The Fisher exact test was used to test the relationship between presence or absence of posterior PVWM involvement and the presence of some UL functionality (defined as class 1, 2, or 3 UL impairment).
5 percent had PVWM involvement while 53 percent had minimal (<25%) or no ahPCG involvement (Table).
The extent of involvement of the posterior PVWM can be seen in the figures.
The two subjects who did not have PVWM involvement underwent CT scans on the day of the stroke.
This indicates that in half of our subjects, the ahPCG lesion could not account for the paresis, and in the other half, either the ahPCG, the PVWM lesion, or both produced the paresis.
Stroke studies have shown that lesions in the posterior half of the PVWM are associated with paresis and that the pattern of paresis corresponds with the somatotopic localization defined by DTT studies [1-3].
A definitive study would require prospective imaging using stateof-the-art MRI techniques to quantitate damage to the ahPCG, the arm-hand premotor cortex, and the posterior PVWM in relation to the established trajectory of the corticospinal tract.