Smyth MD, Peacock WJ
Muscle Nerve 2000 Feb;23(2):153-163
Univ of California San Francisco, Dept of Neurological Surgery, 505 Parnassus Avenue, Room M-779, Box 0112, San Francisco, California 94143-0112, USA
Many NeuroSurgical procedures have been designed for or applied to the treatment of Spasticity arising from different disorders.
Including Cerebral Palsy, Traumatic, Ischemic, or Hypoxic Brain Injury, Multiple Sclerosis, and Spinal Cord Injury.
NeuroSurgical procedures are primarily aimed at reducing Spasticity by interrupting the Stretch Reflex at various sites along the Spinal Reflex Arc
Or, attempting to increase the Centrally mediated Inhibitory influence on the pool of Motor Neurons in the Anterior Horn.
Surgical interventions for Spasticity can be classified into Peripheral Ablative Procedures, such as: Rhizotomy or Peripheral Neurectomy, and Central Ablative Procedures, such as Cordectomy, Myelotomy, or Stereotactic Procedures.
NonAblative procedures include Peripheral Nerve or Motor Point Blocks, the implantation of Cerebellar or Spinal Stimulators.
And the implantation of SubDural catheters for infusion of pharmacologic agents to increase Inhibitory activity.
Several proposed mechanisms for Spasticity are reviewed so that the rationale for the various surgical interventions for Spasticity described may be better understood.
Copyright 2000 John Wiley & Sons, Inc.
Myelin Oligodendrocytic Basic Protein (MOBP)
Is EncephalitoGenic & A Potential Target Antigen
In Multiple Sclerosis (MS)
Kaye JF, Kerlero de Rosbo N, Mendel I, Flechter S, Hoffman M, Yust I, Ben-Nun A
J NeuroImmunol 2000 Jan 24;102(2):189-98
The Weizmann Institute of Science, Dept of Immunology, Rehovot, Israel
PMID# 10636488; UI# 20100443
Uncovering primary target Antigens in Multiple Sclerosis (MS) is of major significance for understanding the Etiology and PathoPhysiology of the disease, and for designing Immunospecific therapy.
In this study, a synthetic Peptide representing a predicted T-Cell Epitope on Myelin Oligodendrocytic Basic Protein (MOBP) was found to be EncephalitoGenic in C3H.SW mice, inducing Experimental AutoImmune EncephaloMyelitis with an abrupt onset.
Two separate preliminary studies with MOBP Peptides indicated that AutoReactivity to MOBP occurs in MS. These data strongly suggest that MOBP is a highly relevant target in MS and further point to the complexity of Antigen specificities in MS.
Reddy H, Narayanan S, Matthews PM, Hoge RD, Pike GB, Duquette P, Antel J, Arnold DL
Neurology 2000 Jan 11;54(1):236-9
McGill University, Montreal-Neurological Institute, Dept of Neurology and NeuroSurgery, Canada
PMID# 10636158; UI# 20100113
A patient was followed after the new onset of HemiParesis from relapse of MS with serial MR Spectroscopic and Functional MRI.
The association of clinical improvement with recovery of N-AcetylAspartate, a marker of Neuronal integrity, and progressive reduction of abnormally large functional MRI Cortical activation with movement demonstrates that dynamic reorganization of the Motor Cortex accompanies remission of MS.
Filippi M, Bozzali M, Horsfield MA, Rocca MA, Sormani MP, Iannucci G, Colombo B, Comi G
Neurology 2000 Jan 11;54(1):207-13
Univ of Milan, Dept of NeuroScience, Scientific Institute, Ospedale San Raffaele, Italy
PMID# 10636149; UI# 20100104
To evaluate the contribution made by Cervical Cord damage, assessed using a fast Short-Tau Inversion Recovery (fast-STIR) sequence and Magnetization Transfer Ratio (MTR) Histogram analysis to the clinical manifestations of MS.
Previous studies have failed to show significant correlations between the number and extent of T2 Spinal Cord lesions and the clinical status of patients with MS.
Fast-STIR is more sensitive than T2-weighted imaging for detecting Cervical Cord MS lesions.
MTR Histogram analysis provides estimates of the overall disease burden in the Cervical Cord with higher pathologic specificity to the more destructive aspects of MS than T2-weighted scans.
We obtained fast-STIR and Magnetization Transfer (MT) scans from 96 patients with MS (52 with Relapsing/Remitting [RRMS], 33 with Secondary/Progressive [SPMS], and 11 with Primary/Progressive [PPMS] MS and 21 control subjects.
Dual-echo scans of the Brain were also obtained and lesion load measured.
Eighty-one of the patients with MS had an abnormal Cervical Cord scan.
Patients with SPMS had more Cervical Cord lesions and more images with visible Cervical Cord damage than did patients with RRMS or PPMS (p = 0.04).
The entire cohort of patients with MS had lower average MTR of the Cervical Cord (p = 0.006) than control subjects.
Compared to control subjects, patients with RRMS had similar Cervical Cord MTR Histogram-derived measures.
Whereas, those with PPMS had lower average MTR (p = 0.01) and peak height (p = 0.02).
Patients with SPMS had lower Histogram peak height than did those with RRMS (p = 0.03).
The peak position and height of the Cervical Cord MTR Histogram were independent predictors of the probability of having locomotor disability.
We found no correlation between Brain T2 lesion load and any of the Cervical Cord MTR Histogram metrics.
This study shows that the amount and severity of MS pathology in the Cervical Cord are greater in the Progressive forms of the disease.
An accurate assessment of Cervical Cord damage in MS gives information that can be used in part to explain the clinical manifestations of the disease.