Corticospinal tract

ALS is a disorder of the motor neurons and the cortical neurons that provide their input. The disorder is characterized by rapidly progressive weakness and muscle atrophy. Most affected patients die of respiratory compromise and pneumonia after 2 to 3 years. There is prominent loss of motor neurons in the spinal cord and brainstem although the oculomotor neurons are spared. Large pyramidal motor neurons in layer V of motor cortex, which are the origin of the descending corticospinal tracts, are also lost. 

Distinguish between corticospinal tracts and multineuronal tracts... 

The corticospinal tracts originate in the cerebral cortex. Neurons of the primary motor cortex are referred to as pyramidal cells. Most of these neurons axons descend directly to the alpha motor neurons in the spinal cord. In... 

Even in the case of spinal cord injury where application of anti-Nogo antibodies results in regeneration of the cut axons, an additional important element for functional recovery is enhanced fiber growth from the unlesioned fibers, i.e. compensatory plasticity, as discussed above. After high corticospinal tract injury in the rat at the level of the medullary pyramid and treatment with anti-Nogo antibodies, rubrospinal pathways were shown to sprout into deafferented areas of the spinal cord, resulting in high levels of functional recovery, i.e. a functional switch in the remodeled pathway [42]. 

Sicotte, M., Tsatas, O., Jeong, S. Y., Cai, C-Q., He, Z. and David, S. Immunization with myelin or recombinant Nogo-66/MAG promotes axon regeneration and sprouting after corticospinal tract lesions in the spinal cord. Mol. Cell. Neurosci. 23 251-263, 2003. 

Schnell, L., Schneider, R., Kolbeck, R., Barde, Y. A. and Schwab M. E. Neurotrophin-3 enhances sprouting of corticospinal tract during development and after adult spinal cord lesion. Nature 367 170-173,1994. 

Friedreich s ataxia is caused by an intronic triplet repeat expansion. Friedreich s ataxia is an autosomal recessive disorder characterized by progressive ataxia, nystagmus, distal sensory polyneuropathy and corticospinal tract degeneration. It is caused by an unstable expanded GAA repeat in intron 1 of the frataxin gene on chromosome 9ql3. This diminishes expression of frataxin, a mitochondrial iron-storage protein that participates in free radical metabolism [71]. 

Subacute AIDS encephalitis (K3) was detected in adult and pediatric brains. Immunocytochemical analysis of adult and pediatric brains revealed gp 41 im-munoreactivity (78% and 40% respectively). Virtually all adult brains with SAE had gp 41 immunoreactivity in macrophages and microglia. Spinal cords with vacuolar myelopathy or corticospinal tract degeneration had only rare gp 41 positive cells. Brains of aborted fetuses from HIV-1 seropositive women were negative for gp 41 immunocreactivity, but some were positive for HIV-1 by polymerase chain reaction. 

Lie C, Hirsch JG, Rossmanith C, Hennerici MG, Gass A (2004) Clinicotopographical correlation of corticospinal tract stroke a color-coded diffusion tensor imaging study. Stroke 35 86-92... 

Liao D, Cooper L, Cai J, Toole J, Bryan N, Burke G, Shahar E, Nieto J, Mosley T, Heiss G (1997) The prevalence and severity of white matter lesions, their relationship with age, ethnicity, gender, and cardiovascular disease risk factors the ARIC Study. Neuroepidemiology 16 149-162 Lie C, Hirsch JG, Rossmanith C, Hennerici MG, Gass A (2004) Clinicotopographical correlation of corticospinal tract stroke a color-coded diffusion tensor imaging study. Stroke. 35 86-92... 

Recently, using color-coded diffusion tensor imaging five different patterns of corticospinal tract stroke were identified that fall into two clinical subgroups with either little recovery or good recovery. Patients with poor motor recovery had lesions centered in the pyramidal tract (anterior choroidal artery). Patients with good recovery had either very small lesions or lesions located anteriorly or medially (Lie et al. 2004). 

Trauma-induced axonal injury (TAI)is an important feature of human TBI. Some investigations have reported that moderate hypothermia can also reduce the generation of traumatically induced axonal injury (6,13). In one study, moderate hypothermia (32°C/4 h) initiated 10 min or 25 min after injury significantly reduced the number of abnormally stained axonal profiles (6). A study by Koizumi and Povlishock (13) reported that posttraumatic hypothermia (32°C/1 h) initiated as late as 1 h after trauma significantly reduced the density of amyloid precursor protein (APP) immunoreacti ve damaged axons within the corticospinal tract. Together, these data indicate that posttraumatic hypothermia in two models of TBI provides substantial protection in terms of axonal... 

In the cortex and from the cortex, information is conveyed through corticocortical and descending pathways. In particular, information meets in the cortex the sites of origin of the descending motor pathways, including cortical-brain stem pathways and the corticospinal tract. 

A 46-year-old man chronically abused heroin through inhalation and developed a gait disorder with paresthesia of the legs, incontinence, and impotence. MRI scans showed bilateral subcortical lesions and bilateral signal abnormalities in the corticospinal tract and posterior columns. Motor evoked potentials were slow, with prolonged F wave latency, which is evidence of peripheral nerve disease. Multivitamins and high doses of prednisone did not produce benefit. 

This condition was diagnosed as progressive myelopathy affecting only the corticospinal tract and posterior columns, the characteristics of which differ from acute leukoencephalopathy significantly, although both are serious consequences of heroin inhalation. Progressive myelopathy has been reported after heroin insufflation but never after inhalation of vapors. The authors favored an immune mechanism. 

Fig. 23.1. (a) Outline or "mask" of the corticospinal tract shown in (i) coronal, (ii) axial and (iii) sagittal views (Pineiro et al. 2000). (b) Axial MR slices showing the intersection of a stroke with the corticospinal mask, from which the maximum proportion of the mask cross-sectional area occupied by stroke is calculated. The corticospinal mask is shown in dark gray, the stroke in light gray, and the point of intersection between the stroke and the mask in white (Pineiro et al. 2000). 

Binkofski F, Seitz RJ, Arnold S et at (1996). Thalamic metabolism and corticospinal tract integrity determine motor recovery in stroke. Annals of Neurology 39 460-470 Blennerhassett J, Dite W (2004). Additional task-related practice improves mobility and upper limb function early after stroke ... 

Subacute combined degeneration of the spinal cord is from demyelination of the corticospinal tracts and posterior columns of the spinal cord, leading to gait ataxia and loss of position sense and vibratory sense. Peripheral neuropathy leads to loss of cutaneous sensation and tendon reflexes (Savage and Lindenbaum, 1995). 

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