spinal shock stages

Neurology 2000; 54: 1574–1582. Spinal Shock—Comparative Aspects and Clinical Relevance P.M. Smith and N.D. Jeffery Spinal shock is the loss of muscle tone and segmental spinal reflexes that develops caudal to a severe spinal cord injury. 1173185, Differences between Neurogenic Shock and Spinal Shock. Electroencephalogr din Neurophysiol 1977; 43: 160–167. Somatosensory evoked potentials and Hoffmann reflex in acute spinal cord lesions; physiopathological and prognostic aspects. Masliah E, Pagan AM, Terry RD, DeTeresa R, Mallory M, Gage FH . Cell 2002; 110: 223–235. New synapse growth by spinal reflex afferents mediating hyper-reflexia may occur initially via local axonal protein synthesis and local redistribution of axonal structural protein and then subsequently via somal protein synthesis with axonal transport of that protein. Denervation supersensitivity in partially denervated spinal neurons allows initial return of spinal reflexes by 1–3 days. Exp Neurol 1986; 93: 510–521. Spinal Cord 1998; 36: 744–749. Metab Brain Dis 1988; 3: 49–65. Adv Exp Med Biol 2002; 508: 219–226. King VR, Bradbury EJ, McMahon SB, Priestley JV . Prog Brain Res 2002; 137: 389–399. The DPR requires an unusually strong stimulus, in contrast to the Babinski sign or normal plantar response, and is elicited by stroking a blunt instrument upward from the heel toward the toes along the lateral sole of the foot and then continuing medially across the volar aspect of the metatarsal heads. Axon-length-dependent rate of synapse growth would also explain the late appearance of extensor spasms and also interspecies differences in late return of the tibial H-reflex. The study emphasizes the importance of the evolution of reflexes and the relationship of the delayed plantar response (DPR) to prognosis. Brain 1917; 40: 264–401. Voluntary movement is superimposed on this background excitation. Neurotrophin-3 enhances sprouting of corticospinal tract during development and after adult spinal cord lesion. Google Scholar. Functional Recovery in Neurological Disease. In most cases Physiopedia articles are a secondary source and so should not be used as references. The H-reflex latency also increases by 2–4 ms at 1–4 weeks and persists through the later reflex excitability increase at 3–4 months (Figure 1). Schwartzman RJ, Eidelberg E, Alexander GM, Yu J . Atkinson PP, Atkinson JL . The optimal timing likely differs between complete and incomplete SCI. Relationship of altered glutamate receptor subunit mRNA expression to acute cell loss after spinal cord contusion. Diagnosis and Management of Spinal Cord Emergencies. Holdsworth FW . Changes in truncated trkB and p75 receptor expression in the rat spinal cord following spinal cord hemisection and spinal cord hemisection plus neurotrophin treatment. In the initial spinal shock phase of injury, there is urinary retention and detrusor areflexia. Binder MD, Heckman CJ, Powers RK . Functional recovery can occur with sprouting and synapse formation from spared descending motor axons.110 This is accompanied by successful depolarization of lower motor neurons despite reduced numbers of descending motor axons. Synopsis of the Diastaltic Nervous System: or The System of the Spinal Marrow, and its Reflex Arcs; as the Nervous Agent in all the Functions of Ingestion and of Egestion in the Animal Oeconomy. Nat Neurosci 2001; 4 (Suppl): 1207–1214. Stage 4: Refractory Stage of Shock. Krenz NR, Weaver LC . In subjects with chronic incomplete SCI and hyper-reflexia, motor neurons are often either under voluntary control or under reflex control; thus, either one or the other input comes to dominate control over a given motor neuron. Goltz… (believes)…shock may persist for months, even years. The stages … J Neurophysiol 1998; 79: 392–409. Schadt JC, Barnes CD . Viewed as a model for reflex recovery, human tibial H-reflex undergoes sequential changes caudal to spinal cord transection: (1) areflexia due to motoneuron hyperpolarization, (2) reflex re-emergence by 1–3 days due to neuronal transcription–translation yielding denervation supersenshivity, (3) increased reflex excitability at 2–4 weeks and increased latency at 1–4 weeks via disynaptic interneuron or axon-supplied synapse growth, and (4) increased reflex excitability at 3–4 months via primary afferent or soma-supplied synapse growth with less presynaptic inhibition and less H-reflex depression with repetitive stimulation. Other mechanisms may also contribute to spinal shock. Benowitz LI, Goldberg DE, Irwin N . Cardiovascular abnormalities accompanying acute spinal cord injury in humans: incidence, time course and severity. J Neurophysiol 1984; 52: 435–448. J Spinal Cord Med 1996; 19: 215–224. Initial synapse growth allows place holding by long axons, which would otherwise not be able to compete with intrinsic spinal interneurons for vacant synaptic sites. Preserved descending input after incomplete SCI allows some recovery of function, perhaps by the same neuronal mechanisms of denervation supersensitivity and synapse growth that allow the transition from areflexia to hyper-reflexia.111, Both corticospinal inputs and IA afferents increase axon growth in response to the neurotrophin NT3.90, 112, 113, 114, 115, 116 NTs like NT3, promoting both IA afferent and corticospinal neurite growth, could underlie competitive synapse growth. Adv Neurol 1988; 47: 361–385; (review). Fouad K, Metz GA, Merkler D, Dietz V, Schwab ME . Receptor trafficking and the plasticity of excitatory synapses. ‘for about 20 minutes after…severance, neither by mechanical, thermal, nor electrical excitation of the skin innervated from below the point of severance, can any reflex movement at all be elicited’. Goldberger ME, Murray M . Change of vanilloid receptor 1 following neuromodulation in rats with spinal cord injury. In cats with spinal cord transection, the latest changes in cutaneomuscular hyper-reflexia also precede the latest changes in tibial H-reflex hyper-reflexia;55 again, this suggests earlier synapse growth in short-axoned spinal interneurons relaying cutaneomuscular reflexes than in long-axoned Ia afferents relaying the tibial H-reflex. Spinal cord transection produces a long-term increase in GABAB binding in the rat substantia gelatinosa. PubMed  Annu Rev Neurosci 2001; 24: 807–843. Weidner N, Ner A, Salimi N, Tuszynski MH . We present here a new paradigm for spinal shock consisting of four phases: (1) areflexia/hyporeflexia, (2) initial reflex return, (3) early hyper-reflexia, and (4) late hyper-reflexia. The second stage is the initial return of some of the reflexes. Zapata P . Schmidt BJ, Hochman S, MacLean JN . Guttmann L . Tremblay LE, Bedard PJ . Through a better understanding of the underlying mechanisms of spinal shock, we may be able to offer novel interventions that facilitate recovery.14. The physiologist Sherrington8 also recognized the potential for confusion in his description of ‘shock’ and distinguished between circulatory shock and spinal shock. Critical periods may be due to a transient period when many vacant synaptic sites are open to innervation by spared inputs. Skup M, Dwornik A, Macias M, Sulejczak D, Wiater M, Czarkowska-Bauch J . Sherrington CS . Stages of Spinal Shock • Stages: – Phase I (0‐1 day post‐injury): Flaccid paralysis with absent DTR’s. Culmsee C, Stumm RK, Schafer MK, Weihe E, Krieglstein J . Clinical implications of the model are discussed as well. Marked species differences (human, monkey, cat, rat) have been observed in the time-course of functional recovery after incomplete SCI, as well as in the full appearance of spinal hyper-reflexia after complete SCI.105, 111, 119, 155, 156 Traditionally, this was attributed to varying degrees of encephalization across species, but it may actually reflect the longer delay for soma-supported synapse growth in the human and monkey due to longer axons. The motor neuron surface and spinal shock. Chen XY, Wolpaw JR . Autoradiographic localization of substance P receptors in rat spinal cord: effects of experimental spinal transection. Sequential synapse formation mediated by axonal and then somal phases could result in increased H-reflex latency due to persisting slowed conduction in thinner, immature terminal branches. Burke D . Competitive synapse growth has important implications for the timing of interventions. Oxford University Press: New York, 1999. Thompson FJ, Reier PJ, Lucas CC, Parmer R . Following SCI, new synapses may be formed by spinal interneurons, spinal reflex afferents, and spared supraspinal inputs.17 The formation of new synapses could lead to both desirable and undesirable clinical effects. J Physiol (Lond) 2001; 533: 83–89; (Review) (48 refs). Zhang LI, Poo MM . Little JW, Halar EM . Arch Phys Med Rehabil 1991; 72: 408–412. Spinal cord control of movement: implications for locomotor rehabilitation following spinal cord injury. Orlovsky GN, Deliagina TG, Grillner S . Exp Neurol 1993; 123: 35–50. Trends Neurosci 2000; 23: 639–645. Functional desirable new synapse growth can then be reinforced and allowed to mature through soma-supported synapse growth. Evidence of fusimotor function in human spinal shock. Neural prostheses: clinical applications of functional electrical stimulation in spinal cord injury. Acta Physiol Lat Am 1966; 16: 266–277. An additional advantage of the second theory is that an axon phase of synapse growth might serve a place-holding function, allowing the long-axoned neurons to, at least partially, compete with short-axoned neurons. Recovery of voluntary function below incomplete SCI is probably enhanced by activity in both animals119 and humans.120 Exercise can increase NT synthesis in neurons of the spinal cord (BDNF, NT-4)121 and could be the molecular signal for such activity-dependent recovery. Brain Res 2000; 880: 183–186. Ann N Y Acad Sci 1998; 860: 189–202. Leis AA, Zhou HH, Mehta M, Harkey III HL, Paske WC . A recent article by Ditunno et al 3 describes spinal shock and the stages of reflexic recovery. Beattie MS, Leedy MG, Bresnahan JC . Neuron 2002; 35: 1043–1056. Exp Neurol 2001; 168: 283–289. This might also aid selective synapse growth by desired axon populations as specific NTs work on different groups of axons.151 During the recovery period, clinicians must also strive to optimize conditions for new synapse growth, which includes optimizing nutrition, optimizing general health, and minimizing medication use that may compromise synapse growth.152, In contrast to promoting synapse formation by descending motor pathways, an alternative approach is to inhibit synapse growth by segmental reflex inputs. J Neurosci 1997; 17: 5560–5572. Neuroscience 1998; 85: 443–458. Clinicians may need to ‘destabilize’ newly grown synapses by intrinsic spinal neurons to allow regenerating descending axons to establish new synapses.11 This might be accomplished by using botulinum toxin or alcohol injected intramuscularly for ‘somatic stripping’ of synapses on motor neuron soma.154 NT administration or in vivo synthesis may then be required to assure synapse formation by the regenerated axons. Spinal Shock. Neurorehabil Neural Repair 1999; 13: 157–165. Proc Natl Acad Sci USA 2001; 98: 3513–3518. Exp Neurol 1995; 132: 186–193. Also known as spinal shock syndrome, spinal shock is the loss of muscle tone and spinal reflexes below the level of a severe spinal cord lesion[1]. Stage 2 of Spinal Shock: This stage occurs over the next two days and there is gradual return of some of the reflexes below the spinal cord injury. Thus, the absence of all reflexes is uncommonly observed during the initial 24 h if a careful neurological examination is performed.7 A pathologic reflex, the DPR, is usually the first reflex to return and can be observed within hours of injury.7 In most cases, it is transient and disappears within several weeks. Enhanced neocortical neural sprouting, synaptogenesis, and behavioral recovery with D-amphetamine therapy after neocortical infarction in rats. Early locomotor training with clonidine in spinal cats. ‘After the brief interval certain skin reflexes begin to appear; almost always earliest is the adduction-flexion of the hallux, elicitable by stimuli applied to the 3rd, 4th, or 5th digits (plantar surface or sides), or to the skin of the sole, especially on the fibular side’. J Comp Neurol 1974; 158: 19–36. Constable & Company LTD: London, 1906. Velocity-dependent ankle torque in rats after contusion injury of the midthoracic spinal cord: time course. Cadilhac J, Georgesco M, Benezech J, Duday H, Dapres G . Definition. Top Contributors - Cindy John-Chu, Vidya Acharya and Kim Jackson. Segmental reflex pathways in spinal shock and spinal spasticity in man. Little JW, Ditunno Jr JF, Stiens SA, Harris RM . Mendell LM, Munson JB, Arvanian VL . Functional capacity of the isolated human spinal cord. 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. They stated that it develops within 1–6 h following severing of the spinal cord. Sequential mRNA expression for immediate early genes, cytokines, and neurotrophins in spinal cord injury. Below a spinal cord lesion, synaptic endings from axotomized neurons to spinal motor neurons and interneurons degenerate over days and are then replaced by terminal sprouting from neurons below the lesion over weeks to months.16, 17, 31, 84 Replacement synaptic growth may originate from both spinal interneurons and from primary segmental afferents.16, 17, 85, 86, 87 A postulated signal for new synaptic growth is the increase in NTs caudal to a SCI. Neuron 2001; 32: 1013–1026. Wernig A, Muller S, Nanassy A, Cagol E . Winslow EB, Lesch M, Talano JV, Meyer Jr PR . Spinal Stenosis. Article  Brittis PA, Lu Q, Flanagan JG . In complete injuries, the BC can occur simultaneously (16/31) with the DPR, but it often lags behind and may not be evident for several days. Nakamura M, Bregman BS . Hand weakness or numbness can get bad … Exp Neurol 2001; 169: 255–263. Grossman SD, Rosenberg LJ, Wrathall JR . Neurogenic shock (from a broken spinal cord and often called spinal shock) is a rare cause of distributive shock, but has a very distinct pattern of symptoms: ow blood pressure is an early sign (unlike other forms of shock) Hall2 later introduced the term ‘shock’ in 1841: If, in a frog, spinal marrow (cord) be divided… for a very short time no diastolic actions (reflexes) in the extremities (are present, then) the diastolic actions (reflexes) speedily return. Bradyarrhythmias, atrioventricular conduction block, and hypotension occur following cervical lesions due to impaired sympathetic innervation in the setting of preserved cranial nerve (vagus) mediated parasympathetic function. With recovery of reflex function, one of several voiding patterns may develop. CAS  J Neurophysiol 1992; 68: 1473–1486. Injuries to the Spine and Spinal Cord. PubMed  Retrograde signaling in the development and modification of synapses. Cord transection may reduce normal descending inhibition to spinal inhibitory pathways, which could then contribute to the depression of spinal reflexes.28 Later, metabolic or structural changes in spinal neurons could contribute to reflex depression.29, 30 Dendrites of spinal cord neurons retract and many synapses degenerate within 1–3 days following SCI.31, 32 Dendrite retraction and synapse loss in the isolated caudal cord likely reflects impaired release and uptake of neurotrophins and growth factors in hypoactive spinal neurons.31, 32 The hyporeflexia of spinal shock, however, appears immediately after SCI. Spinal shock, first described by Whytt in 1750, is a temporary loss of all neurological activity including motor, sensory and reflex activity below the level of the spinal cord lesion that can occur immediately following the onset of an acute spinal cord injury. The DPR has disappeared in the majority of cases. Serotonergic (5-HT) neurons of the raphe nucleus and noradrenergic (NE) neurons from the locus coeruleus may contribute much of this basal excitatory input.19, 20 5-HT and NE act on spinal motor neurons yielding plateau potentials, which may amplify excitatory inputs including reflex inputs.21, 22, 23 Plateau potentials originate on dendrites and amplify excitatory inputs up to six-fold, thus leading to sustained firing with minimal excitatory input.24 This effect may be due to prolonged activation of Ca2+ channels. Little JW, Harris RM, Lerner SJ . Locomotor capacity attributable to step training versus spontaneous recovery after spinalization in adult cats. Such training may be enhanced by medications such as the noradrenergic α-2-agonist clonidine.138, 139, Functional electrical stimulation is an alternative method for stimulating specific synapses and neuron pools, therefore influencing spinal cord plasticity and performance.140, 141, 142 Additional interventions that might enhance synapse formation by spared descending inputs include medications to increase excitability of spinal neurons (eg 5-HTP, clonidine, TRH, and theophylline),54, 143, 144, 145 stimulants of axon growth (eg inosine),146 stimulants of NT synthesis (eg clenbuterol),147, 148 inhibitors of Nogo and related myelin glycoproteins that block longer-distance axon sprouting,149 and agents that block the intracellular Rho pathway, which inhibits axon growth.150 Adding these interventions in combination with exercise therapies might have a synergistic effect on activity-dependent synapse growth. Monosynaptic and oligosynaptic contributions to human ankle jerk and H-reflex. Eur J Neurosci 1995; 7: 823–829. The proposed model of spinal shock suggests several questions for clinician investigators: Can a quantitative clinical study of spinal reflexes from day 0 to day 365 post-SCI reveal more details of the underlying neuronal mechanisms, similar to Ko et al7 but relying on quantitative measures? Retention of hindlimb stepping ability in adult spinal cats after the cessation of step training. Behav Neurosci 1987; 101: 179–186. Hiersemenzel LP, Curt A, Dietz V . Brain Res 1998; 797: 234–242. Illis LS . This space allows for processes such as bleeding, neoplasm and infection to reach an advanced stage before neurologic sequelae are noted. Basura GJ, Nantwi KD, Goshgarian HG . Spinal shock revisited: a four-phase model. Stage I: Less Responsive Spinal Nerve Cells. Sampson EE, Burnham RS, Andrews BJ . J Neurophysiol 1999; 81: 85–94. Zhang B, Goldberger ME, Wu LF, Murray M . Fitzsimonds RM, Poo MM . Over time, symptoms are likely to become more noticeable and could include one or more of the following: Weakness or numbness. Most DTRs first reappear during this period,7 and they are evident in almost all subjects within 30 days. Mechanisms causing plateau potentials in spinal motoneurones. Little JW . H-reflex and M-response amplitudes were recorded at measured sites over the soleus muscle. Chancellor MB Personal communication, 2002. Stage 3 & 4 of Spinal Shock: In this stage, patient has abnormally strong or increased reflexes (hyperreflexia), which are … Lehmann KG, Lane JG, Piepmeier JM, Batsford WP . During this period, cutaneous (polysynaptic) reflexes such as the BC, the AW, and the CM begin to recover. In complete SCI, any regenerating axons of descending motor pathways are at a disadvantage due to axon length. Llewellyn-Smith IJ, Weaver LC . Activity-dependent learning contributes to motor recovery. Maffiuletti NA, Martin A, Babault N, Pensini M, Lucas B, Schieppati M . Synapse 1993; 14: 263–267. It is an age-related condition of narrowing of the opening of the spinal canal. A review of the clinical literature fails to reveal any reported documentation of the course of recovery of detrusor paralysis; however, most clinicians would estimate the time of bladder recovery determined by cystometrogram to be 4–6 weeks.80 Reports from acute care settings show that vasovagal hypotension and bradyarrhythmias resolve in 3–6 weeks.81, 82 Orthostatic hypotension as a result of standing a tetraplegia subject, however, may persist for 10–12 weeks or longer.83 In contrast, the malignant hypertension of autonomic dysreflexia develops by weeks to months and persists indefinitely. Exp Neurol 1975; 46: 605–615. Electrical activity and development of neural circuits. Cellular delivery of neurotrophin-3 promotes corticospinal axonal growth and partial functional recovery after spinal cord injury. Little JW, Harris RM, Smithson D . Patterns of sprouting and implications for recovery of function. Preshock (nonprogressive phase, stage of compensation): activation of compensatory neurohumoral reflexes in order to maintain vital organ perfusion. Low spinal cord transection at S2 in rat yields an areflexic tail that persists for 2 weeks; the tail then gradually becomes hyper-reflexic to both stretch and cutaneous stimuli.108 Spinal motoneurons below a transection show low-threshold, prolonged, self-sustained motor-unit firing (minutes to hours) in association with hyper-reflexia; this hyperexcitable motoneuron behavior is present by 30 days after cord transection in rats but not at 2 days.23, 108 The late appearance of plateau potentials below SCI is proposed as a factor in late developing hyper-reflexia. Its hallmark is the transient suppression and gradual return of reflex activity caudal to SCI. Neuroscience 2001; 104: 513–521. J Spinal Cord Med 1995; 18: 42–46. Arch Neurol 1963; 9: 127–132. Eur J Pharmacol 1994; 264: 249–257. Nacimiento W, Noth J . Exp Neural 1999; 159: 267–273. Neurogenic shock is different from spinal shock in that spinal shock is often temporary and will last for a day or two, where there is loss of sensory and motor tone, which is also temporary. Demonstrated only in settings of severe spinal cord injury occurring during relative brief period. PubMed Central  When refering to evidence in academic writing, you should always try to reference the primary (original) source. The role of activity blockade on glutamate receptor subunit expression in the spinal cord. J Neurosci Res 1997; 50: 1023–1029. Stages of shock. Feraboli-Lohnherr D, Barthe JY, Orsal D . It can affect the lower back regions and extend to limbs as well as head and neck, producing pain with electric shock feelings. For incomplete SCI, with significant axonal sparing, descending motor axons are present to compete with segmental reflex inputs. Spasticity in rats with sacral spinal cord injury. NMDA receptor-mediated oscillatory properties: potential role in rhythm generation in the mammalian spinal cord. The first stage is usually hyporeflexia, which is the partial or full loss of spinal cord reflexes. Spinal shock manifests as distal areflexia of a transient nature that may last from a few hours to weeks. Spinal Cord 1999; 37: 402–409. Although the H-reflex and Achilles tendon reflex are traditionally considered monosynaptic reflexes, Burke et al92 suggest that disynaptic input contributes as well. Selective increases in some factors and receptors are seen in both neurons and glia.58, 59, 60, 61, 62, 63 The signal that triggers increased expression of NTs, GFs, and NT-Rs and GF-Rs is unknown,64 but lipopolysaccharides from degenerating axons or cytokine release by glia are candidates, as is spinal neuron inactivity.65. An axon-length-dependent rate of synapse growth would explain the two phases of increased H-reflex excitability at 2–4 weeks and at 3–4 months. Guillain G, Barre JA . J Neurotrauma 2000; 17: 203–218. Sherrington1, 8 felt that ‘noci-ceptive’ (polysynaptic) reflexes were depressed for a shorter duration than monosynaptic DTRs. A quantitative analysis of the response of presynaptic boutons to postsynaptic motor neuron axotomy. Jones LL, Oudega M, Bunge MB, Tuszynski MH . Bennett DJ, Gorassini M, Fouad K, Sanelli L, Han Y, Cheng J . Synapse growth by reflex afferents may interfere with synapse growth by descending motor pathways. Ann Neurol 1983; 14: 33–37. Spinal Shock is acute transient stage of spinal cord lesion resulting in flaccid paralysis below the level of injury, with muscular hypotonia and loss of deep tendon and superficial reflexes. Interlimb reflexes and synaptic plasticity become evident months after human spinal cord injury. J Neurotrauma 1998; 15: 451–457. If reversal of symptoms does not occur within 24hrs, it may call for protracted recovery time and lengthened stay in rehabilitation[4]. Differences in H-reflex between athletes trained for explosive contractions and non-trained subjects. https://www.physio-pedia.com/index.php?title=Spinal_Shock&oldid=264539, Defined as systolic blood pressure less than 100 mm Hg with a, Consequent to SCI with associated autonomic dysregulation, Common with cord injuries above T6 level. The stages of shock. J Neurophysiol 1997; 77: 797–811. He also used the term ‘reflex arc’ to describe reflexes.2 Hall was therefore the first to use both the terms ‘spinal shock’ and ‘reflex arc’ and to link the two phenomena.3. In comparison to somal-mediated growth, some synapse growth originates from protein synthesis in axon terminals – a ‘distributed sprouting program’.95, 96, 97 Growth cones have 500–1000 ribosomes that provide a low basal level of protein synthesis, but which yield a marked increase in local protein synthesis in response to NTs. These training effects are similar to the effects of operant conditioning in rats, monkeys, and humans, in which H-reflex amplitude can be increased or decreased over a period of days and weeks.11 Reflex excitability below a SCI may therefore be affected by pre-SCI experience,77, 78 causing AJ to return later in a ballet dancer with low tendon reflex excitability than in an untrained individual. Altered patterns of reflex excitability subsequent to contusion injury of the rat spinal cord. Burke D, Gandevia SC, McKeon B . Changes in NMDA receptor subunit expression in response to contusive spinal cord injury. Lecture on Stages of Shock Shock Stages Nursing NCLEX: Initial, Compensatory, Progressive, Refractory In: Rowell LB, Sheperd JT (eds.) Hulsebosch CE. Of note, human S1 primary afferents have axon lengths of roughly 150 mm versus spinal interneurons with axon lengths of roughly 15 mm. Ditunno et al (2004)[11] proposed a four-phase model of the syndrome. Depressed spinal reflexes caudal to spinal cord injury (SCI), defined as spinal shock, have intrigued clinicians and researchers for more than two centuries. Abnormal reflexes may be present. Spitzer NC . Exp Neurol 2001; 169: 407–415. Muresan V . Axon-length-dependent rate of late synapse growth may also explain markedly differing late reflex changes across species and across differing spinal reflexes. Arch Phys Med Rehabil 1985; 66: 19–22. J Neurotrauma 2002; 19: 1231–1249. This would be compatible with the theory of competitive synapse growth underlying functional recovery and hyper-reflexia.111 The quality of functional recovery would depend largely on the variety and number of descending motor axons spared. Goshgarian HG, Yu XJ, Rafols JA . II. Lovely RG, Gregor RJ, Roy RR, Edgerton VR . From spinal shock to spasticity: neuronal adaptations to a spinal cord injury. – Phase III (4 days –1 month post‐injury): Early hyper‐ J Neurotrauma 1999; 16: 69–84. Exp Brain Res 2000; 133: 233–241. Stimulation of the bronchi by aggressive suctioning of secretions can result in bradyarrhythmias or conduction block. Illis14 suggests spinal shock cannot be adequately described unless it is divided into phases: ‘the first phase of spinal shock (depression of reflexes)… withdrawal of impulses from descending tracts… (is not) acceptable unless it includes the second phase…return of reflexes in an altered form’. With the exponential growth in new knowledge regarding postinjury spinal cord physiology comes an increased understanding of this complex clinical process. The fourth phase of spinal shock occurs between 1 and 6 months postinjury. One axon, many kinesins: What's the logic? Other receptors (ie serotonin 2A, vanilloid VR1) also increase in density by 1–3 days caudal to spinal cord transection.53, 54 Such transcriptional/translational increases in neurotransmitter receptors could explain the initial re-emergence of reflexes. Rho signaling pathway targeted to promote spinal cord repair. Riddoch G . Neurotrophin-3-mediated regeneration and recovery of proprioception following dorsal rhizotomy. Google Scholar. Chemotropic responses of retinal growth cones mediated by rapid local protein synthesis and degradation. Reeves TM, Smith DC . Article  Phys Ther 2000; 80: 477–484. Before we get into the nitty-gritty, let’s talk about the stages of shock. Raven Press: New York, 1988, pp 401–423. Clenbuterol, a beta(2)-adrenoceptor agonist, improves locomotor and histological outcomes after spinal cord contusion in rats. The role of glycine in spinal shock. Kapfhammer JP . Stage of Spinal Shock or Areflexia. PubMed Google Scholar. This is assumed to be the result of a conduction block … J Neurol Neurosurg Psychiatry 1974; 37: 1352–1360. Med Sports Sci 1992; 36: 234–246. The cremasteric reflex is seen in approximately 1/3 of subjects (6/20) in the initial phase.

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