SPINAL SHOCK

SPINAL SHOCKDR. SUMIT KAMBLESENIOR RESIDENT DEPT. OF NEUROLOGYGMC, KOTA

Spinal shock phenomena surrounding physiologic or anatomic transaction of the spinal cord that results in temporary loss or depression of all or most spinal reflex activity below the level of the lesion.

Demonstrated only in settings of severe spinal cord injury occurring during relative brief period.

HISTORY1750-Whytt first described phenomenon.1841- Hall introduced term spinal shock.1890- Bastian defined it as complete severance of the spinal cord that results in total loss of motor and sensory function below the level of the lesion, as well as permanent extinction of tendon reflexes and muscular tone despite the reflex arc remaining intact.Sherrington- 1. Replaced Bastian's use of the term "permanent" with temporary extinction. 2. Polysynaptic reflexes are depressed for shorter duration than monosynaptic.

PATHOPHYSIOLOGIC CHARACTERISTICS OF SPINAL SHOCKSpinal shock may occur up to several hours after the onset of injury.More severe the physiologic or anatomic transection of the spinal cord, the more profound the state of spinal shock.Isolated spinal cord closest to the disruption is the most severely affected-loss of reflex function occurs.Spinal cord segment most distal to the transection may be depressed later.

Farther it is from the site of injury, more likely it will retain some reflex capabilities.Patients with high-level cervical spinal cord injuries are likely to retain distal sacral reflexes such as bulbocavernosus and anal wink despite loss of all other reflexes.Lower the spinal cord injury, more likely that all distal reflexes will be absent.Reflex arcs at the level of spinal cord injury may remain permanently absent if portions or all of the arc components are permanently injured.

Proximal spinal cord may also undergoes changes, and these cephalad effects are known as Schiff Sherrington phenomenon.Transient loss of upper extremity reflexes with upper thoracic spinal cord lesions may be seen.Usually abates after a few hours or days.Tran section of the spinal cord as low as the third lumbar segment affects the excitability of the forelimbs.

DURATION OF SPINAL SHOCKDuration of spinal shock is proportionate to the degree of encephalization in the various species.In frogs and rats it lasts for minutes; in dogs and cats it lasts for 1 to 2 h; in monkeys it lasts for days; and in humans it usually lasts for a minimum of 2 wk. It may be prolonged because of toxic or septic conditions such as urinary tract infections or pressure sores and malnutrition.

Depends on age of the pateint.Higher or proximal the SCI lesion, shorter is the spinal shock duration.Muscle spindle reflexes always return except at vertical spinal cord injury levels, and they generally return in a caudal to cephalad direction.

PROGNOSTIC SIGNIFICANCE-Spinal cord injury with concomitant spinal shock usually has a worse associated prognosis than does the same degree of spinal cord injury without spinal shock. Patients with equivalent degrees of spinal cord injury and spinal shock may do somewhat better if they have early resumption of reflex spinal cord function.

CHARACTERISTIC OF SPINAL SHOCKMotor Effects Paraplegia ,QuadriplegiaLoss of tone -Muscles become flaccidAreflexia - All superficial and deep reflexes are lostSensory Effects -All Sensations are lost below the level of transection Complete lesions above T1 will eliminate all sympathetic outflow.Lesions between T1 and T6 will preserve sympathetic tone in head and upper extremities but deny it to the adrenals and lower extremities.Lesions between T6 and the lumbar cord will preserve adrenal innervation but denervate the lower extremities.

PHASES OF SPINAL SHOCKPHASEPOSSIBLE MECHANISMPhase 1 (0-1 days)Areflexia/ hyporeflexiaLoss of descending facilitationPhase 2(1-3 days)Initial reflex returnDenervation supersensitivityPhase 3 (1-4 weeks)Initial hyper-reflexiaAxon supported synapse growthPhase 4 (1-12 months)Final hyper-reflexiaSoma supported synapse growth

PHASE 1-AREFLEXIA/HYPOREFLEXIA( 0-1DAY) CLINICAL DESCRIPTION-Caudal to SCI, DTRs such as AJ and KJ are absent.Muscles are flaccid and paralysed.Cutaneous ( polysynaptic) reflexes such as BC, AW, and CM begin to recover.Pathological reflex DPR is usually first reflex to return (hours of injury) - TransientBradyarrhythmias, AV block, and hypotension occurs following cervical lessions due to impaired sympathetic innervation.

PHYSIOLOGY-Lost normal background supraspinal excitation.Increased spinal inhibitionLost plateau potentials in spinal neurons due to 5HT loss.Reduced neuronal metabolism. Retraction of dendrites and synapses.

PHASE 2-INITIAL REFLEX RETURN (1-3 DAYS) CLINICAL DESCRIPTION-Cutaneous reflexes becomes stronger.DTRs are still absent, although tibial H-reflex returns by about 24 h.In eldarly DTRs and Babinski sign can appear.

PHYSIOLOGY-Denervation supersensitivity-NMDA receptor upregulation.Inactivity dependent receptor upregulationNT and GF synthesis increases.

Denervation supersensitivity- Supersensitivity to neurotransimitters(a) reduced excitory neurotransmitter reuptake, (b)increased synthesis and insertion of receptors into postsynaptic membrane,(c) decreased removal and degradation of receptors (d) altered synthesis and composition of recepotor subunits.

PHASE 3-EARLY HYPER-REFLEXIA (4 TO 30 DAYS) CLINICAL DESCRIPTON-Most DTRs first reappear during this period, AJ usually precedes KJ.Babinski sign follows recovery of AJ closely. Skeleton muscle tone than recovers slowely after 3-4 weeks.Only in 10% DPRs persists beyond a month.Improvement in vagally mediated bradyarrhythmias and hypotension.Autonomic dysreflexia begin to emerge.

PHYSIOLOGY-New synapse growth to occupy vacated synaptic sites.NT retrogrades signal to elicit synapse growth.Competitive and activity dependent synapse growth.Most synapse growth by short axoned interneuronsLimited synapse growth by long axoned neurons.Plateau potentials , possibly via Ca channel synthesis in spinal neurons.

PHASE 4- SPASTICITY/HYPERREFLEXIA (1-12 MONTHS) CLINICAL DESCRIPTION-DPR disappear in majority cases.Cutaneous reflexes, DTRs and Babinski sign become hyperactive and responds to minimal stimuli.Mass reflex can be elicited in some casesTime of bladder recovery ( 4-6 weeks).Vasovagal hypotension and bradyarrhythmias resolves by 3-6 weeks.Orthostatic hypotension may persists for 10-12 weeks or longer.Autonomic dysreflexia may persists indefinately.

AUTONOMIC DYSREFLEXIA-Characterized by acute elevation in BP coupled with bradycardia/ tachycardia.Usually occurs with injury at and above T6.Symptoms vary from mild headache, blurred vision to life threatening intracranial /subarachnoid hemorrhage, retinal detachment and death.Vasoconstriction from sympathetic activation-dry, pale skin below lesion.Parasympathetic response responsible for sweating, piloerection and flushing above level of injury.

Management-Monitoring heart rate and BP.Patient should be placed in supine position.Inspected for areas of constriction.Relieving bladder and bowel distension.Fast acting antihyertensive- nifedipine, nitrates, captopril.

PHYSIOLOGY-New synapse growth by long axoned neuronsSoma supplied synapse growth via axon transport.Competitive and activity dependent synapse growth.

TIME COURSE AND PATTERN OF REFLEX RECOVERY0-1 day1-3 days1-4 weeks1-12 monthsDPR+++++++/-+/-BC reflex+/-++++++AW reflex+/-++++++CM reflex+/-++++++Babinski sign-+++++Flexor withdrawal reflex-+/-+++++DTR-+/-+++++Tibial H- reflex-+++++++Extensor spasm---+++Reflex neurogenic bladder---+++Autonomic hyperreflexia---+++

PROGNOSTIC FACTORS OF NEUROLOGICAL RECOVERY

Good prognostic factor1.Spinal shock of 1 week, 3.Flexor spasms within three weeks 4. Bedsore within one week5. Persistance of DPR beyond 7 days.

CLINICAL IMPLICATIONS OF SPINAL SHOCKFormation of new synapses could lead to both desirable and undesirable clinical effects.With significant sparing of descending motor inputs, descending axons can sprout, resulting in motor recovery.With minimal sparing, growth of segmental reflexes inputs leads to spasticity, neuropathic pain and less voluntary motor recovery.

During recovery optimized conditions must be provided for new synapse growth-1. Nutrition2. Optimal general health3. Minimizing medication use compromising new synapse growth4. coordinating active exercise and functional training to enhance the underlying synapse growth5.controlling interfering spasticity

Selected activity and electric activation may lead to selected desired synaptic growth.Exercise can increase NT synthesis and could be molecular signal for activity dependant recovery.Functional electrical stimulation is alternative tool.

Additional intervention to enhance synapse formation-1. Medications to increase excitability of spinal neurons (5-HTP, clonidine, TRH, Theophylline)2. Stimulants of axonal growth (inosine)3. Stimulants of axonal synthesis (clenbutorol)4. Inhibition of Glutamate Toxicity (dizocilpine)5.Cell Replacement Strategies

TIMING OF POTENTIAL INTERVENTIONS-Interventions targeted at promoting synapse growth should be applied before available synapse space is occupied by synapses from local segmental neurons mediating spasticity and hyperreflexia.

Spinal v/s neurogenic shockSpinal shockNeurogenic shockDefinitionImmediate temporary loss of total power, sensation and reflexes below the level of injurySudden loss of the sympathetic nervous system signalsBPHypotension Hypotension PulseBradycardiaBradycardiaBulbocavernosus reflexAbsentVariable Motor Flaccid paralysisVariableTime 48-72 hrs immediate after SCIMechanism Peripheral neurons become temporarily unresponsive to brain stimuliDisruption of autonomic pathways loss of sympathetic tone and vasodilation

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REFERENCESSpinal shock revisited: a four phase model International spinal cord society, march 2010Spinal shock review, Mayo clinic proc 1996Bradleys neurology in clinical practice, 6th edition