Neurological manifestations of spinal canal stenosis are characterized by a predominance of subjective symptoms in the form of pain, paresthesia, transient motor disorders on the background of weak severity or absence of neurological signs of damage to the nervous system. The latter are found, as a rule, only at a late stage of the disease in connection with the development of compression-ischemic radiculo-or myelopathy.
In the first place in frequency, specificity and diagnostic significance should be put neurogenic intermittent claudication syndrome, observed in most patients, regardless of the localization of stenosis along the spinal column. The main pathogenetic mechanism of this syndrome is transient ischemia of the spinal cord or its roots due to angiospasm, venous and cerebrospinal hypertension in the vertebral or radicular canal, which increase when moving to a vertical position with the extension of the trunk while walking and standing.
In most cases, neurogenic intermittent claudication can be designated as postural dysbasia, which implies the appearance and preservation of symptoms in the standing position, when walking, when extending the spine, relief, reduction of their severity when bending the spine, leaning forward, in a squatting position. Usually the patient complains of numbness, pain or weakness in the legs, without indicating their connection with the specific situation. Therefore, the patient should be asked direct questions: when, in what position he has symptoms; how far he can go before they occur; what is their duration; what does he do to reduce them.
In stenosis of the cervical vertebral canal, neurogenic intermittent claudication often precedes or is one of the signs of myelopathy. In half of the patients, intermittent lameness of the spinal cord is represented by transient weakness in one or both legs without sensitivity disorders or pathological foot marks. In about a third of cases, along with paresis, there are complaints of numbness, paresthesia in the legs, spreading (when trying to continue walking) in an upward direction to the trunk. In 15% of cases, there are only sensitive disorders without a noticeable decrease in strength in the legs, even less (5%) – transient ataxia and pelvic disorders.
Intermittent claudication syndrome in combination with postural paresthesia, dysesthesia in the chest, abdomen, on the anterolateral surfaces of the thighs is the most common sign of thoracic myelopathy against the background of spinal canal stenosis. In 10% of cases, it may be the only symptom of the disease for many years.
In patients with stenosis of the lumbar vertebral canal intermittent claudication in the majority of cases yudovina, more precisely, associated with damage to the roots of the horse’s tail. Initially, when walking, numbness, paresthesia or pain in one leg appear, which can be designated as a stage of unilateral intermittent lameness. Diffuse pain, absence of objective symptoms of injury of roots can be viewed as alternating the sciatica or sciatica. In rare cases, there is intermittent lumbalgia with muscle-dystonic syndrome, which prevents walking. In the developed stage of the disease, the symptoms of intermittent claudication become bilateral and often asymmetric, the severity and duration of the attack increases, postural weakness in the legs joins, in the supine position; after resting, the strength is sufficient. The presence of permanent motor, reflex or sensory disorders indicates the development of the syndrome of compression of the horse’s tail. Some patients may show incontinence of urine and feces, priapism, which in the beginning, like other manifestations of stenosis, observed during a walk, after a long stay on his feet; occasionally presented as monosimptomnoe. The same applies to transient sensitive ataxia when walking due to a temporary decrease in deep sensitivity in the legs.
Stenosis radicular channel pattern develops radicular intermittent claudication, the symptoms are unilateral, marked numbness, paresthesia, pain limited to the area of root innervation, motor, sensory and reflex disorders the minimum and are selective. As the disease progresses, signs of monoradicular deficiency increase.
In cases of a combination of stenosis of the vertebral and radicular canals, intermittent claudication or radicular pain syndrome may dominate the clinical picture.
Multiple root canal stenosis naturally leads to a kind of intermittent claudication syndrome in combination with painful cramps in large muscle groups, in which, as a rule, fascicular twitches are observed, especially noticeable even after a small physical activity.
Thus, the most vivid and constant manifestation of spinal canal stenosis is neurogenic intermittent claudication, which may be the only syndrome or combined with reflex pain, radicular or spinal disorders. Pure motor variant of intermittent claudication is observed in 1/3 of the cases. 70% yudovina intermittent claudication, bilateral, presence of unilateral symptoms may be evidence in favor of stenosis, or radicular channel to reflect the early stage of spinal stenosis, often monosegmental type.
Neurogenic intermittent claudication syndrome should be differentiated from peripheral vascular intermittent claudication in patients suffering from obliterating endarteritis or atherosclerosis of the legs. Patients complain of increased cold feet. Pain and convulsive contractions of the calf muscles occur during rapid walking, which causes the patient to stop for a few seconds or minutes, after which he can walk several hundred meters to the next attack. Unlike claudication, when the spinal canal stenosis in the squatting position, the pain does not decrease. On the other hand, for relatively mild cases of the disease, the symptom of “pacing” is characteristic, when, as the walk continues, after a while, the vessels adapt to the load, angiospasm is removed and the phenomena of intermittent claudication disappear; with neurogenic claudication, the picture is opposite. Symptoms of peripheral vascular insufficiency increase in cold, wet weather. Feet pale, cold to the touch. Warmth, foot massage relieve pain. Over time, trophic changes develop in the form of thinning, hyperpigmentation of the skin of the feet, shins, brittle nails appear. Reduced or no pulsation of the arteries of the feet. Rheovasography (RVG) confirms the weakening of organic blood flow in the distal legs.
Neurogenic intermittent claudication syndrome should be differentiated with vascular intermittent claudication of the Central type in connection with atherosclerotic occlusion or stenosis of the lower part of the aorta, its bifurcation, as well as stenosis of the iliac or femoral arteries. This can also include rare cases of congenital abdominal aortic stenosis, more common in short women with thin legs. In this group of patients, pain and numbness in the leg when walking are diffuse, often mimic the neurological manifestations of osteochondrosis. The severity of the pain syndrome increases in parallel with the load. The legs are cold, there is a moderate hypotrophy of the muscles of the thighs and legs. The process is often asymmetric, more pronounced in the right leg. Men complain of decreased sexual function. The pulse on the femoral artery is reduced or absent, but may persist on the arteries of the feet. Auscultation detects noise over the aorta or femoral artery. Ultrasound, aortography identify existing vascular pathology. Pain syndrome is more often caused by ischemia of working muscles.
Intermittent claudication is one of the manifestations of McArdle’s disease-glycogenosis, in which a deficiency of muscle phosphorylase leads to a violation of the anaerobic cleavage of glycogen to lactic acid. One of the earliest signs of the disease — arising from walking weakness and pain in the calf muscles. Positive ischemic test on the hands and feet — tourniquet causes tonic cramp. Electromyography (EMG) after exposure to the nerve tetanizing current captures on the background of contracture bioelectric silence. After bouts of tetany detected myoglobinuria. The disease is inherited by autosomal recessive type.
It should be remembered that the syndrome of spinal or caudogenic intermittent claudication may occur in patients with arteriovenous malformations, vascular tumors of the spinal cord, varicose veins of the spine. To identify this pathology, it is necessary to use selective angiography, venography, MG, which should be carried out after the exclusion of spinal stenosis.
Paroxysmal disorders of the peripheral nervous system and spinal cord are peculiar but little-known manifestations of spinal canal stenosis. Bouts dysfunction nervous system in ties with postural provocation — the key to diagnostic primary stage disease. In typical cases, during an awkward movement with extension and rotation of the spine, when jumping or falling from a small height, a push during a sports game, a person suddenly “takes away” his hands or feet, develops paresis or even paralysis of a transient nature. Motor defect with hypotension, hyporeflexia can persist for seconds, minutes, hours or several days. Pathological and meningeal signs are absent.
To paroxysmal motor manifestations are also painful cramps, exciting, as a rule, individual muscle groups, such as the muscles of the shoulder girdle, sternocleidomastoid, trapezoidal, forearm flexors, small muscles of the hands with stenosis of the cervical vertebral canal; intercostal and abdominal muscles with thoracic; calf, popliteal, adductor thigh muscles, quadriceps and gluteal muscles with lumbar and perineal muscles with sacral stenosis. The spasm can be one-or two-sided, more often tonic or tonic-clonic character, myoclonias are less often noted. In some cases, thoracic stenosis convulsion captures paravertebral muscles. Increased mechanical and electrical excitability of muscles, often observed fibrillar and fascicular twitching.
Paroxysmal disorders of sensation may accompany movement disorders occur in isolation or bouts of numbness, hypoesthesia of the limbs, torso. The most typical paresthesia, temperature dysesthesia, itching, shooting pain. Localization of sensory disorders corresponds to the level of stenosis. Monosegmental narrowing of the spinal canal is often manifested by shingles or spotted dysesthesia, which is described by patients as feeling “handcuffs”, “rubber bands”, “barbed wire”, “belt”, “Hoop”, usually with a clear feeling of heat or cold.
Rare manifestations of vertebral stenosis include cases of paroxysmal disorders of the pelvic organs such as urinary incontinence, feces and gases, spontaneous erection, which occur when running, prolonged stay on his feet, hard physical work.
The above motor-sensory disorders in most patients with spinal stenosis can be triggered by the sample with hyperextension of the spine, when the lateralization of symptoms in connection with the narrowing of the radicular canal is further tilt to the affected side. During fixation of the spine in the position of hyperextension (for 30-60 s), the patient appears typical paresthesia, pain, cramps or weakness in the limbs. It is important to note that only half of patients with a positive hyperextension test or a symptom of an intervertebral foramen has a developed intermittent claudication syndrome, even less often-organic neurological signs.
A dramatic variant of decompensation of latent stenosis of the spinal canal is neuropraxia-the development of transient neurological deficit after inadequately mild spinal injury. Often, paresis and paralysis occur at the time of falling on outstretched arms from a small height with minimal acceleration. This can happen as a result of a person tripping over a rock or other obstacle, falling off a Bicycle or while skiing down a mountain. Whiplash car injury, contact sports (Boxing, wrestling), gymnastics, acrobatics, skydiving can also provoke a state of neuropraxia. The essence of this syndrome is the unexpected appearance of a pronounced, but short-term motor defect, which spontaneously disappears after a few minutes, hours, sometimes lasts up to two days. At the time of injury, the patient may feel a burning lightning pain with irradiation along the spine in the limbs, their short-term numbness, paresthesia. Occasionally there is a single delay in urination. When examining the patient, there are no signs of impaired conductivity in the spinal cord, which distinguishes this phenomenon from a concussion of the spinal cord.
In most cases, neuropraxia is observed in cervical stenosis, much less often-with mild trauma of the thoracic and lumbar sections. The main predisposing factor is the constitutional stenosis of the spinal canal, damage is also contributed by the instability of the motor segments due to osteochondrosis, the presence of abnormalities of the vertebrae, hyperlordosis, weakness of the ligamentous and muscular apparatus. Mechanical action on the spinal cord, ponytail and surrounding vessels in a close bony case at the time of injury leads to a functional axonal block. In neuropraxia, neurological disorders are completely reversible.
Permanent neurological deficit due to damage to the roots and directly to the spinal cord is not characteristic of constitutional, abnormal or spondyl-dysplastic stenosis. In such patients, even an absolutely narrow channel can be completely compensated for decades, but its presence makes the nerve structures vulnerable to mechanical stress, which in the case of injury leads to their significant damage with persistent neurological deficiency.
Radicular, radicular-vascular syndromes, myelopathy are, as a rule, signs of combined, degenerative or acquired non-degenerative stenosis, but in these cases the symptoms of prolapse are moderately or weakly expressed. The clinical picture is dominated by symptoms of irritation in the motor (fasciculation, crampy, increased mechanical excitability), sensitive (paresthesia, thermal dysesthesia), vegetative (sympathalgia with vegetative-vascular disorders), reflex (hyperreflexia) areas. Characterized by chronic slowly progressive disease with periods of stabilization, which can last for many years. Persistent paresis of the limbs, conductive sensitivity disorders, sphincter dysfunction are observed in elderly patients with severe degenerative stenosis. In this category of patients, trauma, disc herniation can lead to severe irreversible damage to nerve structures, to progressive myelopathy.
Thus, the clinical nucleus of spinal canal stenosis is represented by a variety of pain, neurodystrophic and vegetative-vascular disorders, which are also usually subcompensated and have little impact on the quality of life of the patient. However, mild trauma, physical overload, chronic stress, pathology of internal organs can decompensate the process.
Progressive dystrophy of the spine, herniated discs, autoimmune inflammation in the roots and membranes of the spinal cord, instability of motor segments, subsequent mechanical and microcirculatory damage to the spinal cord lead to the appearance of signs of neurogenic intermittent claudication, which indicate the possibility of a progredient course of the disease.
With time growing neurodystrophic disorders, formed multiple foci of osteofibrosis with local interspinal tenderness and paravertebral points around joints, condyles, the projection of the sacroiliac joints. Myofascial pain in the long muscles of the back, shoulder and pelvic girdle, popliteal, flounder, adductor muscles of the thigh, in the ileotibial tract are often combined with vegetative-vascular disorders.
The hypokinetic variant of dystonia is manifested by venous stagnation with a feeling of bursting pain, heat, burning in the hands, feet; swelling, hyperemia, cyanosis of the skin are noted.
More often there is a hyperkinetic variant with angiospasm, feeling of chilliness, cold in the hands or feet, pallor of the skin, a decrease in the pulsation of the peripheral arteries. Sweating or dry skin, hypertrichosis, trophic changes of nails, varicose veins can be found in most patients with spinal stenosis. RVG objectifies the decrease in arterial tone, the difficulty of venous outflow in Hypo – or hypertonicity with a decrease in blood filling in the hyperkinetic variant of vascular dystonia. Thermography demonstrates the violation of skin temperatures of different directions and configurations, confirming the involvement of the autonomic nervous system in the process.