THE HIDDEN CONSEQUENCES OF CERVICAL SPINE INJURY
Dnepropetrovsk Medical Academy,
Dnepropetrovsk, Ukraine
The rate of spinal injuries is 4-6 % of all injuries. The proportion of cervical spine injuries (CSI) is up to 46 %. Intense mobility and relative weakness of ligamentous apparatus account for the high rate of dislocations, subdislocations and sprains even in injuries considered as insignificant [1]. Even after mild CSI, patients suffer from pain in the neck during several months. Such pain is accompanied by intense vegetative and vascular disorders, decreasing sensitivity and functional changes in the brain with minimal neurological deficiency. Vertebral dislocation, spinal canal deformation, muscular spasm and local edema result in disorder of topographic and anatomic relationships of the spine, the spinal cord and its roots. An injury is never limited by the region of impaction, but it affects primarily intact adjacent regions leading to formation of more extensive regions of the injury affecting the cerebral structures, the structures in the cervico-occipital region (vertebral arteries, sympathetic plexus, muscular and articular apparatus of the neck). The cervical department of the spinal cord includes the centers responsible for innervation in the upper and lower extremities and diaphragm. Therefore, disorders in their functioning are quite natural and predictable consequences of all CSI. The slightest dislocations of cervical vertebrae and their instability are accompanied by vertebral and basilar insufficiency and other manifestations of disordered cerebral blood flow. The proximity of medulla oblongata determines pathologic initiation of disorders in functioning of the respiratory and cardiovascular centers [2].
The injuries without fractures and complications with clear neurologic symptoms do not attract careful attention of specialists. Sometimes, patients with such injuries do not seek medical advice, i.e. the consequences of such injuries remain hidden and unrecognized for a long time. The most demonstrative example of such injuries is cervical whiplash injury – excessive stretching or tension of muscular and ligamental structures of the cervical spine as result of acceleration and deceleration without fractures of the cervical vertebrae and signs of spinal cord lesions [3].
Whiplash injuries are mainly caused by road traffic accidents: frontal collisions with other car or obstacle (excessive flexion in the cervical spine), hit by a motor vehicle moving behind (excessive extension in the cervical spine in a driver and his/her passengers), lateral collision (combination of flexion and extension with rotatory deformations) [4].
However such injury often appears as result of athletic injuries, mostly in martial arts. Too precipitous, high amplitude flexion, extension and rotation movements in the cervical intervertebral joints appear as result of strong blows to the head. The power of a blow performed by a heavyweight boxer may be above 1,000 kg, a kick by a kickboxer – more than 2,000 kg [5]. Such figures are quite comparable with the power of blows in car accidents. Such injuries remain unrecognized for a long time, because they appear as secondary injuries in maxillofacial injuries in wrestlers and boxers [6].
The same biomechanical conditions appear after unsuccessful falling on the head and the neck as result of throws and hits. Such injury can be a result of neck-lock or long term wrestler's bridge which are common for both training and competition. Similar biomechanics relates to neck injuries in divers. More rarely such injuries appear after fallings or collisions in soccer, hockey, volleyball and gymnastics. It is especially interesting and unexpectedly at first glance that the same results appear in long term steady load in “peaceful” and non-sporting conditions: long term neck position in hyperextension (or in hyperflexion, rotation in any combinations) in performance of professional duties (truck drivers, crane men, tractor operators), during TV watching or sitting at a computer display [7].
One of the pathogenetic factors of CSI is disordered blood circulation in vertebrobasilar basin which worsens the clinical manifestations, favors increasing ischemia in the region of an injury and in the superjacent departments. Even if such complications were absent in the acute period of trauma, they appear in the long term perspective [8, 9]. The most common manifestation of vertebrobasilar insufficiency is vestibulopathy syndrome – dizziness and balance disorder which increase in rotating and tipping the head. High sensitivity of the vestibular analyzer, extensive reflectory associations and features of blood circulation predetermine almost constant presence of symptoms in patients with vertebrogenic vestibulopathy.
The main components of the pathogenetic mechanisms of vertebrogenic vestibulopathy are disorder of the vestibulospinal anatomic relationships, change in perfusion in the vestibular region of the brain stem and the inner ear, as well as vegetative shifts in excitation of the sympathetic plexus of the vertebral artery. The feature of vestibular dysfunction in cervical osteochondrosis is intensity and duration of vegetative responses because of excitation of the sympathetic periarterial plexus of the vertebral artery. Besides dizziness, a lot of patients demonstrate the opticovestibular syndrome in view of instability and appearance of “unpleasant feelings in the head” on looking at moving objects. Along with subjective vestibular symptoms, about a half of patients demonstrate spontaneous nystagmus (small-swinging, horizontal, fatigable). Some patients demonstrate nystagmus of load after tipping or rotation of the head, with the latent period of 15-20 seconds. 20 % of cases are associated with peripheral vestibular syndrome with onsets of systemic dizziness with evident vegetative responses produced by rapid changes in position of the head and cochlear disorders such as noise and insignificant decreasing hearing [10].
The clinical manifestations of vertebrobasilar insufficiency are variable: visual and eye movement disorders such as ambiopia or visual field defect and photopsia in a half of patients. About one third of patients demonstrate movement disorders in view of changing tendon reflexes on the side contrary to vertebrobasilar ischemia. Disordered statics and motion coordination and sensory disorders with changes in fascial skin sensitivity are observed in each fourth patient. Throat and laryngeal reflexes, and disordered functioning of cranial nerves are more rare [11]. Psychoemotional disorders and cephalalgia of various intensity take place in almost all patients with vertebrobasilar insufficiency [12].
Vertebrogenic disorders of cerebral hemodynamics are always accompanied by venous dysfunction even in intact or hemodynamically instable stenosis of brachiocephalic arteries. Such patients mainly complain of headache and fascial edema. Disordered venous return appears as result of compression of vertebral, paravertebral and epidural venous collectors by functionally changed vertebral motional segments. The mechanism of supporting the balance of blood supply-outflow leads to spasm of cerebral arteries with disordered venous return. When arterial spasm becomes generalized, systemic arterial pressure increases predominantly by means of the diastolic component [13].
Disordered hemodynamics in the basin of vertebral arteries and stimulation of the posterior cervical sympathetic nerve cause some complex hypothalamic disorders which supplement the picture of vertebrobasilar insufficiency. Hypothalamic disorders lead to endocrine dysfunctions, dermatologic and allergic diseases, visual and hearing pathology [14]. The ophthalmic artery, which includes the central retinal artery as a branch, is a part of Willis's artery, which is formed from the vessels of vertebrobasilar and carotid basin. Therefore, CSI is associated with visual disorders. Presence of changes in the eye ground indirectly confirms insufficient cerebral perfusion, since such changes show the state of cerebral perfusion to some extent. Besides photopsia, one can register appearance of scotoma and visual field defect conditioned by vasospasm or extravasal compression of small or bigger branches of the magistral vessels of the head and the neck. Significant venous hyperemia and narrowing the arteries (by the type of angiospasm) is observed in 90 % of patients [15]. Functional visual disorders (asthenopia) are common, especially in children [16]. Disordered perfusion of visual nerves cause degenerative and dystrophic processes in the retina accompanied by visual disorders [17].
Arterial hypertension is another common sequence of CSI. One distinguish the vertebrogenic mechanism of increasing arterial pressure including neurogenic and pain mechanisms, change in circulation in the posterior departments of the brain and of the stem structures with development of syndrome of vertebrobasilar insufficiency that is an additional etiopathogenetic factor of developing hypertensive response, disordered vegetative regulation, disarranged microcirculation, and, as result, development of hypoxia. Secondary spasm or compression of magistral arteries having the topological association with the spine is a trigger of endothelial injury by means of blood flow tangential influence on arterial walls and following development of endothelial dysfunction and progressing hypertension [18].
One should note some complications such as vertebrogenic visceropathy. Stimulation of ganglia as result of CSI inevitably causes secretory, motor and trophical disorders in the organs which are reflectory connected to the certain spinal motional segments. At the initial stages of the process the visceral pathology can demonstrate the functional patterns with gradual transition to organic diseases. Vegetative innervation of the internal organs is characterized by multiple segments; therefore, physiological and pathological processes and responses are not limited by a single segment, but they spread to regions of adjoining metamers. There are close relationships between adjacent segments of the spinal cord and ganglions of bordering sympathetic trunks. Preganglionic vegetative fibers come from the cells of lateral horns of the spinal cord. As for sympathetic ganglion, these fibers form the branches and come to several nerve cells which form the postganglionic fibers. The postganglionic fibers head for various organs within the boundaries of various segments [19]. A vertebrogenic pathogenetic mechanism is identified in a half of patients with biliary dyskinesia [20]. As far as the heart is innervated with the cervical segments 3-7, the vertebral visceral syndrome often demonstrate cardialgia and disorders of cardiac rhythm [21].
Even insignificant CSI without disarranged anatomic integrity of the bone-tendon system lead to breakdown of static and coordinatory functions of intervertebral joints by type of functional blockade, which is immediately compensated by development of hypermobility in the adjacent superior and inferior segments. Over time the functional blocks appear in these segments which present a common complication of instability. Therefore, a vicious circle appears. Local overloading in the segment makes negative influence on trophism of the intervertebral disk with promoting the development of degenerative and dystrophic processes and vertebral deformations. Owing to the anatomic integrity of the bone and muscular system, this process is inevitably accompanied by involvement of muscles of the interested region. Initially the participation of muscles is limited by muscular and tonic response. Then some regions of local muscular hypertones and more rough neurodystrophic changes appear in muscles with tonic contraction [22].
Diagnostics of hidden complications of CSI with involvement of cerebral perfusion is realized with ultrasonic techniques [23]. The vertebrogenic origin of the syndrome of vertebrobasilar insufficiency is considered as proved in presence of dynamics of identified complications in tests with turns and inclinations of the head [24].
Both surgical and conservative techniques are used for treating cerebral disorders in the vertebrobasilar basin in case of a vertebrogenic lesion as result of CSI. Each technique has its own advantages. Surgical intervention showed the high efficiency and the advantage for the stenotic lesion of vertebral arteries [25]. Adequate surgical tactics allows interrupting the posttraumatic pathologic chain in view of increasing ischemia in superjacent regions at the background of vertebrobasilar insufficiency. The results of the studies prevent active usage of excessive manipulation in reduction of a dislocation by means of leveraged mechanisms, because it can result in worsening vascular disorders [26]. In cases of evident absence of vertebral arterial stenosis it is preferable to realize the complex use of conservative techniques [27]. Minimal intensity of degenerative changes in the vertebral motional segments is associated with higher clinical efficiency of the combination of dry extension of the cervical spine, massaging the collar zone and wearing the cervical collar for patients with cervical spine injuries. Vertebral reposition, which is efficient in instability, is less efficient in presence of evident anatomic changes such as spondylosis, spondylarthrosis, decreasing height of the intervertebral disks with their dislocation to the spinal canal [28]. The differentiated approach to choice of a treatment method is properly provided by usage of magnetic resonance imaging [29]. The efficiency of conservative treatment is usually conducted according to the findings of doppler technique [30].
CONCLUSION
Summing up the results of the analysis of the problem of hidden complications of CSI one should make a conclusion about necessity of proper examination for all patients with such injuries, with obligatory usage of ultrasonic and tomographic techniques. Success in prevention of long term complications consists in early diagnostics and differentiated treatment.