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PubMed2000

Abdominal decompression for suspected fetal compromise/pre-eclampsia.

BACKGROUND: Abdominal decompression was developed as a means of pain relief during labour. It has also been used for complications of pregnancy, and in healthy pregnant women in an attempt to improve fetal wellbeing and intellectual development. OBJECTIVES: The objective of this review was to assess the effects of antenatal abdominal decompression for maternal hypertension or impaired fetal growth, on perinatal outcome. SEARCH STRATEGY: The Cochrane Pregnancy and Childbirth Group trials register and the Cochrane Controlled Trials Register were searched. Date of last search: February 1998. SELECTION CRITERIA: Randomised or quasi-randomised trials comparing abdominal decompression with no decompression in women with pre-eclampsia and/or fetuses thought to be compromised. DATA COLLECTION AND ANALYSIS: Eligibility and trial quality were assessed by one reviewer. MAIN RESULTS: Three studies were included, all with the possibility of containing serious bias. Therapeutic abdominal decompression was associated with the following reductions: persistent pre-eclampsia (relative risk 0.36, 95% confidence interval 0.18 to 0.72); fetal distress in labour (relative risk 0.37, 95% confidence interval 0.19 to 0.71); low birthweight (relative risk 0.50, 95% confidence interval 0.40 to 0. 63); Apgar scores less than six at one minute (relative risk 0.26, 95% confidence interval 0.12 to 0.56); and perinatal mortality (relative risk 0.39, 95% confidence interval 0.22 to 0.71). REVIEWER'S CONCLUSIONS: Due to the methodological limitations of the studies, the effects of therapeutic abdominal decompression are not clear. The apparent improvements in birthweight and perinatal mortality warrant further evaluation of abdominal decompression where there is impaired fetal growth and possibly for women with pre-eclampsia.

Female↗

PubMed2000

Abdominal decompression in normal pregnancy.

BACKGROUND: Abdominal decompression was developed as a means of pain relief during labour. It has also been used for complications of pregnancy, and in healthy pregnant women in an attempt to improve fetal wellbeing and intellectual development. OBJECTIVES: The objective of this review was to assess the effects of prophylactic abdominal decompression on admission for pre-eclampsia, fetal growth, perinatal morbidity and mortality and childhood development. SEARCH STRATEGY: The Cochrane Pregnancy and Childbirth Group trials register and the Cochrane Controlled Trials Register were searched. Date of last search: February 1999. SELECTION CRITERIA: Randomised trials comparing abdominal decompression with dummy decompression or no treatment in healthy pregnant women. DATA COLLECTION AND ANALYSIS: Eligibility and trial quality were assessed by one reviewer. MAIN RESULTS: Three studies were included. There was no difference between the abdominal decompression groups and the control groups for low birth weight (relative risk 0.69, 95% confidence interval 0.27 to 1.77) and perinatal mortality (relative risk 2.47, 95% confidence interval 0.77 to 7.92). There were no differences in admission for pre-eclampsia, Apgar score and childhood development. REVIEWER'S CONCLUSIONS: There is no evidence to support the use of abdominal decompression in normal pregnancies. Future research should be directed towards the use of abdominal decompression during labour, and during complicated pregnancies.

Female↗

PubMed1994

Simultaneous active compression-decompression and abdominal binding increase carotid blood flow additively during cardiopulmonary resuscitation (CPR) in pigs.

The effects of adding active compression-decompression and abdominal binding separately or combined to standard compression CPR was tested in a randomized cross-over design during ventricular fibrillation in eight pigs. The flow and pressure effects of the two techniques appeared to be additive with no interference between the two. Carotid blood flow increased 22% with active compression-decompression, 34% with abdominal binding and 59% with the combination compared to flow with standard compression. Peak antegrade carotid flow occurred in early systole with retrograde flow in early diastole and close to zero in late diastole with no profound alterations induced by active decompression or abdominal binding. Abdominal binding increased the intrathoracic pressure during the compression phase as estimated from the esophageal pressure, while active decompression caused a negative esophageal pressure during the decompression phase. Neither active decompression nor abdominal binding caused any changes in the coronary perfusion pressure, nor in the left ventricular transmural pressure except for a rise in mid-diastolic pressure with active decompression.

Animals↗

PubMed1994

Active compression-decompression resuscitation: effect on resuscitation success after in-hospital cardiac arrest.

OBJECTIVES: The purpose of this study was to test the hypothesis that active compression-decompression would improve resuscitation success in human subjects after cardiac arrest. BACKGROUND: Active compression-decompression cardiopulmonary resuscitation is a new method that improves cardiopulmonary hemodynamic function in animal models and humans after cardiac arrest. METHODS: We conducted a prospective randomized clinical trial in patients with in-hospital cardiac arrest. Patients were assigned to receive standard manual or active compression-decompression cardiopulmonary resuscitation. The primary study end points were spontaneous return of circulation, 24-h survival and survival to hospital discharge. RESULTS: Fifty-three consecutive patients after cardiac arrest undergoing 64 resuscitation attempts were studied (30 women, 23 men; mean [+/- SD] age 71 +/- 13 years, range 38 to 96). Spontaneous return of circulation was observed in 24 (47%) of 53 patients and was increased in patients receiving active compression-decompression compared with those receiving standard manual cardiopulmonary resuscitation (15 [60%] of 25 vs. 9 [32%] of 28, respectively, p = 0.042); 24-h survival was increased (12 [48%] of 25 vs. 6 [21%] of 28, respectively, p = 0.041); and there was a trend toward improved survival to hospital discharge (6 [24%] of 25 vs. 3 [11%] of 28, respectively, p = 0.198) when active compression-decompression was compared with standard manual cardiopulmonary resuscitation. CONCLUSIONS: Active compression-decompression cardiopulmonary resuscitation improves return of spontaneous circulation and 24-h survival after in-hospital cardiac arrest. Active compression-decompression cardiopulmonary resuscitation appears to be a beneficial adjunct to standard manual cardiopulmonary resuscitation.

Aged↗

PubMed1991

Treatment of pseudotumor cerebri by primary and secondary optic nerve sheath decompression.

We performed optic nerve sheath decompression in 53 patients (101 eyes) with pseudotumor cerebri and visual loss. Sixty-nine eyes (85 patients) with acute papilledema uniformly had improved visual function after optic nerve sheath decompression. Of 32 eyes with chronic papilledema (18 patients), only ten had improved visual function after optic nerve sheath decompression. This difference was significant (P = .0001). Thirteen eyes required secondary or tertiary optic nerve sheath decompression after an initial successful result. Eleven of 13 eyes had improved visual function after repeat optic nerve sheath decompression. We believe that patients with acute papilledema and visual loss should be offered optic nerve sheath decompression, and if symptoms recur, repeat optic nerve sheath decompression is a safe and effective treatment option.

Acute Disease↗

PubMedDate not supplied

Treatment of acute nontoxic megacolon during colonoscopy: tube placement versus simple decompression.

The study compares the efficacy of colonoscopic decompression versus decompression and tube placement in the treatment of Ogilvie's syndrome. Nine patients were treated with a single colonoscopic decompression which resulted in four recurrences. In contrast, there were no recurrences observed in 11 patients who underwent decompression and subsequent tube placement (p less than 0.05). There was no morbidity observed from either decompression or tube placement. Tube placement added less than 10 min of additional procedure time to the colonoscopy. The tube utilized in this study was an enteroclysis tube with sideholes cut in the distal 20 cm. The tube was easily inserted over a Teflon-coated flexible guide wire inserted through the colonoscope into the cecum following decompression. This study demonstrates that colonoscopic decompression followed by tube placement is the preferred treatment modality for acute nontoxic megacolon.

Acute Disease↗

PubMed1997

The risk of diplopia following orbital floor and medial wall decompression in subtypes of ophthalmic Graves' disease.

We preoperatively divided 58 ophthalmic Graves' disease patients into types I and II categories before two-wall orbital decompression. Type I classification was given to patients who had no diplopia and essentially normal versions. Type II classification was assigned to patients with restrictive motility loss and diplopia within 20 degrees of the primary position. Ocular motility was assessed before and after two-wall orbital decompression. Only one of 25 type I patients (4%) experienced diplopia after orbital decompression, while seven of 14 (50%) (p = 0.001) type II patients without preoperative primary-position diplopia had primary diplopia postoperatively. Of 12 type II patients who had preoperative primary-position diplopia, esotropia increased by an average of 12.4 diopters postoperatively. Vertical deviation increased an average of 13.4 diopters for 10 patients who underwent unilateral two-wall decompression. The likelihood of new or worsening diplopia in all type II patients following decompression was 22 of 36 (61%). We conclude that adverse motility change following two-wall orbital decompression is rare in type I disease patients, but it occurs 61% of the time in type II disease patients. Predicting preoperatively which patients are likely to develop adverse motility change and diplopia may help clarify indications and risks of orbital decompression surgery in patients with ophthalmic Graves' disease.

Adolescent↗

PubMedDate not supplied

Lumbar spinal instability (olisthesis) after extensive posterior spinal decompression.

Twenty-seven patients who underwent extensive posterior spinal decompression procedures were reviewed to investigate the incidence, the clinical significance and contributing factors of the postdecompression olisthesis, and indication for spinal fusion at the time of extensive decompression. Eleven patients were female and 16 were male. The mean age was 49.4 years. Twenty-two patients were treated with extensive decompression and spinal fusion, and five patients were treated with decompression alone without spinal fusion. The average follow-up time was 2 1/2 years (1-4 1/2). The incidence of newly developed postdecompression olisthesis was 3.7% (1/27) and all four patients with preoperative spondylolisthesis progressed further postoperatively. The author was neither able to identify definitive contributing factors for olisthesis, nor able to confirm the previously reported factors: young age, normal disc heights, and multiple level decompression in this review study. The incidence rate of pseudarthrosis was high (27.3%) after the extensive posterior decompression and fusion. The concomitant spinal fusion is not routinely indicated to patients with extensive posterior spinal decompression. Furthermore, it does not appear to be effective in prevention of olisthesis. The concomitant spinal fusion should be exceptional rather than routine.

Adult↗

PubMed1994

Axon regeneration after decompression of the conus medullaris.

STUDY DESIGN: The effect of acute spinal stenosis (simulating fracture) and decompression of stenosis on axon regeneration was evaluated in an animal model. OBJECTIVES: Clinical function and quantitative histomorphometry were used to gain insight into the clinicopathologic effects of acute spinal stenosis and decompression. SUMMARY OF BACKGROUND DATA: Decompression of extrinsic compression after thoracolumbar fractures has been suggested to maximize recovery of neurologic function. Clinical studies seem to support this, but the histologic results of decompression are poorly understood. METHODS: Experimental spinal stenosis was created in 5 female beagle dogs, followed by decompression in three of the beagles at 6 weeks. Clinical function and histologic appearance were analyzed using a monoclonal antibody to neurofilaments. RESULTS: Stenosis consistently produced significant neurologic deficit and axon degeneration within motor roots distal to the stenosis. Decompression resulted in improved neurologic function and a tendency for the axons to return to normal number and volume based on quantitative histomorphometry. CONCLUSION: This study provides an animal model and functional and histologic data that support the use of decompression of acute spinal stenosis of 50% or more canal compromise at the level of the conus medullaris and a neurologic deficit. This may be seen clinically in thoracolumbar fractures.

Animals↗

PubMed1999

The influence of spinal canal narrowing and timing of decompression on neurologic recovery after spinal cord contusion in a rat model.

STUDY DESIGN: The effect of spinal canal narrowing and the timing of decompression after a spinal cord injury were evaluated using a rat model. OBJECTIVE: To evaluate whether progressive spinal canal narrowing after a spinal cord injury results in a less favorable neurologic recovery. Additionally, to evaluate the effect of the timing of decompression after spinal cord injury on neurologic recovery. SUMMARY OF BACKGROUND DATA: Results in previous studies are contradictory about whether the amount of canal narrowing or the timing of decompression after a spinal cord injury affects the degree of neurologic recovery. METHODS: Forty adult male Sprague-Dawley rats were equally divided into a control group, in which spacers of 20%, 35%, and 50% were placed into the spinal canal after laminectomy, and an injury group in which the spacers were placed after a standardized incomplete spinal cord injury. After spacer removal, neurologic recovery in both was monitored by Basso, Beattie, Bresnahan (BBB) Locomotor Rating Scale (Ohio State University, Columbus, OH) motor scores and transcranial magnetic motor evoked potentials for 6 weeks followed by histologic examination of the spinal cords. Subsequently, 42 rats were divided into five groups in which, after spacer placement, the time until decompression was lengthened 0, 2, 6, 24, and 72 hours. Again, serial BBB motor scores and transcranial magnetic motor evoked potentials were used to assess neurologic recovery for 6 weeks until the animals were killed for histologic evaluation. RESULTS: Spacer placement alone in the control animals resulted in no neurologic injury until canal narrowing reached 50%. All of the control groups (spacer only) exhibited significantly better (P < 0.05) motor scores compared with the injury groups (injury followed by spacer insertion). Within the injury groups the motor scores were progressively lower as spacer sizes increased from the no-spacer group to the 35% group. The results in the 35% and 50% groups were not statistically different. The results of the time until decompression demonstrated that the motor scores were consistently better the shorter the duration of spacer placement (P < 0.05) for each of the time groups (0, 2, 6, 24, and 72 hours) over the 6-week recovery period. Histologic analysis showed more severe spinal cord damage as both spinal canal narrowing and the time until decompression increased. CONCLUSION: The results in this study present strong evidence that the prognosis for neurologic recovery is adversely affected by both a higher percentage of canal narrowing and a longer duration of canal narrowing after a spinal cord injury. The tolerance for spinal canal narrowing with a contused cord appears diminished, indicating that an injured spinal cord may benefit from early decompression. Additionally, it appears that the longer the spinal cord compression exists after an incomplete spinal cord injury, the worse the prognosis for neurologic recovery.

Animals↗

PubMed1994

Optic nerve sheath decompression for the treatment of visual failure in chronic raised intracranial pressure.

The records of all patients undergoing optic nerve sheath decompression for visual failure in chronic raised intracranial pressure performed over a 15 year period have been reviewed. The aim was to study the visual outcome and relation to any shunting procedures. Fourteen patients (20 eyes) were identified in whom follow up information of at least one year was available. Eleven patients had benign intracranial hypertension (idiopathic intracranial hypertension) and three had dural venous sinus occlusive disease. Eight patients had unilateral surgery and six had bilateral surgery. Visual acuity and fields either improved or stabilised in 17 out of 20 eyes and three deteriorated. Of the eight patients undergoing unilateral surgery, the other eye remained stable in seven and deteriorated in one. Four patients required optic nerve sheath decompression despite previous shunting or subtemporal decompression. Five patients required shunts or subtemporal decompression after optic nerve sheath decompression because of persistent headache in three cases and for uncontrolled visual failure in two cases. No patients lost vision as a direct consequence of surgery. It is concluded that optic nerve sheath decompression is a safe and important therapeutic option in the management of chronic raised intracranial pressure complicated by visual loss. Vision can be saved after shunt failure, and in other cases may be maintained without the need for a shunt. Shunts may still be required, however, after optic nerve sheath decompression, especially for persistent headache.

Adult↗

PubMedDate not supplied

Equalization of amniotic fluid volumes after decompression amniocentesis for treatment of the twin oligohydramnios-polyhydramnios sequence.

OBJECTIVE: To measure acute and chronic changes in the placenta and amniotic fluid associated with performance of decompression amniocentesis in pregnancies with the twin oligohydramnios-polyhydramnios sequence (TOPS). METHODS: Amniotic fluid pressures, placental thickness, placental perfusion, and amniotic fluid volumes were measured in each sac of a monochorionic diamniotic twin gestation before and after decompression amniocentesis. Indigo carmine was injected into the polyhydramnic sac after decompression, and fluid from the oligohydramnic sac was sampled after equilibration. Spectrophotometric analysis of amniotic fluid specimens was performed for dye detection. Amniotic fluid volume and placental perfusion studies were repeated 1 week later. RESULTS: Three patients with TOPS were enrolled, and decompression amniocentesis was performed in the midtrimester. After decompression, amniotic fluid volume decreased in the polyhydramnic sac, amniotic fluid pressures decreased in both sacs, placental thickness increased, and umbilical artery Doppler velocimetry was unaffected. The amniotic fluid volume increased acutely in only one oligohydramnic sac after decompression, and ultrasonographic examination, amniotic fluid spectrophotometric analysis, and placental pathologic examination all identified interfetal membrane disruption as the etiology. CONCLUSIONS: Decompression amniocentesis as a treatment for TOPS does not result in acute or chronic changes in the amniotic fluid volume of the oligohydramnic sac in the absence of interfetal membrane disruption.

Adult↗

PubMedDate not supplied

Arthroscopic shoulder decompression development and application. A five year experience.

The purpose of this study was to critically evaluate the results of 80 consecutive subacromial decompressions in 76 patients with impingement syndrome and to assess the value of arthroscopy for subacromial decompression. The average followup was 32 months. The charts, radiographs, and clinical findings of all patients were reviewed. There were 57 males and 19 females, with a mean age of 41 years. Subjective, objective, and functional results were assessed. The greatest improvement was seen in the areas of pain with activity, pain at night, and use of medications. Impingement signs had decreased significantly at final followup. The procedure allowed an early return to work and competitive athletics. Repeat surgery was necessary in eight cases: three full thickness rotator cuff repairs, two stabilization procedures, two open debridements, and one biceps tenodesis and excision of the distal clavicle. An important finding was the number of unsuspected diagnoses that were made during arthroscopy. Twelve patients had significant labral tears, seven patients had complete rotator cuff tears, four patients had biceps tendon fraying, and two patients had loose bodies in the glenohumeral joint. In most of these shoulders the intraarticular lesions would not have been diagnosed by open subacromial decompression. Radiographic evaluation suggested that the "outlet view" can be helpful in determining depth of bony resection and may be a prognostic indicator. Patients who underwent simple decompression rather than bony resection tended to be younger and had less Stage III impingement changes, and they generally had a slightly better final outcome. Patients who had compensation injuries generally had a poorer outcome. In reviewing our results, it appears that arthroscopic subacromial decompression can be a successful alternative to open decompression. The key to success for closed decompression is related to 1) accurate diagnosis, 2) selective treatment, 3) adequate bone resection when required, and 4) repair of full thickness rotator cuff tears in the active patient. Postoperative rehabilitation, which includes early range of motion, is critical.

Acromion↗

PubMed1991

Intraoperative monitoring of the facial nerve during decompressive surgery for hemifacial spasm.

In 11 consecutive patients, intraoperative electromyographic (EMG) recordings were made from the facial muscles during microvascular decompression for hemifacial spasm. In one patient, recordings could not be obtained for technical reasons, and two patients had no abnormality. In the remaining eight patients, the abnormal response resolved before decompression in two, resolved immediately at the time of decompression in five, and failed to resolve in one. All patients were relieved of their hemifacial spasm. In the five patients whose abnormalities resolved at the time of decompression, there was a precise intraoperative correlation between decompression of the nerve and disappearance of the abnormal EMG response. In three cases, this was a useful guide to the need to decompress more than one vessel. These results confirm the findings of Møller and Jannetta, support the use of this technique for intraoperative monitoring of facial nerve decompression procedures, and provide strong circumstantial evidence that vascular cross-compression is an important etiological factor in hemifacial spasm.

Electromyography↗

PubMed1994

Microvascular decompression for trigeminal neuralgia caused by vertebrobasilar compression.

Thirty-one (2%) of 1404 consecutive patients with typical trigeminal neuralgia who underwent microvascular decompression between 1972 and 1993 were found to have vascular compression by the vertebral artery (VA) or the basilar artery (BA). Compared to the remaining 1373 patients, this subgroup was older (mean age 62 vs. 55 years, p < 0.001), was predominantly male (68% vs. 39%, p < 0.002), demonstrated left-sided predominance (65% vs. 39%, p < 0.002), was more likely to be hypertensive (65% vs. 18%, p < 0.001), and was more likely to have ipsilateral hemifacial spasm (16% vs. 0.6%, p < 0.001). The trigeminal nerve was compressed by the VA in 18 cases (the VA alone in three and the VA plus other vessels in 15), the BA in 12 cases (the BA alone in four and the BA plus other vessels in eight), and the vertebrobasilar junction in one case. Twenty-nine of the 31 patients underwent vascular decompression of the trigeminal nerve, one had a complete trigeminal root section, and one underwent partial root section with vascular decompression of the remaining nerve. All 31 patients were pain-free, off medication immediately after surgery, and this pain-free, medication-free status was maintained at 1 year after surgery in 96% of cases, at 3 years in 92%, and at 10 years in 86%, based on life-table analysis. Minor trigeminal hypesthesia/hypalgesia was present preoperatively in 52%. New or worsened minor hypesthesia/hypalgesia developed in 41% of patients, while transient diplopia as well as hearing loss developed in 23% and 13% in the overall series, respectively. No patient developed major trigeminal sensory loss or masseter weakness after vascular decompression alone. There was no operative mortality. Vascular decompression is an effective treatment for patients with trigeminal neuralgia who have vertebrobasilar compression of the trigeminal nerve. Patients should be warned that decompression of a tortuous vertebrobasilar system carries a higher risk of mild trigeminal dysfunction, diplopia, and hearing loss than standard microvascular decompression.

Age Factors↗

PubMed1995

Microvascular decompression for hemifacial spasm.

The authors report the results of 782 microvascular decompression procedures for hemifacial spasm in 703 patients (705 sides), with follow-up study from 1 to 20 years (mean 8 years). Of 648 patients who had not undergone prior intracranial procedures for hemifacial spasm, 65% were women; their mean age was 52 years, and the mean preoperative duration of symptoms was 7 years. The onset of symptoms was typical in 92% and atypical in 8%. An additional 57 patients who had undergone prior microvascular decompression elsewhere were analyzed as a separate group. Patients were followed prospectively with annual questionnaires. Kaplan-Meier methods showed that among patients without prior microvascular decompression elsewhere, 84% had excellent results and 7% had partial success 10 years postoperatively. Subgroup analyses (Cox proportional hazards model) showed that men had better results than women, and patients with typical onset of symptoms had better results than those with atypical onset. Nearly all failures occurred within 24 months of operation; 9% of patients underwent reoperation for recurrent symptoms. Second microvascular decompression procedures were less successful, whether the first procedure was performed at Presbyterian-University Hospital or elsewhere, unless the procedure was performed within 30 days after the first microvascular decompression. Patient age, side and preoperative duration of symptoms, history of Bell's palsy, preoperative presence of facial weakness or synkinesis, and implant material used had no influence on postoperative results. Complications after the first microvascular decompression for hemifacial spasm included ipsilateral deaf ear in 2.6% and ipsilateral permanent, severe facial weakness in 0.9% of patients. Complications were more frequent in reoperated patients. In all, one operative death (0.1%) and two brainstem infarctions (0.3%) occurred. Microvascular decompression is a safe and definitive treatment for hemifacial spasm with proven long-term efficacy.

Adolescent↗

PubMed1992

Wide versus selective decompression in the operative treatment of lumbar spinal stenosis.

The early post-operative results of wide versus selective decompression in a group of 64 patients with lumbar spinal stenosis were studied with the aim of ascertaining whether a more limited approach gives comparable results to the more traditional method of wide decompression. Wide decompression involved complete removal of a vertebral lamina at the stenotic level. Selective decompression refers to removal of the lower part of the superior lamina and the upper part of the inferior lamina at the stenotic level together with limited facetectomies. Patients were compared with respect to post-operative relief of back pain and sciatica/claudication as well as the ability to return to their pre-morbid level of functional activity. Follow up ranged from 4 months to 26 months. Results showed that both wide and selective decompression were able to achieve complete or considerable relief of symptoms and return to pre-morbid level of activity in 74% to 84% of patients. The results in the 2 groups were not statistically different. It appears that within the first 2 years of surgery, the vast majority of our post-decompression patients had good results regardless of whether wide or selective decompression was used.

Adult↗

PubMed1991

1991 Volvo Award in experimental studies. Cauda equina syndrome: neurologic recovery following immediate, early, or late decompression.

An animal model of cauda equina syndrome was developed. Neurologic recovery was analyzed following immediate, early, and delayed decompression. Five experimental groups, each containing six dogs, were studied. Compression of the cauda equina was performed in all 30 dogs following an L6-7 laminectomy. The cauda equina was constricted by 75% in each group. The first group was constricted and immediately decompressed. The remaining groups were constricted for 1 hour, 6 hours, 24 hours, and 1 week, respectively, before being decompressed. Somatosensory evoked potentials were performed before and after surgery, before and immediately after decompression, and 6 weeks following decompression. Daily neurologic exams using the Tarlov grading scale were performed. At 6 weeks postdecompression, all dogs were killed, and the neural elements analyzed histologically. Following compression, all 30 dogs had significant lower extremity weakness, tail paralysis, and urinary incontinence. All dogs recovered significant motor function 6 weeks following decompression. The dogs with immediate decompression generally recovered neurologic function within 2-5 days. The dogs receiving 1-hour and 6-hour compression recovered within 5-7 days. The dogs receiving 24-hour compression remained paraparetic 5-7 days, with bladder dysfunction for 7-10 days and tail dysfunction persisting for 4 weeks. The dogs with compression for 1 week were paraparetic (Tarlov Grade 2 or 3) and incontinent during the duration of cauda equina compression. They recovered to walking by 1 week and Tarlov Grade 5 with bladder and tail control at the time of euthanasia. Immediately after compression, all five groups demonstrated at least 50% deterioration of the posterior tibial nerve evoked potential amplitudes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗