Permanent flaccid paraplegia in children with thoracic spinal cord injury

Boltshauser, Eugen; Isler, W; Bucher, H. U.; Friderich, H

doi:10.1038/sc.1981.46

Cited by 10 publications

(4 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This commonly translates into the immediate but usually transient extinction of most spinal reflex responses, including stretch reflexes, which manifests itself clinically by an initial flaccidity 139, 177, 218. In a minority of cases, flaccidity persists chronically after occurrence of a central lesion, e.g., with some spinal cord infarcts25, 132, 193 or cerebral lesions 177. Persistent flaccidity is often associated with a greater degree of paresis and poorer outcome,36, 79, 82, 133, 177, 197, 221 although this is not always the case 159, 201.…”

Section: Immediate Effects Of Central Lesionmentioning

confidence: 99%

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes

2005

View full text Add to dashboard Cite

Spastic paresis follows chronic disruption of the central execution of volitional command. Motor function in patients with spastic paresis is subjected over time to three fundamental insults, of which the last two are avoidable: (1) the neural insult itself, which causes paresis, i.e., reduced voluntary motor unit recruitment; (2) the relative immobilization of the paretic body part, commonly imposed by the current care environment, which causes adaptive shortening of the muscles left in a shortened position and joint contracture; and (3) the chronic disuse of the paretic body part, which is typically self-imposed in most patients. Chronic disuse causes plastic rearrangements in the higher centers that further reduce the ability to voluntarily recruit motor units, i.e., that aggravate baseline paresis. Part I of this review focuses on the pathophysiology of the first two factors causing motor impairment in spastic paresis: the vicious cycle of paresis-disuse-paresis and the contracture in soft tissues.

show abstract

Section: Immediate Effects Of Central Lesionmentioning

confidence: 99%

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes

2005

View full text Add to dashboard Cite

show abstract

“…5 By recording CMAPs of tibial and peroneal motor nerves in patients with paraplegia the extent and severity of a lesion of intramedullary anterior horn cells of the conus medullaris and motor nerve ®bres of the cauda equina due to traumatic/nontraumatic damage can be quantitatively assessed. 6 However, the time course and the characteristic of pathological motor nerve conduction studies and its diagnostic and prognostic signi®cance in acute paraplegic patients has not yet been evaluated.…”

Section: Introductionmentioning

confidence: 99%

Diagnostic and prognostic value of compound motor action potential of lower limbs in acute paraplegic patients

2000

View full text Add to dashboard Cite

Objectives: To evaluate the diagnostic and prognostic contribution of motor nerve conduction studies (NCS) in addition to neurological examination in patients with acute paraplegia. Methods: In 79 patients with acute onset of paraplegia due to traumatic or ischaemic damage of the conus medullaris/cauda equina (conus/cauda) or lesion of the mid-thoracic spinal cord (epiconal) neurological (initial and follow-up clinical motor and sensory scores; outcome of ambulatory capacity determined at least 6 months post-trauma) and electrophysiological examinations (motor nerve conduction velocity (MNCV) and compound motor action potential (CMAP) of tibial and peroneal nerves) were performed in parallel. Results: Severe axonal motor neuropathies were signi®cantly caused by conus/cauda lesions (loss of tibial CMAP in 71% and of peroneal CMAP in 68%) compared to patients with epiconal lesion (no loss of tibial CMAP and abolished peroneal CMAP in 14%). The CMAPs were deemed acutely pathological 4 ± 14 days post-trauma and were indicative of the severity of conus/cauda lesion while the MNCV remained normal. Follow-up recordings (up to 1 year post trauma) revealed no signi®cant change in the CMAP values. The clinical examination according to the American Spinal Injury Association (ASIA protocol) in contrast to the CMAP values was signi®cantly related to the outcome of ambulatory capacity. Conclusions: In contrast to patients with an epiconal SCI almost all patients with damage of the conus/cauda present a severe axonal neuropathy of the tibial and peroneal nerves. Pathological CMAPs develop as early as 1 ± 2 weeks after onset of acute paraplegia. They allow, at an early stage, to di erentiate between conus/cauda or epiconal lesion and to assess the severity of conus/cauda lesion. Thereafter follow-up examinations remain stable and a developing worsening of peripheral nerve or spinal cord function, eg due to post-traumatic syringomyelia, may be indicated by a secondary deterioration of CMAP values. The clinical examination, according to the ASIA protocol, in acute paraplegia patients, in contrast to the motor nerve conduction studies, is of prognostic value in predicting the outcome of ambulatory capacity.

show abstract

“…In the two patients with ischemic spinal cord injury and contusio spinalis respectively no abnormalities could be demonstrated in myelography, CT-scan nor MRI. Normal findings from myelography and MRI are known (2,6). The absence of demonstrable findings can be explained by the fact that the pathophysiological processes are taking place on an electri• cal, chemical or ultra-structurallevel (5).…”

Section: Discussionmentioning

confidence: 99%