SEARCH · PubMed Health

Results for “COMPRESSION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources

PubMed2003

Delayed neuronal damage related to microglia proliferation after mild spinal cord compression injury.

In order to investigate the mechanism of delayed progressive or secondary neuronal damage after the spinal cord injury, we developed a mild-compression injury model in the rat thoracic spinal cord. Our compression device consists of a soft silicone point of contact to the dura, in order to prevent violent injury that may cause axonal tears or hemorrhages in the spinal cord. Since rats often assume a 'standing' posture, i.e. raising head with lifting their fore-limbs, damage to the thoracic spinal cord was evaluated by measuring the frequency of 'standing', which effectively indicates hind limb function. Twenty-four hours after compression by a 20 g weight for 10 or 20 min, the standing frequency of the injured rat was almost the same as that of sham animals that underwent laminectomy without compression. However, the standing frequency decreased with time; the frequency of standing at 72 h was approximately 30-50% that of sham animals. In the compressed spinal cord tissue, microglial cells, detected by lectin staining, proliferated with time. An enormous amount of microglia was observed at 48 and 72 h after compression, although only a small amount of cells were positive to lectin staining at 24 h after the compression. These results suggest that our mild-compression spinal cord injury model showed late-onset or delayed neuronal damage that may be related to pathological microglia proliferation.

Animals↗

PubMed2002

A comparison of chronic pain behavior following local application of tumor necrosis factor alpha to the normal and mechanically compressed lumbar ganglia in the rat.

To study the role of inflammatory cytokines in the initiation and persistence of radiculopathy as seen in humans, tumor necrosis factor alpha (TNF-alpha) was administered either to normal, uninjured L5 dorsal root ganglia (DRG) of rats via a hole drilled through the transverse process, or to chronically compressed L5 DRG via a hollow stainless steel rod inserted into the intervertebral foramen. In other experiments, a mixture of soluble TNF receptors (sTNF-Rs: sTNF-RIplus minussTNF-RII) was locally delivered to the chronically or acutely compressed DRG to neutralize the activity of endogenous TNF-alpha. Behavioral tests of mechanical allodynia were performed before and after TNF-alpha administration. Infusion of the normal DRG with TNF-alpha at a rate of 1 microl/h for 7 days induced ipsilateral mechanical allodynia (i.e. decreased mechanical withdrawal threshold) that lasted about 2 weeks. Infusion of the compressed DRG did not alter compression-induced allodynia within the first operative week but substantially enhanced the ipsilateral allodynia after the first postoperative week. Neutralizing the activity of endogenous TNF-alpha of the compressed DRG with sTNF-Rs reduced allodynia for 3 days, but was subsequently without effect. Similar results were obtained when sTNF-Rs were chronically administrated at the acutely compressed ganglion. Results demonstrated that exogenous TNF-alpha causes pain and mechanical allodynia when deposited at the normal DRG, and further enhances the ongoing allodynia when administrated at the compressed DRG. Results also suggest that endogenous TNF-alpha contributes to the early development of mechanical allodynia in rats with chronic DRG compression.

Animals↗

PubMed2003

Chronic inflammation and compression of the dorsal root contribute to sciatica induced by the intervertebral disc herniation in rats.

The pathophysiological mechanisms underlying sciatica and back pain are not well understood. In the present study, a sciatica model was developed to investigate the contributions of inflammation and compression of the dorsal root (DR). The procedure used autologous disc to apply direct pressure to the L5 DR (disc compression, DC group). For control, five additional groups were included: (1). mechanical compression of L5 DR without disc (compression, CP group); (2). epidurally placed disc without mechanical compression (disc group); (3). epidurally placed nucleus pulposus (NP) without mechanical compression (NP group); (4). epidurally placed annulus fibrosus (AF) without mechanical compression (AF group) and (5). sham group. The paw withdrawal latency to heat stimulation, paw withdrawal threshold to mechanical stimulation, body weight, and motor function were determined pre- and post-surgery. It was observed that all experimental groups with the exception of the sham group showed a progressive and prolonged mechanical hyperalgesia with the DC group having the strongest effect. Furthermore, the disc group showed a greater mechanical hyperalgesia with earlier onset in comparison with the CP group and disc, AF, and NP groups developed thermal hyperalgesia in addition to mechanical hyperalgesia following surgery. Finally, rats in all groups showed normal motor function and body weight increase. These data suggest that this model is suitable to investigate the mechanisms of sciatica and inflammation as well as mechanical compression is involved in the pathogenesis of this condition. Moreover, AF and NP may contribute similarly to the development of sciatica and back pain.

Animals↗

PubMed1988

Evaluation of microsurgical internal neurolysis in a primate median nerve model of chronic nerve compression.

This study evaluates the effect of internal neurolysis on a chronically compressed primate median nerve as compared with a simple decompression procedure. In 11 adult, cynomologous monkeys, the median nerve in the carpal tunnel was banded with a silicone tube. After 6 months of nerve compression (mild to moderate compression in our model) in eight monkeys, a microneurosurgical internal neurolysis was carried out on the median nerve of one hand and a simple decompression (removal of band) was carried out on the median nerve of the other hand. Histologic, morphologic, and electrophysiologic evaluation was carried out 6 months later. Six control animals were similarly evaluated after 0, 6, and 12 months of nerve compression. The degree of compression produced was not severe in that it did not cause Wallerian degeneration. Histologic and electrophysiologic improvement was produced in both treatment groups over the two chronically compressed groups (6 and 12 months of compression). While internal neurolysis did not cause intraneural scarring or nerve fiber damage as compared with simple decompression alone, there was no difference noted between the effects of these two treatment methods on the chronically compressed nerve.

Animals↗

PubMed1997

Consolidation mechanisms of pharmaceutical solids: a multi-compression cycle approach.

PURPOSE: The consolidation behavior of various pharmaceutical solids were characterized using compression-cycle profiles. Compression-cycle profiles for both uncompacted powder and formed tablets were obtained. These profiles were used to qualitatively and quantitatively characterize the consolidation mechanism of pharmaceutical solids. METHODS: An Instron Universal Testing apparatus and a specially instrumented die coupled with a computerized data acquisition system were utilized to measure the upper-punch pressure and the corresponding die-wall pressure during the compression cycle. RESULTS: Compression cycle profiles were obtained for a variety of pharmaceutical materials. Based on these profiles, parameters such as hysteresis areas, loading slopes, and unloading slopes were calculated for the materials studied. CONCLUSIONS: Materials that consolidate by plastic deformation have similar compression cycle profiles for the first and subsequent compression cycles indicating that the plastic deformation process occurs to the same extent on the first as well as subsequent compression cycles. For brittle materials, the brittle fracture process occurs during the first compression cycle. During subsequent cycles the tabletted material does not undergo further yield or failure and primarily undergoes elastic deformation. Low molecular-weight polyethylene glycol is an excellent model material for plastically deforming materials, whereas sucrose or sodium citrate are excellent examples of materials that consolidate by brittle fracture.

Compressive Strength↗

PubMed2006

Evaluation of the effect of JPEG and JPEG2000 image compression on the detection of diabetic retinopathy.

AIMS: To compare the effect of classic Joint Photographic Experts Group (JPEG) and JPEG2000 compression algorithms on detection of diabetic retinopathy (DR) lesions. METHODS: In total, 45 colour fundus photographs obtained with a digital nonmydriatic fundus camera were saved in uncompressed Tagged Interchanged Files Format (TIFF) format (1.26 MB). They were graded jointly by two retinal specialists at a 1 month interval for soft exudates, hard exudates, macular oedema, newvessels, intraretinal microvascular abnormalities (IRMA), and retinal haemorrhages and/or microaneurysms. They were compressed to 118, 58, 41, and 27 KB by both algorithms and 24 KB by classic JPEG, placed in random order and graded again jointly by the two retina specialists. Subjective image quality was graded, and sensitivity, specificity, positive and negative predictive values, and kappa statistic were calculated for all lesions at all compression ratios. RESULTS: Compression to 118 KB showed no effect on image quality and kappa values were high (0.94-1). Image degradation became important at 27 KB for both algorithms. At high compression levels, IRMA and HMA detection were most affected with JPEG2000 performing slightly better than classic JPEG. CONCLUSION: Performance of classic JPEG and JPEG2000 algorithms is equivalent when compressing digital images of DR lesions from 1.26 MB to 118 KB and 58 KB. Higher compression ratios show slightly better results with JPEG2000 compression, but may be insufficient for screening purposes.

Algorithms↗

PubMed1998

Fibrocartilage in tendons and ligaments--an adaptation to compressive load.

Where tendons and ligaments are subject to compression, they are frequently fibrocartilaginous. This occurs at 2 principal sites: where tendons (and sometimes ligaments) wrap around bony or fibrous pulleys, and in the region where they attach to bone, i.e. at their entheses. Wrap-around tendons are most characteristic of the limbs and are commonly wider at their point of bony contact so that the pressure is reduced. The most fibrocartilaginous tendons are heavily loaded and permanently bent around their pulleys. There is often pronounced interweaving of collagen fibres that prevents the tendons from splaying apart under compression. The fibrocartilage can be located within fascicles, or in endo- or epitenon (where it may protect blood vessels from compression or allow fascicles to slide). Fibrocartilage cells are commonly packed with intermediate filaments which could be involved in transducing mechanical load. The ECM often contains aggrecan which allows the tendon to imbibe water and withstand compression. Type II collagen may also be present, particularly in tendons that are heavily loaded. Fibrocartilage is a dynamic tissue that disappears when the tendons are rerouted surgically and can be maintained in vitro when discs of tendon are compressed. Finite element analyses provide a good correlation between its distribution and levels of compressive stress, but at some locations fibrocartilage is a sign of pathology. Enthesis fibrocartilage is most typical of tendons or ligaments that attach to the epiphyses of long bones where it may also be accompanied by sesamoid and periosteal fibrocartilages. It is characteristic of sites where the angle of attachment changes throughout the range of joint movement and it reduces wear and tear by dissipating stress concentration at the bony interface. There is a good correlation between the distribution of fibrocartilage within an enthesis and the levels of compressive stress. The complex interlocking between calcified fibrocartilage and bone contributes to the mechanical strength of the enthesis and cartilage-like molecules (e.g. aggrecan and type II collagen) in the ECM contribute to its ability to withstand compression. Pathological changes are common and are known as enthesopathies.

Adaptation, Physiological↗

PubMedDate not supplied

In vitro mechanical compression induces apoptosis and regulates cytokines release in hypertrophic scars.

Hypertrophic scars resulting from severe burns are usually treated by continuous elastic compression. Although pressure therapy reaches success rates of 60-85% its mechanisms of action are still poorly understood. In this study, apoptosis induction and release of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) were evaluated in normal (n = 3) and hypertrophic (=7) scars from burns after in vitro mechanical compression. In the absence of compression (basal condition) apoptotic cells, scored using terminal deoxyribonucleotidyl transferase assay, were present after 24 hours in the derma of both normal scar (23 +/- 0.4% of total cell) and hypertrophic scar (11.3 +/- 1.4%). Mechanical compression (constant pressure of 35 mmHg for 24 hours) increased apoptotic cell percentage both in normal scar (29.5 +/- 0.4%) and hypertrophic scar (29 +/- 1.7%). IL-1beta released in the medium was undetectable in normal scar under basal conditions while in hypertrophic scar the IL-1beta concentration was 3.48 +/- 0.2 ng/g. Compression in hypertrophic scar-induced secretion of IL-1beta twofold higher compared to basal condition. (7.72 +/- 0.2 ng/g). TNF-alpha basal concentration measured in normal scar medium was 8.52 +/- 4.01 ng/g and compression did not altered TNF-alpha release (12.86 +/- 7.84 ng/g). TNF-alpha basal release was significantly higher in hypertrophic scar (14.74 +/- 1.42 ng/g) compared to normal scar samples and TNF-alpha secretion was diminished (3.52 +/- 0.97 ng/g) after compression. In conclusion, in our in vitro model, mechanical compression resembling the clinical use of elastocompression was able to strongly increase apoptosis in the hypertrophic scar derma as observed during granulation tissue regression in normal wound healing. Moreover, the observed modulation of IL-1beta and TNF-alpha release by mechanical loading could play a key role in hypertrophy regression induced by elastocompression.

Adolescent↗

PubMed2004

Histopathologic changes in oculomotor nerve and ciliary ganglion in aneurysmatic compression injuries of oculomotor nerve.

BACKGROUND: Bilateral common carotid artery ligation (BCCAL) increases vertebrobasilar blood flow and leads to increased luminal pressure, luminal enlargement, wall thinning, convolutions and sometimes aneurysm formation in posterior circulation arteries, especially the posterior communicating arteries (PcomA). PcomA aneurysms compress the oculomotor nerves. The principal aim of this investigation is to examine the histopathologic results of the compressive effect of PcomA aneurysms on the oculomotor nerves (OMN) and on ciliary ganglions (CG). METHODS: When we observed the effects of BCCAL on the posterior circulation arteries of the brain in fifteen ligated rabbits after sacrifice, we noticed aneurysm formation on these arteries in three rabbits. These aneurysms developed on the PcomAs compressed the oculomotor nerves. These compressed nerves and normal oculomotor nerves together with their ciliary ganglions were examined histopathologically. RESULTS: A PComA aneurysm developed in three rabbits from 15 ligated animals and these aneurysms compressed the oculomotor nerves on the same side. Partial peripheral necrosis and axonal loss were seen on the compressed oculomotor nerves. Concomitantly, cellular loss and necrosis were also observed on their ganglions. CONCLUSION: Bilateral common carotid artery ligation may lead to PcomAs and these aneurysms could compress the oculomotor nerves. Compression injuries of oculomotor nerve may cause cellular injury and necrosis on both oculomotor nerves and ciliary ganglions.

Animals↗

PubMed1989

Resistance to axonal degeneration after nerve compression in experimental diabetes.

To determine the effect of diabetes on the development of axonal degeneration after acute nerve compression, the mobilized peroneal nerves of rats with streptozotocin-induced diabetes and of control rats were compressed at 150 mmHg (1 mmHg = 133 Pa) for 30 min by using specially devised cuffs. At three intervals after compression--3 days, rats diabetic for 31 wk; 14 days, diabetic for 6 wk; and 24 days, diabetic for 31 wk--groups of nerves were studied to assess numbers and sizes of fibers above, at, and below the cuff and to assess frequency of fiber degeneration in teased fibers from nerve distal to the cuff. Teased fibers with pathologic abnormalities were more frequent in nerves from controls than in nerves from diabetic rats in all three groups but the difference was statistically significant only at 3 and 14 days after compression. The lack of significant difference at 24 days may be explained by higher rates of disappearance of degenerating products and of fiber regeneration at 24 than at 3 and 14 days. This study provides evidence that in addition to delaying the reported functional deficit of vibratory detection threshold and conduction block during nerve compression, diabetes also may partially prevent axonal injury. Low nerve myo-inositol concentration did not predispose diabetic nerve to acute compression injury. If these results also apply to human diabetes and if repeated acute compression is involved in the genesis of fiber degeneration in entrapment, then a higher frequency of entrapment neuropathy among diabetics might be due to mechanisms other than increased susceptibility of fibers to acute compression--e.g., possibly to greater constriction of nerve due to pathologic alterations of the carpal ligament.

Animals↗

PubMed1990

Structural alterations of nerve during cuff compression.

Whether compression nerve injury is due to ischemia, direct mechanical injury, or both remains unsettled. To assess structural changes of nerve during compression, peroneal nerves of rats were compressed at various pressures for different times, and the structural alterations were stopped by simultaneous in situ and perfusion fixation. The structural changes observed during a few minutes of compression cannot be explained by ischemic injury because the pathologic alterations characteristic of ischemia take many hours to develop and in any case are different from the ones found here. The pressure- and time-related structural changes observed in the present study under the cuff were (i) decrease in fascicular area and increase in fiber density due to expression of endoneurial fluid; (ii) compression and expression of axoplasm, sometimes to the point of fiber transection; (iii) lengthening of internodes; and (iv) obscuration of nodes of Ranvier due to cleavage and displacement of myelin and overlapping of nodes by displaced loops of myelin. At the edges of the cuff the changes were (i) increase of fascicular area probably from expressed endoneurial fluid; (ii) widening of nodal gaps, perhaps mainly from translocated axonal fluid; and (iii) disordered structure of axoplasm. We suggest that the process of paranodal demyelination and axonal transection are linked, occur during the act of compression, and are due to shear forces. The initial event is expression of endoneurial fluid, followed by compression and expression of axoplasm and cleavage and displacement of layers of myelin. Conceivably, with prolonged cuff compression ischemic injury might be found to be superimposed on mechanical injury.

Animals↗

PubMed2006

Effects of the method of preparation on the compression, mechanical, and release properties of khaya gum matrices.

A study has been made of the compression properties of khaya gum matrices and the effects of drug concentration and method of preparation of the material on the compression, mechanical and the drug release characteristics of the matrices. Khaya gum matrix tablets were prepared by direct compression and wet granulation methods. The compression properties of the formulations were assessed using the equations of Heckel and Kawakita. The mechanical properties of the tablets were evaluated using crushing strength and friability of the tablets, whereas the release properties of the tablets were evaluated by using the disintegration and dissolution times. The results obtained show that khaya gum deformed mainly by plastic deformation. The compression properties of the formulations were affected by the concentration of the drug and the method of preparation of the materials for compression. Tablets prepared by wet granulation showed faster onset and higher amount of plastic deformation during compression than those prepared by direct compression. Tablets containing dicalcium phosphate showed higher mechanical strength and disintegration and dissolution times. Wet granulation also increased the mechanical strength of the tablet without significantly affecting the drug release characteristics from the matrix tablets. Thus, the wet granulation method could be useful in the preparation of khaya gum matrix tablet with acceptable mechanical properties and drug release properties.

Calcium Phosphates↗

PubMed2003

Synaptic blockade plays a major role in the neural disturbance of experimental spinal cord compression.

We analyzed dynamic processes of neural excitation propagation in the experimentally compressed spinal cord using a high-speed optical recording system. Transverse slices of the juvenile rat cervical spinal cord were stained with a voltage-sensitive dye (di-4-ANEPPS). Two components were identified in the depolarizing optical responses to dorsal root electrical stimulation: a fast component of short duration corresponding to pre-synaptic excitation and a slow component of long duration corresponding to post-synaptic excitation. In the directly compressed dorsal horn, the slow component was attenuated more (attenuated to 37.4 +/- 9.1% of the control) than the fast component (to 70.5 +/- 14.9%) (p < 0.01) at 400 msec after stimulation. Depolarizing optical responses to compression and to chemical synaptic blockade were similar. There was a regional difference between white matter (attenuated to 86.2 +/- 10.5%) and gray matter (to 72.6 +/- 10.4%) (p < 0.03) in compression-induced changes of the fast components; neural activity in the white matter was resistant to compression, especially in the dorsal root entry zone. Depolarizing optical signals in the region adjacent to the directly compressed site were also attenuated; the fast component was attenuated to 77.6 +/- 10.4% and the slow component to 31.8 +/- 11.3% of the control signals (p < 0.01). Spinal cord dysfunction induced by purely mechanical compression without tissue destruction was virtually restored with early decompression. We suggest that a disturbance of synaptic transmission plays an important role in the pathophysiological mechanisms of spinal cord compression, at least under in vitro experimental conditions of juvenile rats.

Animals↗

PubMed1995

Free radical damage in acute nerve compression.

Nerve compression causes injury by local ischemia and direct mechanical distortion. Peripheral nerves in diabetes mellitus are more prone to injury than those of nondiabetics. We sought to determine whether reperfusion-induced, oxygen-derived free radical injury occurs in peripheral nerves subjected to acute compression in normal and chronically diabetic rats. Female Sprague-Dawley rats weighing 250 to 275 g (N = 347) were divided into two groups: normal and streptozocin-induced diabetics. A total of 187 normal and 160 diabetic nerves were analyzed. After 8 weeks of untreated hyperglycemia, the sciatic nerves of normal and diabetes mellitus rats were subjected to one of three operations: a sham operation, 24-hour compression alone, and 24-hour compression followed by 1-hour reperfusion (CR). Nerve compression was established by banding the right sciatic nerve with a Silastic tubing, 1 cm long and 0.62 mm internal diameter, which was secured with 6-0 nylon suture. In the CR group, after 24 hours of compression, the tubings were released for 1 hour to permit reperfusion. Nerve tissue within the zone of compression underwent biopsy examination and was frozen for subsequent analysis. Blood flow to the nerve was quantified by injecting fluorescein (10 mg/kg intravenously) 10 minutes before harvest and measuring tissue levels fluorometrically. Compression with the Silastic tubing significantly reduced neural blood flow by 75%. Blood flow improved but failed to return to baseline levels after tubing release in diabetes mellitus nerves while perfusion returned to baseline in non-diabetes mellitus nerves. Nerve homogenate was assayed for malonyldialdehyde, an indicator of lipoperoxidation, as well as enzymes of cellular defense and glucose metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1998

Role of reactive oxygen species in optic nerve compression injury: a preliminary study.

Optic nerve compression is one of the complications in craniofacial surgery and blepharoplasty. We have shown previously that acute and chronic nerve compression produce significant tissue injury in rat sciatic nerve. In the present study the optic nerve was evaluated for possible ischemia/reperfusion injury after acute compression in an animal model. Male New Zealand White rabbits were used in the experiment. The optic nerve was subjected to 2-hour compression followed by reperfusion for 1 hour. Nerve compression was established by banding the optic nerve with silastic tubing. The compressed optic nerve was assayed for malondialdehyde, an indicator of lipid peroxidation, measured as thiobarbituric acid reactive substances (TBARS). The TBARS levels increased significantly to 2.5 times normal, from 37+/-6 pmoles per milligram tissue (N=6) to 90+/-12 pmoles per milligram tissue dry weight (N=5) in the compressed/reperfused nerve (p < 0.05). Much of these increases were prevented by treatment with deferoxamine, an iron chelator and antioxidant. The results indicate that optic nerve is injured by acute compression followed by reperfusion. The nerve compression injury appears to be due to reactive oxygen species and can be ameliorated by treatment with free radical scavengers.

Animals↗

PubMed2003

Endoscopic and transconjunctival orbital decompression for thyroid-related orbital apex compression.

OBJECTIVE: To evaluate the efficacy and safety of a combined endoscopic and transconjunctival orbital decompression in patients with thyroid-related orbitopathy with orbital apex compression. STUDY DESIGN: Retrospective review. METHODS: A sequential series of patients with thyroid-related orbitopathy presenting with orbital apex compressive myopathy with and without optic neuropathy who were undergoing combined endoscopic and transconjunctival decompression by the same surgeons from 1992 to 2001 was reviewed. Patients were regularly evaluated preoperatively and postoperatively over a 3- to 55-month period to record the effects of this approach on visual acuity, Hertel exophthalmometry, and diplopia. Complications and secondary ophthalmological procedures were reviewed. RESULTS: Between 1992 and 2001, 72 combined endoscopic and transconjunctival decompressions were performed on 41 patients with orbital apex compression. Visual acuity improved in 89.3% of the patients with compressive optic neuropathy (P <.0005) and in 34.1% of those without neuropathy. Proptosis was reduced by 3.65 mm, on average. There was one case of transient intraoperative cerebrospinal fluid extravasation at the site of the optic nerve decompression, and one patient developed epistaxis. CONCLUSIONS: The study supports the treatment of thyroid-related orbital apex compression with and without compressive optic neuropathy by a combined transconjunctival and endoscopic approach. This approach offers short hospital stays, excellent visual recovery, and minimal complications in patients with thyroid-related orbital apex compressive myopathy and related compressive optic neuropathy. The beneficial effects observed in the patients with visual loss continued to improve over time and were significant (P <.001).

Adult↗

PubMed1997

Lower urinary tract symptoms in lumbar root compression syndromes: a prospective survey.

STUDY DESIGN: A prospective, observational survey. OBJECTIVES: To describe lower urinary tract symptoms in uncomplicated lumbar root compression syndromes with special reference to prevalence, nature, and severity, and to analyze whether the occurrence of lower urinary tract symptoms correlates with age, pain, analgesic intake, or the type and level of compression. SUMMARY OF BACKGROUND DATA: Lower urinary tract symptoms with lumbar root compression are well known in the classic but rather rare cauda equina syndrome. However, micturition difficulties seem to be far more frequent in lumbar root compression syndromes. METHODS: One hundred eight male patients admitted for surgery for lumbar disc herniation or spinal stenosis were investigated with an extensive questionnaire about their micturition. RESULTS: Fifty-five percent had significant lower urinary tract symptoms. Eighty percent of the patients with spinal stenosis had symptoms. Thirty-three patients had irritative symptoms, 36 had obstructive symptoms, and 23 had retention symptoms. Twenty-four had severe symptoms. Median compression resulted in more symptoms than paramedian compression. There was no correlation between age, level of compression, drug intake, or pain score and lower urinary tract symptoms. CONCLUSIONS: Lower urinary tract symptoms of mixed type occur with a high prevalence in male patients with lumbar root compression syndromes referred for neurosurgical evaluation and treatment.

Adult↗

PubMed1998

Compression of the upper cervical spinal cord causing symptoms of brainstem compromise. A case report.

STUDY DESIGN: A case is reported in which a flexion-induced compression of the upper cervical spinal cord caused symptoms of brainstem compromise in the absence of radiographic evidence of osseous instability. OBJECTIVES: A 41-year-old woman developed postoperative cervical instability with flexion-induced neurologic symptoms referable to the brainstem. The instability was caused by direct compression at the third cervical vertebral body, which in turn was caused by differential movements between the neuraxis and skeletal elements in the upper cervical spine. SUMMARY OF BACKGROUND DATA: Pathologic processes at the craniocervical junction may cause brainstem compromise with neurologic symptoms. The mechanism of brainstem involvement is usually either vertebrobasilar insufficiency or direct mechanical compression. In cases where the brainstem is compressed by skeletal elements, the compressing osseous structures usually are the walls of the foramen magnum or the odontoid process, or, less frequently, the atlas or axis vertebrae. Symptoms of brainstem dysfunction caused by dynamic compression at the level of the third cervical vertebra in the absence of hindbrain herniation are unusual and, to the best of the authors' knowledge, have not been described previously. METHODS: The patient underwent initial examination, evaluation, and periodic follow-up examination with magnetic resonance imaging from the time of her first visit until 26 months after the surgical treatment. The patient experienced postsurgical instability with dynamic compression by the C3 vertebral body, which caused brainstem compromise. Surgical treatment consisted of decompressive C3 corpectomy and fusion of C2 to C6, supplemented by anterior fixation. RESULTS: After undergoing surgical decompression of C3, reconstruction, and anterior internal fixation of C2 to C6, the patient had dramatic neurologic improvement. Diplopia, paresthesia, and nystagmus disappeared immediately after surgery. Swallowing difficulties, hoarseness, and vertigo improved gradually. At follow-up examination 26 months after surgery, the patient was asymptomatic. Magnetic resonance imaging showed good position of the construct, with no evidence of compression of the spinal cord or brainstem. CONCLUSIONS: Instability of the cervical spine may result in symptoms of brainstem dysfunction, even in the absence of hindbrain herniation. This instability is explained by the differential movement between the bony structures and neuraxis in the upper cervical region. Diagnosis and adequate management of this instability alleviates the neurologic symptoms and prevents possible hazardous complications.

Adult↗