Back pain and epidural spinal cord compression

1988 ◽  
Vol 3 (2) ◽  
pp. 191-197 ◽  
Author(s):  
David W. Bates ◽  
James B. Reuler
1992 ◽  
Vol 78 (6) ◽  
pp. 397-402 ◽  
Author(s):  
llan G. Ron ◽  
Irith Reider ◽  
Nelly Wigler ◽  
Samario Chaitchik

Primary spinal epidural lymphoma (Stage I) is diagnosed predominantly late after a long prodromal phase of local back pain resulting in spinal cord compression. The use of CT and NMR images in the early stage of investigation and their analysis may help to diagnose these cases prior to the appearance of neurologic deficit. We report on 2 patients who presented with prolonged localized back pain with sudden symptoms of spinal cord compression. CAT scan and NMR imaging demonstrated the characteristic appearance of lymphoma. Decompressive laminectomy supported the diagnosis. Radiotherapy treatment to the region of the non-Hodgkin's lymphoma resulted in complete resolution. Thereafter, systemic chemotherapy with CHOP achieved a good response.


2017 ◽  
Vol 27 (3) ◽  
pp. 341-345 ◽  
Author(s):  
Arnold H. Menezes ◽  
Patrick W. Hitchon ◽  
Brian J. Dlouhy

A family with familial spinal extradural arachnoid cyst is presented. A 14-year-old boy had an extensive T-8 through L-2 dorsal extradural arachnoid cyst with spinal cord compression and slowly progressive myelopathy. His mother had presented 4 years earlier with acute excruciating back pain due to the combination of a lumbar extradural arachnoid cyst at L2–4 and an extruded disc at L3–4. The literature is reviewed in light of the pathogenesis, imaging, and surgical technique required for treatment.


2010 ◽  
Vol 3 (3) ◽  
pp. 291-295 ◽  
Author(s):  
L. M. Kampschreur ◽  
E. K. Hoogeveen ◽  
J. W. op den Akker ◽  
J. J. Beutler ◽  
T. Beems ◽  
...  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Giulia Salomone ◽  
Milena La Spina ◽  
Giuseppe Belfiore ◽  
Gregoria Bertuna ◽  
Laura Cannavò ◽  
...  

Abstract Background Spinal cord compression (SCC) is an uncommon, severe complication of Hodgkin lymphoma (HL), occurring in 0.2% of cases at the onset and in 6% during disease progression. We present a teenager with SCC with clinical onset of HL; her pre-existing neurological abnormalities covered the presence of an epidural mass, which could have misled us. Case presentation A 13-year-old girl presented with a three-month history of lower back pain and degrading ability to walk. She suffered from a chronic gait disorder due to her preterm birth. A magnetic resonance imaging of the spine revealed an epidural mass causing collapse of twelfth thoracic vertebra and thus compression and displacement of the spinal cord. Histological examination with immunohistochemical analysis of the epidural mass demonstrated a classic-type Hodgkin lymphoma. Early pathology-specific treatment allowed to avoid urgent surgery, achieve survival and restore of neurological function. Conclusions Children and adolescents with back pain and neurological abnormalities should be prioritized to avoid diagnostic delay resulting in potential loss of neurological function. SCC requires a prompt radiological assessment and an expert multidisciplinary management.


1929 ◽  
Vol 25 (7-8) ◽  
pp. 852-854
Author(s):  
I. Tsimkhes

Doctor. V. I. Nizner. Demonstration of the patient after laminectomy for a spinal fracture. B-th, a worker, 35 years old, fell from a staircase 372 meters high. Dizziness, vomiting, back pain, stulag and urine retention. Swelling in the area of the spinous processes of the 12th thoracic and 1st lumbar vertebrae. Spinal cord compression and spinal injury in the lumbar region are suspected.


Author(s):  
Tony El Murr

A 59 year old male with a past medical history of cholecystectomy and essential hypertension, presented to the emergency department with severe back pain, abdominal discomfort, poor appetite, generalized fatigue and progressive weight loss of 10 kgs over a three-month period. He has never been a smoker and drinks alcohol occasionally. He has no known allergies and no familial history of cancer. His current home medication includes beta blocker; angiotensin receptor blocker and low dose acetylsalicylic acid. His back pain started two months prior to presentation; it is not well localized to specific vertebra, not irradiating to lower limbs and sometimes related to weight lifting and cough. It is rarely exacerbated at night. His orthopedic surgeon attributed it to osteoarthritis since the patient used to practice hard manual work and weights lifting at his shop. He has been treated since that time with NSAIDs, muscle relaxant and opioids without complete analgesic response. At presentation, he had no fever, chills or night sweats. He had no urinary or sexual complaints that would suggest prostatic disease and was otherwise asymptomatic. The physical examination showed diffuse pain on lumbar vertebral percussion and abdominal tenderness in the right upper quadrant. He has no skin lesions and no palpable peripheral lymph nodes. His neurologic examination was also normal. On admission, significant laboratory findings showed hemoglobin 11.8 g/dl, platelets of 97,000 k/ul, white blood count 4,400 k/ul, ESR=40, creatinine 0.4 mg/dl,CRP 7.5 mg/L, lactate dehydrogenase 2256 U/L, alanine aminotransferase (ALAT) 70 U/L, gamma-glutamyl transferase (GGT) 1500 U/L, total bilirubin 2.32 mg/dl, and a creatine kinase (CK) 167 U/L. Prostatic specific antigen (PSA) was normal and equal to 1.17 ng/ml. Peripheral smear displayed normal pattern and thyroid tests were all within normal ranges. He was negative for salmonellosis, brucellosis and HIV. Tuberculin PPD test was negative as well. His chest X-ray was normal and abdominopelvic ultrasound showed only multiple liver nodules and mild prostate hypertrophy without ascites or significant abdominal lymph nodes. Lumbar MRI done one week before his admission revealed multiple vertebral lytic lesions without spinal cord compression. PET/CT done on the third day at hospital revealed a significant uptake of radiotracer by multiple small nodules in the right lung, in the liver and by multiple lymph nodes within the abdominal cavity. Moreover there were many lytic lesions in the dorsal and lumbar vertebrae. Surprisingly, the scan also showed focal, intense uptake of the prostate with a SUVmax of 8, 28 with evidence of seminal vesicles invasion. Both gastroscopy and colonoscopy was normal as well as his brain MRI. Ultrasound-guided liver nodules biopsies performed on the fifth day after stopping the acetylsalicylic acid revealed neuroendocrine small cell carcinoma as it showed immunohistochemical (IHC) positivity for synaptophysin and CD56. IHC was negative for TTF1 and PSA. Ultrasound-guided biopsy of the prostate was not performed for medical reasons as on his hospital day 7, the patient started feeling numbness and muscle weakness in his lower limbs more severe on the left side associated with urinary incontinence and revealing a spinal cord compression by secondary bone lesions. Regarding this rapidly progressive disease, high dose dexamethasone subcutaneous therapy and ten sessions of focused proton beam radiotherapy has been conducted on daily basis to release the spinal cord compression without significant improvement. Meanwhile, and based on liver biopsy findings, treatment by octreotide 100mg S/C twice daily was started, followed by chemotherapy with Carboplatin, Etoposide, and Atezolizumab (TECENTRIQ) 1200mg. Few days after, the patient developed severe prolonged pancytopenia requiring blood and platelets transfusions and treatment with double dose of granulocyte stimulating growth factor. His prolonged neutropenia was complicated by CMV colitis with unretractable diarrhea, bilateral pneumonia and pseudomonas aeroginosa septicemia. After one month of large spectrum antibiotics, antiviral and antifungal treatment, and while he was still neutropenic, bone marrow biopsy revealed severe infiltration by neuroendocrine small cell carcinoma. The patient was still deteriorating clinically and showing further weight and appetite loss, total muscle weakness and asthenia. At this point, he was no longer a candidate for chemotherapy but only symptomatic treatment was maintained. He died 45 days after his admission.


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