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The developing brain possesses a high potential for neuroplasticity. Yet, this remarkable potential of (re-)organization is not a general principle. It seems to vary among different functional systems. Here, we show that distinct brain structures involved in somatosensory processing are already prenatally determined so that a pre- or perinatally acquired (congenital) brain damage of such structures results in a persistent somatosensory deficit. Eleven patients with hemiparesis due to congenital cortico-subcortical unilateral stroke who showed versus not showed a somatosensory deficit were contrasted with magnetic resonance imaging lesion–behavior mapping. The brain areas which were typically damaged in patients with a somatosensory deficit but typically spared in patients without a somatosensory deficit were located in the primary and secondary somatosensory cortex (S1, S2) as well as the inferior parietal cortex directly neighboring S1 and S2. The results argue for an early functional determination of primary and secondary somatosensory cortex, without substantial capacities for (re-)organization. They demonstrate that cortical damage of these areas cannot be compensated by shifting the functional representation to undamaged parts of the cortex.