Astereognosis and Dissociated Loss of Frontal or Parietal Components of Somatosensory Evoked Potentials in Hemispheric Lesions

Abstract

Detailed clinical sensory and motor signs were correlated case by case with somatosensory evoked potentials (SEP) in 22 selected patients with a single circumscribed hemisphere lesion. The lesions collectively mapped out a variety of cerebral sites from the anterior frontal to the posterior parietal regions. SEPs were averaged from 8 standard scalp sites with an earlobe reference electrode, so that parietal N20-P27-P45 were differentiated from prerolandic P22-N30 SEP components. SEP wave forms to stimulation on the unaffected side served as the patient's own control. A complete parietal lesion produced contralateral hemianaesthesia without upper motor neuron signs and eliminated the parietal N20-P27-P45 while the prerolandic P22-N30 persisted at usual latencies. The neural generators for the N20 and the P22 components are thus distinct. It is also proposed that direct, short latency pathways convey somatosensory inputs to the motor cortex, independently of connections via parietal areas 2 and 5. Enhancement of P22-N30 after chronic parietal lesions suggests collateral reinnervation by residual inputs after partial deafferentiation of prerolandic cortex. Small postcentral lesions produced astereognosis (with preserved tactile and deep sensation) and reduced or eliminated the N20 and P27 SEP components, but did not affect the P22-N30 components. Precentral lesions with severe hemiplegia (but not prefrontal lesions) eliminated the prerolandic P22-N30 SEP components and did not alter the parietal N20-P27-P45 components. The data are pertinent to the understanding of the pathophysiology of somatosensory deficits and for the diagnostic use of SEPs in cerebral lesions.

Congruency of body-related information induces somatosensory reorganization

“…Notably, this somatosensory modulation was observed at early latencies, with 22 suppressive effects measured for the P50 component that is known to originate from the primary somatosensory cortex (SI; Mauguière et al, 1983;Allison et al, 1989a;Ishibashi et al, 2000). We therefore concluded that a coherent representation of the body, housed in occipital or multisensory parietal areas and driven by vision of the hand, might promote an on-line reorganization of somatotopic maps, enhancing intracortical inhibitory connections in SI.…”

The Determination of Sensory Deficits in Children With Hemiplegic Cerebral Palsy

“…The methodology for the evaluatlon of sensation was not specified. The parietal SEP component IS not linked to pain and temperature (Maugiere et al, 1983), and therefore should not have been included in the sensations evaluated.…”

“…and SEP abnormalities. Maugiere et al (1983) studied the relationship between motor and sensory deficits to specific SEP abnormalities in 22 subjects. Eight sensory modalities and 2 apraxias were assessed.…”

Potencial evocado somato-sensitivo em crianças com pontas evocadas por estímulo somato-sensitivo no eletrencefalograma

“…É bem conhecido que esses componentes com amplitude elevada são encontrados em pacientes com epilepsia mioclônica progressiva, mas, também ocorrem em outras afecções do SNC 4,[24][25][26][27][28][29][30] . Esse aumento de amplitude dos componentes corticais do PES pode representar uma hiperexcitabilidade do córtex somato-sensitivo correspondente ao possível local epileptogênico 29 .…”