STUDY - Technical - New Dacian's Medicine
Cervical
and Back Pain (2)
Translation Draft
We've now reached the "famous" lumbar discopathy.
We've now reached the "famous" lumbar discopathy.
It
is a common cause of chronic or recurrent lumbar or lower limb
pain, frequently occurring at levels L4 - L5 and L5 - S1,
without "losing" the involvement of higher levels that is
rarer.
The cause of disc disease is often unknown. Degeneration of the pulpy nucleus and fibrous ring, which increases with age, can be asymptomatic or painful. Sneezing, coughing or unimportant movement can cause the prolapse of the pulpy nucleus and the push of the weakened and brittle posterior fibrous nucleus. In severe discopathy, the nucleus can pass through the ring (herniate) or can be removed and reach as free fragment in the vertebral canal.
Symptoms of a broken intervertebral disc are pain, abnormal position and limitation of spine movements (especially flexion) or root pain. The appearance of root pain may suggest the involvement of one or more roots.
A sensitivity disorder with localization on a dermatoma (paresthesia, hyper or hyposensitivity) or asymmetrical reduction or loss of deep tendinous reflexes are more suggestive of a specific root lesion than the appearance of pain.
Motor abnormalities (focal muscle weakness or fasciculation, muscle atrophy) occur less frequently, but the appearance of a myotomal paternal impairment may suggest the specific involvement of a nerve root.
Lumbar discopathy is usually one-sided, but bilateral involvement can be found in large central disc hernias, which compress several nerve roots at the same level. Reflective, sensory, motor and pain-distribution elements related to specific lesions of the roots of the lombosacrate nerves are multiple.
When assessing it should be borne in mind that abscesses or epidural tumors may produce a syndrome similar to herniated disc. Fever, constant pain and lack of positional influence, sphincter abnormalities or signs of medullary distress suggest an etiology other than lumbar discopathy. Bilateral absence of the achilles reflex may occur normally in the elderly or may be a sign of bilateral S1 radiculopathy. The absence of a deep osteotendinous reflex or local loss of sensitivity may be due to damage to a nerve root, but injury to other levels along the nerve is not excluded.
For example, the absence of the patellar reflex may be due to femoral neuropathy rather than damage to the root of the L4 nerve. A decrease in localized sensitivity in the foot or distal lateral portion of the calf may be due to a peronial neuropathy rather than damage to the root of the L5 nerve.
When present, paresthesia can occur throughout the root distribution territory or only in a distal portion of the nerve root territory. "Weakness" may be due to poor training (weakness in running) associated with radicular pain, real asthenia or both.
Electromyography (EMG) can differentiate true weakness from that caused by lack of training: Asymmetric muscle atrophy may reflect chronic loss of motor axons associated with nerve root, nerve injury or muscle decommissioning.
There are 5 indications for surgery: 1. progressive motor deficiency by nerve root injury, 2. progressive damage demonstrated by EMG and nerve conduction studies, 3. altered function of the colon or bladder or other signs of medullary disease, 4. disabling root pain present despite conservative treatment of at least one month and 5. recurrent disabling pain despite conservative treatment (the latter two are more subjective and better established).
Degeneration of the intervertebral disc without the franchise expulsion of the disc tissue can give rise to low dorsolumbar pain, with pain in the lower limb very small or even absent or sometimes pain in the lower limb, with small or absent lumbar discomfort. There are no signs of nerve root involvement, but low back pain can irradiate in the thigh or lower limb.
Lumbar disc syndromes are usually one-sided, but large central disc hernias (with or without the expulsion of a large, free fragment in the vertebral canal) can cause bilateral symptoms and signs. Central and large disc hernias can cause ponytail syndrome, with bilateral signs and symptoms by involving lombosacrate roots.
The diagnosis is certain when all the signs and symptoms indicating disc pain with radiculopathy are presented. When a single symptom is present (especially low back pain), the specific diagnosis can be difficult (MRI investigation of the spine providing excellent intravertebral and adjacent soft tissue anatomy images, some lateral retouch or bone hole lesions can be viewed with sufficient clarity and in TC myelographic studies).
Of course there are other causes of low back pain such as spinal stenosis, facet hypertrophy, lumbar adhesive arachnoiditis and back fall syndrome.
Spinal stenosis is caused by a narrow vertebral canal, symptoms including back pain and lower limb (usually bilateral), caused by gait or orthostatism (pseudoclaudication) and improved by sitting or decubit dorsal positions. Localized weakness, loss of sensitivity or changes in reflexes may occur.
Unlike vascular claudication, symptoms are usually caused by orthostatism without walking. Unlike disc disease, symptoms are usually improved in the sitting position. Severe neurological deficits, including paralysis and urinary incontinence, occur in a small number of cases. Spinal stenosis is acquired in 75% of congenital cases or occurs by association between congenital and acquired factors.
Congenital forms (acondroplasia, idiopathic) are characterized by short and thick pedicules, which produce both anteroposterior (central) stenosis of the vertebral canal and stenosis of the lateral recesses. Acquired factors that may contribute to spinal stenosis include degenerative diseases (spondylose, spondylolistesis, scoliosis), trauma, spinal surgery (postlaminectomy, welding), metabolic or endocrine diseases (epidural lipomatosis, osteoporosis, acromegaly, renal osteodystrophy, hypoparathyroidism) and Paget's disease.
MRI and TC myelography provide the best description of anatomical changes. Conservative treatment includes non-steroidal anti-inflammatory drugs (NSAIDs), exercise programs and symptomatic treatment of pain exacerbation.
Surgical treatment is taken into account when medical treatment does not sufficiently relieve pain to allow daily activities or when neurological signs of outbreak are present (of the 65 to 80% of patients treated surgically, more than 75% have an improvement of lower back or lower limb pain but the remaining approximately 25% have developed recurrent stenosis at the same vertebral level or at an adjacent one , up to 5 years after the initial intervention, recurrent symptoms usually responding to a second surgical decompression).
Unilateral hypertrophy of the articular facet can cause root pain exacerbated and improved by many of the factors that also influence disc radiculopathy, patients often having low back pain and RPI sign (localized muscle weakness, hyporeflection and loss of sensitivity may occur). MRI, TC myelography and surgical exploration can visualize hypertrophy of the upper and lower facets. Foraminotomy and facetectomy can relieve back and lower limb pain in the long term in 80 to 90% of patients.
Lumbar adhesive arachnoiditis with radiculopathy is the result of a fibrosis process following a local tissue inflammatory response to subarachnoid space damage. Fibrosis will produce adhesions of the nerve roots, which will cause low back and lower limb pain, associated with reflex, motor and sensory deficits.
The classic clinical picture occurs in a patient with multiple lumbar surgery or after myelography with oily substances (Pantopeque). Myelography-induced arachnoiditis have become rare, with other causes being chronic spinal infections, spinal cord injuries, intrathecal haemorrhages, intrathecal injection of steroids or anesthetics or foreign bodies.
MRI is the method of selection for demonstrating arachnoiditis. Nerve roots can all adher centrally or join dura mater on the periphery or cause accumulations of cerebrospinal fluid (CRL) in the tecal sac, which may prevent the roots from being viewed.
Current treatments are not satisfactory and sometimes the cause of low back pain remains unknown. Some patients have undergone multiple interventions for disc disease, but continue to have pain and disability. The initial indication for surgery in disc disease is questionable when there is only low back pain, with no clear neurological signs and a minor swelling of the disc, revealed at TC or MRI. Scores based on neurological signs, psychological factors, physiological studies and imaging studies were compiled to minimize the possibility of unsuccessful surgery and to avoid selecting patients with a psychological profile with poor functional results.
Now let's move on to arthritis, spinal arthritis being a major cause of cervical and back pain.
For starters, I'm going to tackle spondylosis. Osteoarthritis of the spine occurs in old age and involves primarily the cervical and lombosacrate spine, patients often accusing pain starting from the spine, accentuated by movement and associated with stiffness and limitation of movements.
The relationship between clinical symptoms and radiological elements is often inconsistent, intense pain exists when radiological diagnostic elements are minimal and large osteophytes are viewed in asymptomatic patients of middle or elderly age. Hypertrophied facets and osteophytes can compress nerve roots into lateral recesses or intervertebral holes.
Osteophytes that arise from the vertebral body can cause central stenosis of the vertebral canal. Decreasing the height of the intervertebral disc decreases the vertical dimensions of the intervertebral hole, causing the compression of the nerve root at that level by the lowered pedicle.
Osteoarthritis changes in the lumbar spine can sometimes cause compression of the horsetail. Degenerative spondylisthesis (slip of a vertebral body on the underlying vertebra) most often occurs at the L5 - S1 level and can further contribute to root compression. Surgical procedures should be considered only after conservative failure.
Ankylosing spondylitis is a distinct form of arthritisl spinal disease that typically presents with insidious lypose and buttock pain in a man under 40 years of age and is associated with morning lumbar redness, nocturnal low back pain, unimproved rest pain, increased VSH and the presence of antigens.
In the initial stages, differential diagnosis includes tumors and infections, but the back pain in ankylosing spondylitis improves characteristically with exercise. With the course of the disease, the loss of normal lumbar lordosis and the exaggeration of thoracic cystosis are observed. Inflammation and erosion of the peripheral fibers of the fibrous ring at the point of contact with the vertebral body are followed by ossification and bone growth.
These bone growths (sindesmopites) bind the adjacent vertebral bodies and produce decreased mobility of the spine for anterior flexion, lateral flexion and extension.
The radiological characteristics of the disease are periarticular destructions, subsequent sclerosis of sacroiliac joints and the joining of the vertebral bodies by bone growths, resulting in characteristic " bamboo column", immobile and welded.
Stress fractures of spontaneously ankylosed posterior bone elements of the rigid and osteoporosis column can produce focal spine pain and medullary compression or ponytail syndrome. Sometimes atlanto-axial subluxation occurs with medullary compression. Bilateral ankylosis of the ribs of the spine and a decrease in the height of the thoracic vertebrae can be causes of severe respiratory dysfunction.
I've only got a little bit left and I'm going to get the neck pain... Tomorrow's post.
The cause of disc disease is often unknown. Degeneration of the pulpy nucleus and fibrous ring, which increases with age, can be asymptomatic or painful. Sneezing, coughing or unimportant movement can cause the prolapse of the pulpy nucleus and the push of the weakened and brittle posterior fibrous nucleus. In severe discopathy, the nucleus can pass through the ring (herniate) or can be removed and reach as free fragment in the vertebral canal.
Symptoms of a broken intervertebral disc are pain, abnormal position and limitation of spine movements (especially flexion) or root pain. The appearance of root pain may suggest the involvement of one or more roots.
A sensitivity disorder with localization on a dermatoma (paresthesia, hyper or hyposensitivity) or asymmetrical reduction or loss of deep tendinous reflexes are more suggestive of a specific root lesion than the appearance of pain.
Motor abnormalities (focal muscle weakness or fasciculation, muscle atrophy) occur less frequently, but the appearance of a myotomal paternal impairment may suggest the specific involvement of a nerve root.
Lumbar discopathy is usually one-sided, but bilateral involvement can be found in large central disc hernias, which compress several nerve roots at the same level. Reflective, sensory, motor and pain-distribution elements related to specific lesions of the roots of the lombosacrate nerves are multiple.
When assessing it should be borne in mind that abscesses or epidural tumors may produce a syndrome similar to herniated disc. Fever, constant pain and lack of positional influence, sphincter abnormalities or signs of medullary distress suggest an etiology other than lumbar discopathy. Bilateral absence of the achilles reflex may occur normally in the elderly or may be a sign of bilateral S1 radiculopathy. The absence of a deep osteotendinous reflex or local loss of sensitivity may be due to damage to a nerve root, but injury to other levels along the nerve is not excluded.
For example, the absence of the patellar reflex may be due to femoral neuropathy rather than damage to the root of the L4 nerve. A decrease in localized sensitivity in the foot or distal lateral portion of the calf may be due to a peronial neuropathy rather than damage to the root of the L5 nerve.
When present, paresthesia can occur throughout the root distribution territory or only in a distal portion of the nerve root territory. "Weakness" may be due to poor training (weakness in running) associated with radicular pain, real asthenia or both.
Electromyography (EMG) can differentiate true weakness from that caused by lack of training: Asymmetric muscle atrophy may reflect chronic loss of motor axons associated with nerve root, nerve injury or muscle decommissioning.
There are 5 indications for surgery: 1. progressive motor deficiency by nerve root injury, 2. progressive damage demonstrated by EMG and nerve conduction studies, 3. altered function of the colon or bladder or other signs of medullary disease, 4. disabling root pain present despite conservative treatment of at least one month and 5. recurrent disabling pain despite conservative treatment (the latter two are more subjective and better established).
Degeneration of the intervertebral disc without the franchise expulsion of the disc tissue can give rise to low dorsolumbar pain, with pain in the lower limb very small or even absent or sometimes pain in the lower limb, with small or absent lumbar discomfort. There are no signs of nerve root involvement, but low back pain can irradiate in the thigh or lower limb.
Lumbar disc syndromes are usually one-sided, but large central disc hernias (with or without the expulsion of a large, free fragment in the vertebral canal) can cause bilateral symptoms and signs. Central and large disc hernias can cause ponytail syndrome, with bilateral signs and symptoms by involving lombosacrate roots.
The diagnosis is certain when all the signs and symptoms indicating disc pain with radiculopathy are presented. When a single symptom is present (especially low back pain), the specific diagnosis can be difficult (MRI investigation of the spine providing excellent intravertebral and adjacent soft tissue anatomy images, some lateral retouch or bone hole lesions can be viewed with sufficient clarity and in TC myelographic studies).
Of course there are other causes of low back pain such as spinal stenosis, facet hypertrophy, lumbar adhesive arachnoiditis and back fall syndrome.
Spinal stenosis is caused by a narrow vertebral canal, symptoms including back pain and lower limb (usually bilateral), caused by gait or orthostatism (pseudoclaudication) and improved by sitting or decubit dorsal positions. Localized weakness, loss of sensitivity or changes in reflexes may occur.
Unlike vascular claudication, symptoms are usually caused by orthostatism without walking. Unlike disc disease, symptoms are usually improved in the sitting position. Severe neurological deficits, including paralysis and urinary incontinence, occur in a small number of cases. Spinal stenosis is acquired in 75% of congenital cases or occurs by association between congenital and acquired factors.
Congenital forms (acondroplasia, idiopathic) are characterized by short and thick pedicules, which produce both anteroposterior (central) stenosis of the vertebral canal and stenosis of the lateral recesses. Acquired factors that may contribute to spinal stenosis include degenerative diseases (spondylose, spondylolistesis, scoliosis), trauma, spinal surgery (postlaminectomy, welding), metabolic or endocrine diseases (epidural lipomatosis, osteoporosis, acromegaly, renal osteodystrophy, hypoparathyroidism) and Paget's disease.
MRI and TC myelography provide the best description of anatomical changes. Conservative treatment includes non-steroidal anti-inflammatory drugs (NSAIDs), exercise programs and symptomatic treatment of pain exacerbation.
Surgical treatment is taken into account when medical treatment does not sufficiently relieve pain to allow daily activities or when neurological signs of outbreak are present (of the 65 to 80% of patients treated surgically, more than 75% have an improvement of lower back or lower limb pain but the remaining approximately 25% have developed recurrent stenosis at the same vertebral level or at an adjacent one , up to 5 years after the initial intervention, recurrent symptoms usually responding to a second surgical decompression).
Unilateral hypertrophy of the articular facet can cause root pain exacerbated and improved by many of the factors that also influence disc radiculopathy, patients often having low back pain and RPI sign (localized muscle weakness, hyporeflection and loss of sensitivity may occur). MRI, TC myelography and surgical exploration can visualize hypertrophy of the upper and lower facets. Foraminotomy and facetectomy can relieve back and lower limb pain in the long term in 80 to 90% of patients.
Lumbar adhesive arachnoiditis with radiculopathy is the result of a fibrosis process following a local tissue inflammatory response to subarachnoid space damage. Fibrosis will produce adhesions of the nerve roots, which will cause low back and lower limb pain, associated with reflex, motor and sensory deficits.
The classic clinical picture occurs in a patient with multiple lumbar surgery or after myelography with oily substances (Pantopeque). Myelography-induced arachnoiditis have become rare, with other causes being chronic spinal infections, spinal cord injuries, intrathecal haemorrhages, intrathecal injection of steroids or anesthetics or foreign bodies.
MRI is the method of selection for demonstrating arachnoiditis. Nerve roots can all adher centrally or join dura mater on the periphery or cause accumulations of cerebrospinal fluid (CRL) in the tecal sac, which may prevent the roots from being viewed.
Current treatments are not satisfactory and sometimes the cause of low back pain remains unknown. Some patients have undergone multiple interventions for disc disease, but continue to have pain and disability. The initial indication for surgery in disc disease is questionable when there is only low back pain, with no clear neurological signs and a minor swelling of the disc, revealed at TC or MRI. Scores based on neurological signs, psychological factors, physiological studies and imaging studies were compiled to minimize the possibility of unsuccessful surgery and to avoid selecting patients with a psychological profile with poor functional results.
Now let's move on to arthritis, spinal arthritis being a major cause of cervical and back pain.
For starters, I'm going to tackle spondylosis. Osteoarthritis of the spine occurs in old age and involves primarily the cervical and lombosacrate spine, patients often accusing pain starting from the spine, accentuated by movement and associated with stiffness and limitation of movements.
The relationship between clinical symptoms and radiological elements is often inconsistent, intense pain exists when radiological diagnostic elements are minimal and large osteophytes are viewed in asymptomatic patients of middle or elderly age. Hypertrophied facets and osteophytes can compress nerve roots into lateral recesses or intervertebral holes.
Osteophytes that arise from the vertebral body can cause central stenosis of the vertebral canal. Decreasing the height of the intervertebral disc decreases the vertical dimensions of the intervertebral hole, causing the compression of the nerve root at that level by the lowered pedicle.
Osteoarthritis changes in the lumbar spine can sometimes cause compression of the horsetail. Degenerative spondylisthesis (slip of a vertebral body on the underlying vertebra) most often occurs at the L5 - S1 level and can further contribute to root compression. Surgical procedures should be considered only after conservative failure.
Ankylosing spondylitis is a distinct form of arthritisl spinal disease that typically presents with insidious lypose and buttock pain in a man under 40 years of age and is associated with morning lumbar redness, nocturnal low back pain, unimproved rest pain, increased VSH and the presence of antigens.
In the initial stages, differential diagnosis includes tumors and infections, but the back pain in ankylosing spondylitis improves characteristically with exercise. With the course of the disease, the loss of normal lumbar lordosis and the exaggeration of thoracic cystosis are observed. Inflammation and erosion of the peripheral fibers of the fibrous ring at the point of contact with the vertebral body are followed by ossification and bone growth.
These bone growths (sindesmopites) bind the adjacent vertebral bodies and produce decreased mobility of the spine for anterior flexion, lateral flexion and extension.
The radiological characteristics of the disease are periarticular destructions, subsequent sclerosis of sacroiliac joints and the joining of the vertebral bodies by bone growths, resulting in characteristic " bamboo column", immobile and welded.
Stress fractures of spontaneously ankylosed posterior bone elements of the rigid and osteoporosis column can produce focal spine pain and medullary compression or ponytail syndrome. Sometimes atlanto-axial subluxation occurs with medullary compression. Bilateral ankylosis of the ribs of the spine and a decrease in the height of the thoracic vertebrae can be causes of severe respiratory dysfunction.
I've only got a little bit left and I'm going to get the neck pain... Tomorrow's post.
What
can I wish you but trust, love and gratitude?
Dorin, Merticaru