Biomedical subjects

Helena Brisby

Publications and source records attributed to Helena Brisby.

8 recordsLinked to original sources

PubMed2007

Patients' satisfaction with provided care/information and expectations on clinical outcome after lumbar disc herniation surgery.

STUDY DESIGN: A prospective study of patients undergoing lumbar disc herniation surgery. OBJECTIVES: To assess patients' satisfaction with care/preoperative information, if expectations on surgical results and ability to return to work are related to baseline characteristics, and/or can predict self-reported outcome. Self-reported outcome was compared with objective outcome. SUMMARY OF BACKGROUND DATA: Patients' expectations on treatment results have been discussed as a predictive factor for postoperative outcome and satisfaction demonstrated to be directly related to patient expectations. METHODS: The study includes 148 patients, 46% women, mean age 40 (range 18-66). Before and 2 years after surgery, questionnaires about given information/care, expected/present work ability, and expectations on/obtained improvement of physical functions/symptoms (leg and back pain, sensibility, and muscle function) were filled in. The visual analog scale leg pain, Zung Depression Scale, and Oswestry Disability Index were used as baseline characteristics. At 2-year follow-up, self-reported and objective outcome was assessed. RESULTS: Satisfaction with given information/care were reported by 46% and 82%, respectively. Zung Depression Scale related to expectations on leg pain recovery (P = 0.022), work ability (P = 0.046), and satisfaction with given information (P = 0.031). Patients who expected to return (76%) and not return (24%) to work, returned in 78% and 26%, respectively (P = 0.021). A high agreement between self-reported outcome and objective outcome were found (P < 0.001). CONCLUSIONS: Patients undergoing lumbar disc herniation surgery are mostly satisfied with provided care before and after surgery, however, less satisfied with information provided. Further, patients with preoperative positive expectations on work return and realistic expectations on pain and physical recovery have a greater chance to be satisfied with the surgical results.

Adult↗

PubMed2007

Differentiation of human mesenchymal stem cells and articular chondrocytes: analysis of chondrogenic potential and expression pattern of differentiation-related transcription factors.

Mesenchymal stem cells (MSCs) are a candidate for replacing chondrocytes in cell-based repair of cartilage lesions. However, it has not been clarified if these cells can acquire the hyaline phenotype, and whether chondrocytes and MSCs show the same expression patterns of critical control genes in development. In order to study this, articular chondrocytes and iliac crest derived MSCs were allowed to differentiate in pellet mass cultures. Gene expression of markers for the cartilage phenotype, helix-loop-helix (HLH) transcription factors, and chondrogenic transcription factors were analyzed by real-time PCR. Matrix production was assayed using biochemical analysis for hydroxyproline, glycosaminoglycans, and immunohistochemistry for collagen types I and II. Significantly decreased expression of collagen type I was accompanied by increased expression of collagen types IIA and IIB during differentiation of chondrocytes, indicating differentiation towards a hyaline phenotype. Chondrogenesis in MSCs on the other hand resulted in up-regulation of collagen types I, IIA, IIB, and X, demonstrating differentiation towards cartilage of a mixed phenotype. Expression of HES1 increased significantly during chondrogenesis in chondrocytes while expression in MSCs was maintained at a low level. The HLH gene HES5 on the other hand was only detected in chondrocytes. Expression of ID1 decreased significantly in chondrocytes while the opposite was seen in MSCs. These findings suggest that chondrocytes and MSCs differentiated and formed different subtypes of cartilage, the hyaline and a mixed cartilage phenotype, respectively. Differentially regulated HLH genes indicated the possibility for HLH proteins in regulating chondrogenic differentiation. This information is important to understand the potential use of MSCs in cartilage repair.

Adult↗

PubMed2006

Pathology and possible mechanisms of nervous system response to disc degeneration.

Degeneration of the intervertebral disc is clinically considered to be an important source of pain in patients with low-back pain. Disc deterioration and/or degeneration may influence the nervous system by stimulation of nociceptors in the anulus fibrosus, causing nociceptive pain that is often referred to as discogenic pain. The stimulation of the nociceptors may be of mechanical or inflammatory origin. Deterioration of a disc with loss of normal structure and weight-bearing properties may lead to abnormal motions that cause mechanical stimulation. This theory is supported by the fact that patients commonly experience an increase in pain with weight-bearing and certain movements. In addition, an ingrowth of vessels and nerve fibers into deeper layers of the anulus fibrosus has been observed in degenerated discs. A large number of inflammatory and signaling substances, such as tumor necrosis factor and interleukins (interleukin-1beta, interleukin-6, and interleukin-8), may also play a role in the development of back pain. Independent of stimulus of the nociceptors, the pain impulses are conducted through myelinated A delta fibers and unmyelinated C fibers to the dorsal root ganglion and continue by way of the spinothalamic tract to the thalamus and the somatosensory cortex. In response to stimulation of the nociceptors in the disc, the somatosensory system may increase its sensitivity, resulting in a nonfunctional response; that is, normally innocuous stimuli may generate an amplified response (peripheral sensitization). When disc degeneration leads to a disc herniation, the adjacent nervous system structures, such as the nerve roots or the dorsal root ganglion, can be affected, causing neuropathic pain of mechanical or biochemical origin. Disc deterioration also influences other spinal structures, such as facet joints, ligaments, and muscles, which can also become pain generators. Thus, disc degeneration may be responsible for the development of chronic low-back pain without being the actual pain focus. Both nociceptive and neuropathic pain can be modulated at higher centers, both at the spinal and the supraspinal levels (central sensitization). The altered magnitude of perceived pain is often referred to as neural plasticity and is considered to play a critical role in the evolution of chronic pain. Together with the complexity of the nervous system and pain modulation mechanisms, psychological aspects may also play a role in the response of the nervous system in patients with chronic low-back pain caused by disc degeneration.

Chronic Disease↗

PubMed2004

Cerebrospinal fluid biomarkers in experimental spinal nerve root injury.

STUDY DESIGN: Cerebrospinal fluid biomarkers were evaluated in a setup using established pig models to mimic clinical disc herniation. OBJECTIVES: To investigate biomarkers for nerve tissue injury, inflammation, and pain in cerebrospinal fluid after mechanical compression and/or nucleus pulposus application to spinal nerve roots. SUMMARY OF BACKGROUND DATA: The association between mechanical compression, biochemical effects of nucleus pulposus, and nerve root injury in degenerative disc disorders is incompletely investigated. METHODS: The unilateral S1 nerve root was exposed in 20 pigs. The animals were divided into four groups (n = 5 each): 1) slow-onset mechanical compression with an ameroid constrictor; 2) autologous nucleus pulposus application; 3) mechanical compression plus nucleus pulposus; and 4) sham operation. After 1 week, 6 mL of cerebrospinal fluid was collected, and four structural nerve proteins, neurofilaments, S-100, glial fibrillary acidic protein, neuron-specific enolase, the proinflammatory cytokine interleukin-8, the neurotransmitter nociceptin, and substance P endopeptidase activity were analyzed using immunoassays. RESULTS: The concentration of neurofilament was increased in the mechanical compression group (17.0 microg/L +/- 5.0) and in the mechanical compression plus nucleus pulposus group (19.8 +/- 12.1 microg/L) compared with the sham group (0.9 +/- 0.9 microg/L) and the nucleus pulposus group (0.4 +/- 0.1 microg/L) (P < 0.01 for both). The concentration of nociceptin was increased significantly in the mechanical compression group (24.0 +/- 8.6 fm/mL) and in the mechanical compression plus nucleus pulposus group (31.2 +/- 6.6 fm/mL) compared with the sham group (7.0 +/- 1.3 fm/mL) (P < 0.05 and P < 0.01, respectively). A correlation was found between concentrations of neurofilament and nociceptin (r = 0.50, P < 0.05). There were no intergroup differences regarding glial fibrillary acidic protein, neuron-specific enolase, S-100, interleukin-8, or substance P endopeptidase activity. CONCLUSIONS: The present study demonstrates increased concentrations of neurofilament and nociceptin in cerebrospinal fluid after nerve root compression. A simultaneous application of nucleus pulposus did not increase the response.

Animals↗

PubMed2004

When is spinal pain "neuropathic"?

Although one cannot always determine when a patient's persistent pain is neuropathic, the issues are becoming clearer. Patients with spinal pain need to be examined carefully and the persistence of pain should not necessarily be considered to indicate a continuing search for a nociceptive focus. Similarly, continuing pain following successful surgery may be caused by persistent spinal or central neurologic changes. New methods for characterizing the site of neural changes will develop--functional MRI and PET scanning are now characterizing brain activity and will possibly yield results soon that will be helpful in the clinic. Further work needs to be done to identify which clinical features lead to better responses to agents for the treatment of neuropathic pain. New, more specific agents with actions focused on the specific parts of neural transmission are being developed. These include agents (such as growth factors) that will cure, not just suppress, the pathologic pain generators and pathways in patients with persistent pain.

Humans↗

PubMed2004

Cell therapy for disc degeneration--potentials and pitfalls.

Disc degeneration is considered a major source of pain in patients with chronic low back pain. Novel strategies to cure or decrease the symptoms and increase the patient's quality of life and function are under development. Until recently conservative treatment and fusion surgery were the main therapeutic options. Disc prostheses are undergoing clinical evaluation. The potential for cell transplantation to the intervertebral disc with mature autologous disc cells, chondrocytes, or stem cells is in early stages of investigation. Cell transplantation potentially can increase proteoglycan production and induce disc regeneration or slow down the degeneration process. In animal models, transplantation of autologous disc cells and chondrocytes (derived from costal cartilage) has been demonstrated to be feasible and may slow disc degeneration.

Animals↗

PubMed2003

Nerve root injuries in patients with chronic low back pain.

In conclusion, the nerve roots and the DRG play an important role in the pain mechanisms of patients suffering from chronic low back pain. Signs of demyelination and increased sensitization for stimuli occurs after a direct nerve root trauma, and the plasticity for the DRG also may change the response to a given peripheral stimuli when repeated frequently over a long period of time. The regeneration mechanisms of spinal nerve roots and DRG regarding function are slow, and the final grade of recurrence depends on the degree of injury. The limited regeneration mechanisms for nerve injury and the fact that "established chronic pain centers" are hard to influence after a long pain history favor an aggressive strategy for pain management. Today, a number of treatment strategies exist for chronic low back pain patients (with or without a diagnosed nerve root injury). These strategies include physiotherapy, nonsteroid anti-inflammatory drugs (NSAIDs), steroids, analgesics of different types and administration routes, surgery, and other sorts of invasive treatments. Further knowledge about the nerve root, DRG, and the rest of the nervous system in these patients is necessary; for understanding how and when to treat patients with chronic low back pain, we need to understand more about what we are trying to treat.

Chronic Disease↗

PubMed2002

Glycosphingolipid antibodies in serum in patients with sciatica.

STUDY DESIGN: Serum antibody titers against 10 different glycosphingolipids were investigated by enzyme-linked immunosorbent assay in three groups of patients: patients with acute sciatica (Group IA, radicular pain for 32 +/- 36 days, n = 68), a subgroup of these patients 4 years later (Group IB, n = 23), and patients undergoing lumbar discectomy because of disc herniation (Group II, n = 37). OBJECTIVES: To investigate the immunologic response in sciatica patients by analyzing circulating autoantibodies against glycosphingolipids, molecules highly expressed in cells from the nervous system, and the possible correlation of such antibodies to clinical and imaging findings as well as to subjective symptoms. SUMMARY OF BACKGROUND DATA: The titers of glycosphingolipid antibodies are elevated in neurologic diseases with autoimmune stimulation such as Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy. METHODS: Antiglycosphingolipid antibodies were assayed by a microtiter enzyme-linked immunosorbent assay method. Antibody titers were related to a healthy population by a method that judges all positive results (positive result = patient sera/pooled blood donor serum >2, at titer 1/400) as indicating a pathologic condition. RESULTS: Increased levels of circulating antibodies against one or more glycosphingolipids were detected in 71% of patients with acute sciatica, in 61% of sciatica patients at a 4-year follow-up visit (eight antigens analyzed) and in 54% in patients undergoing discectomy. These frequencies were somewhat higher than, and in the last group similar to, those reported for generalized nervous system disorders with autoimmune involvement. In the acute sciatica patients, positive neurologic findings were associated with increased levels of two of the examined antibodies: 3'LM1 (immunoglobulin M and/or immunoglobulin G), P = 0.023, and GD1a (immunoglobulin M), P = 0.017. CONCLUSION: The presence of glycosphingolipid antibodies in patients with sciatica and disc herniation suggests an activation of the immune system and thus a process possibly involved in the pathophysiology of sciatica. The autoimmune response was not limited to antibodies against one specific glycosphingolipid target; rather, an overall increase in autoantibodies against nervous system-associated glycosphingolipids was observed. These results encourage further studies of the pathophysiologic and clinical relevance of autoimmune responses in patients with sciatica and disc herniation.

Acute Disease↗