Spinal Shock

1/23/2008

 

Question:  What are aspects of spinal shock?

 

 

<1> PMID: 15037862

Journal Article. Research Support, Non-U.S. Gov't. Research Support, U.S. Gov't, Non-P.H.S.. Research Support, U.S. Gov't, P.H.S.. Review.

Spinal Cord. 42(7):383-95, 2004 Jul.

Spinal shock revisited: a four-phase model.[see comment]. [Review] [156 refs]

<2> PMID: 10762496

Clinical Trial. Journal Article. Research Support, Non-U.S. Gov't.

Neurology. 54(8):1574-82, 2000 Apr 25.

From spinal shock to spasticity: neuronal adaptations to a spinal cord injury.

<3> PMID: 8637263

Journal Article. Review.

Mayo Clinic Proceedings. 71(4):384-9, 1996 Apr.

Spinal shock. [Review] [79 refs]

 

 

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<1>

Unique Identifier [PMID]: 15037862

Authors: Ditunno JF. Little JW. Tessler A. Burns AS.

Institution: Department of Rehabilitation Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA.

Title: Spinal shock revisited: a four-phase model.[see comment]. [Review] [156 refs]

 

Source: Spinal Cord. 42(7):383-95, 2004 Jul.

Abstract: Spinal shock has been of interest to clinicians for over two centuries. Advances in our understanding of both the neurophysiology of the spinal cord and neuroplasticity following spinal cord injury have provided us with additional insight into the phenomena of spinal shock. In this review, we provide a historical background followed by a description of a novel four-phase model for understanding and describing spinal shock. Clinical implications of the model are discussed as well. [References: 156]

 

Publication Type: Journal Article. Research Support, Non-U.S. Gov't. Research Support, U.S. Gov't, Non-P.H.S.. Research Support, U.S. Gov't, P.H.S.. Review.
 

 

<2>

Unique Identifier [PMID]: 10762496

Authors: Hiersemenzel LP. Curt A. Dietz V.

Institution: Swiss Paraplegic Centre, University Hospital Balgrist, Zurich, Switzerland.

Title: From spinal shock to spasticity: neuronal adaptations to a spinal cord injury.

 

Source: Neurology. 54(8):1574-82, 2000 Apr 25.

Abstract: OBJECTIVE: To investigate the adaptational changes in excitability of spinal neuronal circuits below the level of lesion from spinal shock to spasticity in patients with spinal cord injury (SCI). METHODS: More than 6 months after an acute SCI, clinical follow-up examinations were paralleled by electrophysiologic recordings with tibial nerve stimulation (M-wave, F-wave, H-reflex, and flexor reflex). RESULTS: During spinal shock, the loss of tendon tap reflexes and flaccid muscle tone were associated with low persistence of F-waves and loss of flexor reflexes, whereas H-reflexes were already elicitable. During the transition to spasticity, the reappearance of tendon tap reflexes and muscle tone and the occurrence of spasms was associated with the recovery of F-waves and flexor reflex excitability, whereas the H-to-M ratio remained about stable over months. At later stages (2 to 6 months after SCI) when clinical signs of spasticity became established, the electrophysiologic measures showed little change. In paraplegic patients, in contrast to tetraplegic patients, M-wave and flexor reflex amplitudes even decreased. CONCLUSIONS: The late decrease in M-wave and flexor reflex amplitude in paraplegic patients suggests a secondary impairment/degeneration of premotoneuronal circuits and of motoneurons. The divergent course of clinical signs of spasticity and their probable neuronal correlates indicates the occurrence of non-neuronal changes contributing to spasticity.

Publication Type: Clinical Trial. Journal Article. Research Support, Non-U.S. Gov't.
 

 

<3>

Unique Identifier [PMID]: 8637263

Authors: Atkinson PP. Atkinson JL.

Institution: Department of Neurology, Mayo Clinic Rochester, MN 55905 USA.

Title: Spinal shock. [Review] [79 refs]

 

Source: Mayo Clinic Proceedings. 71(4):384-9, 1996 Apr.

Abstract: The term "spinal shock" applies to all phenomena surrounding physiologic or anatomic transection of the spinal cord that results in temporary loss or depression of all or most spinal reflex activity below the level of the injury. Hypotension due to loss of sympathetic tone is a possible complication, depending on the level of the lesion. The mechanism of injury that causes spinal shock is usually traumatic in origin and occurs immediately, but spinal shock has been described with mechanisms of injury that progress over several hours. Spinal cord reflex arcs immediately above the level of injury may also be severely depressed on the basis of the Schiff-Sherrington phenomenon. The end of the spinal shock phase of spinal cord injury is signaled by the return of elicitable abnormal cutaneospinal or muscle spindle reflex arcs. Autonomic reflex arcs involving relay to secondary ganglionic neurons outside the spinal cord may be variably affected during spinal shock, and their return after spinal shock abates is variable. The returning spinal cord reflex arcs below the level of injury are irrevocably altered and are the substrate on which rehabilitation efforts are based. [References: 79]

Publication Type: Journal Article. Review.

 

 

 

 

 

Resident Report / Department of Medicine & Grady Branch Library

Emory University School of Medicine

2007 Edition

Participating Faculty:  Carlos Del Rio MD  / Joyce Doyle MD / Lorenzo Difrancesco MD / Rachel Del Favero MD / Lewis Satterwhite  MD

Contact: Karl Woodworth 

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