1. Twenty-seven patients with a Brown-SeÌquard syndrome resulting from trauma have been studied, fourteen of the left side of the cord and thirteen of the right. There were sixteen gunshot wounds and eleven closed injuries. 2. The prognosis for recovery is much better than the initial catastrophic nature of the symptoms and signs would indicate. 3. The pattern of recovery is discussed in detail and the long and rather tedious course of the treatment is indicated. 4. Spasticity on the side worse affected still presents a difficult problem, but a less severe one than that presented by flaccid paralysis.
Patients with spinal cord injuries have been seen to have increased healing of attendant fractures. This for the main has been a clinical observation with laboratory work confined to rats. While the benefits in relation to quicker fracture healing are obvious, this excessive bone growth (heterotopic ossification) also causes unwanted side effects, such as decreased movement around joints, joint fusion and renal tract calculi. However, the cause for this phenomenon remains unclear. This paper evaluates two groups with spinal column fractures – those with neurological compromise (n=10) and those without (n=15), and compares them with a control group with isolated long bone fractures (n=12). Serum was taken from these patients at five specific time intervals post injury (1 day, 5 days, 10 days, 42 days (6 weeks) and 84 days (12 weeks)). These samples were then analysed for levels of Transforming Growth Factor-Beta (TGF-β using the ELISA technique. This cytokine has been shown to stimulate bone formation after both topical and systemic administration. Results show TGF-β levels of 142.79+/-29.51 ng/ml in the neurology group at 84 days post injury. This is higher than any of the other time points within this group (p=0.009 vs. all other time points, ANOVA). Furthermore, this level is also higher than the levels recorded in the no neurology (103.51+/-36.81 ng/ml) and long bone (102.28=/-47.58 ng/ml) groups at 84 days post-injury (p=0.009 and p=0.04 respectively, ANOVA). In conclusion, the results of this work, carried out for the first time in humans, offers strong evidence of the causative role of TGF-β in the increased bone turnover and attendant complications seen in patients with acute spinal cord injuries.
Patients with spinal cord injuries have been seen to have increased healing of attendant fractures. This for the main has been a clinical observation with laboratory work confined to rats. While the benefits in relation to quicker fracture healing are obvious, this excessive bone growth (heterotopic ossification) also causes unwanted side effects, such as decreased movement around joints, joint fusion and renal tract calculi. However, the cause for this phenomenon remains unclear. This paper evaluates two groups with spinal column fractures – those with neurological compromise (n=10) and those without (n=11), and compares them with a control group with isolated long bone fractures (n=10). Serum was taken from these patients at five specific time intervals post injury (1 day, 5 days, 10 days, 42 days (6 weeks) and 84 days (12 weeks)). These samples were then analysed for levels of Transforming Growth Factor-Beta (TGF-ß) using the ELISA technique. This cytokine has been shown to stimulate bone formation after both topical and systemic administration. Results show TGF-ß levels of 142.79+/−29.51 ng/ml in the neurology group at 84 days post injury. This is higher than any of the other time points within this group (p<
0.001 vs day 1, day 5 and day 10 and p=0.005 vs 42 days, ANOVA univariate analysis). Furthermore, this level is also higher than the levels recorded in the non neurology (103.51+/−36.81 ng/ml) and long bone (102.28=/−47.58 ng/ml) groups at 84 days post injury (p=0.011 and p=0.021 respectively, ANOVA univariate analysis). There was statistically significant difference in TGF-ß levels seen between the clinically more severely injured patients, ie complete neurological deficit and the less severely injured patients, ie incomplete neurological deficit. In conclusion, the results of this work, carried out for the first time in humans, offers strong evidence of the causative role of TGF-ß in the increased bone turnover and attendant complications seen in patients with acute spinal cord injuries.
Decubitus ulcers are found in approximately 4.7% of hospitalized patients, with a higher prevalence (up to 30%) among those with spinal cord injuries. These ulcers are often associated with hip septic arthritis and/or osteomyelitis involving the femur. Girdlestone resection arthroplasty is a surgical technique used to remove affected proximal femur and acetabular tissues, resulting in a substantial defect. The vastus lateralis flap has been employed as an effective option for managing this dead space. The aim of this study was to evaluate the long-term outcomes of this procedure in a consecutive series of patients. A retrospective single-center study was conducted from October 2012 to December 2022, involving 7 patients with spinal cord injuries affected by chronic severe septic hip arthritis and/or femoral head septic necrosis as a consequence of decubitus ulcers over trochanter area. All patients underwent treatment using a multidisciplinary approach by the same surgical team (orthopedic and plastic surgeons) along with infectious disease specialists. The treatment consisted of a one-stage procedure combining Girdlestone resection arthroplasty with unilateral vastus lateralis flap reconstruction, alongside targeted antibiotic therapy. Complications and postoperative outcomes were assessed and recorded. The mean follow-up period was 8 years (range 2-12).Aim
Method
Patients with spinal cord injuries have been seen to have increased healing of attendant fractures. This for the main has been a clinical observation with laboratory work confined to rats. While the benefits in relation to quicker fracture healing are obvious, this excessive bone growth (heterotopic ossification) also causes unwanted side effects, such as decreased movement around joints, joint fusion and renal tract calculi. However, the cause for this phenomenon remains unclear. This paper evaluates two groups with spinal column fractures – those with neurological compromise (n=10) and those without (n=11), and compares them with a control group with isolated long bone fractures (n=10). Serum was taken from these patients at five specific time intervals post injury (1 day, 5 days, 10 days, 42 days (6 weeks) and 84 days(12 weeks)). These samples were then analysed for levels of Transforming Growth Factor-Beta (TGF-b) using the ELISA technique. This cytokine has been shown to stimulate bone formation after both topical and systemic administration. Results show TGF-b levels of 142.79+/−29.51 ng/ml in the neurology group at 84 days post injury. This is higher than any of the other time points within this group (p<
0.001 vs. day 1, day 5 and day 10 and p=0.005 vs. 42 days, ANOVA univariate analysis). Furthermore, this level is also higher than the levels recorded in the no neurology (103.51+/−36.81 ng/ml) and long bone (102.28=/−47.58 ng/ml) groups at 84 days post injury (p=0.011 and p=0.021 respectively, ANOVA univariate analysis). There was statistically significant difference in TGF-b levels seen between the clinically more severely injured patients i.e. complete neurological deficit and the less severely injured patients i.e. incomplete neurological deficit. In conclusion, the results of this work, carried out for the first time in humans, offers strong evidence of the causative role of TGF-b in the increased bone turnover and attendant complications seen in patients with acute spinal cord injuries.
Increased bone turnover and fracture healing is associated with acute spinal cord injuries. Experimental work to date has been confined to animal models. While the benefits in relation to quicker fracture healing are obvious, this excessive bone growth (heterotopic ossification) also causes unwanted side effects, such as decreased movement around joints, joint fusion and renal tract calculi. This paper evaluates two groups of patients with spinal column fractures – those with neurological compromise and those without, and compares them with a control group with isolated long bone fractures. Serum was taken from these patients at 10 days post injury and was analysed for the known osteogenic cytokines Insulin-like Growth Factor-1 (IGF-1) and Transforming Growth Factor-b1 (TGF-b1) as well as being added to an osteoblast cell culture line to analyse cell proliferation. The results for the IGF-1 show a higher level in the neurology group compared to the no neurology group (p=0.038). In the TGF-B1 assay, the neurology group has a lower level than the other two groups (p<
0.0001 and p=0.002 respectively). However, when this group is subdivided into patients with complete and incomplete neurology, it can be seen that the levels of the complete group are elevated, although not significantly so (p=0.228). All three groups stimulated markedly increased osteoblast cell proliferation versus a control group (p=0.086, p=0.005 and p=0.002 respectively). However, the neurology group is significantly lower than the other two groups (p=0.007 and p=0.001 respectively). Furthermore the complete group causes a lower proliferation rate than the incomplete group (p=0.539). In conclusion, at 10 days post injury when the acute inflammatory reaction is subsiding and new bone is being laid down, patients with acute spinal cord injuries have increased bone turnover. This increase is being indirectly mediated by IGF-1, and more elevated levels with more severe neurological compromise suggest a contributory role of TGF-b1. Direct stimulation of osteoblasts does not appear to have any role to play in this accelerated bone healing.
Patients with spinal cord injuries have been seen to have increased healing of attendant fractures. This for the main has been a clinical observation with laboratory work confined to rats. While the benefits in relation to quicker fracture healing are obvious, this excessive bone growth (heterotopic ossification) also causes unwanted side effects, such as decreased movement around joints, joint fusion and renal tract calculi. However, the cause for this phenomenon remains unclear. This paper evaluates two groups with spinal column fractures – those with neurological compromise (n=10) and those without (n=11), and compares them with a control group with isolated long bone fractures (n=10). Serum was taken from these patients at five specific time intervals post injury (24hrs, 120hrs, 10 days, 6 weeks and 12 weeks). The time period most closely related to the end of the acute inflammatory reaction and the laying down of callus was the 10-day post injury time period. Serum samples taken at this time period were analysed for IGF-1 and TGF-β levels, both known to initiate osteoblastic activity, using ELISA kits. They were also exposed to an osteoblast cell culture line and cell proliferation was measured. Results show that the group with neurology has increased levels of IGF-1 compared to the other groups (p<
0.14, p<
0.18 respectively, Student’s t-test) but had lower TGF- (p<
0.05, p<
0.006) and osteoblast proliferation levels (p<
0.002, p<
0.001), despite having a significantly higher cell proliferation than a control group (p<
0.0001). When the neurology group is subdivided into complete (n=5) and incomplete (n=5), it was shown that the complete group had higher levels of both IGF-1 and TGF-. This trend is reversed in the osteoblast proliferation assay. This work, for the first time in human subjects, identifies a factor which may be regulating this complication of acute spinal cord injuries, namely IGF-1. Furthermore, the observed trend in the two cytokines seen in the complete neurology group may suggest a role for TGF-β. However, the results do show that a direct mediation of this unwanted side effect of spinal cord injuries is unlikely as seen in the proliferation assay. Further work remains to be done to fully understand the complexities of the excessive bone growth recognised in this patient group.
Patients with spinal cord injuries have been seen to have increased healing of attendant fractures. While the benefits are obvious, this excessive bone growth also causes unwanted side effects, such as decreased movement around joints, joint fusion and renal tract calculi. However, the cause for this phenomenon remains unclear. This paper evaluates two groups with spinal column fractures – those with neurological compromise (n=10) and those without (n=15), and compares them with a control group with isolated long bone fractures (n=12). Serum was taken from these patients at five specific time intervals post injury (1 day, 5 days, 10 days, 42 days (6 weeks) and 84 days(12 weeks)). These samples were then analysed for levels of Transforming Growth Factor-Beta (TGF-.) using the ELISA technique. This cytokine has been shown to stimulate bone formation after both topical and systemic administration. Results show TGF-.; levels of 142.79±29.51 ng/ml in the neurology group at 84 days post injury. This is higher than any of the other time points within this group (.0.009 vs. all other time points, ANOVA). Furthermore, this level is also higher than the levels recorded in the no neurology (103.51±36.81 ng/ml) and long bone (102.28±47.58 ng/ml) groups at 84 days post injury (p=0.009 and p=0.04 respectively, ANOVA). In conclusion, the results of this work, carried out for the first time in humans, offers strong evidence of the causative role of TGF-.; in the increased bone turnover and attendant complications seen in patients with acute spinal cord injuries.
This basic science study attempts to explain why patients with spinal cord injuries have been seen to display increased healing of attendant fractures. For the main part, this has been a clinical observation with laboratory work confined to rats. While the benefits in relation to quicker fracture healing are obvious, this excessive bone growth (heterotopic ossification) also causes unwanted side effects, such as decreased movement around joints, joint fusion and renal tract calculi. However, the cause for this phenomenon remains unclear. This paper evaluates two group with spinal column fractures – those with neurological compromise (n=10) and those without (n=11), and compares them with a control group with isolated long bone fractures (n=10). Serum was taken from these patients at five specific time intervals post injury (24hrs, 120hrs, 10 days, 6 weeks and 12 weeks). The time period most closely related to the end of the acute inflammatory reaction and the laying down of callus was the 10-day post injury time period. Serum samples taken at this time period were analysed for IGF-1 and TGF-ß levels, both known to initiate osteoblastic activity, using ELISA kits. They were also exposed to an osteoblast cell culture line and cell proliferation was measured. Results show that the group with neurology has increased levels of IGF-1 compared to the other groups (p<
0.14, p<
0.18 respectively, Student’s t-test) but had lower TGF-ß (p<
0.05, p<
0.006) and osteoblast proliferation levels (p<
0.002, p<
0.0001). When the neurology group is subdivided into complete (n=5) and incomplete (n=5), it was shown that the complete group had higher levels of both IGF-1 and TGF-ß. This trend is reversed in the osteoblast proliferation assay. This work, for the first time in human subjects, identifies a factor which may be regulating this complication of acute spinal cord injuries, namely IGF-1. Furthermore, the observed trend in the two cytokines seen in the complete neurology group may suggest a role for TGF-ß. However, the results do show that a direct mediation of this unwanted side effect of spinal cord injuries is unlikely as seen in the proliferation assay. Further work remains to be done to fully understand the complexities of the excessive bone growth recognised in this patient group.
Traumatic central cord syndrome (CCS) typically follows a hyperextension injury and results in motor impairment affecting the upper limbs more than the lower, with occasional sensory impairment and urinary retention. Current evidence on mortality and long-term outcomes is limited. The primary aim of this study was to assess the five-year mortality of CCS, and to determine any difference in mortality between management groups or age. Patients aged ≥ 18 years with a traumatic CCS between January 2012 and December 2017 in Wales were identified. Patient demographics and data about injury, management, and outcome were collected. Statistical analysis was performed to assess mortality and between-group differences.Aims
Methods
Acute spinal cord injury (SCI) is most often secondary to trauma, and frequently presents with associated injuries. A neurological examination is routinely performed during trauma assessment, including through Advanced Trauma Life Support (ATLS). However, there is no standard neurological assessment tool specifically used for trauma patients to detect and characterize SCI during the initial evaluation. The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) is the most comprehensive and popular tool for assessing SCI, but it is not adapted to the acute trauma patients such that it is not routinely used in that setting. Therefore, the objective is to develop a new tool that can be used routinely in the initial evaluation of trauma patients to detect and characterize acute SCI, while preserving basic principles of the ISNCSCI. The completion rate of the ISCNSCI during the initial evaluation after an acute traumatic SCI was first estimated. Using a modified Delphi technique, we designed the Montreal Acute Classification of
Acute spinal cord injury (SCI) is most often secondary to trauma, and frequently presents with associated injuries. A neurological examination is routinely performed during trauma assessment, including through Advanced Trauma Life Support (ATLS). However, there is no standard neurological assessment tool specifically used for trauma patients to detect and characterize SCI during the initial evaluation. The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) is the most comprehensive and popular tool for assessing SCI, but it is not adapted to the acute trauma patients such that it is not routinely used in that setting. Therefore, the objective is to develop a new tool that can be used routinely in the initial evaluation of trauma patients to detect and characterize acute SCI, while preserving basic principles of the ISNCSCI. The completion rate of the ISCNSCI during the initial evaluation after an acute traumatic SCI was first estimated. Using a modified Delphi technique, we designed the Montreal Acute Classification of
Acute spinal cord injury (SCI) is most often secondary to trauma, and frequently presents with associated injuries. A neurological examination is routinely performed during trauma assessment, including through Advanced Trauma Life Support (ATLS). However, there is no standard neurological assessment tool specifically used for trauma patients to detect and characterize SCI during the initial evaluation. The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) is the most comprehensive and popular tool for assessing SCI, but it is not adapted to the acute trauma patients such that it is not routinely used in that setting. Therefore, the objective is to develop a new tool that can be used routinely in the initial evaluation of trauma patients to detect and characterize acute SCI, while preserving basic principles of the ISNCSCI. The completion rate of the ISCNSCI during the initial evaluation after an acute traumatic SCI was first estimated. Using a modified Delphi technique, we designed the Montreal Acute Classification of
Aim: To determine whether timing of intervention affects neurological outcome after spinal cord injury resulting from rugby cervical facet dislocations. Methods: An observational study on 57 rugby players who were admitted to a