EPIDEMIOLOGY AND CLINICAL FEATURES

Lesions causing CP and location (Table 2.1a,b)

BCP has been caused by all kinds of lesions at any level along the spinothalamoparietal path, from brainstem to cortex, a fact already appreciated in the 1930s (Garcin 1937; DeAjuraguerra 1937; Riddoch 1938). These include rapidly or slowly developing processes, apparently without differences in probability of triggering CP (but systematic studies have not been conducted), compressive or disruptive/distractive (these latter perhaps being more often associated with CP).

Stroke, either hemorrhagic or ischemic, is the commonest cause of BCP (without differences between the two); dismayingly, iatrogenic CP is not rare. In agreement with their known incidence, in all studies, infarcts are more common than hemorrhages (roughly 4:1).

When the lesion is thalamic, Vc is always involved (the case of Gonzales et al. [1992] had signs of capsular involvement). Contrary to previous belief, one third or even less of BCP cases are purely thalamic (e.g., Hirato et al. 1993; Andersen et al. 1995; Tasker 2001b; Widar et al. 2002; Oliveira et al. 2002; see also Schmahmann 2003) and complete thalamic syndromes are exceptional. CP does not arise following thalamic lesions only damaging the kinesthetic afferent pathway and probably the spindle afferent pathway as well (Ohye 1998). In all other cases, lesions are cortico-subcortical, in the brainstem, capsulothalamic or lenticulocapsular, or diffuse. Most CPSP is supratentorial (roughly 80%; Tasker 2001).

All cortical lesions responsible for CP involve, exclusively or in combination, the parietal lobe, and specifically SI (and also SII) (e.g., Bassetti et al. 1993).