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Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease characterized by multiorgan involvement with diverse clinical presentations. Central nervous system involvement in neuropsychiatric syndromes of SLE (NPSLE), such as cerebrovascular disease and myelopathy, is a major cause of morbidity and mortality in SLE patients. The concomitant occurrence of myelopathy, cerebrovascular disease, and peripheral neuropathy in a patient with SLE has not yet been reported. We report on a 41-year-old woman with SLE who showed motor and sensory impairment with urinary retention and was diagnosed with cervical myelopathy and acute cerebral infarction by spine and brain magnetic resonance imaging and peripheral neuropathy by electrodiagnostic examination. Even though pathogenesis of NPSLE is not well elucidated, we assume that increased antibodies of anti-double stranded DNA (anti-dsDNA), presence of lupus anticoagulant and hypertension are risk factors that have caused neuropsychiatric lupus in this patient.
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Myotonic dystrophy is the most common autosomal dominant myopathy in adults. Our patient, a 41 year-old female suffering from myotonic muscular dystrophy, developed upper thoracic myelopathy due to hypertrophy of the ligamentum flavum and the posterior longitudinal ligament. She had a typical hatchet face and ptosis with "head hanging forward" appearance caused by neck weakness. Motor weakness, sensory changes and severe pain below T4 level, along with urinary incontinence began 3 months ago. Genetic and electrodiagnostic studies revealed myotonic dystrophy type 1. Magnetic resonance imaging of the spine showed loss of cervical lordosis and spinal cord compression due to hypertrophied ligamentum flavum and posterior longitudinal ligament at T1 to T3 level. We concluded that her upper thoracic myelopathy was likely related to the thickness of the ligamentum flavum and posterior longitudinal ligament due to repetitive mechanical stress on her neck caused by neck muscle weakness with myotonic dystrophy.
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Spinal dural arteriovenous fistula is a rare vascular lesion of the spinal cord associated with progressive myelopathy. Symptoms include progressive gait dysfunction, weakness, sensory loss, and bowel and bladder dysfunction. Because these symptoms overlap with other common causes of myelopathy and the disease is rare, spinal dural arteriovenous fistula is often not suspected and the time to diagnosis is long. We report the case of a 60-year-old woman who presented with progressive lower limb weakness and gait disturbance diagnosed as spinal dural arteriovenous fistula involving a fractured L1 vertebral body.
Citations
Methods: Thirty nine patients who underwent cervical decompression and fusion for cervical myelopathy were studied. Preoperatively, gait disturbance was present in all patients. The patients were evaluated with Nurick classification, Functional Independence measure (FIM) score and gait analysis using three dimensional motion analyzer before surgery, 1 week and 3 months after surgery.
Results: In the Nurick classification there was statistically significant change but no significant change in FIM score after surgery. In the gait analysis there were statistically significant improvements in all the linear parameters, kinetic (ankle plantarflexion moment) and kinematic (knee range of motion in swing phase) parameters (p＜0.05).
Conclusion: This study suggests that gait analysis can be used as a quantitative tools of postoperative gait improvement in patient with cervical myelopathy. (J Korean Acad Rehab Med 2003; 27: 58-62)
Ischemic myelopathy is a rare and uncommon disease than the cerebral ischemia. Ischemia of spinal cord usually occur in the midthoracic regions (T4-T8). The major arteries supplying spinal cord are anterior and posterior spinal arteries. Anterior spinal artery is more responsible for the ischemic change of the spinal cord. We report a 45 years old man with ischemia of the spinal cord and acute renal failure due to rhabdomyolysis following the heavy alcohol ingestion. (J Korean Acad Rehab Med 2002; 26: 631-634)
Organophosphate is known to damage both the peripheral and central nervous system. We report a case of organophosphate-induced peripheral polyneuropathy with myelopathy. A 46 years old woman who had ingested a large amount of insecticide (organophosphate) was transported to our hospital. Following medical treatment, she was transferred to the Department of Rehabilitation Medicine 1 month later. Upon admission to rehabilitation medicine, the patient was quadriplegic with markedly decreased muscle tone and strength. Electrodiagnostic examination revealed low amplitude of sensory nerve action potential (SNAP), unevokable compound muscle action potential in distal muscles and abnormal spontaneous activities with needle
electromyography, which were compatible with peripheral polyneuropathy. Three months later, motor and sensory function of upper extremities were normalized. The muscle tone of lower extremity increased to Ashworth grade II. Follow-up electrodiagnostic examination revealed normalization of SNAP and disappearance of spontaneous activities, but somatosensory evoked potential which were initially normal, revealed prolonged P40 latencies in the lower extremities. These electrophysiological findings were thought to result from the spinal cord lesion and correlated with clinical findings. We diagnosed the patient as peripheral polyneuropathy with delayed myelopathy induced by organophosphate. (J Korean Acad Rehab Med 2002; 26: 113-116)
Ischemic myelopahty of spinal cord after cardiac arrest is rarely reported. In general brain stem and spinal cord is less vulnerable to ischemic injury than cerebrum and cerebellum. Ischemic myelopathy usually occurs in the midthoracic region (T3∼T8) and rarely reported after cardiac arrest.
In this case previously healthy 62 year old patient suffered from cardiac arrhythmia for a few days and then developed cardiac arrest and sustained paraplegia due to ASIA class B spinal cord injury. After paraplegia MRI showed predominant involvement of the anterior horn cell area in the midthoracic region.
We present two patients with a cerebral palsy who developed cervical myelopathy long from term involuntary movements. Frequently instability with a premature onset of spondylosis of the cervical spine is found in an athetoid cerebral palsy patient. These structural abnormalities appear to be related to the athetoid motion of neck in a cerebral palsy. The combination of a disk degeneration and listhetic instability with a narrow canal predisposes these patients for the relatively rapid progression to a devastating neurological defect. Early surgical management is a treatment of choice for the cervical myelopathy associated with an athetoid cerebral palsy.
Chronic progressive radiation myelopathy(CPRM) is a rare but serious complication of radiation therapy. It's exact cause is unknown and the diagnosis is usually made based on the exclusion of other causes of myelopathy. Magnetic resonance imaging(MRI) with gadolinium- diethylenetriamine pentaacetic acid(DTPA) enhancement seems to be useful for the diagnosis of CPRM. There is no known effective treatment and the complication is irreversible.
We report a case of CPRM after radiation therapy for subglottic cancer which was not respond to high-dose steroid therapy with review of literature.
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