Cortex sensorimotor

M. A. Franceschini, S. Fantini, J. H. Thompson, J. P. Culver, and D. A. Boas. Hemodynamic evoked response of the sensorimotor cortex measured noninva-sively with near-infrared optical imaging. Psychophysiology, 40 548-560, 2003. 

Sensorimotor deficits imitating peripheral nerve involvement were reported (Back and Mrowka 2001). Ulnar and median nerve-like deficit were due to infarcts located in the thalamus and the corona radiate (Lampl et al. 1995). We have seen two patients with radial nerve-like deficits due to cortical ischemic lesions of the cortical presentation of the hand in the motor cortex. Normal nerve conduction velocity and MRI help to clarify these cases. 

PEM is one of the most frequent cancer-associated syndromes. This complex disorder usually affects several areas of the CNS. Cerebellar and brain stem disorders, as well as limbic encephalitis, are the most common clinical presentations of PEM [31, 32], Focal involvement of the sensorimotor cortex has been described in a few cases [33], and PEM may manifest as epileptic seizures or epilepsia partialis continua [33, 34], or as extrapyramidal symptoms [35], Two-thirds of the patients are affected in both the CNS and the peripheral nervous system. The predominant feature in more than half of these is SN [32, 36], hence the commonly used term is PEM/SN. Autonomic dysfunction is common in PEM/SN patients [36], often presenting as gastrointestinal dysmotility [37]. 

Despite the limitations of fMRI outlined above, fMRI studies have shown similar findings to those of positron emission tomography studies in recovery after stroke (Yozbatiran and Cramer 2006 Rijntjes 2006). Increased ipsilateral primary sensorimotor cortical activity with posterior displacement of the ipsilesional focus of activity, bilateral supplementary motor area activation and premotor cortical activation occurs after stroke with use of the affected hand in comparison with use of the unaffected hand (Weiller et al. 1992 Cramer et al. 1997 Cao et al. 1998 Pineiro et at 2001). Specifically, in patients with capsular or other subcortical stroke, good recovery is related to enhanced recruitment of the lateral premotor cortex of the lesional hemisphere and lateral premotor and, to a lesser extent, primary sensorimotor and parietal cortex of the contralateral hemisphere (Gerloff et al. 2006). 

The mechanisms of motor recovery vary according to location of the lesion cortical iirfarcts are associated with activation of the contralateral primary sensorimotor cortex, whereas subcortical infarcts appear to activate the bilateral primary sensorimotor cortex (Kwon et al. 2007). Several studies indicate that worse motor performance is related to a greater amount of contralesional activation (Calautti et al. 2007) and that patients who activate the ipsilesional primary motor cortex early had a better recovery of hand function (Loubinoux et al. 2007). Repetitive peripheral magnetic stimulation increases the activation of the parieto-premotor network and thereby might have a positive conditioning effect for treatment (Struppler et al. 2007). In addition to changes in the activation pattern of the... 

Abou-Donia et al, 2002). Intramuscular injection of 0.1 and 1.0 mg/kg for 7 days, followed by a 30-day observational period, resulted in sensorimotor deficits in rat behavior, differential levels of NO, and increased acetylcholinesterase activity in the cortex of animals dosed with 1 mg/kg, suggesting multiple exposures to low doses of uranyl acetate caused prolonged neurobehavioral deficits in rats after the initial exposure has ceased, similar to the exposures of Gulf War veterans (Abou-Donia et al, 2002). 

Sorensen JC, Dalmau I, Zimmer J, Finsen B (1996) Microglial reactions to retrograde degeneration of tracer-identified thalamic neurons after frontal sensorimotor cortex lesions in adult rats. Exp Brain Res 112 203—212. 

Reports of neurological adverse effects after tetanus immunization have appeared (8). The most common reported complication is a polyneuropathy. In the majority of cases the onset occurred within 14 days of the last injection, and ranged in severity from a single nerve palsy to profound sensorimotor involvement of the nervous system, including cord and cortex. Recovery was usually complete (eight of 10 patients with onset at less than 14 days after injection) but three patients with onset at more than 14 days from injection had only partial recovery. 

Alzheimer C, Schwindt PC, Crill WE 1993a Modal gating of Na channels as a mechanism of persistent Na current in pyramidal neurons from rat and cat sensorimotor cortex. J Neurosci 13 660-673... 

Waxman We don t know the full answer. We have looked at two other areas in experimental autoimmune encephalitis (EAE) where neurons send axons through tracts that are demyelinated. We have looked at red nucleus neurons that send their axons down the spinal cord, and we have looked at sensorimotor cortex neurons. We do not see changes that are nearly as dramatic as what we see in the cerebellum. We are in the midst of doing a survey of the entire neuraxis. 

Stafstrom CE, Schwindt PC, Chubb MC, Crill WE 1985 Properties of persistent sodium conductance and calcium conductance of layer V neurons from cat sensorimotor cortex in vitro. J Neurophysiol 53 153-170... 

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