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Diseases of the spinal cord.pptx
- 1. Diseases of thespinal cord Dr.Chala R(MD) March 2022 1
- 2. Introduction • Diseases ofthe spinal cord are frequently devastating. • They produce quadriplegia, paraplegia, and sensory deficits far beyond the damage as the spinal cord contains, in a small cross-sectional area, almost the entire motor output and sensory input of the trunk and limbs. • Many spinal cord diseases are reversible if recognized and treated at an early stage • Knowledge of relevant spinal cord anatomy is often the key to correct diagnosis 2
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- 5. SYMPTOMS AND SIGNS •Sensory symptoms often include paresthesias; may begin in one or both feet and ascend. Sensory level to pin sensation or vibration often correlates well with location of transverse lesions. May have isolated pain/temperature sensation loss over the shoulders (“cape” or “syringomyelic” pattern) or loss of sensation to vibration/position sense on one side of the body and pain/temperature loss on the other (BrownSéquard hemicord syndrome). • Motor symptoms are caused by disruption of corticospinal tracts that leads to quadriplegia or paraplegia with increased muscle tone, hyperactive deep tendon reflexes, and extensor plantar responses. With acute severe lesions, there may be initial flaccidity and areflexia (spinal shock). • Autonomic dysfunction includes primarily urinary retention; should raise suspicion of spinal cord disease when associated with back or neck pain, weakness, and/ or a sensory level. • Interscapular pain may be first sign of midthoracic cord compression; radicular pain may mark site of more laterally placed spinal lesion; pain from lower cord (conus medullaris) lesion may be referred to low back. 5
- 6. SPECIFIC SIGNS BYSPINAL CORD LEVEL • Approximate indicators of level of lesion include the location of a sensory level, a band of hyperalgesia/hyperpathia at the upper end of the sensory disturbance, isolated atrophy or fasciculations, or lost tendon reflex at a specific spinal cord segment. 6
- 7. Lesions Near theForamen Magnum • Weakness of the ipsilateral shoulder and arm, → • followed by weakness of ipsilateral leg,→ • then contralateral leg, → • then contralateral arm, often with respiratory paralysis. • There is often suboccipital pain spreading to the neck and shoulders 7
- 8. Cervical Cord • Bestlocalized by noting pattern of motor weakness and areflexia; • Upper cervical cord lesions produce quadriplegia and weakness of the diaphragm. • The uppermost level of weakness and reflex loss with lesions at shoulder (C5), the biceps(C5–6); brachioradialis (C6), finger and wrist extensors and triceps(C7); and finger, and wrist flexion(C8). • Horner’s syndrome (miosis, ptosis, and facial hypohidrosis) may accompany a cervical cord lesion at any level. 8
- 9. Thoracic Cord • ThoracicCord Lesions here are localized by the sensory level on the trunk and, if present, by the site of midline back pain. • Useful markers of the sensory level on the trunk are the nipples (T4) and umbilicus (T10). • Leg weakness and disturbances of bladder and bowel function accompany the paralysis. • Lesions at T9-T10 paralyze the lower—but not the upper— abdominal muscles, resulting in upward movement of the umbilicus when the abdominal wall contracts (Beevor’s sign) 9
- 10. Lumbar Cord • Upperlumbar cord lesions paralyze hip flexion and knee extension and abolish the patella reflex, whereas • lower lumbar lesions affect foot and ankle movements, knee flexion, and thigh extension, while abolishing the ankle jerks. • Lumbar Cord Lesions at the L2-L4 spinal cord levels paralyze flexion and adduction of the thigh, weaken leg extension at the knee, and abolish the patellar reflex. • Lesions at L5-S1 paralyze only movements of the foot and ankle, flexion at the knee, and extension of the thigh, and abolish the ankle jerks (S1). 10
- 11. Sacral Cord (ConusMedullaris) • The conus medullaris is the tapered caudal termination of the spinal cord, comprising the sacral and single coccygeal segments. • The distinctive conus syndrome consists of , The bulbocavernosus (S2-S4) and anal (S4-S5) reflexes are absent . 11
- 12. Cauda Equina (Clusterof Nerve Roots Derived from Lower Cord) • Lesions below spinal cord termination at the L1 vertebral level produce a flaccid, areflexic, asymmetric paraparesis with possible bladder/bowel dysfunction and sensory loss below L1; pain is common and projected to perineum or thighs. • . By contrast to lesions of conus medullaris, the lesions of the cauda equina, the nerve roots derived from the lower cord, are characterized by low back and radicular pain, asymmetric leg weakness and sensory loss, variable areflexia in the lower extremities, and relative sparing of bowel and bladder function. • Mass lesions in the lower spinal canal often produce a mixed clinical picture with elements of both cauda equina and conus medullaris syndromes. 12
- 13. INTRAMEDULLARY AND EXTRAMEDULLARY SYNDROMES •Spinal cord disorders may be intramedullary (arising from within the substance of the cord) or extramedullary (compressing the cord or its blood supply). • Extramedullary lesions often produce radicular pain, early corticospinal signs, and sacral sensoryloss. • Intramedullary lesions produce poorly localized burning pain, less prominent corticospinal signs, and often spare perineal/sacral sensation 13
- 14. ACUTE AND SUBACUTESPINAL CORD DISEASES • Symptoms of the cord diseases that evolve over days or weeks are focal neck or back pain, followed by various combinations of paresthesias,sensory loss, motor weakness, and sphincter disturbance. • Compressive and Noncompressive Myelopathy 14
- 15. DISTINGUISHING COMPRESSIVE FROM NONCOMPRESSIVEMYELOPATHY •The first priority is to exclude treatable compression of the cord by a mass lesion. • The common causes are tumor, epidural abscess or hematoma, herniated disk, and spondylitic vertebral pathology. • Epidural compression due to malignancy or abscess often causes warning signs of neck or back pain, bladder disturbances, and sensory symptoms that precede the development of paralysis. Spinal subluxation, hemorrhage, and noncompressive etiologies such as infarction are more likely to produce myelopathy without antecedent symptoms. • Magnetic resonance imaging (MRI) with gadolinium, centered on the clinically suspected level, is the initial diagnosticprocedure if it is available; 15
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- 17. COMPRESSIVE MYELOPATHIES • Neoplasticspinal cord compression : Most are epidural in origin, resulting from metastases to the adjacent spinal bones. • Almost any tumor can be responsible: breast, lung, prostate, kidney, lymphoma, and myeloma most frequent. • Thoracic cord most commonly involved. Initial symptom is usually back pain, worse when recumbent, with local tenderness preceding other symptoms by many weeks. • Spinal cord compression due to metastases is a medical emergency; in general, therapy will not reverse paralysis of >48 h duration. 17
- 18. • Spinal epiduralabscess: Triad of fever, localized midline dorsal spine or neck pain, and progressive limb weakness; once neurologic signs appear, cord compression rapidly progresses. • Spinal epidural hematoma: Presents as acute focal or radicular pain followed by variable signs of a spinal cord or conus medullaris disorder. • Acute disk herniation: Cervical and thoracic disk herniations are less common than lumbar. 18
- 19. NONCOMPRESSIVE MYELOPATHIES • Themost frequent causes of noncompressive acute transverse myelopathy are spinal cord infarction; systemic inflammatory disorders,including SLE and sarcoidosis; demyelinating diseases, including multiple sclerosis (MS); neuromyelitis optica (NMO); postinfectious or idiopathic transverse myelitis, which is presumed to be an immune condition related to acute disseminated encephalomyelitis ;and infectious (primarily viral) causes. • After spinal cord compression is excluded, the evaluation generally requires a lumbar puncture and a search for underlying systemic disease . 19
- 20. • Spinal cordinfarction: Anterior spinal artery infarction produces paraplegia or quadriplegia, sensory loss affecting pain/temperature but sparing vibration/position sensation (supplied by posterior spinal arteries), and loss of sphincter control. • Onset sudden or progressive, evolving over minutes or a few hours. Associated conditions:Aortic atherosclerosis, dissecting aortic aneurysm, vertebral artery occlusion or dissection in the neck, aortic surgery, or profound hypotension. • Therapy is directed at the predisposing condition. Lumbar drainage of spinal fluid is sometimes used prophylactically during aortic surgery but has not been studied systematically. 20
- 21. CHRONIC MYELOPATHIES • Spondyliticmyelopathies: One of the most common causes of gait difficulty in the elderly. Presents as neck and shoulder pain with stiffness, radicular arm pain, and progressive spastic paraparesis with paresthesias and loss of vibration sense; in advanced cases, urinary incontinence may occur. A tendon reflex in the arms is often diminished at some level. Diagnosis is best made by MRI. Treatment is surgical . • Vascular malformations: An important treatable cause of progressive or episodic myelopathy. May occur at any level; diagnosis is often suggested by contrastenhanced MRI , but is confirmed by selective spinal angiography. Treatment is embolization or surgery with occlusion of the major feeding vessels. • Retrovirus-associated myelopathies: Infection with human T-cell lymphotropic virus I (HTLV-I) may produce a slowly progressive spastic paraparesis with variable pain, sensory loss, and bladder disturbance; diagnosis is made by demonstration of specific serum antibody. Treatment is symptomatic. A progressive vacuolar myelopathy may also result from HIV infection. • Syringomyelia: Cavitary expansion of the spinal cord resulting in progressive myelopathy; may be an isolated finding or associated with protrusion of cerebellar tonsils into cervical spinal canal (Chiari type 1). Classic presentation is loss of pain/ temperature sensation in the neck, shoulders, forearms, or hands with areflexic weakness in the upper limbs and progressive spastic paraparesis; cough headache,facial numbness, or thoracic kyphoscoliosis may occur. Diagnosis is by MRI; treatment is surgical and often unsatisfactory. 21
- 22. • Multiple sclerosis:Spinal cord involvement is common and is a major cause of disability especially in progressive forms of MS . • Subacute combined degeneration (vitamin B12 deficiency): Paresthesias in hands and feet, early loss of vibration/position sense, progressive spastic/ataxic weakness, and areflexia due to associated peripheral neuropathy; mental changes and optic atrophy may be present along with a serum macrocytic anemia. Diagnosis is confirmed by a low serum B12 level, elevated levels of homocysteine and methylmalonic acid. Treatment is vitamin replacement beginning with 1 mg of IM vitamin B12 repeated at regular intervals or by subsequent oral treatment. • Hypocupric myelopathy: Clinically nearly identical to subacute combined degeneration (above) except there is no neuropathy. Low levels of serum copper and usually ceruloplasmin make the diagnosis. Some cases are idiopathic and others follow GIprocedures that hinder absorption; excess zinc ingestion is another cause. Treatment is oral copper supplementation. 22
- 23. • Tabes dorsalis(tertiary syphilis): May present as lancinating pains, gait ataxia,bladder disturbances, and visceral crises. Cardinal signs are areflexia in the legs,impaired vibration/position sense, Romberg sign, and Argyll Robertson pupils which fail to constrict to light but accommodate. • Familial spastic paraplegia: Progressive spasticity and weakness in the legs occurring on a familial basis; may be autosomal dominant, recessive, or X-linked. Morethan 30 different loci identified. • Adrenomyeloneuropathy: X-linked disorder that is a variant of adrenoleukodystrophy. Usually, affected males have a history of adrenal insufficiency and then develop a progressive spastic paraparesis. Diagnosis made by elevated very long chain fatty acids in plasma and in cultured fibroblasts. No therapy is clearly effective although bone marrow transplantation and nutritional supplements 23
- 24. COMPLICATIONS Bladder dysfunction withrisk of urinary tract infection; bowel dysmotility; pressure sores; in high cervical cord lesions, mechanical respiratory failure; paroxysmal hypertension or hypotension with volume changes; severe hypertension and bradycardia in response to noxious stimuli or bladder or bowel distention; venous thrombosis and pulmonary embolism. 24