 12 (parietal CP) Bogousslavsky et al. (1988) 25 Graff-Radford et al. (1985) Michel et al. 3. Age of onset (CPSP only) 30 13 157 107 43 Kong et al. (2004) Widar et al. (2004) 18 thalamocortical Kameda et al. (2004) 10 brainstem Greenspan et al. 7 (26À72, median 55); nr in 2 pts Spinal vs. 019) 12 spinal Garcia-Larrea et al. 5) 119 Weimar et al. (2002) Widar et al. 5 (40À96, median 74) 8 Bowsher (2001) Lampl et al.

2002) Bowsher (2001) Kumral et al. 8% LMI 80% ? 5% of pts 1 pt with possible CPSP was eliminated from study because pain appeared 108 mos (9 yrs, 4 yrs in the text) after stroke 16 pts with bilateral thalamic infarction. CPSP in 1 pt 3 mos after the stroke LMI pts: onset of sensory symptoms immediate to 6 mos after the stroke. 9%). 1%) symptoms developed after 6 mos and in one case the time span between stroke and the onset of symptoms was unknown. 5 days) 6 stroke pts. Early-onset CPSP contralateral to the ischemic lesion þ delayed ipsilateral sensory symptoms mirroring the site of the most severe CPSP (without new ischemic lesions).

6. 6) Right-sided lesions predominate among CPSP patients at both thalamic and cortical levels. This difference is most likely not due to a difficulty of communication after left lesions (moreover, right lesions may cause hemineglect and anosognosia more frequently). It should not depend on simple prevalence of right strokes either, since men, but much less women, show CPSP laterality. 7. 7) Data are available only for thalamic vascular strokes. The hypothesis that CP correlates with the size, rather than the site, of the lesion is a time-honored one, but available data are conflicting.

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Central Pain Syndrome: Pathophysiology, diagnosis and management by Sergio Canavero

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