Spinal Cord II

Control of visceral function Lateral corticospinal tracts –Volitional control of breathing Lateral columns –Volitional control of micturition –Automatic control of Micturition Breathing Sweating Blood pressure

Urinary Bladder Dysfunction Depends on level and severity of injury With Spinal Shock –Areflexic bladder Acute urinary retention Lesion of cauda equina or S2 to S4 –Areflexic (paralytic) bladder continues Sacral parasympathetic motor neurons Afferent pathways Both

Spinal cord injury above level of sacral micturition reflexes –Hyperreflexic or spastic bladder usually develops –Loss of conscious awareness of bladder –Bladder capacity is decreased –Increased bladder pressure –Incomplete emptying –Urine retention

Increased risk of: –UTI –Urinary stone formation –Upper urinary tract degeneration

Causes of spinal cord injury that commonly produce urinary dysfunction SCI MS Tumors Tabes dorsalis due to syphilis

Genital Dysfunction Genital system –Spinal LMN (usually bilateral innervation) –Sensory afferents –Ascending and descending pathways (ALS) Spinal cord: lower lumbar and sacral –Lesion here Disrupt erection and ejaculation

Lesion above T12 –Psychogenic erections abolished –Reflexive erections may persist in LMN intact –Ejaculation occurs in only a small proportion of patients with significant spinal cord injury

Breathing Main Muscles –Diaphragm: C3-C5 –Intercostal: T1-T12 Assist with normal inspiration High volume expiration –Abdominal muscles: T6-T12 Assist with expiration

Accessory muscles –Sternocleidomastoid: C1-C3 –Scalenes: C4-C11 –Trapezius: C1-C4, CN XI

Effect of SCI on breathing Lumbar – little effect Thoracic –Impair cough, little effect on normal breathing Lower cervical –More effects on breathing C5 or higher –Affect diaphragm C3 or higher –Bilateral diaphragm paralysis –Require artificial ventilation

Voluntary breathing patterns Corticospinal tracts Lesion can block voluntary breathing, but automatic breathing can remain intact with discrete lesion

Automatic breathing Ventrolateral white matter Lesion – high cervical lesion –May stop breathing when asleep Sleep apnea

Classification of SCI

Etiology Complete vs. Incomplete Deficits Anatomical criteria

Complete Lesions Sensory and motor tracts in SC are disrupted Sensory and motor function severely disrupted below level of lesion Sensory systems –Radicular pain –Local vertebral pain –Segmental paresthesias

Motor Effects of a complete lesion Spinal shock –Areflexia –Flaccid paralysis After spinal shock resolves –Hypertonia –Hyperreflexia –Spasticity –Plantar extensor signs (Babinski sign)

At level of injury LMN signs –Paresis –Atrophy –Fasciculations –Areflexia

Autonomic dysfunction Spastic bladder Bowel constipation Anhidrosis – decreased sweating Trophic skin changes Impaired temperature control Vasomotor instability

Incomplete Injuries to the Spinal Cord Specific signs and symptoms depend on specific regions of white and gray matter that are lesioned Often include both segmental signs and vertical tract signs

Anterior Cord Syndrome Spinal Cord Losses –Anterior 2/3 rd of spinal cord Anterior horn (LMN) Corticospinal tracts Spinothalamic tracts Etiology –Ischemia (anterior spinal artery) –Infarction –Trauma Flexion type injury Acute traumatic disk herniation

Anterior Cord: Signs and Symptoms Losses below level of lesion –Motor control –Pain and temperature sensation Intact sensations –Discriminative touch –Vibration sense –Proprioception

Posterolateral Cord Syndrome Bilateral degeneration of dorsal and lateral columns Etiology –Subacute combined degeneration of SC Severe vitamin B12 deficiency AIDS Pernicious anemia –Chronic syphilis – Dorsal column syndrome

Posterior Column Syndrome: S & S Loss of fine touch, proprioception, and vibration sense Marked sensory ataxia causes by loss of proprioceptive pathways

Posterolateral Cord Syndrome: S&S Parathesias in feet Impaired vibration sense and proprioception in legs –Sensory ataxia Motor dysfunction –Spastic weakness –Hyperreflexia –Babinski’s signs Pain and temperature sensation intact

Central Cord Syndrome Lesion in central part of spinal cord –Lesion can expand Etiology –Severe hyperextension injury of neck –Tumor –Postradiation myelopathy –Infarction –Syringomyelia

Central cord S & S First region injured is usually the spinothalamic fibers as they cross the midline of the spinal cord –Bilateral loss of pain and temperature sensation at the level of the injury –Normal tactile sense Lesion also damages ventral horn –Usually upper extremity because injury is often in cervical cord Corticospinal fibers for UE are more medial and usually affected first In general, UE usually more involved than LE

Brown-Sequard Syndrome Lateral cord syndrome (hemisection) Etiology –Multiple sclerosis –Tumor –Syringomyelia –Penetrating wound of spinal cord

Brown-Sequard S & S At level of lesion, motor (LMN) and sensory lost ipsilateral Pain and temperature –Lost contralateral below lesion Discriminative touch, vibration, conscious proprioception –Lost ipsilateral below lesion Upper motor neuron –Ipsilateral below lesion

Etiology of SCI Inflammatory diseases Vascular disorders Tumors Trauma

Inflammatory disease (Myelitis) Usually microbial cause Transverse myelitis (SC alone) –Weakness and numbness of feet (less often the hands and arms) –Difficulty in emptying the bladder –Develop over several days –Symptoms usually remain stable, and then slowly improve

Vascular disorders Arterial obstruction or hemorrhage Dissecting arterial aneurysm Complication of vascular surgery Vascular malformations –Arteriovenous malformations When symptomatic usually produce slowly progressing signs of cord compression or ischemia Injury by general hypoxia/ischemia or hypotension (cardiac arrest or hemorrhage)

Tumors Less common than brain tumors –Most are benign and compress the cord Extradural metastasis are most common of all spinal tumors (lung, breast, prostate) Usual symptoms –Sensorimotor spinal tract symptoms – compression Asymmetric spastic Impaired pain and thermal sensation weakness Dorsal column signs – paresthesias Loss of voluntary bowel and bladder control –Radicular-spinal cord syndrome – includes radicular pain

Trauma 8-10,000 each year –MVA 50% –Falls 20% –Sports-related 14% –Gunshot or stab wounds 13% Gender and age –80% Male, 16 and 30 years old

SCI Trauma Most commonly at: –Cervical spine –Thoracolumbar junction

Mechanism of Injury Direct –With or without injury to vertebral column –Stab wounds, small penetrating missles Indirect –More common –Force directed to cord by way of vertebral column –Often injury to spine and spinal cord Can have fractures, dislocations or subluxations of the spine Often both direct and indirect –High-velocity missles, fracture/dislocations

Open vs. Closed injuries Depends on integrity of dura Open (penetrating) –Penetrating injury –Direct or sharp violence Closed (nonpenetrating) –Indirect or blunt trauma –More common type of injuries

Cervical spine More vulnerable to trauma (2/3 rd of injuries) –Exposure –Relatively poor mechanical stability –Weight of head Spinal canal is largest at C1/2 level, so there is some safety built in –About 75% of patients with C1-2 fractures have no neurological damage

Below C2, canal narrows –Most narrow between C4 and C6 Lower cervical cord or nerve root injuryusually due to: –compression from: Vertebral body fracture Disc herniation –Stretching due to excessive movement between vertebrae

Forces causing injury –Flexion Auto accident Most consistently results in neurological damage –Vertical compression Injury most often at C4-5 –Hyperextension

Thoracic spine Stiffest and most mechanically stable due to ribs SCI here are less common than in cervical region, but more likely to be complete –Spinal canal is narrowest in this region –Vulnerable to compression and flexion injury –Also more vulnerable to vascular injury

Thoracolumbar spine 2 nd most frequent site of injury –Junction between stiff thoracic region and flexible lumbar region Factors that reduce the severity of injury –Spinal canal widens between T11 and L2 –Spinal cord ends at L1/L2, so more likely that the cauda equina rather than spinal cord will be injured

Lower lumbar spine and sacrum Stabilized by strong paraspinal and abdominal muscles Most common injury – fall from heights producing vertical compression, followed by flexion injury and penetrating wounds Usually incomplete: good vascular supply, wide spinal canal, and that the cauda equina is present here

Pathophysiology Damage greatest at level of injury, but may extend several levels above and below Neurological damage –Initial injury –Secondary reactions which begin within hours of the initial trauma and lead to edema, ischemia, demyelination and necrosis of spinal cord

Mechanism of secondary injury Hemorrhage Ischemia Local electrolyte derangements Inflammatory reactions (glucocorticoids) Local accumulation of various bioreactive substances

Long term changes in SCI Necrotic tissue removed (resorption) Replaced by: –Scar tissue –Cysts or cavities

Classification of SCI Paraplegia –Partial or complete paralysis of all or parts of the trunk and both LE –Results from lesions in the thoracic and lumbar spinal cord or sacral roots Quadriplegia –Partial or complete paralysis of all four extremities and the trunk, including the respiratory muscles –Results from lesions in the cervical cord

Level of the lesion Most distal uninvolved nerve root segment with normal function –Complete: no sensory or voluntary motor control below the level of neurological injury –Incomplete: Some preservation of sensory or motor function below the level of the lesion Note that most asymmetrical with regard to motor and sensory losses –May need to identify a level of the lesion on each side

SCI and Autonomic Dysfunction During spinal shock –Neural control of pelvic organs is depressed Atonic bowel and bladder –Overfilling and overflow leaking After spinal shock resolves –Reflexive control –No voluntary control –No sensation of filling

More serious autonomic complications Autonomic dysreflexia Poor thermoregulation Orthostatic hypotension

Autonomic Dysreflexia AKA Mass reflex Overactivation of sympathetic nervous system Can occur in people with SCI at T6 and above

Stimulus: anything irritating –Full bladder or bowel –Fold in sheet Response –Activation of sympathetic NS –Descending fibers that can shut down the sympathetic NS are lost

S & S Rapid increase in blood pressure –Can be very high Pounding headache Emptying of bladder Flushing of skin and sweating about level of injury Decreased heart rate –Why?

Treatment Remove the irritating stimulus Drugs

Body temperature regulation Which division of ANS? With spinal cord injury –Reflexive sweating may be intact –Thermoregulative sweating impaired below level of injury –May have compensatory excessive sweating above the level of the injury