PubMed Health⌕ Search

Biomedical subjects

G Anson

Publications and source records attributed to G Anson.

3 recordsLinked to original sources

Microsurgical correction of facial asymmetry in 60 consecutive cases.

Restoring soft-tissue contour in patients with facial asymmetry is a difficult problem for plastic surgeons. We report our experience with 57 consecutive patients who underwent 60 microvascular free flaps for the correction of facial asymmetry between July of 1989 and June of 1994. Etiologies of facial asymmetry included hemifacial microsomia, hemifacial atrophy, postradiation sequelae, burns and trauma, and selected congenital anomalies. Thirty-eight patients were reconstructed with a customized parascapular flap incorporating extensions of dorsal thoracic fascia. Other donor sites utilized were as follows: six superficial inferior epigastric flaps, three myocutaneous flaps, seven muscle flaps, and six fasciocutaneous flaps with bone. To correct facial asymmetry, the recipient site was dissected through a limited preauricular incision whenever feasible, and the superficial temporal artery and vein were used as recipient vessels. A monitoring skin paddle was rarely used. There were no flap losses in this series. Six patients experienced a postoperative hematoma, three of which were drained at the bedside. Limited skin slough occurred in three patients. No donor-site complications other than hypertrophic scarring were encountered. Flap revisions were performed in 22 of the 57 patients to maximize aesthetic results. Based on our experience, we feel that the operative approach presented here allows excellent and stable correction of facial asymmetry due to a variety of etiologies. Furthermore, this technique is applicable to other congenital craniofacial deformities such as Treacher-Collins syndrome and orbital-facial clefts.

Adolescent↗

Cortical cell assemblies: a possible mechanism for motor programs.

The concept of a motor program has been used to interpret a diverse range of empirical findings related to preparation and initiation of voluntary movement. In the absence of an underlying mechanism, its exploratory power has been limited to that of an analogy with running a stored computer program. We argue that the theory of cortical cell assemblies suggests a possible neural mechanism for motor programming. According to this view, a motor program may be conceptualized as a cell assembly, which is stored in the form of strengthened synaptic connections between cortical pyramidal neurons. These connections determine which combinations of corticospinal neurons are activated when the cell assembly is ignited. The dynamics of cell assembly ignition are considered in relation to the problem of serial order. These considerations lead to a plausible neural mechanism for the programming of movements and movement sequences that is compatible with the effects of precue information and sequence length on reaction times. Anatomical and physiological guidelines for future quantitative models of cortical cell assemblies are suggested. By taking into account the parallel re-entrant loops between the cerebral cortex and basal ganglia, the theory of cortical cell assemblies suggests a mechanism for motor plans that involve longer sequences. The suggested model is compared with other existing neural network models for motor programming.

Journal Article↗