Spinal shock revisited: a four-phase model

Ditunno, John F.; Little, James W.; Tessler, Alan; Burns, Anthony S.

doi:10.1038/sj.sc.3101603

Cited by 382 publications

(275 citation statements)

References 146 publications

(180 reference statements)

Supporting

Mentioning

256

Contrasting

Unclassified

Order By: Relevance

“…Hall observed similar aspects in patients who suffered spinal cord (paraplegia) and brain (hemiplegia) lesions he examined clinically 1,2 . This notion of (neural) shock was accepted and further extended to the brain.…”

Section: On Shock and Beyondmentioning

confidence: 65%

Shock, diaschisis and von Monakow

Engelhardt

Gomes²

2013

Arq. Neuro-Psiquiatr.

View full text Add to dashboard Cite

The concept of shock apparently emerged in the middle of the 18th century (Whyett) as an occurrence observed experimentally after spinal cord transection, and identified as "shock" phenomenon one century later (Hall). The concept was extended (Brown-Séquard) and it was suggested that brain lesions caused functional rupture in regions distant from the injured one ("action à distance"). The term "diaschisis" (von Monakow), proposed as a new modality of shock, had its concept broadened, underpinned by observations of patients, aiming at distinguishing between symptoms of focal brain lesions and transitory effects they produced, attributable to depression of distant parts of the brain connected to the injured area. Presently, diaschisis is related mainly to cerebrovascular lesions and classified according to the connection fibers involved, as proposed by von Monakow. Depression of metabolism and blood flow in regions anatomically separated, but related by connections with the lesion, allows observing diaschisis with neuroimaging.

show abstract

Section: On Shock and Beyondmentioning

confidence: 65%

Shock, diaschisis and von Monakow

Engelhardt

Gomes²

2013

Arq. Neuro-Psiquiatr.

View full text Add to dashboard Cite

show abstract

“…Soon after the injury (hours to days) there is a transient state of hypoexcitability of the isolated spinal cord, known as 'spinal shock', which is associated with flaccid paralysis of the muscles and absent tendon reflexes, in addition to impairment of spinal autonomic function. 19 Coincident with spinal shock there is dilatation of the blood vessels, particularly those in the skin, which (combined with impaired autonomic reflexes) often results in profound hypotension, and is termed 'neurogenic shock'. 20,21 Over time (days to weeks) the spinal shock resolves, but SCI patients are frequently troubled with sudden falls in blood pressure upon postural change, or following prolonged periods of sitting (orthostatic hypotension) characterised by dizziness, lightheadedness or even syncopal events.…”

Section: Physiology and Neuroanatomy Of Cardiovascular Controlmentioning

confidence: 99%

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

2005

View full text Add to dashboard Cite

Motor and sensory deficits are well-known consequences of spinal cord injury (SCI). During the last decade, a significant number of experimental and clinical studies have focused on the investigation of autonomic dysfunction and cardiovascular control following SCI. Numerous clinical reports have suggested that unstable blood pressure control in individuals with SCI could be responsible for their increased cardiovascular mortality. The aim of this review is to outline the incidence and pathophysiological mechanisms underlying the orthostatic hypotension that commonly occurs following SCI. We describe the clinical abnormalities of blood pressure control following SCI, with particular emphasis upon orthostatic hypotension. Possible mechanisms underlying orthostatic hypotension in SCI, such as changes in sympathetic activity, altered baroreflex function, the lack of skeletal muscle pumping activity, cardiovascular deconditioning and altered salt and water balance will be discussed. Possible alterations in cerebral autoregulation following SCI, and the impact of these changes upon cerebral perfusion are also examined. Finally, the management of orthostatic hypotension will be considered.

show abstract

“…After both human and experimental SCI, the initial trauma leads to an instantaneous, often complete, neurological deficit below the injury level. The initial flaccid paralysis and subsequent return of reflexes observed in the hours and days after SCI are collectively referred to clinically as ''spinal shock'' (Ditunno et al, 2004). Axons that remain intact immediately after the trauma are unable to conduct action potentials until the delicate microenvironment and axonal membrane potentials are restored.…”

Section: Introductionmentioning

confidence: 99%

Diffusion Tensor Imaging at 3 Hours after Traumatic Spinal Cord Injury Predicts Long-Term Locomotor Recovery

Kim

Loy

Wang

et al. 2010

Journal of Neurotrauma

View full text Add to dashboard Cite

Accurate diagnosis of spinal cord injury (SCI) severity must be achieved before highly aggressive experimental therapies can be tested responsibly in the early phases after trauma. These studies demonstrate for the first time that axial diffusivity (ljj), derived from diffusion tensor imaging (DTI) within 3 h after SCI, accurately predicts long-term locomotor behavioral recovery in mice. Female C57BL=6 mice underwent sham laminectomy or graded contusive spinal cord injuries at the T9 vertebral level (5 groups, n ¼ 8 for each group). In-vivo DTI examinations were performed immediately after SCI. Longitudinal measurements of hindlimb locomotor recovery were obtained using the Basso mouse scale (BMS). Injured and spared regions of ventrolateral white matter (VLWM) were reliably separated in the hyperacute phase by threshold segmentation. Measurements of ljj were compared with histology in the hyperacute phase and 14 days after injury. The spared normal VLWM determined by hyperacute ljj and 14-day histology correlated well (r ¼ 0.95). A strong correlation between hindlimb locomotor function recovery and ljj-determined spared normal VLWM was also observed. The odds of significant locomotor recovery increased by 18% with each 1% increase in normal VLWM measured in the hyperacute phase (odds ratio ¼ 1.18, p ¼ 0.037). The capability of measuring subclinical changes in spinal cord physiology and murine genetic advantages offer an early window into the basic mechanisms of SCI that was not previously possible. Although significant obstacles must still be overcome to derive similar data in human patients, the path to clinical translation is foreseeable and achievable.

show abstract

Spinal shock revisited: a four-phase model

Cited by 382 publications

References 146 publications

Shock, diaschisis and von Monakow

Shock, diaschisis and von Monakow

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

Diffusion Tensor Imaging at 3 Hours after Traumatic Spinal Cord Injury Predicts Long-Term Locomotor Recovery

Contact Info

Product

Resources

About