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PubMed1994

Pathological findings associated with trigeminal neuralgia caused by vascular compression.

Vascular compression of the trigeminal nerve root accounts for more than 80% of intractable cases of trigeminal neuralgia, but the pathogenesis is still debated. The authors report the ultrastructural changes in the trigeminal nerve root of a patient with trigeminal neuralgia, at the point of compression by a large, medially placed petrosal vein, and compare these with the findings in six cases of trigeminal neuralgia not related to vascular compression. Vascular compression of the trigeminal nerve root was associated with focal loss of myelin and close apposition of the demyelinated axons with few intervening astrocytic processes. No inflammatory cells were present. Immunoelectron microscopy for glial fibrillary acid protein confirmed that astrocyte processes were largely confined to the periphery of the lesion. Of the other six rhizotomy specimens, only one, from a patient with multiple sclerosis, showed demyelination with intervening astrocyte processes, perivascular lymphocytes, and lipid-laden macrophages. These findings support the hypothesis that ephaptic transmission plays a role in the pathogenesis of trigeminal neuralgia related to vascular compression.

Adult↗

PubMed2004

Endoscope-assisted microsurgery for microvascular compression syndromes.

OBJECTIVE: To discuss the results of endoscope-assisted surgery in microvascular decompression (MVD) of Cranial Nerves (CNs) V, VII, and VIII. METHODS: Neuroendoscopy was used as an adjunct to the surgical microscope in the MVD of the trigeminal (17 patients), facial (10 patients), and vestibulocochlear (1 patient) nerves in a series of 28 consecutive patients. After a standard microsurgical approach to CNs V, VII, and VIII, the endoscope was used to inspect all aspects of neural anatomy, to assess vascular compression, and to check the results of the decompression. Endoscope use was graded in four categories: Grade I, used but no definite role; Grade II, visualization assisted; Grade III, procedure assisted; and Grade IV, primary role. The usefulness of the endoscope was evaluated in each case. RESULTS: The endoscope was useful in visualizing the anatomy in all cases. It was especially useful in establishing trigeminal vein compression of CN V in Meckel's cave; observing multiple sources of vascular compression; ensuring adequate decompression after cauterization of vein, insertion of the Teflon felt, or a pexy procedure; and permitting observation of the compression of CN VII at the root exit zone by small arteries and veins. In six patients with trigeminal neuralgia, the trigeminal vein was cauterized and divided by using endoscopic vision only because the venous compression was not completely visualized with the microscope. During a follow-up period of 6 to 52 months (mean, 29 mo; median, 40 mo), all patients were asymptomatic and receiving no medication. CONCLUSION: The endoscope is a useful adjunct to MVD in the treatment of trigeminal neuralgia, hemifacial spasm, and disabling positional vertigo or tinnitus.

Arterioles↗

PubMed2006

High-resolution three-dimensional magnetic resonance angiography and three-dimensional spoiled gradient-recalled imaging in the evaluation of neurovascular compression in patients with trigeminal neuralgia: a double-blind pilot study.

OBJECTIVE: To assess the value of high-resolution three-dimensional (3D) time-of-flight (TOF) magnetic resonance (MR) angiography and gadolinium (Gad)-enhanced 3D spoiled gradient-recalled imaging in the visualization of neurovascular compression in patients with trigeminal neuralgia. METHODS: Forty-eight patients with unilateral trigeminal neuralgia underwent high-resolution 3D TOF MR angiography. After administration of a contrast agent, a 3D spoiled gradient-recalled sequence (3D Gad) was run. Images were reviewed by a radiologist blinded to clinical details. All patients underwent microvascular decompression surgery. Microdissection of the trigeminal nerve and compressing vessels was videotaped during surgery and reviewed by surgeons uninvolved in patient care. Results from neuroradiological studies were then compared with findings on operative videotapes. RESULTS: MR angiography in combination with 3D Gad imaging identified surgically verified neurovascular contact in 42 of 46 (91%) symptomatic nerves. The offending vessel (artery, vein) was correctly identified in 31 of 41 cases (sensitivity, 76%; specificity, 75%). Neurovascular compression was observed in 71% of asymptomatic nerves with a trend toward greater compression severity on the symptomatic nerve (P < 0.09). Agreement between the direction of neurovascular contact defined by 3D TOF MR angiography and 3D Gad and findings at surgery was good (kappa = 0.78; 95% confidence interval, 0.61-0.94). CONCLUSION: Double-blind assessment of surgical and neuroradiological findings confirms that neurovascular compression can be visualized with good sensitivity in patients with trigeminal neuralgia by 3D TOF MR angiography in combination with Gad-enhanced 3D spoiled gradient-recalled sequences. Anatomic relationships defined by this method can be useful in predicting surgical findings.

Adult↗

PubMed2003

Mechanical anisotropy of the human knee articular cartilage in compression.

Articular cartilage exhibits anisotropic mechanical properties when subjected to tension. However, mechanical anisotropy of mature cartilage in compression is poorly known. In this study, both confined and unconfined compression tests of cylindrical cartilage discs, taken from the adult human patello-femoral groove and cut either perpendicular (normal disc) or parallel (tangential disc) to the articular surface, were utilized to determine possible anisotropy in Young's modulus, E, aggregate modulus, Ha, Poisson's ratio, v and hydraulic permeability, k, of articular cartilage. The results indicated that Ha was significantly higher in the direction parallel to the articular surface as compared with the direction perpendicular to the surface (Ha = 1.237 +/- 0.486 MPa versus Ha = 0.845 +/- 0.383 MPa, p = 0.017, n = 10). The values of Poisson's ratio were similar, 0.158 +/- 0.148 for normal discs compared with 0.180 +/- 0.046 for tangential discs. Analysis using the linear biphasic model revealed that the decrease of permeability during the offset compression of 0-20 per cent was higher (p = 0.015, n = 10) in normal (from 25.5 x 10(-15) to 1.8 x 10(-15) m4/N s) than in tangential (from 12.3 x 10(-15) to 1.3 x 10(-15) m4/N s) discs. Based on the results, it is concluded that the mechanical characteristics of adult femoral groove articular cartilage are anisotropic also during compression. Anisotropy during compression may be essential for normal cartilage function. This property has to be considered when developing advanced theoretical models for cartilage biomechanics.

Adult↗

PubMed2004

Elimination of the friction effects in unconfined compression tests of biomaterials and soft tissues.

The mechanical properties of biomaterials and soft tissues are determined conventionally using unconfined compression tests. In such tests, frictionless specimen/platen contact in unconfined compression tests has to be assumed in determining the material properties of the materials. Previous theoretical analysis demonstrated, however, that the effects of the friction at the specimen/platen contact interface on the measured stress responses are non-negligible. In this study, a computational approach was proposed to eliminate the effects of friction. The friction coefficient between the specimen and the compression platens is measured first. Using a finite element model, the stress-strain relationship, without the influence of the friction effects, can be derived from the experimental data obtained in conventional unconfined compression tests. In order to validate the proposed approach, unconfined compressive tests of rubber have been performed.

Algorithms↗

PubMed1998

The compressive strength of articular cartilage.

Articular cartilage provides the smooth bearing surfaces in freely moving (synovial) joints. Its mechanical properties are important because structural failure of cartilage is closely associated with joint disorders, including osteoarthritis. Some mechanical properties of cartilage are well characterized, but little is known about its compressive strength. A technique for measuring cartilage compressive strength is evaluated, and an overview of experiments which relate strength to stiffness and tissue hydration is given. Specimens of bovine articular cartilage-on-bone, approximately 15 mm square, were loaded on a hydraulic materials testing machine using flat impermeable indentors. Linear-ramp loading/unloading cycles of 1 s duration, and of increasing severity, were applied until failure was evident on force-displacement graphs. Some specimens were tested following a 30 min period of creep loading. Inkstaining and histology were used to locate the site of initial damage to each specimen. Specimen failure occurred first in the cartilage surface layer at a nominal applied stress of 14-59 MPa (mean 35.7 MPa). Mechanical properties were little affected by specimen or indentor size, provided both remained within defined limits, and compressive strength could be measured to an accuracy of approximately +/- 5 per cent. Compressive stiffness was a significant predictor of strength, but only if it was measured at high levels of stress. Strength increased following creep-induced water loss, and initial mechanical damage could propagate under moderate cyclic loading. This technique for measuring cartilage compressive strength has potential for investigating the causes of cartilage failure in vivo.

Animals↗

PubMed2005

Effect of compression on interaction between 1,4-dihydropyridine compounds and lactose monohydrate.

Manidipine dihydrochloride or benidipine hydrochloride will change to hydrate form in part, when differential scanning calorimetric (DSC) measurement is carried out together with lactose monohydrate. This interaction was accelerated by compressing their mixture. It can be suggested that the interaction may cause by the disruption of crystal structure of lactose monohydrate due to compression to set free of water molecules. A new DSC peak at 170 degrees C, which was not observed in each component, appeared in DSC measurement of a mixture. This will be based on hydrate formed by the interaction, i.e., movement of water molecules. The profile of the plotting of the DSC peak area ratio before and after compression against the compression force changed by the molar ratio of lactose monohydrate in a mixture. In the case of low molar ratio of lactose monohydrate, profiles for manidipine dihydrochloride and benidipine hydrochloride differed from each other. This will be because manidipine dihydrochloride is stickier than benidipine hydrochloride. The profile for manidipine dihydrochloride became more gradual and showed lag compression force region when the amount of addition of the lubricant, magnesium stearate in a mixture increased. The endothermic peak area at 170 degrees C for manidipine dihydrochloride was larger than that for benidipine hydrochloride. It should be suggested that benidipine hydrochloride is easier to be transformed to its hydrate than manidipine dihydrochloride.

Compressive Strength↗

PubMed2001

MRI in the diagnosis and treatment of suspected malignant spinal cord compression.

It remains unclear whether MRI is essential in all patients with suspected malignant spinal cord compression (MSCC), or whether some patients can be treated on the basis of plain radiographic findings and neurological examination. A prospective study was carried out of 280 consecutive patients with suspected MSCC, and the results of neurological examination plus plain radiographs were compared with MRI. 201 patients had MSCC (186 extradural, 5 intradural extramedullary and 10 intramedullary) and 11 patients had thecal sac compression without evidence of spinal cord compression. 25% of patients with MSCC had two or more levels of compression, 69% of these involving more than one region of the spine. A paraspinal mass was noted at the site of extradural spinal cord compression in 28%, and only one-third of these were detected on plain radiography. Focal radiographic changes and consistent neurology were present in 91 (33%) patients who had not had previous radiotherapy. MRI confirmed the presence of MSCC in 89/91 patients (specificity and positive predictive value of radiographic/clinical findings 98%) and the level of disease in all. MRI led to a change in the radiotherapy plan in 53% of patients (21% major change). The sensory level when present was four or more segments below the MRI level in 25/121 (21%) patients, and two or more levels above in 8/121 (7%) patients. Although focal radiographic abnormalities with consistent neurological findings, when present, accurately predicted the presence and level of MSCC, whole spine MRI is indicated in most patients with suspected MSCC because the additional information may alter the management plan. Treatment may be appropriately initiated on the basis of focal radiographic changes and consistent neurology if MRI is contraindicated or delayed, and in patients with a poor prognosis. In patients in whom there are no focal radiographic abnormalities and consistent neurological findings, urgent MRI is mandatory before radiotherapy is commenced.

Adult↗

PubMed1988

Vertigo caused by basilar artery compression of the eighth nerve.

Vascular compression syndromes in the posterior cranial fossa have become well described clinical entities, especially for the fifth and seventh cranial nerves. Jannetta has proposed vascular compression of the eighth nerve as the etiology of hearing loss, tinnitus, and vertigo in some patients. The case that follows illustrates a clear-cut example of vestibular symptoms arising from vascular compression of the eighth nerve. The patient involved had disabling peripheral vertigo refractory to medical management. Magnetic resonance imaging documented a tortuous basilar artery compressing the eighth nerve on the involved side. This was confirmed at surgery, and a selective section of the vestibular nerve provided complete relief of disabling symptoms and preservation of hearing. The authors describe the details of this case and the enigma of eighth nerve symptoms due to vascular compression.

Basilar Artery↗

PubMed2006

Dynamic compression augments interstitial transport of a glucose-like solute in articular cartilage.

Solute transport through the extracellular matrix is essential for cellular activities in articular cartilage. Increased solute transport via fluid convection may be a mechanism by which dynamic compression stimulates chondrocyte metabolism. However, loading conditions that optimally augment transport likely vary for different solutes. To investigate effects of dynamic loading on transport of a bioactive solute, triangular mechanical loading waveforms were applied to cartilage explants disks while interstitial transport of a fluorescent glucose analog was monitored. Peak-to-peak compression amplitudes varied from 5-50% and frequencies varied from 0.0006-0.1 Hz to alter the spatial distribution and magnitude of oscillatory fluid flow. Solute transport was quantified by monitoring accumulation of fluorescence in a saline bath circulated around the explant. Individual explants were subjected to a series of compression protocols, so that effects of loading on solute desorption could be observed directly. Maximum increases in solute transport were obtained with 10-20% compression amplitudes at 0.1 Hz; similar loading protocols were previously found to stimulate chondrocyte metabolism in vitro. Results therefore support hypotheses relating to increased solute transport as a mediator of the cartilage biological response to dynamic compression, and may have application in mechanical conditioning of cartilage constructs for tissue engineering.

Animals↗

PubMed2004

Pronator syndrome and other nerve compressions that mimic carpal tunnel syndrome.

The purpose of this clinical commentary is to provide a comprehensive review of compressive neuropathies that may mimic carpal tunnel syndrome, provide the clinician with information to differentially diagnose these median nerve compression sites, and provide an evidence-based opinion regarding conservative intervention techniques for the various compression syndromes. While rare in comparison to carpal tunnel syndrome, pronator syndrome and anterior interosseous nerve syndrome are proximal median nerve compressions that may be suspected if a patient with carpal tunnel syndrome fails to respond to conservative or surgical intervention. Differential diagnosis is based largely on the symptoms, patterns of paresthesia, and specific patterns of muscle weakness. Due to the relative rarity of pronator syndrome and anterior interosseous nerve syndrome, few controlled studies exist to determine the most effective treatment techniques. Based on sound anatomical and biomechanical considerations, anecdotal experience, and available research, however, treatment strategies for pronator syndrome and anterior interosseous nerve syndrome compression neuropathies can be divided into 4 major categories: (1) rest/immobilization, (2) modalities, (3) nerve gliding, and (4) nonconservative treatment.

Carpal Tunnel Syndrome↗

PubMed1997

Effects of alpha-phenyl-N-tert-butyl nitrone (PBN) on compression injury of rat spinal cord.

alpha-Phenyl-N-tert-butyl Nitrone (PBN) is a free radical scavenger which recently has proved to be neuroprotective in experimental studies on focal cerebral ischemia and infarction. We therefore studied the effect of this drug in a model of moderate compression injury to rat spinal cord at the midthoracic level. The compound was given intraperitoneally 0.5 h before (100 mg/kg b.w) and at 1.5 h (50 mg/kg b.w) and 3.5 h (50 mg/kg b.w) after compression. Treated animals and controls (vehicle alone) were allowed to survive for 1 or 9 days following trauma. The functional outcome was tested by the inclined plane method and the motor performance score. By using MAP2 immunostaining the number of nerve cell bodies in the ventral horn and the ratio of MAP2 immunostained area to area of whole section of the cord were assessed to detect loss of neurons and loss of dendrites in the compressed segment. beta APP and PGP9.5 immunostaining was used to demonstrate axonal lesions. Treated and control rats showed at day 1 when tested with the inclined plane method a marked reduction of the capacity angle. This abnormality recovered gradually over the following days and was normalized at day 9. The motor performance score showed a marked reduction at day 1 which almost normalized at day 9. There was no difference regarding the functional outcome between rats given PBN and controls in none one of these functional tests. The spinal cord of normal rats presented immunoreactivity to MAP2 in nerve cell bodies and dendrites but not in axons and other structures. Following compression there was at day 1 and 9 a marked loss of MAP2 immunoreactivity in dendrites and nerve cell bodies. We could not detect any difference between the PBN and the control rats regarding the degree of cell loss or degree of reduction of dendrite staining. No difference between the two groups was seen with the axonal immunostainings (beta APP and PGP9.5). In conclusion, our study did not reveal any neuroprotective effect of PBN on the functional outcome and morphology (immunostaining to MAP2, beta APP and PGP9.5) in this model of moderate compression trauma to rat spinal cord.

Amyloid beta-Protein Precursor↗

PubMed1979

Experimental acute balloon compression of the spinal cord. Factors affecting disappearance and return of the spinal evoked response.

Acute balloon compression of the thoracic spinal cord for 15, 7, 5, 3, and 1 minute in monkeys caused immediate disappearance of the spinal evoked response and complete focal ischemia of the compressed segment in all animals. Only the animals in the 1-minute group, however, demonstrated return of the evoked response. These data, coupled with data from previous experiments of slow balloon compression of the spinal cord and spinal cord ischemia, suggest that the major pathological substrate for neural dysfunction after balloon compression of the spinal cord, be it acute or slow, is physical injury of the neural membrane, irrespective of blood flow changes. These findings also suggest that the ability of that membrane to recover is related to rapidity and length of time of compression. Focal changes in blood flow do not appear to be significant in this mechanism.

Acute Disease↗

PubMed1982

Ultrastructural changes in rat peripheral nerve following pneumatic tourniquet compression.

The sciatic nerves of 12 male rats were examined in the electron microscope 14 days after pneumatic tourniquet compression. Tourniquet pressure was maintained at 300 mmHg for varied lengths of time (30 minutes to 3 hours). Nerves compressed for 30 minutes showed very mild fissuring of the myelin without axonal degeneration. Examination of nerves compressed for 1 to 3 hours showed progressively more varied and extensive damage. Changes included splaying of myelin lamellae, axonal shrinkage with periaxonal edema. Schwann cell hypertrophy, and an increase in the number of microtubules and mitochondria per unit area. The myelin sheaths of some fibers, compressed for more than 2 hours, were completely ruptured. These changes resemble nerve lesions which could be induced by a variety of experimental procedures. Ultrastructural changes produced by tourniquet compression are apparently time-related and affect large-diameter nerves more profoundly than smaller-diameter nerves. The data reported provide an explanation for delayed muscle rehabilitation experienced by patients who have undergone extremity surgery with pneumatic tourniquet application. The evidence presented suggests that the incidence of tourniquet palsy may be far greater than previously recognized.

Animals↗

PubMed1993

Serotonergic manipulations in experimental neoplastic spinal cord compression.

The effects of differing strategies of serotonergic manipulation on vascular permeability, prostaglandin E2 (PGE2) synthesis, and the clinical course are evaluated in an experimental model of neoplastic spinal cord compression in rats. Serotonergic manipulations include in vivo inhibition of serotonin (5-HT) synthesis by p-chlorophenylalanine (p-CPA) and in vivo blockage of serotonin type 2 (5-HT2) receptors either by the selective antagonist ketanserin or by cyproheptadine. In paralyzed rats, the ratio of 5-hydroxyindole-3-acetic acid (5-HIAA) to 5-HT is significantly elevated in the compressed segments, suggesting that 5-HT utilization is increased. Treatment with p-CPA attenuates spinal 5-HT levels by 62.8% +/- 5.1% (mean +/- standard deviation) and reduces the elevated 5-HIAA:5-HT ratio to the normal value. The increased synthesis of PGE2 observed in the compressed cord is unaffected by p-CPA or ketanserin treatment but is markedly attenuated by cyproheptadine. Ketanserin reduces the 10-fold increase in spinal cord permeability observed in paralyzed rats in a clearly dose-related manner. If given at the first sign of neurological dysfunction, ketanserin delays the onset of paraplegia with the 1-mg/kg dose being clearly superior. Cyproheptadine and p-CPA also reduce the increased permeability and protract the course to paraplegia. A comparison of the effect of dexamethasone, indomethacin, cyproheptadine, p-CPA, and ketanserin reveals that they protract the disease course by 48%, 57%, 60%, 64%, and 78%, respectively. These data suggest that 5-HT2 receptors mediate some of the deleterious vascular consequences observed in the compressed spinal cord by a mechanism not coupled with PGE2 synthesis. A potential benefit of serotonergic manipulations for the acute treatment of neoplastic spinal cord compression is suggested.

Animals↗

PubMed1994

Cervicomedullary compression in achondroplasia.

Six patients with achondroplasia and symptoms suggestive of cervicomedullary junction compression are reviewed; these included three females and three males, with an average age of 8 years (range 7 months to 30 years). The mean duration of symptoms prior to intervention was 1.9 years. Symptoms included occipitocervical pain, ataxia, incontinence, apnea, and respiratory arrest. Radiological investigations consisted of plain films with flexion and extension views, pluridirectional tomography, thin-section computerized tomography, and magnetic resonance imaging. Typical findings included marked foramen magnum stenosis, ventrolateral cervicomedullary junction compression secondary to central and paramesial basilar invagination, and dorsal cervicomedullary junction compression secondary to ligamentous hypertrophy and invagination of the posterior atlantal arch. All patients underwent posterior fossa decompression and atlantal laminectomy. Surgery consistently revealed marked dorsal and paramesial overgrowth of the rim of the rim of the foramen magnum, with thickening and invagination of the atlantal posterior arch and a dense fibrotic epidural band resulting in dorsal cervicomedullary compression. Intraoperative ultrasonography was used to determine the extent of decompression required. Three patients required duraplasty. Three patients had concurrent hydrocephalus, two of whom had undergone ventriculoperitoneal shunting prior to surgical decompression of the posterior fossa. One patient developed a pseudomeningocele postoperatively, requiring serial lumbar punctures before it resolved. No patient developed craniovertebral instability following decompression. Improvement or resolution of symptoms was noted in all patients, with an average follow-up period of 4.8 years. Thus, cervicomedullary compression in patients with achondroplasia can be successfully treated with dorsal decompression of the craniovertebral junction. Dense epidural fibrotic bands are frequently noted in these cases and must be aggressively released to ensure satisfactory decompression.

Achondroplasia↗

PubMed2005

A novel dynamic model for experimental spinal cord compression.

OBJECT: The goal of this study was to develop a novel dynamic model for experimental spinal cord compression that closely approximates neoplastic epidural compression of the spinal cord in humans. METHODS: In 30 New Zealand white rabbits, the thoracic spine was exposed via a posterior approach. On each side of one vertebral lamina a small hole was drilled caudal to the articular process. A silicone band was passed through these holes, forming a loop. The spinal dura mater was exposed via an interlaminar approach. The loop was brought into contact with the dura mater and fixed in its position encircling 270 degrees of the circumference of the spinal cord. Thereafter, the loop was gradually tightened at set times by pulling at the ends of the band and fixing them again in their new position. The spinal cord was thus increasingly compressed in a circular and dynamic manner. Neurological deficits of various degrees were created in all animals in the compression group, and the compressive effect of the loop was reliably demonstrated on MR imaging. After decompression of the spinal cord, the neurological deficits were reversible in the majority of animals, and MR imaging revealed either no signal changes or only circumscribed ones within the cord. In contrast, MR images obtained in animals that did not recover revealed the occurrence of extensive chronic myelopathy. CONCLUSIONS: This novel model features reproducibility of paresis and neurological recovery. It is a dynamic model simulating circular tumor growth and is characterized by its easy, straightforward, and cost-saving applicability.

Animals↗

PubMedDate not supplied

Compressive ulnar neuropathies at the elbow: I. Etiology and diagnosis.

Ulnar nerve compression at the elbow can occur at any of five sites that begin proximally at the arcade of Struthers and end distally where the nerve exits the flexor carpi ulnaris muscle in the forearm. Compression occurs most commonly at two sites-the epicondylar groove and the point where the nerve passes between the two heads of the flexor carpi ulnaris muscle (i.e., the true cubital tunnel). The differential diagnosis of ulnar neuropathies at the elbow includes lesions that cause additional proximal or distal nerve compression and systemic metabolic disorders. A complete history and a thorough physical examination are essential first steps in establishing a correct diagnosis. Electrodiagnostic studies may be useful, especially when the site of compression cannot be determined by physical examination, when compression may be at multiple levels, and when there are systemic and metabolic problems.

Diagnosis, Differential↗