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PubMed1997

Degeneration of the pyramidal tracts in patients with amyotrophic lateral sclerosis. A premortem and postmortem magnetic resonance imaging study.

To investigate focal hyperintensity in the internal capsule (IC) on magnetic resonance images (MRIs) and its clinical significance, 80 patients with amyotrophic lateral sclerosis (ALS) and 80 sex- and age-matched normal control subjects were studied. On T2-weighted images, hyperintense foci were found in the posterior part of the posterior limb (PL) of the IC in 41 (51%) of 80 control subjects. However, no subject showed increased signal intensities on proton density-weighted images. Hyperintense foci were also observed in the posterior part of the PL of the IC on T2-weighted images in 52 (65%) of 80 ALS patients and on proton density-weighted images in 26 (65%) of 40 ALS patients; the abnormally intense foci were seen at the same anatomical location in the IC as those in the normal control subjects. On postmortem MRI, the abnormally intense foci were found in the posterior part of the PL of the IC in the formalin-fixed brains from 9 ALS patients. Three normal control subjects did not show signal intensity changes on postmortem MRI. On histological examination of 9 ALS brains, distinct myelin pallor and gliosis were found in the posterior third of the PL of the IC. Proton density-weighted images appear to be useful to distinguish neuropathological changes in the corticospinal tract of ALS patients.

Adult↗
PubMed1978

Developing role of sensorimotor cortex and pyramidal tract neurons in contact placing in kittens.

Unilateral or bilateral removal of kitten sensorimotor (SM) cortex prior to the fourth postnatal week was followed by recovery of contact placing (CP) to stimulation of any of the four forepaw cutaneous fields. However, immediately after a removal under ethyl chloride, CP was depressed contralaterally, especially to lateral stimulation (lateral CP). When the operated kitten aged to 5--9 weeks, the likelihood of CP secondarily declined contralateral to the SM cortical extirpation, but was restored by administration of d-amphetamine. An initial extirpation after the fifth postnatal week was followed by a severe deficit in CP. 2. Cooling the SM cortex, internal capsule or bulbar pyramid during the 2nd and 3rd week was followed by reversible, contralateral loss of lateral CP, extension of the forelimb and, later, by reduced movements. Lateral CPs were often hypermetric prior to loss. By contrast, cooling SM cortex in the first week was usually ineffective. Thus, during the 2nd week, lateral CP developed a dependence on SM cortex, and in particular on PT neurons. 3. After a delay usually of 1 or more min, cooling the SM cortex reduced the resting discharge of individual neurons in buried motor cortex; the antidromic conduction time in PT neurons was significantly increased and the spike height was reduced.

Animals↗