Theme: Examination of the patient with neurological symptoms

of vertebral osteochondrosis.

 

Neurological signs of lumbar and cervical osteochondrosis.

 

      Among all the spinal diseases associated with neurological signs the most common are degenerative – dystrophic processes such as osteochondrosis and spondiloarthrosis.

      Osteochondrosis (OC) is one of the most common diseases. About 80% of all people have attacks of low back or cervical pain during their life – time. It takes 68% of all temporary working disability ieurology.

      Spinal osteochondrosis is a degenerative lesion of cartilage – between vertebral disc associated with reactive changes ieighbouring vertebras, between vertebral joints and connecting apparatus.

Osteochondrosis can occur in any segment of the spine

Osteochondrosis can occur in any segment of the spine

Osteochondrosis can occur in any segment of the spine, i.e. in the cervical spine, thoracic spine and lumbar spine. This is in most cases a creeping process that involves back pain which initially only occurs during exertion. This degeneration increases significantly with age. Back pain is very common in adults. To a certain extent, signs of degeneration in the spine are normal signs of ageing. For example, marginal serrations associated with spondylolysis in 90 % of men over 50. Only a certaiumber of these cases are also clinically relevant, i.e. associated with pain for the patient. A disease occurs when massive changes result in severe problems unusually early on. This tendency is possibly promoted by the civilised lifestyle. It results in degeneration in the vertebral joints, causes wear and tear to the cartilage on the joints and leads to arthritis. The result is stiffening of the joint and the formation of marginal ridges. The end stage of osteochondrosis ultimately results in the complete stiffening of the mobile segments affected.

Osteochondrosis is a pathological process, at the heart of which there is metabolism violation in the spine, and especially in the intervertebral discs. In this connection, such terms as dystrophic and degenerate (process, phenomenon) are applied in relation to the osteochondrosis in the medical literature. Arrival and adequate nutrients’ perception in the intervertebral disc is reduced at the osteochondrosis. Deficiency of water, amino acids and trace elements appear. Water deficiency is influenced on the amortized (elastic) disc function. A condition of the pulposis core and fibrous disc’s ring changes.

Disc is flattened and protruded (prolapsed) step by step, under influence of even usual loads. Then a break of the fibrous disc ring and prolapse of a disc’s particle in the place of the least mechanical resistance (disc herniation) are possible.
Illustrations: Y.Y. Popelyansky, “Orthopedic neurology (vertebral neurology)”, 2003

Etiology of osteochondrosis

According to the main modern theory – osteochondrosis is a polyfactorial disease that develops in case of two conditions:

1.    Decompensation of trophic systems. It is associated with other diseases (those of gastro – intestinal tract, liver, pancreas, and enzyme – associated diseases). All of these diseases lead to the disorders of homeostasis

2.    Local excessive load on spinal segments. They can be explained by inborn peculiarities of spinal cord (sacralization, lumbalization, narrow spinal canal).

 

Pathogenesis of osteochondrosis

    Usually osteochondrosis is developed at the age of 30 – 50. The main pathological process begins in between vertebral discs. Disc consists of pulp nuclei, fibrous ring and hyaline plate. Disc is a natural amortisseur.

The first stage. Because of certain factors (such as dysmetabolism, arthritis and so on) degenerative changes of pulp nuclei develop. That means destruction of chondrocytes with releasing of hyaluronidaze, chondrocakhepsines, and papaini. That causes destruction and depolimerization of muckopolisacharide complex. As a result pulp nuclei looses its hydrophilous properties, becomes small and mobile.

The second stage. There are degenerative changes in fibrous ring. During the movements the main load is on the internal structures of fibrous ring. They broke and cause disc protrusion. The last can be developed later in disc hernia.

The third stage. There are changes of hyaline plates that are called subchondral sclerosis. In this stage reactive process is developed. Disc hernia is vasculated, fibroused and later osteophytes are growing along the bodies of vertebras. In case of spinal segments increased mobility the reactive changes ieighbouring bodies of vertebra and joints are developed. It is known as associated spondiloarthrosis.

 

 

 

 

How do these changes come about?
	The mobile segment of the spinal column consists of two adjacent vertebral bodies, their vertebral arches and connecting joints, the intervertebral disc between them, and the complex ligamentous system connecting the vertebral bodies. If we see the mobile segment as a double column, the vertebral bodies form the anterior column in static terms and the vertebral joints and arches form the posterior column. The healthy, elastic intervertebral disc dampens the forces acting upon these structures.
	Mobile segment of the spinal column Mobile segment of the spinal column, cross-sectional view
	The intervertebral disc is subject to a natural aging process: it shrinks, loses its elasticity and grows thinner. This increasing loss in intervertebral space height results in morphological changes to the entire mobile segment. The degenerated intervertebral disc no longer elastically absorbs the applied forces, and pressure is increasingly shifted directly to the base and upper plates of the adjacent vertebral bodies. The first consequence of this increased pressure is an increase in bone mineral density (sclerosis) of the base and upper plates of the vertebral bodies, a condition called osteochondrosis or osteochondritis.
	Osteochondrosis of the lumbar spine with a loss in height of the intervertebral space and sclerosis of the base and upper plates.
	The reduced thickness of the intervertebral disc alters the stability of the mobile segment. The changes in tensile and stretch stimuli and increasing amount of direct pressure on the end plates of the vertebral bodies results in progressive intervertebral disc degeneration. This results in the formation of new bony substance as added support. The new substance takes the form of a bony outgrowth at the edge of the vertebral body. This process of bony reformation of the vertebral body is known as spondylosis.

 

 

X –ray signs of osteochondrosis

1.    Low height of between vertebral discs.

2.    Sclerosis of final plates.

3.    Osteophytes on the edges of vertebras’ bodies. They are located perpendicularly to the spinal axis.

4.    Local scoliosis.

5.    Spondilolisthesis – dislocation of neighbouring vertebras’ bodies.

6.    Local cyphosis  (instead of lordosis)

     At distorted spondilosis (as a result of degenerative – dystrophic changes in long spinal ligaments) there are osteophytes, which are located parallelly to the spinal axis along the spinal cord and there is no changes of vertebral discs height.

Fig. Osteochondrosis and spondylosis of cervical spine. The intervertebral disc is thinner, base and cover plates are sclerosedm bony support reactions are evident along the edgesof the vertebral bodies.

Between vertebral disc’s hernia can be located in different places according to the spinal canal. These positions are:

·         Medial (clinical features of horse tail lesion)

·         Paramedial (a little bit out side the medial position – several radixes are compressed)

·         Posterior – medial (much more out side the medial position – 1 or 2 radixes are compressed)

·         Foraminal (near the foramina vertebral – 1 radix is compressed)

 

 

Pathogenesis of neurological signs 

1.    Irritation of vessels and nerves with vascular spasm

2.    Compression of vascular – nervous complex

3.    Edema (perivascular edema and radicular edema)

4.    Reactive process of neibouring structures (straining of muscles)

5.    Autoimmune reactions (a part of disc becomes antigen)

According to the nervous structures that are involved in case of disc’s hernia there are compressive and reflex syndromes.

Compressive syndrome occurs at compression and deformation of radix, vessels and spinal cord.

Reflex syndrome occurs at irritation of different receptors (such as Lushka nerve). That means reflex muscular – tonic disturbances, extension of muscles, and pain at palpation of muscles. That is usually the reason of local pain and pain in distance. Such zones of pain are called trigger zones. Pathogenetical process in these zones is known as neuroosteofibrosis, the painful nodes in muscles are called nodes of Kornelius, muscular hypertonus – hypertonus of Muller.

 

Neurological signs of osteochondrosis at lumbar – sacral level

 

Classification

I.    Reflex syndromes

·         Lumbago (backache)

·         Lumbalgia

·         Lumbar ischialgia (muscular – tonic, neuro – dystrophic,  autonomic vascular)

II.   Compressive radicular syndromes.

III. Compressive vascular radicular – spinal syndromes (radicular ischemia)

1.    Acute

A.   Transient

B.   Strokes

2.    Chronic ischemic myelopathy

    

All the neurological signs of osteochondrosis have common symptoms  – the symptoms of vertebrogenous syndrome. 

 

Vertebrogenous syndrome points that the pathological process is associated with spinal cord.

·         Limitation of movements in lumbar – sacral part of spinal cord (bending forward, backward) and increasing of pain while movements, coughing and laughing.

·         Protective straining of long back muscles

·         Extension of lumbar lordosis, cyphosis in lumbar – sacral division.

·         Scoliosis, sometimes with rotation

·         Painful paravertebral points

·         Painful vertebral processes

·         Discharge – postures and symptoms

Ø  Knee – elbow position

Ø  While standing the patient keeps his leg aside in order to make the load less on his leg

Ø  While lying in the bed he bends his leg in all joints.

·         The symptoms of spinal cord instability (it is difficult for the patient to stand, to wash himself, but it is much more easier to walk)

 

 

 

 

I.    Reflex syndromes on lumbar – sacral level are divided into:

·         muscular – tonic

·         vascular

·         neuro- dystrophic

      Clinically all the reflex syndromes at lumbar – sacral level can be divided into:

1. Lumbago

2. Lumbalgia

3. Lumbar ischialgia

1.    Lumbago   It is acute, sudden, attack – like low back pain. It usually begins at lifting something heavy, catching cold or sometimes spontaneously. Pain is very severe and the patient stays in the same position for a long time. At first the pain cannot be localized. Later the patient can localize it and refers the pain to the low back region. It lasts for 1 – 3 up to 6 days.

2.    Lumbalgia The pain is not so severe. It has subacute or chronic character. It lasts for weeks or even months. The pain can be increased or decreased according to different factors.

3.    Lumbar ischalgia The source of pain impulse is receptor. The pain irradiate into hips, leg.

The points of pain:

·         Pain along the crista iliaca

·         The point of iliosacral joint

·         The point of m. gluteus minimus (just under the crista iliaca)

·         The point of m. gluteus medius (1 sm lower)

·         The point under the backside fold

·         Trochanter os iliaca

·         Along the ischiadic nerve (the posterior surface of hip and fossa subpoplitea)

 

The symptoms of strain

·         Lasegue’s symptom – in case of straining and lifting the leg the low back pain appears

 

·         Neri symptom – there is pain in leg at bending head forward

·         Matskevych symptom – there is pain in the anterior surface of the leg at knee bending while lying on abdomen

·         Wasserman symptom – the same clinical picture at lifting the leg

·         Sequar symptom – there is pain on posterior surface of leg at foot flexing

·         Turin symptom – the same clinical picture at toe’s flexing

·         Bechterev’s symptom – there is pain at knee – flexed leg extension

·         Dejerine’s symptom – there is pain in posterior surface of the leg at coughing, sneezing

 

Types of lumbar ischalgia

1.    Muscle – tonic

2.    Neurodystrophic

3.    Autonomic – vascular

 

1.    Muscle – tonic Clinical features are connected with secondary lesion of nerves according to the compressive – ischemic type, the type of tunnel syndrome as a result of muscles spasm and straining.

A. Piriformis syndrome M. Piriformis is located under m. gluteus maximus. It is attached to the internal edge of Trochanter Major and anterior surface of sacroiliac joint.

       Under the muscle sacroilial ligament is situated. Between the muscle and the ligament nervus ischiadicus and a. ischiadica are located. These structures can be irritated or compressed at long – lasted straining of m. Piriformis.

 

Piriformis syndrome is an uncommoeuromuscular disorder that is caused when the piriformis muscle compresses the sciatic nerve. The piriformis muscle is a flat, band-like muscle located in the buttocks near the top of the hip joint. This muscle is important in lower body movement because it stabilizes the hip joint and lifts and rotates the thigh away from the body. This enables us to walk, shift our weight from one foot to another, and maintain balance. It is also used in sports that involve lifting and rotating the thighs — in short, in almost every motion of the hips and legs.

The sciatic nerve is a thick and long nerve in the body. It passes alongside or goes through the piriformis muscle, goes down the back of the leg, and eventually branches off into smaller nerves that end in the feet. Nerve compression can be caused by spasm of the piriformis muscle.

 Symptom of Bone – Bobrovnikova

 

Clinical features:

·         Painful palpation of Trochanter major

·         Painful m.Piriformis

·         Symptom of Soobrase (painful cross-legged position)

·         Symptom of Bone – Bobrovnikova (painful abduction of leg)

·         Popelyansky intermittent claudication (while walking the patient is forced to sit down because of the pain. That is the result of spasm of the vessels

Except the Popelyansky intermittent claudication there are also:

v  Myelogenic intermittent claudication 

v  Caudal intermittent claudication 

v  Intermittent claudication  at obliterated endarteriitis

• Insignificant sphincter disorders (pause before the urination) as a result of n. pudendus irritation

• Insignificant signs of n. ischiadicus lesion (muscles hypotrophy, low Achille reflex, hyposthesia, pain)

 in anatomic relationships with the surrounding structures were found.

Fig. —40-year-old man with piriformis syndrome. Unenhanced axial T1-weighted MR image of sacrum shows accessory fibers of right piriformis muscle (a) overlying right S2 nerve (arrow) and attaching medially. Note that accessory fibers of right piriformis muscle and right S2 nerve are of normal signal intensity. p = normal left piriformis muscle at sacral attachment.

 

Fig. —40-year-old man with piriformis syndrome. Unenhanced oblique coronal T1-weighted MR image shows accessory fibers of right piriformis muscle (a) anterior to and obscuring right S2 nerve. p = normal right and left piriformis muscles

 

2. Neurodystrophic form of lumbar ischialgia is a sign of neuromyofibrosis.There are:

A. Sacroiliac periartrosis – pain and limitation of movements in hip joint. The patients cannot run and so on.

 

B. Knee joint periartrosis– sudden pain in knee joint

 

C. Popliteal syndrome It is the result of neuroosteofibrosis in popliteal fossa in the place of m. ischiocrural attachment.

Clinical features:

·         Pain in fossa poplitea while patient’s standing, palpation

·         Cramps – sudden painful tonic straining of m. Triceps surae

Pains in m. soleus

 

D. Coccygodynia Pain is in the coccyx’s region. The last is connected with sacrum via discs. Degenerative changes in disc; straining and painful pelvic muscles cause coccygodynia. Usually it is observed at pregnancy, after childbirth, at long sitting.

Clinical features:

1.    long lasting aching pains

2.    paresthesia in coccyx region, which is increased at sitting, defecation and decreased at standing

3.    that often leads to patients’ depression

 

E. Neurodystrophic changes of Achille tendon (it is very rare)

The peculiarity of neurodystrophic changes is:

·         One side lesion on the side of lumbar ischialgia

·         The lesion of large joints

·         Connection of exacerbation with low back pain

 

3. Autonomic – vascular form of lumbar ischialgia

·         Vasospastic

·         Vasoparetic

·         Mixed

Clinical features: It appears on background of low back pain, freezing and cyanosis, hyperhydrosis, insignificant autonomic – trophic changes of lower extremities (hyperkeratosis, dryness of skin, edema).

II. Compressive radicular syndromes ( radiculopathy)

Hernia of intervertebral discs in lumbar region causes compression of L5 – S1 radixes, sometimes L3 – L4. In compressed radixes there are edema, venous stasis, aseptic inflammation. Clinical features of radiculopathy consist of clinical features of lumbar ischialgia and symptoms of radix’s loss of functions.

 

Clinical features of radiculopathy.

1.    Radix L5 ( Disc L4 – L5)

·         Pain in the external edge of hip, on the anterior –external surface of crus until the internal surface of foot and great toe

·         Sensory disorders (hypalgesia, analgesia) in the same zones

·         Paresis of great toe extensors and foot extensors

·         Hypotonia and hypotrophy on the anterior surface of crus

·         The patient cannot stand on heels

 F

 

2.    Radix S1 (Disc L5 – S1)

·         Pain in external – posterior surface of hip, crus, foot, the IV –th and Vth toes

·         Sensory disorders (hypalgesia, analgesia) in the same zones

·         Paresis of toes flexors

·         Absent or low Achille reflex

 

3.    Radix L4 (Disc L3 – L4)

·         Pain in anterior – internal surface of hip

·         Sensory disorders (hypalgesia, analgesia) in the same zones prevail over motor ones

·         Weakness of m. Quadriceps femoris

·         Hypotrophy of m. Quadriceps femoris

·         Knee reflex is low or sometimes increased

4.    Radix L2 – L3

    Compression of these radices is very rare. Clinical features include pain and sensory disorders on anterior – medial surface of hip.

·         Symptoms of Matskevych, Wasserman

·         Low knee reflex

·         Weakness of m. Quadriceps femoris

·         Cruralgia

·         Symptoms of lesion of horse tail

·         Irradiation of pain into lower part of abdomen, genital organs

Syndrome of compression of horse tail It is created by radix L2 – S5. It is observed at hernia of discs L4 – L5.

Clinical features:

·         Significant pain in legs

·         Sensory and motor disorders in certain zones of innervation

·         Pelvic disorders (incontinence of urine and feces)

 

III. Compressive vascular radicular – spinal syndromes on lumbar level

There are:

1.      Acute vascular – radicular syndromes (transient, strokes)

2.      Chronic (chronic myelopathy)

 

Acute These ones are observed at disc’s hernia, narrow spinal canal, as a result of spondilolisthesis.

Transient

1.    Myelogenic Popelyansky intermittent claudication (transient ischemia of conus and epiconus)

Clinical features:

·         Weakness in legs without pain during long lasting walking

·         Paresthesia

·         Micturition

 

2.    Caudal intermittent claudication of Verbista (transient ischemia of horse tail radices)

Clinical features:

·         Pain in feet, cruses, anal region

·         Weakness in feet

·         Retention of urine

Symptoms last for about 5 – 7 minutes

 

Strokes

They are developed rapidly after long lasting lumbalgia or lumbar ischialgia. There are such forms as:

A. Paralysis ischias (at radix spinal artery L5 – S1 compression)

Clinical features:

·         Foot weakness without sensory disorders

·         Absence of Achille and sole reflex

B. Syndromes of cone ischemia (S3 – S5)

·         Anesthesia of ano-genital zone

·         Pelvic disorders (retention of urine)

C. Syndromes of epicone ischemia (L4 – S2)

·         Flaccid feet paralysis

·         Absence of Achille reflexes

·         Sensory disorders in zones L4 – S2

D. Syndromes of cone and epicone ischemia

·         Paresis and paralysis of lower extremities, much more expressed in distal parts

·         Sensory disorders in zones L4 – S5

·         Pelvic disorders

E. Syndrome of a. Adamkevych

·         Central or peripheral paralysis (paresis) of lower extremities

·         Conductive sensory disorders from umbilicus and downwards

·         Pelvic disorders according to the central type

·         Bed –sores

 

Chronic compressive vascular syndromes – dyscirculative myelopathy.

    It occurs at graduate compression of spinal vessels, hypertrophy of ligamentum flavum.

Lumbar compressive spinal syndromes are very rare. Compressive myelopathy occurs at discs hernia. There are such syndromes:

 

A. Epicone syndrome (It occurs at protrusion of Th10 – L1 discs with lesion of L4 – L5 – S1 – S2 segments).

Clinical features:

·         Low back pain with irradiation in posterior surface of leg

·         Feet paresis

·         Hypotonic and hypotrophic crus’ muscles

·         Absence of Achille and sole reflexes

B. Cone syndrome It occurs at protrusion of L1 – L2 discs with lesion of S3 – S5 segments.

Clinical features:

·         Perineum anesthesia

·         True urine, feces incontinence and sometimes its retention

·         Bed – sores. These signs are dominant

 

Neurological signs of osteochondrosis at cervical level

Anatomical peculiarities of cervical part of the spinal cord

A. C1 and C2 vertebras are joined without between vertebral discs. Rotation is dominating movement in these vertebras.

B.  The body of C3 and the rest cervical vertebras aren’t separated by the disc completely. Disc is only in anterior and posterior part. There are also hook – like processes. Before them artery is located, after them nerve is situated.

C.  Transversal processes of cervical vertebras have transversal holes. These holes are used by vertebral artery to come through.

D.   If there are some changes in between vertebral discs, the main pressure is on hook –like processes, the artery and nerve.

 

Classification of neurological signs of osteochondrosis on cervical level

1.    Reflex symptoms.

·         Stiff neck

·         Cervicalgia

·         Cervical cranialgia

·         Cevical brachialgia

v  Muscle – tonic syndrome

v  Autonomic – vascular syndrome

v  Neurodystrophic

2.    Compressive radicular syndrome

3.    Compressive – spinal syndrome

4.    Compressive vascular radicular – spinal syndrome

·         Acute

v  Transient

v  Strokes

·         Chronic ischemic myelopathy

5.    A. vertebralis syndrome (radiculopathy of C8 radix, disc C7 – C8)

 

 

 

 

1.    Reflex syndromes

Stiff neck It is sudden acute pain ieck that lasts from several days up to 1 – 2 weeks.

Cervicalgia It is severe dull pain in cervical part of the spinal cord. Usually it appears in the morning, while coughing. There are signs of vertebrogenous syndrome in cervical level  – limitation of movements in cervical part of the spinal cord, painful paravertebral points and vertebral processes. There are positive symptoms of muscles straining.

 

Cervical cranialgia.

It is the result of:

1.    Irritation of a. vertebralis sympathetic plexus – posterior cervical sympathetic syndrome.

2.    Irritation of cervical muscles, fibrous tissues receptors.

Clinical features of posterior cervical sympathetic syndrome:

·         Cranialgia – occipital pain with irradiation in temporal, parietal   parts

·         Vestibulo – cochlear disturbances – dizziness, vomiting

·         Eyes symptoms – eyes pain, tears

·         Autonomic upper quadrant syndrome – asymmetry of blood pressure, temperature, pulse, sensation, cardiac pain and so on

 

 

      Cervical brachialgia.

1.    Muscle – tonic form

2.    Neurodystrophic form

3.    Autonomic – vascular one

 

1.    Muscle – tonic form It can manifest as:

Scalenus – syndrome It is connected with straining of m. scalenus. The muscle starts from transversal processes C3 – C4 and it is attached to the first rib. There are subclavian artery, vein and lower truncus of brachial plexus between the muscle and the rib.

 

The scalene muscles are three paired muscles of the neck, located in the front on either side of the throat, just lateral to the sternocleidomastoid. There is an anterior scalene (scalenus anterior), a medial scalene (scalenus medius), and a posterior scalene (scalenus posterior). They derive their name from the Greek word skalenos and the later Latin scalenus meaning “uneven”, similar to the scalene triangle in mathematics, which has all sides of unequal length. These muscles not only have different lengths but also considerable variety in their attachments and fiber arrangements. As you will see from the descriptions below, these muscles are in a very crowded place and are related to many important structures such as nerves and arteries that run through the neck.

The scalenes run deep to the sternocleidomastoid. They all start at the cervical vertebra and run to the first to second ribs. The anterior scalene runs almost vertically and its upper part is concealed by the SCM and the lower part is concealed by the clavicle. Along its medial border runs the carotid artery. The internal jugular vein, the intermediate tendon of the omohyoid, the phrenic nerve; and the transverse cervical and scapular arteries all lie between the anterior scalene and the sternocleidomastoid (in front of scalene behind the SCM). Between the muscle and the clavicle runs the subclavian vein. The rear of the muscle, its posterior border, makes contact with the brachial plexus nerve roots, which run between it and the medial scalene.

Just behind the anterior scalene is the scalenus medius, referring to the “middle” muscle. This muscle forms part of the floor of the posterior triangle of the neck². The front of the muscle runs close the the brachial plexus and the upper two thoracic nerve roots run through it. It makes contact with the levator scapulae in the rear, and the dorsal scapular nerve and transverse cervical artery pass between the two. The upper two roots of the long thoracic nerve go through the muscle. Only the anterior and medial scalene can be palpated.

 

The Scalene Muscle Group

The posterior scalene is much shorter than the other two, and only starts at the lower cervical vertebra, where it attaches via two three tendinous slips. Whereas the first two attach to the first rib, the medius attaches to the second rib. Some texts refer to a fourth scalene muscle, the scalenus minor. This variant does not always occur on both sides of the neck, but may be present in up to one-third of people. This normal variation may have implications in thoracic outlet syndromes, as does the scalenus anterior, resulting in a syndrome known as Scalenus Anterior sydrome or Scalenus Anticus syndrome (another name for the anterior muscle). The brachial plexus and the subclavian artery, as mentioned above, pass between the anterior scalene and the middle scalene. When present, the minimus inserts between the scalenus anterior and medius, passing behind the subclavian artery while the scalene anterior passes over and in front of it.

Origins: The Anterior Scalene (front scalene) originates on the anterior tubercles of the transverse processes of the third or fourth to the sixth cervical vertebrae.

The Scalenus Medius (middle scalene) originates on the posterior tubercles of the transverse processes of the first or second to seventh cervical vertebrae.

The Scalenus Posterior (rear scalene) attaches by two or three tendons from the posterior tubercles of the transverse processes of the the fifth or sixth to the seventh cervical vertebra (the last two or three).

Insertions: The scalenus anterior inserts onto the scalene tubercle and cranial crest of the firt rib, in front of the subclavian groove. The middle scalene inserts onto the cranial surface of the first rib, between the scalene tubercle and the subclavian groove. The posterior scalene inserts onto the outer surface of the second rib.

Actions: As above, the scalenes function as fixers and elevators of the first and second ribs during inspiration. The anterior and medial scalenes elevate the first rib and the posterior scalene elevates the second rib.

It is generally accepted that, acting unilaterally, they flex the head to the same side and acting bilaterally the flex the head forward (cervical flexion). Their roles as rotators of the neck given differently by different texts. Some report that all three scalenes rotate the head to the same side and some report that they all rotate it to the opposite side. Some report different functions for each scalene. According to Buford, et al., a multiple single-subject study on anesthetized macaques and human cadaver follow up revealed all three muscles as contralateral rotators of the cervical spine (rotating the head to the opposite side). The scalenes also help to laterally stabilize the neck, which is especially suited to the scalenus posterior.

Strength Training and Scalene Strain

When you strain on a heavy lift, such as a barbell squat, you may find yourself holding your breath while tensing the muscles in your shoulder and chest area. This can strain the scalenes. Learn to take your breaths into the diaphragm (discussed more below) and don’t tense your neck, or crane if forward when lifting. Although it is a good idea to keep the shoulders pinned back during most lifting exercises, do not exaggerate this and do not excessively puff the chest out and up.

Scalene Referred Pain Patterns

Any of the scalene muscles may refer pain to any of the associated areas but some are more likely to send pain to certain areas than others. Pain in the chest is referred in two finger-like projections to the pectoral region down to about the level of the nipple. This pain is more likely to be caused by trigger points in the lower part of the scalenus medius or posterior.

 

Scalene Trigger Points and Referred Pain Patterns

Shoulder pain from scalene TP’s is not deep in the joint, but superficial and more to the deltoid muscle. This pain extends down the front and back of the arm, skipping the elbow and occurring again in the radial forearm, thumb, and index finger. This pain pattern of the upper extremity is more likely to be caused by TP’s in the upper part of the scalenus anterior and medius.

Pain is sometimes referred to the back, over the upper half of the inner border of the scapula and the interscapular region, caused by TP’s in the anterior scalene. The scalenus minimus is associated with a more rare referred pain pattern in the lateral part of the arm, from the top of the deltoid down to the elbow, but again skipping the elbow itself. The pain reappears in the back of the forearm (dorsal area), wrist, hand, and all five fingers, becoming very concentrated in the thumb. There may be occasional numbness in the thumb.

Clinical features:

·         There are pains above and under clavicle at the muscle straining

·         There are pains at head movements with irradiation in the arm

·         Edema in above clavicle region

·         Positive Adson test – during the arm adduction there is pain over a. subclavia and slow pulsation in a. radialis

·         Weakness of hand

·         Tenar hypotrophy

·         Hypalgesia of the hand ulnar surface

·         Hand edema

·         Paleness of the hand

 Side-Bending Scalene Stretch

It may be helpful to apply a hot pack or heating pad across the neck for 10 to 15 minutes before performing this stretch. Between stretches, use proper diaphragmatic breathing, taking deep, slow, breaths, to relax the neck.

·         Lie supine (face up) in your bed or on the floor

·         Lower and anchor the shoulder of the side to be stretched by placing that side’s hand under your buttock

·         Bring the opposite hand over your head so that your fingers make contact with the top of the ear.

·         Gently pull the head and neck so that it tilts to the opposite side of the side you want to stretch, relaxing your neck muscles as you do so. Try to pull your ear down to your shoudler.

·         Now, you will rotate your head, and the degree of rotation will determine which scalene is targeted.

o    To target the posterior scalene, turn your face toward the arm that is pulling

o    To target the anterior scalene, turn your face away from the pulling arm.

o    To target the middle scalene, look straight up at the ceiling, or just slightly toward the pulling arm.

·         Concentrate your efforts on the muscle that feels the tightest when you rotate your head to target that muscle

Hold the stretch for around six slow seconds

M. pectoralis minor syndrome At this muscle straining the distal part of vascular – nervous trunk is pressed.

Clinical features:

·         Pain in anterior thoracic part and in ulnar surface of hand

·         Hand weakness

·         IV – th – V – th fingers parasthesia

 

 

 

 

2. Neurodystrophic form of cervical brachialgia

·         Shoulder – scapula periartrosis

·         Shoulder – hand syndrome

·         Epicondilosis

 

Shoulder – scapula periartrosis is the result of muscle – tonic and neurodystrophic tissue disorders.

Clinical features:

·         Pain and limitation of movements in shoulder

·         Painful palpation of caput os humeri

·         Limitation of arm movements (the patient cannot comb his hair)

·         The symptom of frozen shoulder

·         M. deltoideus, m. supraspinatus and infraspinatus atrophy

    There are two stages of this syndrome – algic and dystrophic. In the dystrophic stage not only active movements are limited but the passive ones also.

 

 

Shoulder – hand syndrome This syndrome includes clinical features of shoulder – scapula periartrosis and autonomic – trophic changes of hand.

This syndrome, formerly reflex sympathetic dystrophy or causalgia, is a chronic systemic disease characterized by severe pain, swelling, and changes in the skin. CRPS is expected to worsen over time. It often initially affects an arm or a leg and often spreads throughout the body; 92% of patients state that they have experienced a spread and 35% of patients report symptoms in their whole body. Recent evidence has led to the conclusion that Complex Regional Pain Syndrome is a multifactorial disorder with clinical features of neurogenic inflammation, nociceptive sensitisation (which causes extreme sensitivity or allodynia), vasomotor dysfunction, and maladaptive neuroplasticity, generated by an aberrant response to tissue injury.^[3] Treatment is complicated, involving drugs, physical therapy, scrambler therapy, psychologic treatments and neuromodulation and usually unsatisfactory, especially if begun late.

CRPS is associated with dysregulation of the central nervous system and autonomic nervous system resulting in multiple functional loss, impairment and disability.

 

  Clinical features of algic stage:

  ·  Severe hand pain

·         Edema, hyperemia and cyanosis

·         Hyperesthesia

·         Decreased muscle strength and limitation of movements

Clinical features of dystrophic stage:

·         Muscle atrophy

·         Osteoporosis on X – rays examinations

 

 

 

Fig. Shoulder – hand syndrome 

 

 

 

Shoulder epicondilosis It is very common in tennis players.

Clinical features:

·         Elbow pain

·         Insignificant hypalgesia on external surface of hand

 

3. Autonomic – vascular form

Clinical features are the same as in case of lumbar ischialgia.

 

II.      Compressive radicular syndromes on cervical level

 

1. Radiculopathy C6 radix (C5 – C6 discs)

• Pain, parasthesia and hypalgesia on anterior external surface of arm

• Weakness, hypotrophy of m. biceps brachii

• Absent or low flex elbow reflex

 

2. Radiculopathy C7 radix (C6 – C7 discs)

• Pain, parasthesia and hypalgesia

• Weakness, hypotrophy of m. triceps brachii

• Low extensor elbow reflex

 

3. Radiculopathy C8 radix (C7 – C8 discs)

• Pain, parasthesia and hypalgesia

• Low extensor elbow and carpo – radial reflex

 

III.    Compressive spinal syndromes

      Clinical features are developed during several months or years, sometimes rapidly, acutely.

Clinical features:

1.    The syndrome of bilateral ventral compression of spinal cord

·         Flaccid upper paralysis

·         Central lower paralysis

·         Conductive sensory disorders

·         Pelvic disturbances

2.    Syndrome of lateral column compression

·         Flaccid upper paralysis

·         Central lower paralysis

·         Conductive sensory disorders on the opposite side

 

IV.   Compressive vascular radicular – spinal syndromes.

1.    Acute

A.   Transient

B.   Stroke

2.    Chronic

 

1.    A. Transient – Sensory and motor disorders are liquidated in course of 1 – 2 weeks.

 B. Stroke (It is acute ischemia of radix or spinal cord)

·         At radix artery compression radix stroke is developed

·         At anterior spinal artery compression only anterior 2/3 of spinal diameter are injured.

 

2.    Chronic – cervical myelopathy

·         Anterior horns lesion syndrome

·         Lateral columns syndrome

·         LAS – syndrome

·         Syringomyelia syndrome

   

V.     Vertebral artery syndrome

1.    Drop – attacks (reticular formation ischemia)

2.    Syncope (pyramidal tract ischemia)

 

Additional methods of diagnostics

1.    Spinal X – ray – examination

2.    CT and MRI of spinal cord

X-rays

Stage of instability (pseudospondylolisthesis at L4/5)

X-rays of the segments of the spine are always performed in 2 planes when the patient is standing, with functional images also possibly taken from the side.

Computed tomography (CT) of the spine is currently occupied an important place in the diagnosis of diseases of the lumbar spine, in particular disc herniation in osteochondrosis. Computed Tomography (CT) of the spine compared with other radiological methods of investigation has several advantages – the method neinvaziven, provides a clear visualization of bony structures, discs, ligaments and soft tissues.

Computed tomography (CT) of the spine demonstrated direct signs of disc herniation and other elements are narrowed spinal canal and intervertebral foramen, can clearly identify their location, size and relationship to surrounding anatomic structures.

Magnetic resonance imaging (MRI),

The MRI is preferable over CT. Tomography (imaging in ‘slices’) makes it possible to evaluate spinal canal, nerves, bones, musculature, ligaments and oedema in the spine, as well as spinal canal stenosis and instability.

Magnetic resonance imaging (MRI) of the lumbosacral spine – this is one of the most promising and rapidly improving techniques of modern neuroradiology.

By magnetic resonance angiography (MRI) of lumbosacral spine doctor is able not only to investigate the structural and pathological changes of the spine on an MRI, but also to assess the physico-chemical, pathophysiological processes of the spinal cord as a whole or its individual structures (nerve roots) to conduct functional studies of spinal cord, to perform magnetic resonance angiography, does not require direct puncture of the artery.

Using magnetic resonance imaging (MRI) of the lumbosacral spine can be reliably assess the condition of the intervertebral disc (herniation and protrusion) and joints (spondylarthrosis, spondylosis, ankylosing spondylitis).

Myelography

This contrast medium study of the spinal segment is advisable if functional narrowing of the spinal canal is suspected.

Neurological investigation including nerve conduction velocities (NCV) and electromyography (EMG) is advisable.

 

 

X-ray signs of ostheocondrosis

 

 Magnetic resonance imaging (MRI) of the lumbosacral spine, sagittal projection.

 

 Retrolistesis

 

Treatment

Treatment of an osteochondrosis is referred mainly on elimination of a painful syndrome, disturbance of function of roots of a spinal cord and the prevention of advance of dystrophic process in structures of a backbone.

1.     Orthopedic

Orthopedic methods of influence on a backbone at an osteochondrosis include: treatment by position, application of bandages, corsets, headholders, traction treatment (extension by means of various devices, self-extension, extension in water in a combination to a fangotherapy), etc.

 

2.    Medicines:

·         At edema: Euphyllinum 2.4% 10.0; Lasix 2.0; Dexamethasonum 4 – 8 mg; NaCl 0.9% 200.0 i/v by drops

·         Platiphillinum, No – spa, Baralginum

·         Analgesics  – Reopirini, Voltareni 2.5% 3.0; Tramadol, Aminasini

·         Non steroids medicines– Ketanov, Dicloberl, Movalis, Ranselex, Celecoxib

·         Myorelaxants – Midocalm, Baclofen

·         Chondro- protectors – Rumalon

·         Vitamins and biostimulators

·         Physical methods

In a complex of the medical actions referred on a cupping of a painful syndrome, often include reflexotherapy, cryotherapy (for example, an irrigation of morbid area Aether chloratus) or applications of the preparations causing a hyperemia, the anesthesia, possessing antiinflammatory action.

Widely use a physiotherapy, including treatment by dry fever, the irradiation in erythema doses, diadynamic and impulse currents, an inductothermy, an electrophoresis of solutions of anesthetics, ultrasonic therapy or its combination to introduction of medicinal preparations, etc.

To elimination of a painful syndrome quite often apply light massage of muscles of a back or a neck. If are available neiro trophic disturbances or paresises, appoint massage of a corresponding extremity. With this purpose it is possible to use technics is reflex-segmentary and acupressure to spend underwater massage.

The Wide circulation was received with the manipulation referred on elimination hurt and arising at dystrophic process in a backbone of biomechanical disturbances.

During weakening a painful syndrome, especially at chronic recurring process, it is recommended sanatorium treatment of an osteochondrosis with the purpose of liquidation of the residual phenomena and prophylaxes of exacerbations. Mud, hydrosulphuric, radon baths are shown.

3.Surgical treatment of osteochondrosis of the spine

Surgical treatment is always the last treatment option available. There are cases where surgery is is a must. Examples of this include paralysis of the bladder or rectum caused by narrowing of the spinal canal or a slipped disc.

 

The main indications:

·         Horse tail compression

·         Long lasting (3 – 6 months) pains

·         Huge hernia (over 15 mm)

·         Acute compression of radicular – spinal artery

 

The following surgical techniques are available

·         Minimal invasive surgery to increase the width of the spinal canal

·         Minimal invasive implantation of an intervertebral disc prosthesis (cervical spine and lumbar spine)

·         Dynamic systems (lumbar spine)

·         Minimal invasive surgical fusion from the rear (dorsal) or the front (ventral), alone or in combination with TLIF (transforaminal lumbar interbody fusion) or PLIF (posterior lumbar interbody fusion) in combination with percutaneous instrumentation (lumbar spine)

4.    Sanatorium

 

Prevention

1.    Hypokinesia prevention

2.    Moderate physical activity

3.    Treatment of chronic diseases

 

VASCULAR DISEASE OF THE SPINAL CORD

 

When compared to cerebrovascular disease, vascular disease of the spinal cord is uncommon, a fact that does not support the unsubstantiated claim that the spinal cord has a “poor blood supply.” The blood sup­ply to the spinal cord is adequate in a healthy individ­ual with ample reserve and the capacity for develop­ment of substantial collateral circulation. There are many common factors in vascular disease of the brain and spinal cord (i.e., atherosclerosis). However, be­cause of a unique blood supply, a number of addi­tional factors may produce vascular disease of the cord.

 

ANATOMY

 

 

 

Arterial Supply of the Spinal Cord

The anterior spinal artery runs the entire length of the spinal cord and is located in the anterior ventral sul­cus of the cord. At the cranial end, the anterior spinal artery arises from the fourth portion of the vertebral artery and descends over the ventral surface of the medulla toward the midlineto join the anterior spinal artery from the opposite side. The two vessels are usually small but have the capacity for hypertrophy and are a potential source of collateral circulation to the medulla and spinal cord. The anterior spinal artery is reinforced by three anterior, anastomotic(medullary) arteries in the cervical area. These ves­sels take origin from the vertebral artery, the deep cervical artery, and the costocervical or ascending cervical artery and usually join the anterior spinal artery at the level of C3, C6 and C8, respectively. The thoracic portion receives one or two anastomotic ves­sels, which arise from intercostal arteries. The most common site is at T4 or T5. The thoracolumbar por­tion of the anterior spinal artery is joined by the great anterior anastomotic artery of Adamkiewicz, which arises anywhere between the levels of T8 and L4 on the left side in about 80 percent of cases. This vessel receives blood from the aorta via the lower intercostal or lumbar arteries. In its course over the cauda equina the anterior artery is joined by branches from the lumbar, iliolumbar, lateral, and medial sacral arteries.

The anterior spinal artery is not a continuous vessel. Rather, it should be regarded as a series of anastomotic systems fed by anastomoticarteries such as the artery of Adamkiewicz. This physiological concept suggests that the arterial system of the spinal cord is similar to the arterial systems of the brain and brainstem.

The branches of the anterior spinal artery are of two types.

1.    Central arteries penetrate the median fis­sure and branch alternately to the right or to the left with an occasional bifurcating vessel. These branches extend to the anterior horn, where they divide into a rich capillary network and form a plexus involving the anterior horn cells, the gray commissure, the lat­eral horn, and the base of the posterior horn. The cap­illaries from this system also penetrate the white mat­ter and anastomose with branches of the centripetal system. There is further anastomosis through inter­segmental arterioles, which extend upward and down­ward in the cord, forming a connection between adja­cent segmental arterial systems.

2.    The centripetal system arises from the an­terior spinal artery and extends around the periphery of the spinal cord as far as the posterior nerve root. These vessels give rise to numerous penetrating radial arteries, which enter the white matter and anastomose with the capillaries of the central system.

The posterior spinal arteries constitute an irreg­ular system that traverses the length of the spinal cord immediately posterior to the entrance of the posterior nerve root. These vessels are reinforced by 12 to 16 small posterior anastomotic arteries. The posterior spinal system anastomoses superiorly with the verte­bral arteries and inferiorly with the anterior spinal artery through many fine arterioles surrounding the terminal portion of the spinal cord and cauda equina. The posterior horns of the spinal cord and the poste­rior columns, which constitute the posterior third of the spinal cord, are supplied by penetrating vessels arising from numerous superficial anastomotic ves­sels joining the two posterior spinal arteries.

 

Venous Drainage of the Spinal Cord

The intrinsic drainage of the spinal cord occurs through a central venous system and a radial group of veins.

The central veins of the spinal cord converge toward the anterior median fissure and enter the ante­rior median spinal vein. The radial veins pass to the surface of the cord, where a plexus is formed. This plexus drains into the anterior median spinal vein.

The posterior one-third of the spinal cord is also drained by a series of radial veins into a posterior plexus. Blood from the anterior medial spinal vein and from the posterior plexus of veins enters a series of anastomotic veins, which penetrate the dura and enter the internal and external vertebral plexi. These systems extend throughout the length of the spinal canal and anastomose with the vena cava, the azygos, and thehemiazygos systems. Such an arrangement allows blood to be channeled into the pelvic plexus of veins and into the dural sinuses and cerebral veins at the level of the foramen magnum.

 

SPINAL CORD INFARCTION

Definition

Spinal cord infarction results from inadequate blood supply to the spinal cord parenchyma.

 

Etiology and Pathology

The development of spinal cord infarction is influ­enced by a number of anatomical, physiological, and pathological factors, including:

1.    Site of occlusion. The farther from the cord the occlusion occurs, the better the chance of de­veloping collateral circulation.

2.    Anatomical variation. The greater the number of anastomotic vessels to the cord, the better the chance of avoiding infarction should ananasto­motic vessel or its parent vessel become occluded.

3.    Onset of occlusion. Gradual occlusion of a vessel permits the development of collateral circula­tion and is less likely to cause infarction than rapid occlusion. A decrease in perfusion pressure in the anastomotic vessels produces spinal cord ischemia and increases the chance of infarction.

4.    Systemic   blood  pressure.   Hypotension due to cardiac arrest or acute blood loss decreases perfusion pressure and increases the chance of infarc­tion.

5.    Hypoxia.   Chronic   hypoxia   results   in lower  arterial  oxygen  tension   and  increases  the chance of infarction. Acute hypoxia caused by car­diac or pulmonary arrest may result in infarction.

6.    Atherosclerosis. Progressive atherosclero­sis involving the aorta, anastomotic vessels, or the spinal arteries reduces blood flow to the cord and in­creases the chances of infarction.

7.    Inflammation.   Arteritis   (syphilis,   giant cell arteritis, or polyarteritis nodosa) of the anasto­motic vessels or the anterior spinal artery and its branches will increase the chance of thrombosis and infarction.

8.    Embolism.  Emboli can arise from the heart   or   become   detached   from   atherosclerotic plaques in the aorta, iliac vessels, vertebral, inter­costal, or lumbar arteries and enter the circulation of the spinal cord. Cartilaginous embolism from the nu­cleus pulposus of a herniated intervertebral disc has been reported.

9.    Trauma. The spinal arteries and anasto­motic vessels are susceptible to trauma. Fracture dis­location, cervical subluxation, spondylosis, and disc protrusion may produce damage to the intercostal, lumbar, or anastomotic vessels.

10. Anastomotic arteries may be occluded by a dissecting aneurysm of the aorta or by surgical pro­cedures for aortoiliac occlusive disease.

11. Sickle cell disease with progressive nar­rowing and thrombosis of the anastomotic arteries, or anterior spinal arteries, may lead to ischemia and in­farction.

The pathology of ischemia shows some varia­tion according to the site of the involved vessel. When the aorta is involved, there may be occlusion at the origin of the intercostal or lumbar arteries due to aortic aneurysm, dissecting aneurysm of the aorta, thrombosis, or surgical procedures of the aorta. The vertebral arteries are susceptible to thrombosis owing to atherosclerosis, after cervical injury or chiropractic manipulation, which can cause occlusion or dissect­ing aneurysm of the vertebral arteries. Intercostal and lumbar arteries are occasionally injured in thora­coplasty and resection of an aortic aneurysm. An anastomotic artery may be occluded following trauma to the spine or the development of primary ormetastatic tumors of the spine. There may be involve­ment due to osteomyelitis of the spine or tuberculous osteomyelitis (Pott’s disease). In addition, the vessel may be involved by an arteritis in syphilis or collagen vascular diseases. Anterior and posterior spinal arter­ies may be occluded because of trauma with fracture dislocation of the spine or pressure from a herniated lumbar disc. The anterior spinal artery is particularly susceptible to compression in cases of cervical spondylosis.

The pathological changes in infarction of the spinal cord resemble those seen in ischemic infarc­tion of the brain with necrosis of the gray matter fol­lowed by astroglial proliferation and formation of a glial scar.

 

Clinical Features

All of the signs and symptoms of spinal cord infarc­tion can be attributed to a lesion within the distribu­tion of the occluded vessel.

Transient ischemic attacks of the cervical spinal cord may resemble “drop attacks” without loss or im­pairment of consciousness, and are usually attributed to ischemia of the medullary pyramids. Intermittent attacks can also occur in coarctation of the aorta with an associated “steal” of blood from the spinal cord. Shunting of blood to a low resistance vascular mal­formation in the spinal cord may produce temporary ischemia in the surrounding area. Intermittent com­pression of the spinal cord in patients with spinal stenosis can produce temporary symptoms of cord isch­emia.

The onset of transient ischemia may be sudden or gradual, with deficits developing in an hour or less. Motor symptoms can consist of abrupt onset of quad-riplegia or paraplegia presenting with sudden loss of tone in all four limbs and a drop attack. The less acute episodes consist of numbness, pain, tingling, aching, and cramping below the level of the cord in­volvement, with limb weakness and loss of bladder and bowel function followed by recovery over several hours.

When the anterior spinal artery is occluded, in­farction may occur some distance from the site of oc­clusion, in an area of cord that is a boundary zone be­tween two anastomotic arteries. In this case, there is initial flaccid paralysis and loss of reflexes with a sensory level displaying loss of pain and temperature sensation below the area of infarction. Sphincter con­trol is lost, with bladder and bowel paralysis. The ini­tial flaccidity is followed by a gradual development of spasticity, hyperreflexia, and bilateral extensor plantar responses.³ Occlusion of the cervical anastomoticbranch of the anterior spinal artery produces a combi­nation of upper and lower motor neuron abnormali­ties. There are weakness and wasting of muscles in the upper limb supplied by the appropriate anterior horn cells at the level of the infarct with flaccid quadriparesis progressing gradually to spastic para­paresis and loss of pain and temperature sensation be­low the level of the lesion.

Infarction in the thoracic cord produces a flac­cid paraplegia with gradual progression to spastic paraparesis and impairment or loss of bladder con­trol. This is associated with a dissociated sensory loss and eventually with some return of bladder function.

Lesions of the lumbosacral cord tend to pro­duce flaccid paraparesis because of destruction of the motor neurons of the anterior horn cells at this level. A dissociated sensory loss and incomplete involve­ment of bowel and bladder function are apparent.

It is not unusual to encounter incomplete in­farction of the spinal cord. The effects of infarction depend on the efficiency of the collateral circulation, and only small segments of the anterior two-thirds of he spinal cord may be irreversibly damaged after oc­clusion of the anterior spinal artery or its branches.

Posterior spinal artery occlusion is very rare. Syphilitic arteritis is believed to have been the major cause of this condition in the past. However, trauma, infection, or compression of the posterior spinal ar­teries may compromise the circulation sufficiently to produce infarction of the posterior one-third of the spinal cord. The clinical picture is tabetic-like, with progressive ataxia and loss of vibration and position sense. Tendon reflexes are depressed or absent. There may be retention of urine with painless distention of the bladder. Spinal cord compression should be relieved and infection controlled by appropriate antibiotic therapy. Urinary retention or incomplete emptying can be managed with intermittent self-catheterization. Gait may be improved by physical therapy.

 

Table 12-1

Differential diagnosis: cord infarction, transverse myelitis, epidural abscess

Infarction	Transverse myelitis	Epidural abscess
Age
Elderly, unless some unusual	Any age	Any age
easily identifiable condition
exists (e.g., syphilis)
Pain
Acute onset, radicular	Yes. Often interscapular with	Yes. At site of abscess
distribution	radiation into the abdomen
	and lower limbs
Onset of spasticity
Acute onset, initially flaccid	May be acute or insidious	Insidious onset, spastic lower
followed by development of	onset. May be prolonged	extremities                           j
spasticity	flaccidity	r
Spinalfluid		<■
Normal	Abnormal. Inflammatory cells	Abnormal. Xanthochromic if
	and elevated protein content	complete block,
		polymorphonuclear
		leukocytosis, protein
		elevated, glucose normal
Peripheral nerve involvement
None (except diabetic	Yes. Lesion may involve nerve	None (except diabetic
neuropathy)	roots	neuropathy)
Dissociated sensory loss
Yes	Unusual	No
X-ray spine
Normal	Normal	Osteomyelitis in some cases
Myelography
Normal	Normal	Extradural compression, may
		be a complete block
MRI scan
Abnormal, round Hypointensity Tl	Hypointensity Tl	Obstructed epidural space by
Hyperintensity T2	Hyperintensity T2	enhancing mass
Areas in acute infarction	Areas in white matter

 

 

Diagnostic Procedures

1.  Lumbar puncture. The cerebrospinal fluid (CSF) is normal in appearance, and there is little or no cellular response. The protein content may be elevated.

2.  Magnetic resonance imaging (MRI) will show a round area of hypointensity of Tl-weighted im­ages and hyperintensity on T2-weighted images in an acute ischemic infarction of the spinal cord. This changes to a strand-like abnormality with negative enhancement after infusion of gadolinium several weeks later.

 

Differential Diagnosis

Table 12-1 differentiates cord infarction, transverse myelitis, and epidural abscess.

 

Treatment

Treatment is as for cerebral infarction.

 

Prognosis

Many patients with spinal cord infarction show grati­fying return of function in the lower limbs and con­siderable improvement in bowel and bladder function over a period of several months. Prevention of further infarction depends on the control of precipitating fac­tors discussed in Chapter 8. Patients with atheroscle­rosis run a high risk of coronary artery disease and cerebral thrombosis.

 

INTERMITTENT CLAUDICATION OF THE SPINAL CORD

Intermittent ischemia of the spinal cord or cauda equina may result in transient pain, weakness, and numbness in one or both lower limbs during exercise. The disorder is believed to result from narrowing of the spinal canal, herniation of a lumbar disc, or lum­bar spondylosis, leading to spinal stenosis that results in pressure on the spinal cord or cauda equina. A sim­ilar ischemic effect can occur in aortoiliac occlusive disease. Patients with this condition develop aching in one or both calves followed by paresthesias of one or both feet while walking. Continued walking may result in foot drop. Examination reveals that the cir­culation of both lower limbs is adequate. There is ex­aggeration of tendon reflexes if the spinal cord is in­volved. Radiography, MRI, or computed tomography (CT) scanning of the lumbosacral spine will show the presence ofosteoarthritis and narrowing of interverte­bral disc spaces. Surgical removal or herniated discs and decompression of the spinal stenosis will result in improvement.

 

CHRONIC ISCHEMIA OF THE SPINAL CORD

It is likely that change in the cervical cord in some in­dividuals with cervical spondylosis are due to a com­bination of compression of the cord and ischemia of the cord due to compression of the vasculature. This would account for the development of symptoms in­dicating damage to the cord above and below the site of the lesion.

 

ARTERIOVENOUS MALFORMATION OF THE SPINAL CORD

Definition

Most arteriovenous malformations (AVMs) involving the spinal cord are low-flow conditions. Symptoms are probably the result of increased venous pressure and cord ischemia.

 

Pathology

Spinal AVMs are categorized into four types. Type 1 (dural arteriovenous fistula) is divided into types la and lb.

Type la, the most common type of spinal AVM, is usually found on the dorsal aspect of the thoracic spinal cord or the conus medullaris. There is a single arterial feeder entering the dura at the dural root sleeve. The arteriovenous fistula lies within the dura and the venous outflow drains intradurally into an ar-terialized vein extending several segments above and below, draining into the venous plexus on the dorsal surface of the spinal cord. Type lb AVMs are similar to la AVMs but have multiple additional feeders at one or two adjacent levels that communicate with the dural nidus. Type 2 (glomus) AVMs have a nidus lying within the spinal cord and are fed by multiple feeders from the anterior spinal and posterior spinal arteries. Type 3 (juvenile) AVMs are rare. They are intermedullary but have extramedullary and occasional extraspinal extensions. Type 4 AVMs (intra- or perimedullary fistulae) are intradural extramedullary fistulas fed by the anterior and posterior spinal arteries and are found outside the spinal cord. There are three subdivisions: type 4a, simple extramedullary fistulae; type 4b, intermediate in size extramedullary and supplied by one or more feeders; and type 4c, giant AVMs fed by the anterior spinal artery and draining into a greatly dilated and tortuous plexus of veins. The high-flow shunting may lead to a form of vascular steal from the intrinsic spinal cord arterial supply and cause ischemia of the spinal cord.

 

Clinical Features

Most patients with an AVM of the spinal cord experi­ence pain at the level of the lesion or in the lower limbs. The pain may be constant or episodic and is often of an unpleasant burning quality. Some pa­tients show progressive spastic paraparesis with or without evidence of a lower motor neuron lesion. This is typical of the type la dural arteriovenous fistula, which produces a chronic myelopathy sec­ondary to increased venous pressure and impaired ve­nous drainage from the spinal cord.⁸ Urgency, fre­quency, and incontinence are present in about two-thirds of patients. Sensory deficits occur below the level of the lesion and affect all sensory modali­ties. The neurological deficits tend to progress in astepwise fashion over a period of months or years. Sudden paraplegia from hemorrhage or infarction may occur at any time. Rupture of an AVM with spinal subarachnoid hemorrhage is unusual but has been reported.⁹

 

Diagnostic Procedures

1.  The MRI will demonstrate the site of the malfor­mation and the presence of any hemorrhage.

2.  Superselective arteriography is needed to demon­strate the extent of the AVM, its feeding vessels, and its type.

 

Treatment

Direct removal of the AVM is the treatment of choice in type 1 malformations. The best results with type 2 AVMs are probably obtained withpreoperative em­bolization and subsequent surgical resection. Because type 3 AVMs are intermedullary and extramedullary, they require feederligation embolization and partial resection.

A small type 4 AVM can be removed surgi­cally; those of medium size require embolization and surgical excision, whereas large type 4 AVMs are treated by embolization alone. Embolization is, however, followed by a recanalization in some cases.¹¹

 

VENOUS SPINAL CORD INFARCTION

Three types of venous infarction of the spinal cord have been recognized: embolic, hemorrhagic, and nonhemorrhagic. Embolic infarctions are associ­ated with venous embolism elsewhere, such as pul­monary embolism, and produce sudden back pain with symmetrical dysfunction and dissociate sensory loss. Hemorrhagic infarctions have equally sudden onset with back pain or radicular pain, progressive neurological dysfunction, and a high mortality rate. Nonhemorrhagic infarction is more gradual and pain­less, with neurological signs evolving over several weeks.

Venous spinal cord infarction is often diag­nosed as a transverse myelitis. Angiography may be helpful and MRI scanning will help to rule out hem­orrhage. Nonhemorrhagic cases should be treated with anticoagulation.