In many patients with chronic pain there is often a disparity between the degree of analgesic relief claimed by the patient and the ability to function better. The reasons for this are presented in a construct that suggests areas for consideration in any patient who is being considered for chronic analgesic use. Issues that influence perceived benefit are outlined. The importance of drug tolerance, dosage compliance, and patient’s involvement in treatment are stressed. The use of contracts as an integral part of documented patient participation is outlined. Mechanisms that help in the handling of difficult patients are described. The use of physician extenders, anticipation of inappropriate patient behaviors, and prior expression of sanctions are shown to be helpful. The use of medications as part of the multidimensional care of the patient with chronic pain is discussed. This article presents practical solutions for difficulties encountered in managing patients with chronic pain.
{"title":"Drug Therapy for Chronic Pain","authors":"Joel Seres1","doi":"10.1055/s-2004-830013","DOIUrl":"https://doi.org/10.1055/s-2004-830013","url":null,"abstract":"In many patients with chronic pain there is often a disparity between the degree of analgesic relief claimed by the patient and the ability to function better. The reasons for this are presented in a construct that suggests areas for consideration in any patient who is being considered for chronic analgesic use. Issues that influence perceived benefit are outlined. The importance of drug tolerance, dosage compliance, and patient’s involvement in treatment are stressed. The use of contracts as an integral part of documented patient participation is outlined. Mechanisms that help in the handling of difficult patients are described. The use of physician extenders, anticipation of inappropriate patient behaviors, and prior expression of sanctions are shown to be helpful. The use of medications as part of the multidimensional care of the patient with chronic pain is discussed. This article presents practical solutions for difficulties encountered in managing patients with chronic pain.","PeriodicalId":287382,"journal":{"name":"Seminars in Neurosurgery","volume":"34 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2004-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126816499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
First described in the 16th century, phantom limb pain (PLP) describes the painful sensations resulting from a lost body part, classically a lost limb. This article reviews the incidence, clinical course, pathophysiology, and current treatment options for PLP. The reported incidence of PLP varies widely from 0.5 to 90% because of sampling biases and the lack of differentiating PLP from stump pain or phantom sensations. The clinical course is rapid with symptoms typically occurring within the first week of limb loss and persisting for up to 2 years or more. Although both psychiatric and peripheral causes have been proposed, recent studies suggest a primary role of the central nervous system in the genesis of PLP. Treatment of PLP remains difficult, with no single modality sufficient to manage the pain. Optimal management currently involves a multidisciplinary approach involving physical treatments, pharmacologic intervention, and psychiatric therapy. Surgical options remain limited although novel interventions such as motor cortex stimulation may be beneficial.
{"title":"Phantom Limb Pain","authors":"Paul Park1, Oren Sagher1","doi":"10.1055/s-2004-830019","DOIUrl":"https://doi.org/10.1055/s-2004-830019","url":null,"abstract":"First described in the 16th century, phantom limb pain (PLP) describes the painful sensations resulting from a lost body part, classically a lost limb. This article reviews the incidence, clinical course, pathophysiology, and current treatment options for PLP. The reported incidence of PLP varies widely from 0.5 to 90% because of sampling biases and the lack of differentiating PLP from stump pain or phantom sensations. The clinical course is rapid with symptoms typically occurring within the first week of limb loss and persisting for up to 2 years or more. Although both psychiatric and peripheral causes have been proposed, recent studies suggest a primary role of the central nervous system in the genesis of PLP. Treatment of PLP remains difficult, with no single modality sufficient to manage the pain. Optimal management currently involves a multidisciplinary approach involving physical treatments, pharmacologic intervention, and psychiatric therapy. Surgical options remain limited although novel interventions such as motor cortex stimulation may be beneficial.","PeriodicalId":287382,"journal":{"name":"Seminars in Neurosurgery","volume":"43 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2004-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126559544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The vast majority of meningiomas are benign neoplasms potentially curable with complete surgical resection. Radiotherapy is typically the adjuvant therapy of choice, once surgical options have been depleted, for recurrent or residual meningiomas requiring further therapy. Unfortunately, some meningiomas, not only atypical and malignant tumors but also benign tumors, recur despite maximal therapy with surgery and radiation. Thus, another effective form of adjuvant therapy is required in a small proportion of meningiomas. The most common chemotherapeutic agents in clinical practice are hormonal antagonists, targeting receptors known to be expressed by meningiomas, such as mifepristone, tamoxifen, medroxyprogesterone acetate (MPA), and pegvisomant. More recent evidence has suggested that hydroxyurea and interferon-(cid:2) may be more effective therapy than hormonal antagonists for benign meningiomas. In contrast, malignant meningiomas are treated more like sarcomas with standard chemotherapeutic agents such as ifosfamide, doxorubicin, cisplatin, and dacarbazine. This article reviews the chemo-and biotherapeutic options available in the adjuvant therapy of meningiomas.
{"title":"Chemotherapy and Biological Therapy for Meningiomas","authors":"S. Hentschel, I. McCutcheon","doi":"10.1055/s-2004-828933","DOIUrl":"https://doi.org/10.1055/s-2004-828933","url":null,"abstract":"The vast majority of meningiomas are benign neoplasms potentially curable with complete surgical resection. Radiotherapy is typically the adjuvant therapy of choice, once surgical options have been depleted, for recurrent or residual meningiomas requiring further therapy. Unfortunately, some meningiomas, not only atypical and malignant tumors but also benign tumors, recur despite maximal therapy with surgery and radiation. Thus, another effective form of adjuvant therapy is required in a small proportion of meningiomas. The most common chemotherapeutic agents in clinical practice are hormonal antagonists, targeting receptors known to be expressed by meningiomas, such as mifepristone, tamoxifen, medroxyprogesterone acetate (MPA), and pegvisomant. More recent evidence has suggested that hydroxyurea and interferon-(cid:2) may be more effective therapy than hormonal antagonists for benign meningiomas. In contrast, malignant meningiomas are treated more like sarcomas with standard chemotherapeutic agents such as ifosfamide, doxorubicin, cisplatin, and dacarbazine. This article reviews the chemo-and biotherapeutic options available in the adjuvant therapy of meningiomas.","PeriodicalId":287382,"journal":{"name":"Seminars in Neurosurgery","volume":"41 3","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2003-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114114094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ossification of the posterior longitudinal ligament (OPLL) is characterized by heterotopic bone formation in spinal ligaments through endochondral mechanisms. Although the etiology remains obscure, the pathogenesis of OPLL appears to involve inheritance of OPLL-related HLA genes in patients with this genetic predisposition. Onset of symptoms is often insidious except in patients who present after a trauma. Imaging evaluation usually will include magnetic resonance imaging and computed tomography (CT), with CT providing the most information about the extent of OPLL. Operative treatment for myelopathy from OPLL is often indicated. Operations for OPLL may be divided into two types, anterior and posterior approaches. Evidence suggesting better outcomes after anterior approaches for OPLL have increasingly led surgeons to favor that approach when feasible. In a patient where the OPLL is limited to three or fewer vertebral segments, an anterior decompression should be considered. Patients with OPLL that is continuous and involves more than three levels should be considered for a posterior decompression or a combined anterior and posterior decompression and reconstruction.
{"title":"Ossification of the Posterior Longitudinal Ligament","authors":"Daniel Surdell Jr., B. White","doi":"10.1055/s-2003-41148","DOIUrl":"https://doi.org/10.1055/s-2003-41148","url":null,"abstract":"Ossification of the posterior longitudinal ligament (OPLL) is characterized by heterotopic bone formation in spinal ligaments through endochondral mechanisms. Although the etiology remains obscure, the pathogenesis of OPLL appears to involve inheritance of OPLL-related HLA genes in patients with this genetic predisposition. Onset of symptoms is often insidious except in patients who present after a trauma. Imaging evaluation usually will include magnetic resonance imaging and computed tomography (CT), with CT providing the most information about the extent of OPLL. Operative treatment for myelopathy from OPLL is often indicated. Operations for OPLL may be divided into two types, anterior and posterior approaches. Evidence suggesting better outcomes after anterior approaches for OPLL have increasingly led surgeons to favor that approach when feasible. In a patient where the OPLL is limited to three or fewer vertebral segments, an anterior decompression should be considered. Patients with OPLL that is continuous and involves more than three levels should be considered for a posterior decompression or a combined anterior and posterior decompression and reconstruction.","PeriodicalId":287382,"journal":{"name":"Seminars in Neurosurgery","volume":"68 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2003-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125637815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Multilevel corpectomy for decompressing the spinal cord to treat cervical spondy-lotic myelopathy has become commonplace. Correlation of preoperative radiographic findings with intraoperative anatomy will ensure adequate decompression and lessen complications. Reconstruction with cadaveric fibula or bone-filled titanium cages combined with a locking cervical plate has reduced donor site morbidity and long-term construct failure to near zero for two-level corpectomies. Three or more levels may best be reconstructed by both anterior and posterior instrumentation. One of the more common complications of this operation is hoarseness and that may be lessened with endotracheal tube deflation during retraction. Most of the complications of surgery are minor (including dysphagia), improve with time, and are well tolerated by the patient. The preoperative myelopathic gait improves in 50% and upper extremity weakness/spasticity improves in 70% of patients.
{"title":"Multilevel Corpectomy for Cervical Spondylotic Myelopathy","authors":"S. Shapiro","doi":"10.1055/s-2003-41144","DOIUrl":"https://doi.org/10.1055/s-2003-41144","url":null,"abstract":"Multilevel corpectomy for decompressing the spinal cord to treat cervical spondy-lotic myelopathy has become commonplace. Correlation of preoperative radiographic findings with intraoperative anatomy will ensure adequate decompression and lessen complications. Reconstruction with cadaveric fibula or bone-filled titanium cages combined with a locking cervical plate has reduced donor site morbidity and long-term construct failure to near zero for two-level corpectomies. Three or more levels may best be reconstructed by both anterior and posterior instrumentation. One of the more common complications of this operation is hoarseness and that may be lessened with endotracheal tube deflation during retraction. Most of the complications of surgery are minor (including dysphagia), improve with time, and are well tolerated by the patient. The preoperative myelopathic gait improves in 50% and upper extremity weakness/spasticity improves in 70% of patients.","PeriodicalId":287382,"journal":{"name":"Seminars in Neurosurgery","volume":"49 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2003-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123863668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Treatment of Invasive Pituitary Adenomas","authors":"A. Krisht, Alfonso Fuentes-Pinillos","doi":"10.1055/s-2001-33623","DOIUrl":"https://doi.org/10.1055/s-2001-33623","url":null,"abstract":".","PeriodicalId":287382,"journal":{"name":"Seminars in Neurosurgery","volume":"38 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130020405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Management of Growth Hormone-Secreting Adenomas: An Update","authors":"N. Oyesiku","doi":"10.1055/s-2001-33620","DOIUrl":"https://doi.org/10.1055/s-2001-33620","url":null,"abstract":".","PeriodicalId":287382,"journal":{"name":"Seminars in Neurosurgery","volume":"7 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129284933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Management of Cushing's Disease: An Update","authors":"K. Post, K. Yao, Jane Walsh","doi":"10.1055/s-2001-33621","DOIUrl":"https://doi.org/10.1055/s-2001-33621","url":null,"abstract":".","PeriodicalId":287382,"journal":{"name":"Seminars in Neurosurgery","volume":"57 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115454732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Treatment of Pituitary Tumors: An Update","authors":"A. Krisht","doi":"10.1055/S-2001-33616","DOIUrl":"https://doi.org/10.1055/S-2001-33616","url":null,"abstract":"","PeriodicalId":287382,"journal":{"name":"Seminars in Neurosurgery","volume":"42 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127319562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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