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PubMed1996

The effect of early craniocervical decompression on functional outcome in neonates and young infants with myelodysplasia and symptomatic Chiari II malformations: results from a prospective series.

The indications for hindbrain decompression in neonates and young infants with spinal dysraphism who experience brain stem dysfunction in association with Chiari II malformations have remained controversial. This largely reflects the fact that the postoperative outcome in such patients has often been poor, which has supported the belief that much of the brain stem compromise in these patients is congenital and inherently irreversible. However, in a previous retrospective review of our operative results between 1975 and 1989, we noted that a significant component of the brain stem dysfunction in these children was an acquired phenomenon that potentially was reversible with prompt operative intervention. Accordingly, we hypothesized that with early craniocervical decompression, excellent functional outcome could be achieved in a majority of neonates and young infants with symptomatic Chiari II malformations. On the basis of this premise, we prospectively treated all such patients since 1989 with urgent brain stem decompression after other potential causes for brain stem dysfunction, such as progressive hydrocephalus, had been ruled out. All children underwent limited suboccipital craniectomies, cervical laminectomies extending beneath the inferior extent of the cerebellar tissue, and dural decompressions. The outcome in these patients has been favorable in comparison with previous studies. Ten of the 13 children treated according to this protocol recovered normal or nearly normal brain stem function shortly after decompression; 1 child had mild residual unilateral lower cranial nerve paresis. None of these children required a tracheostomy for ventilatory support, and only one required a temporary gastrostomy. The other three children all exhibited bilateral vocal cord paralysis and severe central hypoventilation by the time decompression was performed and failed to have any meaningful recovery of function. We conclude that early recognition of the symptoms of brain stem compromise in neonates and young infants with spinal dysraphism coupled with urgent evaluation and decompression are effective in producing prompt resolution of the brain stem dysfunction in most affected patients. Conversely, the prognosis for recovery is poor in children who exhibit bilateral vocal cord paralysis by the time of decompression.

Arnold-Chiari Malformation↗
PubMed1991

Decompression comparison of N2 and O2 in rats.

We have previously reported that O2 in the breathing gas mixture contributed significantly to the risk of decompression sickness (DCS) in rats after rapid (less than 10 s) decompression to the surface from depth. The rate of O2 uptake was extremely fast (less than 1 min estimated for equilibrium after a pressure change) compared to much slower rates for He and N2. To further define the role that O2 plays in diving, the present investigation examined decompression outcome in unanesthetized male albino rats after 60-min N2-O2 dives (1-3 atm abs O2, depth 6.26 or 7.26 atm abs). Slower decompression profiles were used to determine the elimination rates of N2 and O2 as pressure was reduced and included "stops" of up to 20 min. The probability of DCS was modeled using the maximum likelihood technique. O2 again contributed significantly to the risk of DCS, although O2 was eliminated very rapidly during decompression; the washout of N2 was considerably longer. These findings support the view that O2 can add significantly to decompression risk. However, this phenomenon may not normally be encountered during human diving operations where relatively slower decompression and lower PO2's are used.

Animals↗
PubMed1979

Evaluation of standard decompression schedule by agarose gel method.

The Standard Decompression Schedule was evaluated by the method of bubble formation in agarose gel, the result of which can be summarized as follows: 1) The number of bubbles formed in agarose gel corresponded well with the exposed pressure. 2) The technique of this method was simple and the number of bubbles was accurately counted. 3) Eventually, this method was useful for examining the decompression schedules. 4) It is not always safe to follow the Standard Decompression Schedule in some pressure conditions. 5) As to the period of time that a person is able to tolerate a high pressure condition, the prescription of the Standard Decompression Schedule is not necessarily correct. 6) The number of bubbles was small by the proper decompression schedule, for example, in the cases of exposure above the 60-meter depth of water. 7) This method can be applied for the prevention of decompression sickness when the agarose gel samples are attached to the workers during the compressed air work. 8) The number of bubbles was inconsistent with the coefficient of body pressure (1. N2 in the body), therefore it is not necessarily safe to rely only on the coefficient of body pressure. 9) To prevent osteonecrosis, the Standard Decompression Schedule is not proper, a deeper first stop and slower ascent being recommended.

Decompression↗
PubMed1985

Air and nitrox saturation decompression: a report of 4 schedules and 77 subjects.

Seventy-seven subjects were decompressed from air or nitrogen-oxygen (nitrox) saturation exposures at 18.3 to 40.2 meters sea water (msw) [60 to 132 feet sea water (fsw)] using four different decompression schedules. A h schedule for decompression from an air saturation-excursion profile at 18.3 msw (60 fsw) resulted in pain-only decompression sickness (DCS) symptoms in 2 of 23 subjects. A 32 and 35 h schedule from a different air saturation profile at 19.8 and 22.9 msw (65 and 75 fsw), respectively, resulted in DCS symptoms in 1 of 24 subjects. A third and fourth schedule for air or nitrox saturation at 40.2 msw (132 fsw) resulted in DCS symptoms in 3 of 12 and 1 of 18, respectively. No serious (type II) symptoms were observed as a result of any of the decompressions. All DCS cases consisted of knee pain occurring either in the last 3 msw of the decompression or shortly after surfacing. Doppler ultrasound monitoring revealed venous gas emboli (VGE) in several subjects, but generally only shallow to 6.1 msw (20 fsw). Results demonstrate an overall DCS incidence of 9%, and all cases were pain-only and localized to the knee. The third schedule (U.S. Navy heliox saturation decompression schedule) seems to produce a higher incidence of DCS than the other schedules when used in air or nitrox exposures. Differentiation between the schedules designed for nitrox was impossible due to the limited number of subjects in each and the variable nature of the exposures.

Adult↗
PubMed1996

[A method for evaluating the safety of decompression regimens for divers].

The authors offer a way of estimation of safety modes of decompression, based on definition of intensity of venous gas embolism (VGE) at each decompression and account of probability of illness of divers in series of tests. Intensity of VGE was determined with the help of ultrasonic gas bubbles Doppler radar. Comparative safety of standard modes of decompression of divers of the Navy was estimated, and also the modes, designed in accordance with mathematical model of decompression, offered by I. A. Voĭtsekhovich (1990), were done. The results testify, that use of ultrasonic radar for estimation of intensity of VGE at decompression and account of average and maximum probability of decompression illness in series of tests of modes permit to receive the comparative characteristic of safety of modes at small number of decompressions.

Adult↗
PubMed1997

Compressed air tunneling and caisson work decompression procedures: development, problems, and solutions.

Multinational experience over many years indicates that all current air decompression schedules for caisson and compressed air tunnel workers are inadequate. All of them, including the Occupational Safety and Health Administration tables, produce dysbaric osteonecrosis. The problem is compounded because decompression sickness (DCS) tends to be underreported. Permanent damage in the form of central nervous system or brain damage may occur in compressed air tunnel workers, as seen on magnetic resonance imaging, in addition to dysbaric osteonecrosis. Oxygen decompression seems to be the only viable method for safely decompressing tunnel workers. Oxygen decompression of tunnel workers has been successfully used in Germany, France, and Brazil. In Germany, only oxygen decompression of compressed air workers is permitted. In our experience, U.S. Navy tables 5 and 6 usually prove adequate to treat DCS in caisson workers despite extremely long exposure times, allowing patients to return to work following treatment for DCS. Tables based on empirical data and not on mathematical formulas seem to be reasonably safe. U.S. Navy Exceptional Exposure Air Decompression tables are compared with caisson tables from the United States and Great Britain.

Decompression↗
PubMed1994

Comparison of haemodynamic effects during venous air infusion and after decompression in pigs.

We have compared haemodynamic effects of venous gas emboli during continuous air infusion into the right atrium and after rapid decompression in pigs. Eight anaesthetized and spontaneously breathing pigs received continuous air infusion at a rate of either 0.05 ml.kg-1.min-1 (six pigs, air infusion group) or 0.10 ml.kg-1.min-1 (two pigs). Another eight pigs (decompression group) underwent a 30-min compression to 5 bar (500 kPa, absolute pressure), followed by a rapid decompression (2 bar.min-1). Haemodynamic variables were measured or calculated, and bubbles in the pulmonary artery were monitored using transoesophageal echocardiography. The results showed less variation in the maximal increase in mean pulmonary arterial pressure (BPa,pulm) during air infusion (0.05 ml.kg-1.min-1) than after decompression, although the mean maximal increase did not differ between the two groups [28.0 mmHg (3.73 kPa), 95% confidence interval (CI) 23.5-32.5, vs 32.0 mmHg (4.27 kPa), 95% CI 25.3-38.7, P = 0.3]. The BPa,pulm stabilized or decreased very slowly after peak values were reached in the air infusion group, whereas the BPa,pulm decreased rapidly during the same period in the decompression group. No significant changes in mean arterial pressure were observed during air infusion (0.05 ml.kg-1.min-1), in contrast to the rapid increase and the subsequent decrease, that appeared after decompression. Finally, the maximal bubble count was much lower in the air infusion group than in most of the pigs in the decompression group. The two pigs that received 0.10 ml.kg-1.min-1 stopped breathing after 5-min infusion, developed arterial hypotension and died.

Animals↗
PubMed2000

Computed chest tomography in an animal model for decompression sickness: radiologic, physiologic, and pathologic findings.

This study was conducted to investigate the early pulmonary effects of acute decompression in an animal model for human decompression sickness by CT and light microscopy. Ten test pigs were exposed to severe decompression stress in a chamber dive. Three pigs were kept at ambient pressure to serve as controls. Decompression stress was monitored by measurement of pulmonary artery pressure and arterial and venous Doppler recording of bubbles of inert gas. Chest CT was performed pre- and postdive and in addition the inflated lungs were examined after resection. Each lung was investigated by light microscopy. Hemodynamic data and bubble recordings reflected severe decompression stress in the ten test pigs. Computed tomography revealed large quantities of ectopic gas, predominantly intravascular, in three of ten pigs. These findings corresponded to maximum bubble counts in the Doppler study. The remaining test pigs showed lower bubble grades and no ectopic gas by CT. Sporadic interstitial edema was demonstrated in all animals--both test and control pigs--by CT of resected lungs and on histologic examination. A severe compression-decompression schedule can liberate large volumes of inert gas which are detectable by CT. Despite this severe decompression stress, which led to venous microembolism, CT and light microscopy did not demonstrate changes in lung structure related to the experimental dive. Increased extravascular lung water found in all animals may be due to infusion therapy.

Acute Disease↗
PubMed1999

The degree of decompressive relief and its relation to clinical outcome in patients undergoing surgery for lumbar spinal stenosis.

STUDY DESIGN: A cross-sectional, clinical study to evaluate surgical decompression of the stenotic area monitored by computed tomographic scan and its relation to clinical variables in patients operated on for lumbar spinal stenosis. OBJECTIVE: To study in patients with lumbar spinal stenosis the influence of the degree of compressive relief on the patients' clinical outcome. SUMMARY OF BACKGROUND DATA: The goal of surgical treatment in lumbar spinal stenosis is to decompress the stenotic area. Although the decompression should be adequate, there are no clear guidelines to determine the extent of necessary decompression. In fact, there is clinical evidence that there is a discrepancy between the surgical outcome in the patient with lumbar spinal stenosis and postoperative radiologic findings. METHODS: In 92 patients with lumbar spinal stenosis who had had no prior back surgery, preoperative and postoperative computed tomographic scans were obtained to determine the degree of decompression. The postoperative scan findings were classified according to the degree of decompression into a no-stenosis group (n = 35), an adjacent-stenosis group (n = 27), and a residual-stenosis group (n = 30). The postoperative instability of the lumbar spine was investigated by functional radiography. The subjective disability of the patients was assessed using the Oswestry score and the severity of pain using the visual analog scale. Walking capacity was evaluated by a treadmill test. The patients' estimations of the results of surgery were classified into groups of satisfied patients and dissatisfied patients. RESULTS: The mean Oswestry score in all 92 patients was 27.1, and mean walking capacity was 630 m. In the satisfied patients, the Oswestry score was 18.8 and in the dissatisfied patients, 34.9 (P < 0.0000). Walking capacity was 690 m and 594 m, respectively. There were 30 patients with postoperative spinal instability, but it had no influence on surgical outcome. There were no differences in the Oswestry score, walking capacity, and patients' satisfaction among the postoperative CT groups. In the linear regression analysis, the satisfied patient corresponded significantly with the Oswestry score. CONCLUSIONS: The satisfaction of the patients with the results of surgery was more important in surgical outcome than the degree of decompression detected on computed tomographic scan.

Cross-Sectional Studies↗
PubMed1999

Effect of decompression enlargement laminoplasty for posterior shifting of the spinal cord.

STUDY DESIGN: A study to measure the shifts of the spinal cords and the effects of decompression laminoplasty in 65 patients with cervical lesions who underwent computed tomographic myelography before and after laminoplasty. OBJECTIVES: To investigate limitations of the spinal cord posterior shift after laminoplasty and to clarify the optimal decompression areas to obtain effective posterior shifting. SUMMARY OF BACKGROUND: Although several types of laminoplasty have been performed, all procedures share the common purpose of posterior decompression. No previous studies have examined the limitations of posterior decompression or the optimal decompression range. METHODS: The distance from the posterior edge of each vertebral body or disc level to the posterior edge of the spinal cord was measured by computed tomographic myelography. After the posterior shift was determined by calculating the difference between pre- and postsurgical distances, the relations between posterior shift and neck alignment, clinical results, and the areas of decompression were analyzed. RESULTS: The spinal cord shift ranged from a maximum of 6.6 mm to a minimum of 0 mm. Clinically, spinal cord shifts greater than 3 mm were associated with good clinical outcomes. Upward or downward advanced laminoplasty was related to larger spinal cord shifts at the upper or lower cervical spine. CONCLUSIONS: A mean spinal cord shift of > 3 mm was associated with good clinical outcomes after laminoplasty. In cases with compressive lesions at the upper or lower cervical spine, extension of decompression one level above or one level below likely results in a greater posterior spinal cord shift at these lesions.

Cervical Vertebrae↗
PubMed1997

Decompression comparison of helium and hydrogen in rats.

The hypothesis that there are differences in decompression risk between He and H2 was examined in 1,607 unanesthetized male albino rats subjected to dives on 2% O2-balance He or 2% O2-balance H2 (depths < or = 50 ATA, bottom times < or = 60 min). The animals were decompressed to 10.8 ATA with profiles varying from rapid to slow, with up to four decompression stops of up to 60 min each. Maximum likelihood analysis was used to estimate the relative decompression risk on a per unit pressure basis (termed "potency") and the rate of gas uptake and elimination, both factors affecting the decompression sickness risk, from a specific dive profile. H2 potency for causing decompression sickness was found to be up to 35% greater than that for He. Uptake rates were unresolvable between the two gases with the time constant (TC) estimated at approximately 2-3 min, leading to saturation in both cases in < 15 min. Washout of both gases was significantly slower than uptake, with He washout (TC approximately 1.5-3 h) substantially slower than H2 washout (TC approximately 0.5 h). It is unknown whether the decompression advantage of the faster washout of H2 or the disadvantage of its increased potency, observed in the rat, would be important for human diving.

Animals↗
PubMed1999

Ventricular pressure monitoring during bilateral decompression with dural expansion.

OBJECT: The management of massive brain swelling remains an unsolved problem in neurosurgery. Despite newly developed medical and pharmacological therapy, the rates of mortality and morbidity caused by massive brain swelling remain high. According to many recent reports, surgical decompression with dural expansion is superior to medical management in patients with massive brain swelling. To show the quantitative effect of decompressive surgery on intracranial pressure (ICP), the authors performed a ventricular puncture and measured the ventricular ICP continuously during decompressive surgery and the postoperative period. METHODS: Twenty patients with massive brain swelling who underwent bilateral decompressive craniectomy with dural expansion were included in this study. In all patients, ventricular puncture was performed at Kocher's point on the side opposite the massive brain swelling. The ventricular puncture tube was connected to the continuous monitor via a transducer device. The ventricular pressure was monitored continuously, during the bilateral decompressive procedures and postoperative period. The initial ventricular ICP was variable, ranging from 16 to 65.8 mm Hg. Immediately after the bilateral craniectomy, the mean ventricular ICP decreased to 50.2+/-16.6% of the initial ICP (range 5-51.5 mm Hg). Additional opening of the dura decreased the mean ICP by an additional 34.5% and reduced the ventricular pressure to 15.7+/-10.7% of the initial pressure (range 0-15 mm Hg). Ventricular pressure measured postoperatively in the neurosurgical intensive care unit was lowered to 15.1+/-16.5% of the initial ICP. The ventricular ICP trend in the first 24 hours after decompressive surgery was an important prognostic factor; if it was greater than 35 mm Hg, the mortality rate was 100%. CONCLUSIONS: Bilateral decompression with dural expansion is an effective therapeutic modality in the control of ICP. To obtain favorable clinical outcomes in patients with massive brain swelling, early decision making and proper patient selection are very important.

Adolescent↗
PubMedDate not supplied

Study of long intestinal tube for decompression of obstructive left colon cancer.

BACKGROUND/AIMS: Recently, several reports have recommended primary resection, rather than a staged operation, for obstructive left colon cancer. However pre-operative decompression is important for reducing complications and improving the curability of primary resection. Among the many pre-operative decompression strategies reported, we selected the long intestinal tube and evaluated the effectiveness of this convenient strategy. METHODOLOGY: A long intestinal tube was inserted pre-operatively for decompression in 27 of 29 patients undergoing resection for obstructive left colon cancer (1991-1995). We retrospectively studied the clinical features (responders vs. non-responders) of the 27 patients. We also compared these 27 with 26 other pre-1990 patients, who did not receive pre-operative decompression, in term of post-operative morbidity. RESULTS: Twelve of the 27 patients were responders; success rate 44.4%. There were no blood profile differences between responders and non-responders, but the time from bowel movement cessation to intestinal tube insertion was 3 days or less in all responders but 4 days or more in non-responders (p<0.001). There was no significant difference in the rate of post-operative morbidity between those with and without pre-operative decompression. CONCLUSIONS: Decompression is likely to be successful, allowing elective primary resection, when initiated within 3 days of bowel movement cessation. However, more than 4 days post-onset, other decompression methods or emergency surgery is necessary.

Adenocarcinoma↗
PubMed1989

Decompression: English tables.

The formulation of decompression procedures has generally been based on the observation that divers can be decompressed without stoppages to surface, from steady-state exposures of about twice the atmospheric pressure. Because decompression sickness rarely develops from this "no-stop decompression", it has been assumed that no gas is liberated. It is therefore assumed, in the calculation of the majority of decompression tables, that using a 2:1 decompression ratio allows the additional gas load from the hyperbaric exposure to be transported to the lungs in solution. Ultrasonic scanning and Doppler techniques have shown that this is not the case. Decompression tables must therefore be formulated so as to take into account the presence of gas, the critical diameter of circulating bubbles and the inherent unsaturation introduced by oxygen.

Decompression↗
PubMed1986

An effect of CO2 on the maximum safe direct decompression to 1 bar from oxygen-nitrogen saturation.

An investigation into the maximum safe decompression step from oxygen nitrogen saturation to 1 bar was carried out with and without the presence of 0.02 bar carbon dioxide. The series, Islander 1, involved 13 teams of 5, fully informed, male volunteers carrying out simulated dives. One group of 6 teams carried out dives in an atmosphere of 0.4 bar oxygen, balance nitrogen (O2-N2); another group of 7 teams used an atmosphere of 0.38 bar oxygen, 0.02 bar carbon dioxide, balance nitrogen (O2-N2-CO2). The dives consisted of a 48-h stay at 1.7 or 1.8 bar to saturate the tissues, followed by decompression to 1 bar air at 0.5 bar/min. Two decompression parameters were studied; the incidence of decompression sickness (DCS) in the 24 h postdecompression, and the incidence and grade of venous gas emboli (VGE) in the first 6 h postdecompression. The grade of VGE was assessed using the Kisman-Masurel scoring system which produces a bubble grade with the subject at rest and after movement. No significant difference was found in the incidence of DCS between the two groups. Twenty subjects were decompressed from 1.7 bar using each mixture, without signs or symptoms of DCS. However, after decompression from 1.8 bar there were 2 cases of DCS in 10 subjects in the O2-N2 group and 2 cases in 15 subjects in the O2-N2-CO2 group. The incidence of detectable VGE was always lower in the O2-N2-CO2 group at both saturation pressures; at 1.7 bar the VGE incidence was lower by 40% (P less than 0.05) at rest and by 55% (P less than 0.001) after movement. At 1.8 bar the reduction was 3% (NS) at rest and 30% (NS) after movement. The results indicate that decompression from 1.8 bar to 1 bar, with or without the presence of 0.02 bar carbon dioxide, is likely to produce more than 5% DCS.

Adult↗
PubMed1983

Hyperbaric exposure during pregnancy in sheep: staged and rapid decompression.

Hyperbaric exposure during pregnancy in sheep: staged and rapid decompression. Undersea Biomed Res 1983; 10(1): 11-15. --Twelve sheep with dated pregnancies were exposed for 20 min to hyperbaric pressure comparable to 165 feet of sea water weekly between the 49th and 133rd days of pregnancy. Six were decompressed in stages and six directly without decompression stops. Those that were decompressed gradually delivered normally at or near term. One lamb was abnormal, but the relationship to pressurization is unclear. Three of those decompressed rapidly aborted dead fetuses, and two others delivered mature, but affected, lambs. Under the conditions of this study staged decompression after repeated hyperbaric exposures protected the fetuses from the destructive effects of rapid decompression. Hyperbaric pressure did not alter gross anatomic development.

Abortion, Incomplete↗
PubMed1997

Reversibility in blood-brain barrier, microcirculation, and histology in rat brain after decompression.

To examine the changes in blood-brain barrier (BBB), cerebral microcirculation, and histology from 15 min to 72 h after decompression, 90 rats were exposed to experimental compression to 6 atm abs air for 90 min and subsequent rapid decompression. The disruption of BBB was examined by Evans blue extravasation. The cerebral microcirculation was demonstrated by perfusion with India ink. The area stained with Evans blue and the regions of defective filling with India ink, observed immediately after decompression decreased in size with time and were undetectable 3-24 h after decompression. The edematous brain tissue with enlarged perivascular space and darkly stained nerve cells also decreased to the uncompressed control level 1-24 h after decompression. These reversible dysbaric changes, however, reappeared 48-72 h after decompression. The different mechanisms, the physicochemical effects of microbubbles, and the maturation phenomenon after temporary brain ischemia induced by dysbaric microbubbles may be involved in the brain damage after decompression sickness.

Animals↗
PubMed1998

[Follow-up monitoring with magnetic resonance tomography after decompressive trephining in experimental "malignant" hemispheric infarct].

Acute ischemia in the complete territory of the carotid or the middle cerebral artery may lead to cerebral edema with raised intracranial pressure and progression to coma and death. Although clinical data suggest benefit for patients undergoing decompressive surgery for massive space occupying hemispheric stroke, little data about the effects of this procedure on morbidity and outcome is available. The experimental data support an early surgical approach. For early and probably most effective treatment of severe, space-occupying cerebral ischemia, the "malignant" character of the brain edema has to be recognized early after onset of vessel occlusion. Hereby magnetic resonance imaging (MRI) may allow to determine the clinical significance of brain edema early after onset, simultaneously allowing to monitor the evolution of ischemia. We performed serial SE-MRI in rats with acute hemispheric infarctions treated by decompressive craniectomy. Focal cerebral ischemia was induced in 36 rats using an endovascular occlusion technique. Decompressive craniectomy was performed 4 and 24 hours after vessel occlusion in groups of 12 animals each. Twelve animals were not treated by decompressive craniectomy (control group). Four, 24, 48, 72 and 168 hours after MCAO all animals were examined with conventional T1- and T2-weighted SE-MRI. Shift of the midline structures and compression of the ventricles were scored. Changes in weight and neurological performance were measured daily. The infarction volume was calculated by triphenyltetrazolium chloride staining 168 hours after MCAO. While mortality in the untreated group was 33.3%, none of the animals treated by a decompressive craniectomy died (mortality 0%). Neurological behaviour, weight loss and infarction volume were significantly better in the animals treated by early decompressive craniectomy (p < 0.05). Four hours after MCAO all untreated animals showed a massive shift of the midline structures and a massive compression of the ventricles; only 7 of 12 animals treated early by craniectomy showed mild mass effects. Correlation of the histological brain damage with T2-weighted MRI 4 hours after MCAO was poor (r = 0.41); later than 24 hours there was a good correlation (r > 0.7). Our results suggest that decompressive craniectomy in malignant cerebral ischemia reduces mortality and significantly improves outcome. If performed early after vessel occlusion, it also significantly reduces infarction size. In the acute phase of hemispheric infarction conventional SE-MRI is not sensitive in estimation of infarction size. Later than 24 hours, conventinal SE-MRI proved to be useful in monitoring brain edema and infarction size in this rat model of malignant hemispheric stroke.

Animals↗