Cohort study of postural sway and low back pain: the Copenhagen City Heart Study.

PURPOSE: Low back pain is a significant health problem with a high prevalence. Studies of smaller cohorts of low back pain patients have indicated increased body sway. The present paper tests the hypothesis of an association between low back pain and postural sway in a large randomly selected population. METHODS: The current study used the fifth examination (2011-2015) of The Copenhagen City Heart Study where 4543 participated. The participants answered a self-administered questionnaire regarding pain, physical activity, smoking, alcohol consumption, education, and other lifestyle factors. Measurement of postural body sway was performed using the CATSYS system. RESULTS: Totally 1134 participants (25%) reported to have low back pain. Subjects with low back pain had higher sway area and sway velocity than subjects without. CONCLUSION: When using multivariate statistical analysis, confounding factors such as male gender, higher age, larger body height, low education level, smoking, and low activity level explained the association between low back pain and postural sway.

Impaired neck motor control in chronic whiplash and tension-type headache.

OBJECTIVES: The purpose of this study is twofold, first to present a new method based on head laser tracking designed to measure head or hand movements and second to further investigate if patients suffering from chronic whiplash or tension-type headache have impaired motor control of neck muscles. MATERIAL AND METHODS: A new laser tracking instrument was designed to measure the ability of a test person to track a reference point moving on the wall by a laser fixed to the forehead or held in the hand. The reference point to be tracked moves in runs of a circle or a square at three different speeds 10, 20, or 30 cm/s. We used a 1 × 1 ×1 m setup geometry to provide head movements well below pain release. Groups of 22 patients diagnosed with chronic whiplash-associated disorder grade 2, 19 patients diagnosed with chronic tension-type headache, and 37 control persons were compared. RESULTS: A small but highly significant dyscoordination of head movements was observed in both patient groups and in whiplash also of the hand. CONCLUSIONS: Our study presents a new method based on laser tracking for precision quantitative measurements of head or hand movements during standardized conditions. The results confirm that motor control of head movements is impaired in both chronic whiplash and tension-type headache, and in whiplash also of the hand. This suggests involvement of the central nervous system in the pathology of these diseases.

Tension-type headache and low back pain reconsidered.

The natural history and clinical course of tension-type headache and non-specific low back pain are reconsidered. By closer examination, these two conditions appear to share several specific clinical features. Both are muscular pain conditions along the spine, they have a preponderance in women, they may occur spontaneously or follow a trivial traumatic incident, and they both have a high risk of chronicity. The affected muscles are tender with tender points. EMG indicates diffuse hyperactivity and abnormal activation pattern, and motor control of the affected muscles and adjacent muscle groups is discoordinated. These shared features suggest analogous pathophysiology involving the neuromotor control of affected and adjacent muscle groups in the cervical and lumbar regions, respectively. As recently suggested for the whiplash disease, we suggest the term spinal dyssynergia for this specific pattern of pathology. This suggestion provides a new perspective for the understanding of these diseases by placing their cause within the central nervous system and not in the spine or spinal musculature. This perspective warrants further clinical, neurophysiological, and neuropharmacological studies of this 'family' of common yet poorly understood clinical muscular pain conditions along the spine.

The Whiplash Disease Reconsidered.

The natural course of the whiplash disease is reconsidered in relation to the predominant view of its cause. It is assumed that a whiplash-type trauma is causing an acute tissue injury such as a distortion or sprain in the neck followed by neck pain and headache, which then tends to become a chronic pain condition. We conclude that the whiplash disease typically evolves following a minor trauma without any signs of a tissue injury. It presents with central neuromotor dysfunction, such as electromyography (EMG) hyperactivity and abnormal activation patterns associated with dyscoordination of the involved and adjacent muscle groups. This indicates a central neurological rather than a peripheral traumatic pathology. This view places the cause of the whiplash disease within the central nervous system, and, in concordance with the EMG abnormalities and motor dyscoordination, we suggest the term cervical spinal dyssynergia for this pathology. It provides a new paradigm for further investigations of this disease as well as a window for possible specific neuropharmacological therapy directed towards dysfunctional neuromotor control.

Blood coagulation and fibrinolysis after experimental subarachnoid hemorrhage.

BACKGROUND: Aneurysmal rebleeding poses a serious risk in patients with subarachnoid hemorrhage (SAH). Studies have shown that antifibrinolytic therapy with tranexamic acid has a dramatic effect on the rate of rebleeding. Therefore, changes in the fibrinolytic system could be hypothesized. METHODS: We have used an experimental SAH rat model to demonstrate serial changes in the haemostatic system as evaluated by Thromboelastography (TEG). RESULTS: In the SAH group, a shorter reaction time (R-time) and higher maximum amplitude (MA) were observed. In the saline group, only a shorter R-time was observed. CONCLUSIONS: The study has shown that a hypercoagulable state is present immediately after experimental SAH is induced as determined by TEG. The reduction in R-time and rise in MA observed in the SAH group indicate that blood in the subarachnoid space is necessary to accomplish a full systemic coagulation response. This abnormality in coagulation profile seems to be a response to the acute traumatic event caused by induction of SAH.

Considerable delay in diagnosis and acute management of subarachnoid haemorrhage.

INTRODUCTION: Rebleeding from subarachnoid haemorrhage (SAH) usually occurs within the first six hours after the initial bleeding. Rebleeding can be prevented effectively with tranexamic acid (TXA). Although a broad consensus has evolved that SAH should be treated as an emergency, it is likely that delays do exist in the diagnosis and treatment of SAH patients. The aim of this study was to prospectively assess the interval between symptom onset, emergency room (ER) admission, initial diagnosis and treatment, and final closure of the aneurysm. MATERIAL AND METHODS: We prospectively studied the time course from the initial bleeding to ER admission, computed tomography (CT), TXA treatment, referral to the neurosurgical department, and to the final closure of the aneurysm. RESULTS: A total of 133 patients with SAH due to ruptured intracranial aneurysms were admitted to two neurosurgical units in Copenhagen, Denmark, during a one-year period. The median time to admission was 60 min. The median delay from admission to CT scan was 55 min. Long pre-hospital delay (p = 0.03) and high Glasgow Coma Scale score on arrival (p = 0.0006) were associated with a longer time to CT scan. The median time from CT scan to initiation of TXA treatment was 50 min. The median time from initial insult to final closure of the aneurysm was 30 hours. CONCLUSION: The present study demonstrates that considerable diagnostic delays exist in connection with CT and TXA treatment after patients' arrival to the ER.

Recovery of anterograde amnesia in a case of craniopharyngioma.

BACKGROUND: Studies of the amnesic syndrome have indicated that telencephalic and diencephalic structures are critical components of the memory system. The exact role of the mammillary bodies (MBs) in human memory remains elusive, since few cases of selective MB damage have been reported. OBJECTIVE: To study a case of severe anterograde amnesia due to a third-ventricle craniopharyngioma with severe MB compression. DESIGN: Case report. SETTING: Neurosurgery clinic of an academic hospital. PATIENT: A 53-year old woman who developed severe anterograde amnesia due to a third-ventricle craniopharyngioma strongly compressing the MBs and, to a lesser extent, the right hippocampus. INTERVENTIONS: Surgical excision of the tumor and neuropsychological testing and positron emission tomography during an associative memory test before and 2 months after tumor removal. A postsurgical magnetic resonance image did not show evidence of damage to the hypothalamus, thalamus, hippocampus, or MBs. MAIN OUTCOME MEASURES: Changes in brain imaging data and results of neuropsychological testing. RESULTS: After tumor removal, the patient showed a complete recovery of memory functions. Performance on the associative memory test was at chance level before surgery and dramatically improved postoperatively. Results of the preoperative positron emission tomographic study showed no activity in memory-related structures. In contrast, a significant blood flow increase occurred in the anterior thalamic nuclei postoperatively. CONCLUSIONS: These behavioral and brain imaging data stress the importance of the MBs in this patient's amnesia. Our data further suggest that the clinical prognosis of decompressing the mammillothalamic tract is excellent, even in cases of massive compression.

Biochemical definitions of disease activity in acromegaly.

UNLABELLED: In acromegaly the therapeutic outcome is difficult to assess and depends on the biochemical method. We have ascertained disease activity in 70 acromegalic patients by means of a GH profile (8 hourly samples) and a single IGF-I measurement as compared to a healthy control group. As an estimate of the "stiffness" of the GH profile we calculated the SD/nadir(GH) from the GH profile. In the control group the following upper normal limits were obtained: IGF-I (microg/l) 217; mean GH (microg/l) 2.16; nadir GH (g/l) 0.3. Based on ROC plot analysis a value of 2.0 for the SD/nadir ratio was used as cut-off. This translated into the following surgical cure rates (%): IGF-I 47; mean GH 77; nadir GH 65; SD/nadir 30. Some of the patients post-surgery had elevated IGF-I levels despite "normal" GH levels. Abnormal SD/nadir versus normal IGF-I and vice versa were recorded in many patients post-surgery. IN CONCLUSION: (1) cure rates of acromegaly depend strongly on the criteria being used and (2) estimates of GH secretion pattern may yield important information about GH status in acromegaly.

Blood flow and ischemia within traumatic cerebral contusions.

OBJECTIVE: To provide evidence of irreversible ischemia in cerebral contusions among patients with severe traumatic brain injuries and to clarify the potential viability of tissue in the pericontusional zone, quantitative regional cerebral blood flow (rCBF) measurements obtained with the xenon-enhanced computed tomographic method were correlated with the areas of contusions, by using image fusion. METHODS: rCBF measurements obtained during the acute phase (mean, 2 d after injury; range, 0-10 d) were statistically correlated with the extent of tissue necrosis identified as focal atrophy on late follow-up computed tomographic scans (mean time after the xenon-enhanced computed tomographic cerebral blood flow investigation, 265 d; range, 30-1047 d). RESULTS: Seventeen patients exhibited 26 traumatic contusions. All contusions progressed to late focal atrophic areas on the follow-up computed tomographic scans. The rCBF values within the traumatic contusions ranged from 0.5 to 22.0 ml/100 g/min, with a mean of 5.9 +/- 5.9 ml/100 g/min. The contusions exhibited a specific rCBF profile, presenting as a core of severe lethal ischemia surrounded by variable but gradually increasing perfusion with increasing distance from the ischemic core. CONCLUSION: The ischemic profile of the contusions, with a pericontusional zone of low rCBF, presents the potential risk of secondary ischemic insults, similar to the risk in the ischemic penumbral zones surrounding areas of acute ischemic stroke.

Rebleeding after aneurysmal subarachnoid hemorrhage: a literature review.

OBJECTIVE: To summarize the current knowledge of the mechanisms leading to rebleeding and the prevention of rebleeding after subarachnoid hemorrhage (SAH). METHODS: A literature search was performed to investigate factors associated with rebleeding after SAH. RESULTS: The review of the literature revealed that rebleeding is a complex and multifactorial event involving hemostasis, pathophysiologic, and anatomic factors. Administration of antifibrinolytics has been shown to have a dramatic effect on the rebleeding rate, so changes in coagulation and fibrinolysis must be involved in rebleeding. CONCLUSIONS: Further studies are warranted before the exact mechanisms leading to rebleeding are established and the optimal preventive measures are made available. At the present time, antifibrinolytic therapy remains the only realistic protective measure during the initial 6 hours after SAH during which the rebleeding rate is highest.

Reduced clot-stability during the first 6 hours after aneurysmal subarachnoid haemorrhage--a prospective case-control study.

INTRODUCTION: Early rebleeding is an important cause of death and disability following aneurysmal subarachnoid haemorrhage (SAH). Recent studies have shown that 50-90% of the rebleedings occurred within the first 6 hours after the primary bleeding. The mechanism leading to rebleeding remains to be established. In the present prospective case-control study we hypothesize that patients with SAH develop a coagulopathy characterized by reduced clot stability during the early period after the initial bleeding. METHODS: Patients with aneurysmal SAH was studied with a dynamic clot lysis assay and markers of fibrinolysis and clot stabilizers in blood samples taken within and after 6 hours after onset of bleeding. Results were compared with blood samples from age and gender matched healthy controls. RESULTS: 36 patients were enrolled, 26 patients had blood samples collected within 6 hours after the initial bleeding whereas 10 patients had blood samples taken later than 6 hours after the initial bleeding. Patients demonstrated significantly reduced clot stability during the first 6 hours after initial bleeding. Fibrinolytic activity was increased during the first 6 hours along with the inhibitors of fibrinolysis whereas the modulators of fibrinolysis were reduced or inactivated. CONCLUSION: During the first 6 hours after SAH patients exhibit reduced clot-stability. Probably a consequence of activated fibrinolysis in combination with reduced or inactivated factor XIII and thrombin-activable fibrinolysis inhibitor.

[Vagoglossopharyngeal neuralgia treated with vascular decompression]. / Vagoglossofaryngeusneuralgi behandlet med mikrovaskulaer dekompression.

This case report describes a 63-year-old man referred with right-sided glossopharyngeal neuralgia. Magnetic resonance imaging (MRI) demonstrated asymmetry of the PICA vessels. A microvascular decompression was performed and complete remission of symptoms followed. After 14 months the neuralgia recurred, this time accompanied by sinus bradycardia/sinus arrest during attacks causing discomfort and syncopes. An MRI now demonstrated an arterial loop at the site of the vagoglossopharyngeal complex leaving the brainstem. After another microvascular decompression, complete remission of symptoms was observed.

[Stroke--an emergency]. / Apopleksi--en akut sygdom.

Treatment for acute stroke has proved effective when initiated in the first few hours after symptom onset. Thrombolysis for acute ischemic stroke has been approved within 3 hours from symptom onset in patients aged 18-80 years. Results from ongoing studies are awaited for selected patients beyond this time and age limit. Haemostatic treatment for patients with intracerebral or subarachnoidal haemorrhage prevent early re-bleeding and early stroke recurrence after TIA or minor stroke can be prevented effectively by carotid endarterectomy within 2 weeks.

[Treatment of acromegaly in Aarhus University Hospital. A retrospective investigation of the period from 1994 to 2004]. / Behandling af akromegali på Arhus Universitetshospital. En retrospektiv opgørelse fra perioden 1994-2004.

INTRODUCTION: Traditional treatment of acromegaly comprises surgery and somatostatin analogs (SA), which however is effective in no more than 80%. New treatments are available which prompted us to follow up our results of surgery and/or SA. PATIENTS AND METHODS: In a retrospective design we followed all 41 patients with newly diagnosed acromegaly at Aarhus University Hospital from 1994 to 2004. 35 patients underwent surgery of whom 10 also received SA. Six patients only received SA. The criteria for cure was a nadir GH level < 0.5 mg/l and/or normalisation of serum IGF-I. RESULTS: The overall cure rate after surgery was 56%. A cure rate of 89% was observed if the tumor size was < 10 mm in maximal diameter. In the surgery-only group serum IGF-I continued to decline when comparing the first and last postoperative levels. Treatment with SA was effective in 40% and a sufficient response with SA as monotherapy was observed in 67%. Serum IGF-I levels were lower in female as compared to male patients both before and after treatment. CONCLUSIONS: 1) The treatment outcome of acromegaly in this population is comparable to international standards. 2) The continuous decline in IGF-I levels as a function of time after surgery, and the gender difference in IGF-I levels must be accounted for when evaluating individual patients. 3) an insufficient response to conventional therapy was observed in 25% of the cases, which is a result that justifies development of new treatment modalities.

["Ultra-early" antifibrinolytic treatment of subarachnoidal bleeding with tranexamic acid]. / Ultratidlig antifibrinolytisk behandling af subaraknoidalblødning med tranexamsyre.

Rebleeding is the biggest risk for patients suffering from subarachnoidal bleeding (SAH) from a ruptured aneurysm, and many resources are spent on early diagnosis and closure of the aneurysm with clip or coils. Recent studies have indicated that the risk of rebleeding is significantly greater in the initial six hours after the first bleeding, i.e., prior to possible closure of the aneurysm. A new prospective randomised study from Sweden indicates that antifibrinolytic treatment with tranexamic acid reduced the incidence of these ultra-early rebleedings from 10.8% to 2.4% and that almost all of this effect was obtained within the first few hours after primary hospital admission. Tranexamic acid treatment was without side effects and was given in standard doses until closure of the aneurysm or alternatively up to three days after the initial bleeding. Naturally, this new treatment has focused on the ultra-early phase of the SAH disease with its enforced acute hospitalization for nonpostponable diagnosis and tranexamic acid treatment. Its implementation is a task for neurosurgical departments in collaboration with regional hospitals and the primary sector.