Iron-silica membranes geochemical plausibility and catalytic potential

Spinal cord lesions may result from different lesions in the cervical and thoracic spines; most commonly these are:

degenerative changes producing stenosis in the cervical spinal canal

disc lesions in the thoracic spinal canal.

In the cervical spine some authors make a distinction between mechanical and vascular causes of myelopathy, and whether it is combined with radiculopathy (Ferguson and Caplan 1 985). Signs and symptoms vary due to different spinal levels being involved.

Cervical

At surgery in the cervical spine, two causes of myelopathy and radicu­

lopathy have been noted: soft or hard disc herniations. Hard discs refer to bony growths, such as foraminal spurs, transverse bony ridges on the vertebral body, uncovertebral exostosis and other degenera­

tive changes that occur with cervical spondylosis (Odom et al. 1958;

Henderson et al. 1983; Mosdal and Overgaard 1 984; Allen 1952).

Spondylotic bars or ridges encroach into the spinal canal, whilst hypertrophying bony tissue from the zygapophyseal or the uncovertebral joints encroach into the foramen (Parke 1 988) . Soft disc herniation, that is cervical disc prolapse, has also been reported to be the cause of radiculopathy and myelopathy (Bertalanffy and Eggert

1988; Young and O'Laoire 1987; O'Laoire and Thomas 1 983).

Cervical spondylotic myelopathy is reported to be the most common cord lesion after middle age (Young 2000) , but cervical spondylotic radiculopathy is more prevalent (Bland 1994; Yu et al. 1 987).

Patients may present with predominantly an upper motor lesion or predominantly a lower motor lesion, but a mixed pattern does occur (Gregorious et al. 1976; Bertalanffy and Eggert 1988). There may be lower motor involvement at the level of the lesion and upper motor neurone below this level (Clark 1 9 9 1 ) . In general, cervical myelopathic symptoms are dependent on the etiologic process and the pathophysiology that is present.

Five categories of cervical spondylotic myelopathy based on neuro­

logical findings have been described in order of decreasing frequency (Crandal and Batzdorf 1 966; Clark 1 9 9 1 ):

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• transverse lesion syndrome - corticospinal, spinothalamic and posterior column involvement

• motor syndrome - corticospinal or anterior horn cell

• central cord syndrome - motor and sensory involvement of upper extremities more than lower extremities

• Brown-Sequard syndrome - unilateral cord lesion, with ipsilateral corticospinal tract involvement and contralateral analgesia below the level of the lesion

• brachialgia and cord syndrome - predominant upper limb pain, with some long tract involvement.

Cord involvement may or may not be symmetrical, so symptoms may be bilateral or unilateral. The tracts most commonly affected are the pyramidal, spinothalamic and posterior column (Yu ^et al. 1987). Cord involvement may be characterised by a deep aching pain and burning sensation (Clark 1 9 9 1 ) . Signs and symptoms are those of an upper motor lesion and spinal pain is not always present .

More commonly myelopathy arises from lesions in the lower cervical spine causing lower limb involvement, with non-dermatomal patterns of muscle weakness and/or sensory disturbance, hyperreflexes, and bladder or bowel dysfunction. Less commonly upper cervical segments are involved and symptoms mainly affect the upper limbs (Clark 1 99 1 ). There are no or minimal symptoms in the legs, but paraesthesia and proprioceptive loss in the hands. Typically the patient complains of numb, clumsy hands and loss of dexterity.

Cases have been reported of mid-cervical lesions causing predomi­

nantly upper extremity signs and symptoms (Shinomiya ^et al. 1994;

Nakajima and Hirayama 1 99 5 ) . Motor loss at deltoid, possibly associated with sensory loss or localised pain, or numbness in the fingers and clumsiness of the hands were predominant symptoms, but examination reveals changes in the lower limbs also. As in other areas, a mixture of lower and upper motor neurone changes may be present.

Onset tends to be insidious, unless trauma is involved, and diagnosis may not be made for several years. The neurological signs and symptoms vary, considerably reflecting the nature and site of the lesion, the rate of progression and the extent of degenerative changes (see Table 8.2).

S E RI O U S S P I N A L PAT H O LOGY

In the cervical spine, as myelopathy is associated with degenerative changes, the patient is likely to be 50 years old or more.

As in other areas of the spine, stenotic symptoms have a static and dynamic, and possibly an ischaemic component (Zeidman and Ducker 1998; Young 2000) . The static factors relate to congenitally narrow canals as well as the degenerative changes of cervical spondylosis, whilst the dynamic component involves the narrowing effect extension has on the spinal canal and intervertebral foramen, and the translation of vertebrae on each other (Nurick 1 972a; Edwards et al. 2003 ; Magnaes 1982). Thus flexion may temporarily relieve symptoms and extension temporarily increase them.

Natural history and treatment options

These patients should not be treated with mechanical forces; they should be referred for further investigations. However, it may be helpful to have an understanding of the natural history and the treat­

ment options available.

Few studies of the natural history of spondylotic myelopathy have been performed (Lees and Turner 1 96 3 ; Nurick 1 972b; Philips 1973) and those that have were small , with dissimilar disability grading systems and outcomes that were not comparable (Zeidman and Ducker 1 998). It has been reported that myelopathy is nearly always a progressive condition (Bohlman and Emery 1 988). In some cases rapid deterioration can occur; once the spinal cord has reached a critical level of compression, trivial trauma may produce sudden and severe symptomatology and neurological deficit (Bohlman and Emery 1 988) . Chronic myelopathy secondary to cervical spondylosis can also occur (Zeidman and Ducker 1 998).

However, although the evidence is of poor quality, it seems that the prognosis for those with cervical myelopathy can be variable. From a review of several early studies, Edwards et al. (2003) concluded that although the majority of patients experienced gradual deterioration in their neurological status, some improved with conservative treat­

ment. A conservative approach to management of cervical myelopathy has been demonstrated to be a viable option, with outcomes as good as surgery, in patients with mild to moderate symptoms and shorter disease duration (Yoshimatsu et al. 200 1 ; Kadanka et al. 2002). (See Surgery for cervical and thoracic problems section in Chapter 9.)

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Thoracic

Thoracic spinal stenosis is rarely mentioned in the literature. It is much less common compared to its incidence in the cervical and lumbar spine, with no information about its natural history (Errico et al. 1997; Kalfas 2000) . One author reports six cases of thoracic myelopathy associated with thoracic spinal stenosis (Barnett et al.

1 987). Thoracic stenosis is usually the result of degenerative changes in the three-joint complex of the spine (disc and zygapophyseal joints) , with hypertrophy of the zygapophyseal joints and osteophyte narrowing of the spinal canal resulting in pain and neurologic symptoms (Errico et al. 1997; Barnett et al. 1 987)

Reports of thoracic spinal cord lesions due to disc herniations are more common. The anatomy of the thoracic spinal canal as well as the blood supply to the thoracic cord predispose to a spinal cord impingement from even a relatively small disc herniation (Errico et al. 1 997)

Thoracic disc herniations are said to make up only 1- 2% of all spinal disc herniations (Kramer 1 990; Arce and Dohrmann 1985; Mellion and Ladeira 200 1 ) . Given the comparatively low proportion of thoracic problems, the large number of these reports suggests the need for greater alertness for this 'red flag' in this region. Disc protrusion in a central posterior direction may affect the spinal cord, which includes about 70% of herniations (Arce and Dohrmann 1 985; Melhon and Ladeira 200 1 ) . Unusual presentations with diffuse symptoms have been reported, such as chronic shoulder pain or buttock and thigh symptoms, which sometimes make it a diagnostic challenge (Wilke et al. 2000; Singer and Edmondston 2000) .

Synopses of the literature have been performed at different dates (Arce and Dohrmann 1 985; Mellion and Ladeira 200 1 ) . Herniations may occur at any segmental level, but the majority occur in the lower thoracic spine and reports of upper thoracic disc herniations are extremely rare (Arce and Dohrmann 1 985; Mellion and Ladeira 200 1 ; Singounas e t a1. l992 ; Arseni and Nash 1 960; Russell 1989) . As the narrowest section of the spinal canal is between T 4 -T9, thoracic disc herniations may affect the cord in a disproportionate way (Kramer 1 990; Logue 1 952; Ravichandran and Frankel 1981).

Presentation will be extremely variable, but three patterns are common (Mellion and Ladeira 200 1 ) :

S E RI O U S S P I N A L PAT H O LOGY

somatic - 10caVradiating pain

radicular pain - band-like chest pain/lower extremity pain

• cord compression signs - motor weakness/sensory disturbances/

bladder and bowel disturbance.

Thoracic disc herniations presenting with somatic and/or radicular symptoms can be given a mechanical evaluation in the normal way, although Failure to respond in the second group may lead to classifi­

cation as an irreducible derangement. The third group is the concern of this section.

Onset has been reported to be insidious in at least 70% of cases (Arce and Dohrmann 1985; Mellion and Ladeira 200 1 ; Russell 1 989). Only in a minority of cases is there a history of acute onset cord signs and symptoms. Most commonly symptoms start as back pain and spread to include more serious sensory and motor symptoms over time, possibly in an episodic way However, back pain may not even be present This means that long delays between onset of symptoms and diagnosis may occur, espeCially as there maybe confusion with visceral disease because of the site of symptoms

Patients with thoracic disc herniations have been misdiagnosed with cardiac, pulmonary, gastrointestinal, renal, cardiac neurosis or psychiatric disorders (Mellion and Ladeira 200 1 ) . Prolonged misdiagnosis as a non-specific complaint may not only lead to inappropriate treatment, but to spinal cord compression and permanent upper motor neurone lesion . There will be a variety of presentations that may or may not include pain, with a mixture of neurological signs and symptoms related to an upper motor lesion (Table 8.2).

As symptoms are due to a disc herniation rather than degenerative changes, as in the cervical spine, the age is usually younger with reported mean ages in the 40s (Mellion and Ladeira 200 1 ).

Disc herniations at upper thoracic levels are rare (Mellion and Ladeira 200 1 ) and are usually manifested by symptoms in the ulnar distribution in the arm and sensory or motor deficit in the hand. A lesion at Tl may be accompanied by the signs of Horner's syndrome (see above). Pain may involve the neck, scapular and anterior upper chest, and there may be reduced reflexes in the upper limb. It has been suggested that as mechanical Tl lesions are so rare, clinicians

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should always be aware of non-mechanical and serious pathology (Mellion and Ladeira 200 1 ) .

Table 8.2 Signs and symptoms associated with spinal cord lesions in the cervical and thoracic spine

Cervical spine ^• non-myotomal weakness/wasting in the hands

Cervical and thoracic spine

• clumsiness of the hands/diminished dexterity

• non-myotomal weakness and atrophy upper limb

• non-dermatomal paraesthesia/numbness upper limb

• Lhermitte's sign -electric shock-type sensation down spine or legs on neck flexion.

• non-dermatomal paraesthesia/numbness in lower limbs

• non-myotomal muscle weakness in lower limbs;

may present initially as stiffness, clumsiness and unsteadiness in the limbs and progress to gail disturbance!broad-based gait

• decreased co-ordination

• flaccid/spastic paraplegia

• increased tone/spasticity

• hyperreflexes

• extensor plantar reflex/positive Babinski sign

• clonus

• bladder, bowel or genital dysfunction -retention!

incontinence/sphincter disturbance.

Source: Yu ^et al. 1987; _Clark 1991; Lestini and Wiesel 1989; Connell and Wiesel 1992; _Arce and Dohrmann 1985; Mellion and Ladeira 2001; _Edwards et al. 2003