Spinal Cord Injuries: Introduction PDF

Spinal cord injuries introduction By Dr. Fatma Said Zidan Lecturer of Physical Therapy for Neurology BUC Objectives Revise anatomy of the spinal cord. Demonstrate causes of spinal cord injuries. Classify spinal cord injures. Des...

Spinal cord injuries introduction By Dr. Fatma Said Zidan Lecturer of Physical Therapy for Neurology BUC Objectives Revise anatomy of the spinal cord. Demonstrate causes of spinal cord injuries. Classify spinal cord injures. Describe clinical picture of spinal cord injuries Anatomy of the spinal cord  Spinal cord The spinal cord is an extension of the brain that runs through spinal canal & ends at the lower border of the 1st lumbar vertebra. It is continuous above with the medulla oblongata and below with the filum terminale. It is divided into 31 segments. Topographical correlation between spinal cord segments and vertebral bodies 1-For cervical vertebrae, add 1. 2-For thoracic1-6 vertebrae, add 2. 3-For thoracic 7-9 vertebrae,add 3 4-Tenth thoracic vertebra→L1 and L2 segments. 5-Eleventh thoracic vertebra→L3 and L4 segments. 6-Twelfth thoracic vertebra→L5 segments 7-First lumbar vertebra→ Sacral and coccygeal segments  Each segment of the spinal cord has four roots; a ventral and a dorsal root for each half. Each dorsal root has an oval swelling called dorsal root ganglion. There are three meningeal layers surround the spinal cord, (superficial) Dura mater > arachnoid mater > pia mater (deep)  The spinal cord is formed of grey matter surrounded by white matter. In the transverse section ; the grey matter resembles the letter H (2 anterior and 2 posterior horns).  The white matter contains ascending and descending nerve fibers arranged into tracts. Corticospinal tract: Ascending tracts:  Causes of spinal cord injuries : Non-traumatic causes (16%): secondary to disease, infection and congenital defects. Trauma (84%): with the most the common occurring as a result of motor vehicle and motor-bike accidents, followed by falls. Sport, in particular, water-based activities and work-related injuries are also common, while violence-related injuries from a gun, stab or war-related injuries are high in some countries. Mechanisms of injury Distraction occurs when the bony spine is hyperextended, as in rapid acceleration and deceleration injuries. Compression results from axial loading, compromising the spinal cord because of encroachment of vertebral body fragments or intravertebral discs  Torsional injuries result from high-impact collisions, which twist and tear spinal cord tissue Penetrating trauma can directly damage the spinal cord. The lower cervical or upper lumbar regions (above and below the thorax, respectively) are vulnerable to this type of injury. Classification of spinal cord injuries:  According to level (site) of lesion: At cervical: tetraplegia (quadriplegia) Below cervical: paraplegia  According to cause: Traumatic Non traumatic: congenital, infection, vascular, neopastic…etc  According to injury (impairment): Complete lesion or incomplete lesion  Classification of spinal cord injuries: A complete spinal cord injury: An incomplete spinal cord has no motor or sensory function injury: in S4 - S5 area of the spinal cord. has some preservation of sensory Motor Function in S4 - S5, reflected and/or motor function in the S4 - S5 by the ability to voluntarily area of the spinal cord. contract the anal sphincter. There are a number of recognized Sensory Function in S4 - S5, patterns of incomplete cord injury. reflected by the appreciation of deep anal pressure or preservation of either light touch or pinprick sensation in the perianal area.  Level of injury: Tetraplegia: A spinal cord injury in the cervical region affects all four limbs (also called quadriplegia). Paraplegia: Spinal cord injuries in the thoracic, lumbar or sacral region affect the lower limbs.  Over 55% of all spinal cord injuries are cervical; the remainder are approximately equally divided between thoracic, lumbar and sacral levels. The most common level of injury is C5, followed by C4, C6 and T12, in that order. Clinical picture: Injuries to the spinal cord are complex, and each individuals injury is unique in terms of the functions affected and therefore the clinical presentation. Signs and symptoms vary depending on where the spine is injured and the extent of the injury but can include loss of power, sensation, respiration, temperature regulation, bladder, bowel and sexual function. Local manifestations: Pain, local tenderness, swelling or deformity at the site of the lesion. Lower motor neuron signs: At the level of the lesion, there is LMNL in a form of motor (muscle weakness or paralysis), sensory (hyposthesia or anesthesia) and sphincters (retention of urine and stool in S3-5 lesions). Upper motor neuron signs: Paralysis: Impaired muscle power below the neurological level of the lesion. It starts by flaccid stage & lasts from several hours to several weeks. This is followed by spastic stage. Contractures are present on the long run.  Below the level of the lesion: 1)The motor manifestations : They depend on whether the cause of the lesion is acute or gradual. If the cause is acute: (inflammatory, vascular or traumatic). It passes by 2 stages: Stage of flaccidity due to neuronal shock: This stage start between 30-60 minutes following a spinal cord injury and lasts from 2 to 6 weeks. Spinal shock is a state of transient physiologic (rather than anatomic) reflex depression of cord function below the level of injury, with associated loss of all sensorimotor functions. Immediately following the lesion there is sudden paralysis, associated with complete loss of tone and absence of reflexes (flaccid paralysis).  Below the level of the lesion: Stage of spasticity due to recovery from the neuronal shock: On recovery from the shock stage, the full picture of U.M.N.L. will be established including: hypertonia, hyperreflexia, positive Babinski sign & may be clonus. If the cause is gradual (e.g. neoplastic): The shock stage is absent, and there will be gradual progressive weakness with hypertonia and hyperreflexia.  Sensory loss: Impaired both superficial and deep sensations below the neurological level of the lesion. Loss of bladder and bowel control: Retention of urine in flaccid stage is followed by incontinence (reflex emptying) in spastic stage below the neurological level of the lesion. Sexual dysfunction: It is closely linked to bladder involvement. Impaired sympathetic outflow: It is more severe in cervical than thoracic level lesion. It leads to impaired temperature control, hypertension and bradycardia. Respiratory problems: Lesions above C4 cause paralysis of diaphragm, Lower cervical lesion causes paralysis of intercostal muscles and abdominal paralysis, this reduces vital capacity.  For example complete lesion at fifth cervical segment (C5) level: 1. Weakness and atrophy of deltoids, supraspinatous and infraspinatous, rhomboids (LMNL). 2. biceps reflex. 3. Hyposthesia or anesthesia in lateral aspect of shoulder. 4. UMNL (motor & sensory (remaining upper limbs, trunk and legs) - autonomic; including sphincters) below C5. There are some common patterns of neurological loss with incomplete spinal cord injury. These are: Central cord lesion Brown-Sequard lesion Anterior cord syndrome Posterior cord syndrome Conus medullaris syndrome Epiconus lesion Central cord syndrome: Central cord lesions commonly occur following hyperextension injuries of the cervical spine in older people with cervical spondylosis. The hyperextension injury causes compression, hypoxia of the central grey matter of the cord, although the peripheral rim of the spinal cord remains intact. Typically, a patient with a cervical central cord lesion has more severe paralysis of the upper limbs than of the lower limbs. Brown-Sequard syndrome: Brown-Sequard lesions occur when one side of the spinal cord is damaged (i.e. lateral hemi-section). They are usually due to penetrating injuries such as gunshot or knife injuries. Anterior cervical cord syndrome This syndrome is usually associated with a flexion injury that damages the anterior two-thirds of the spinal cord. Most often it is caused by vascular insult to the anterior vertebral artery, leaving the two posterior vertebral arteries intact. Typically, a patient with anterior cervical cord syndrome has preservation of light touch and proprioception but not motor function, pain or temperature sensation below the level of the lesion Posterior cord syndrome: Although rare, posterior cord syndrome occurs when there’s damage at the back of the spinal cord. It generally causes a loss of proprioception below the level of injury. However, motor function as well as pain, temperature, and light touch sensations are usually not affected. Conus medullaris syndrome S3,4,5 segment lesion Early urinary incontinence (autonomic bladder) and faecal incontinence. Impotence Impairment of sensation in the saddle- shaped area. No motor or sensory disability in the lower limbs. Epiconus lesion: L4,5 S1,2 SEGMENTS lesion Weakness or paralysis in the lower limbs, in the muscles supplied by L4,5 and S1,2 (dorsiflexors and plantar-flexors of the ankle and toes, the flexors of the knee and the extensors of the hip). The ankle reflex is absent while the knee reflex is intact. Sensory loss from L4 to S2 segment. Bladder disturbances may occur in the form of precipitancy. Cauda equina syndrome: Lower motor neuron lesion Results from injury to cauda equina, lumber and sacral N. roots. Motor weakness of LMN nature of one or both L.Ls (muscles supplied by the affected roots). Sphincteric manifestations are usually late unless the lesion is bilateral and affects mainly S2,3,4 roots (roots of innervation of the bladder).  Cauda equina lesions usually have a painful onset. The pain is radicular and is referred to the lower limbs, either along the femoral distribution when the lesion affects the upper lumbar roots or along the sciatic distribution when the lesion affects the lower lumbar and sacral roots. Later on there is hyposthesia or anaesthesia in the dermatome supplied by the affected root. References: Harvey, Lisa. Management of spinal cord injuries: a guide for physiotherapists. Elsevier Health Sciences, 2008. Singh A, Tetreault L, Kalsi-Ryan S, Nouri A, Fehlings MG. Global Prevalence and Incidence of Traumatic Spinal Cord Injury. Clinical Epidemiology. 2014;6:309.