Capsular Stroke Research Articles

Developmental neuroplasticity in a model of cerebral hemispherectomy and stroke

Cerebral hemispherectomy, a last resort treatment for childhood epilepsy, is a standard procedure which dramatically illustrates the resilience of the brain to extensive damage. If this operation, also mimicking long-term, extensive unilateral capsular stroke, is performed in postnatal cats of up to 60 days of age, there is a remarkable recovery/sparing of neurological functions that is not seen when the lesion occurs during late fetal life or in adulthood. A long-term effect at all ages is loss of neurons in bilateral brain areas remote from the resection site. This is pronounced in adult cats and shows intriguing, paradoxical features in fetal animals, but is substantially attenuated in neonatal cats. Similarly, large-scale reinnervation of subcortical sites (sprouting) by neurons of the remaining, intact hemisphere is prominent in young cats, but not in fetal or adult animals. These and other restorative processes (described herein) in young postnatal animals are matched by relatively higher rates of local cerebral glucose utilization, supporting the notion that they underlie the improved behavioral outcome. Thus, during a critical, defined stage of maturation, presumably common to higher mammals including humans, the brain entirely remodels itself in response to extensive but focal injury. Perhaps the molecular environment allowing for rescue of neurons and enhanced reinnervation at a specific developmental stage could be recreated in subjects with brain lesions at less favorable ages, thereby helping to restore circuitry and spare neurons. However, replacement via transplantation of neurons eliminated by the damage appears to be crucial in attempts to further preserve cells located remotely but yet destined to die or decrease in size. This article presents abundant evidence to show that there is a surprisingly comprehensive long-term morphological remodeling of the entire brain after extensive unilateral damage and that this occurs preferentially during a discrete period of early life. Additional evidence strongly suggests that the remodeling underlies the outstanding behavioral and functional recovery/sparing following early cerebral hemispherectomy. We argue that this period of reduced brain vulnerability to injury also exists in other higher mammals, including man, and suggest ways to enhance restorative processes after stroke/hemispherectomy occurring at other ages.

Respuesta electromiográfica asociada en ictus capsular

Lesions of the pyramidal system are characterized by their effects on qualitative aspects of movement. One of the features of pyramidal defects is the presence of associated movements or synkinesis. We present a case with residual associated electromyographic (EMG) response in a patient who had had a capsular stroke 11 months previously. The patient presented with acute onset of a syndrome of purely motor right hemiparesis (PMH) which improved satisfactorily with complete functional recovery three months later. Eleven months after the acute episode, there was good functional recovery and neurophysiological examination showed the presence of EMG responses associated with the unaffected limb (left hand) when voluntary movements were made with the right hand. The appearance of qualitative alterations of movement associated with pyramidal syndromes and particularly the presence of associated EMG responses in the case of capsular infarct described, may reflect the different processes of reinnervation and functional reorganization which occur following the lesion and which are involved in recovery of motor function.

Motor recovery following capsular stroke. Role of descending pathways from multiple motor areas.

The functional anatomy of motor recovery was studied by assessing motor function quantitatively in 23 patients following capsular or striatocapsular stroke. While selective basal ganglia lesions (caudate and/or putamen exclusively) did not affect voluntary movements of the extremities, lesions of the anterior (plus caudate/putamen) or posterior limb of the internal capsule led to an initially severe motor impairment followed by excellent recovery, hand function included. In contrast, lesions of the posterior limb of the internal capsule in combination with damage to lateral thalamus compromised motor outcome. In experimental tracing of the topography of the internal capsule in macaque monkeys, we found axons of primary motor cortex passing through the middle third of the posterior limb of the internal capsule. Axons of premotor cortex (dorsolateral and post-arcuate area 6) passed through the capsular genu, and those of supplementary motor area (mesial area 6) through the anterior limb. Small capsular lesion can therefore disrupt the output of functionally and anatomically distinct motor areas selectively. The clinically similar motor deficits with a similar course of functional restitution following disruption of these different descending motor pathways indicate a parallel operation of cortical motor areas. They may have the further capability of substituting each other functionally in the process of recovery from hemiparesis.

Capsular stroke as a cause of hemiplegia in infancy

Small, deep lesions of the internal capsule are an uncommon cause of infantile hemiplegia. We report the clinical and radiographic findings of three children with hemiplegia with capsular lesions. Although the etiology of capsular stroke in these children remains uncertain, neither hypertension, coagulopathy, nor vascular malformation was an important factor.