Experimental chronic compressive cervical myelopathy

1993 ◽  
Vol 79 (4) ◽  
pp. 550-561 ◽  
Author(s):  
Ossama Al-Mefty ◽  
H. Louis Harkey ◽  
Isam Marawi ◽  
Duane E. Haines ◽  
Dudley F. Peeler ◽  
...  
Keyword(s):  
Blood Flow ◽  
Spinal Canal ◽  
Morphological Changes ◽  
Clinical Signs ◽  
Magnetic Resonance Images ◽  
Neurological Deficits ◽  
Cervical Cord ◽  
Flow Measurements ◽  
Content Type ◽  
Fine Print

✓ A canine model simulating both cervical spondylosis and its results in delayed progressive myelopathy is presented. This model allowed control of compression, an ongoing assessment of neurological deficits, and evaluation using diagnostic images, frequent electrophysiological tests, local blood flow measurements, and postmortem histological examinations. Subclinical cervical cord compression was achieved in 14 dogs by placing a Teflon washer posteriorly and a Teflon screw anteriorly, producing an average of 29% stenosis of the spinal canal. Four dogs undergoing sham operations were designated as controls. Twelve of the animals undergoing compression developed delayed and progressive clinical signs of myelopathy, with a mean latent period to onset of myelopathy of 7 months. Spinal cord blood flow studies using the hydrogen clearance method showed a significant transient increase in blood flow immediately after compression and a decrease before sacrifice. Somatosensory evoked potential studies indicated progressive deterioration during the period of compression. Magnetic resonance images revealed intramedullary changes. Histological studies showed abnormalities overwhelmingly within the gray matter, including changes in vascular morphology, loss of large motor neurons, necrosis, and cavitation. Axonal degeneration and obvious demyelination were rarely seen. The most profound morphological changes occurred at the site of greatest compression. It is proposed that a momentary arrest of microcirculation occurs during extension of the neck because of loss of the reserve space in the compromised spinal canal. This microcirculatory disturbance is predominant in the watershed area of the cord and mainly affects the highly vulnerable anterior horn cells, leading to neuronal death, necrosis, and eventual cavitation at the junction of the dorsal and anterior horns. Additional supportive evidence of this hypothesis was derived from the literature.

Experimental chronic compressive cervical myelopathy: effects of decompression

1995 ◽  
Vol 83 (2) ◽  
pp. 336-341 ◽  
Author(s):  
H. Louis Harkey ◽  
Ossama Al-Mefty ◽  
Isam Marawi ◽  
Dudley F. Peeler ◽  
Duane E. Haines ◽  
...  
Keyword(s):  
Cervical Myelopathy ◽  
Disease Process ◽  
Cord Compression ◽  
Magnetic Resonance Images ◽  
Pathological Examination ◽  
Cervical Cord ◽  
Spinal Cord Blood Flow ◽  
Flow Measurements ◽  
Content Type ◽  
Fine Print

✓ Twelve dogs developed a delayed onset of neurological abnormalities from chronic cervical cord compression that was characteristic of myelopathy. The animals were divided into two groups and matched according to degree of neurological deficit. Six animals underwent decompression through removal of the anteriorly placed compressive device. Throughout the experiment, serial neurological examinations and somatosensory evoked potential studies were performed on each animal. Spinal cord blood flow measurements were obtained during each surgical procedure and at sacrifice. Magnetic resonance images were obtained after compression and before sacrifice. All animals in the decompressed group showed significant neurological improvement after decompression; no spontaneous improvement in neurological function was seen in the compressed group. On pathological examination, irreversible changes including large motor neuron loss, necrosis, and cavitation were seen in four of the animals in the decompressed group and five in the compressed group. Cervical spondylotic myelopathy in humans is known to respond to decompression; this study provides further evidence that this animal model for chronic compressive cervical myelopathy accurately reflects the disease process seen in humans.

An experimental study of the acute stage of subarachnoid hemorrhage

1983 ◽  
Vol 59 (6) ◽  
pp. 917-924 ◽  
Author(s):  
Ken Kamiya ◽  
Hideyuki Kuyama ◽  
Lindsay Symon
Keyword(s):  
Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Acute Stage ◽  
Flow Measurements ◽  
Content Type ◽  
Baboon Model ◽  
Differential Increase ◽  
Blood Flow Measurements ◽  
Fine Print ◽  
Made In

✓ A baboon model of subarachnoid hemorrhage (SAH) has been developed to study the changes in cerebral blood flow (CBF), intracranial pressure (ICP), and cerebral edema associated with the acute stage of SAH. In this model, hemorrhage was caused by avulsion of the posterior communicating artery via a periorbital approach, with the orbit sealed and ICP restored to normal before SAH was produced. Local CBF was measured in six sites in the two hemispheres, and ICP monitored by an implanted extradural transducer. Following sacrifice of the animal, the effect of the induced SAH on ICP, CBF, autoregulation, and CO2 reactivity in the two hemispheres was assessed. Brain water measurements were also made in areas of gray and white matter corresponding to areas of blood flow measurements, and also in the deep nuclei. Two principal patterns of ICP change were found following SAH; one group of animals showed a return to baseline ICP quite quickly and the other maintained high ICP for over an hour. The CBF was reduced after SAH to nearly 20% of control values in all areas, and all areas showed impaired autoregulation. Variable changes in CO2 reactivity were evident, but on the side of the hemorrhage CO2 reactivity was predominantly reduced. Differential increase in pressure lasting for over 7 minutes was evident soon after SAH on the side of the ruptured vessel. There was a significant increase of water in all areas, and in cortex and deep nuclei as compared to control animals.

Cerebral blood flow measurements and electroencephalograms during carotid endarterectomy

1974 ◽  
Vol 41 (3) ◽  
pp. 310-320 ◽  
Author(s):  
Thoralf M. Sundt ◽  
Frank W. Sharbrough ◽  
Robert E. Anderson ◽  
John D. Michenfelder
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Endarterectomy ◽  
Carbon Dioxide Tension ◽  
Initial Slope ◽  
Flow Measurements ◽  
Content Type ◽  
Blood Flow Measurements ◽  
Electroencephalogram Eeg ◽  
Fine Print

✓ Ninety-three endarterectomies for carotid stenosis were monitored with cerebral blood flow (CBF) measurements, and 113 with both CBF measurements and a continuous electroencephalogram (EEG). Significant CBF increase occurred only when carotid endarterectomy was for a stenosis greater than 90%. A high correlation between CBF and EEG indicated when a shunt was required. To sustain a normal EEG, the CBF ascertained by the initial slope technique must be 18 ml/100 gm/min at an arterial carbon dioxide tension (PaCO2) of 40 torr. The degree of EEG change below this level during occlusion reflected the severity of reduced blood flow and was reversible with replacement of a shunt. The value and limitations of these monitoring techniques and a concept of ischemic tolerance and critical CBF are discussed.

Endovascular occlusion of intracranial vessels for curative treatment of unclippable aneurysms: report of 16 cases

1991 ◽  
Vol 75 (5) ◽  
pp. 694-701 ◽  
Author(s):  
Jonathan E. Hodes ◽  
Armand Aymard ◽  
Y. Pierre Gobin ◽  
Daniel Rüfenacht ◽  
Siegfried Bien ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Posterior Inferior Cerebellar Artery ◽  
Artery Aneurysm ◽  
Neurological Deficits ◽  
Parent Vessel ◽  
Content Type ◽  
Fine Print

✓ Among 121 intracerebral aneurysms presenting at one institution between 1984 and 1989, 16 were treated by endovascular means. All 16 lesions were intradural and intracranial, and had failed either surgical or endovascular attempts at selective exclusion with parent vessel preservation. The lesions included four giant middle cerebral artery (MCA) aneurysms, one giant anterior communicating artery aneurysm, six giant posterior cerebral artery aneurysms, one posterior inferior cerebellar artery aneurysm, one giant mid-basilar artery aneurysm, two giant fusiform basilar artery aneurysms, and one dissecting vertebral artery aneurysm. One of the 16 patients failed an MCA test occlusion and was approached surgically after attempted endovascular selective occlusion. Treatment involved pretreatment evaluation of cerebral blood flow followed by a preliminary parent vessel test occlusion under neuroleptic analgesia with vigilant neurological monitoring. If the test occlusion was tolerated, it was immediately followed by permanent occlusion of the parent vessel with either detachable or nondetachable balloon or coils. The follow-up period ranged from 1 to 8 years. Excellent outcomes were obtained in 12 cases with complete angiographic obliteration of the aneurysm and no new neurological deficits and/or improvement of the pre-embolization symptoms. Four patients died: two related to the procedure, one secondary to rupture of another untreated aneurysm, and the fourth from a postoperative MCA thrombosis after having failed endovascular test occlusion. The angiographic, clinical, and cerebral blood flow criteria for occlusion tolerance are discussed.

Ultrastructural observations of the capsule of chronic subdural hematoma in various clinical stages

1975 ◽  
Vol 43 (5) ◽  
pp. 569-578 ◽  
Author(s):  
So Sato ◽  
Jiro Suzuki
Keyword(s):  
Endothelial Cells ◽  
Subdural Hematoma ◽  
Morphological Changes ◽  
Chronic Subdural Hematoma ◽  
Neurological Deficits ◽  
High Permeability ◽  
Content Type ◽  
Clinical Stages ◽  
Capillary Endothelial Cells ◽  
Fine Print

✓ The authors used light and electron microscope to examine the capsules of chronic subdural hematoma in 33 cases. In cases with neurological deficits, capillary endothelial cells in the capsule had many cytoplasmic protrusions and fenestrations, suggesting high permeability of the capillary wall. Endothelial degeneration was also observed in these cases. These morphological changes were reversed by osmotherapy. Formation of collagen fibrils from fibroblasts in the hematoma capsule was frequently observed in the cases treated by osmotherapy.

Cervical flexion myelopathy: a “tight dural canal mechanism”

1987 ◽  
Vol 66 (6) ◽  
pp. 935-937 ◽  
Author(s):  
Yoshinobu Iwasaki ◽  
Kunio Tashiro ◽  
Seiji Kikuchi ◽  
Mayumi Kitagawa ◽  
Toyohiko Isu ◽  
...  
Keyword(s):  
Morphological Changes ◽  
Cord Compression ◽  
Cervical Cord ◽  
Posterior Border ◽  
Disc Disease ◽  
Content Type ◽  
Neuroradiological Examination ◽  
Cervical Flexion Myelopathy ◽  
Progressive Weakness ◽  
Fine Print

✓ The authors describe a case of flexion myelopathy due to specific morphological changes of the cervical cord, termed a “tight dural canal mechanism.” The patient was an 18-year-old man with progressive weakness and muscle atrophy of the left arm. Neuroradiological examination revealed that the lower cervical cord was compressed during flexion of the cervical spine, but that there was no disc disease or cervical vertebral instability. The cord compression was attributed to a pinching mechanism by the posterior border of the vertebral body and the posterior component of the dura on flexion.

Cerebral arterial blood flow and aneurysm surgery

1977 ◽  
Vol 47 (6) ◽  
pp. 810-818 ◽  
Author(s):  
Helge Nornes ◽  
Per Wikeby
Keyword(s):  
Blood Flow ◽  
Cerebral Artery ◽  
Arterial Blood Flow ◽  
Anterior Portion ◽  
Flow Measurements ◽  
Content Type ◽  
Aneurysm Neck ◽  
Flow Monitoring ◽  
Arterial Blood ◽  
Fine Print

✓ Cerebral arterial blood flow was monitored in 22 patients undergoing surgery for intracranial saccular aneurysms. An electromagnetic flow probe was used to record the internal carotid artery (ICA) flow in the neck or intracranially in seven patients. The ICA flow ranged between 100 and 175 ml/min (average 144 ml/min). Intracranial flow measurements with specially designed probes were made in 17 patients. The middle cerebral artery (MCA) showed flow values between 75 and 120 ml/min (average 97 ml/min). Flow figures recorded from the proximal anterior cerebral artery (ACA) were lower (average 65 ml/min), and had a wider range from 30 to 110 ml/min. Test occlusion of the terminal ICA showed a retrograde flow in the proximal ACA to the MCA ranging from 15 to 125 ml/min (average 78 ml/min). This test was used to investigate the collateral potential of the anterior portion of the circle of Willis, which is essential to the decision of whether to undertake trap ligation procedures in this location. Flow monitoring in the parent vessel was also of use in some patients to assess flow conditions after the clipping of the aneurysm neck.

The “filum intermedium” sign: focal in utero spinal cord infarct and extraspinal thecal sac

1994 ◽  
Vol 81 (6) ◽  
pp. 941-946 ◽  
Author(s):  
Adam N. Mamelak ◽  
Philip H. Cogen ◽  
A. James Barkovich
Keyword(s):  
Spinal Cord ◽  
Spinal Canal ◽  
Spinal Column ◽  
In Utero ◽  
Magnetic Resonance Images ◽  
Radiographic Appearance ◽  
Radiographic Findings ◽  
Content Type ◽  
And Migration ◽  
Fine Print

✓ This report describes the unique case of a child born with paraplegia and a neurogenic bladder who was found to have a dysplastic, nonossified T-12 vertebral body, midline fusion of the T-12 neural arches, obliteration of the spinal canal at T-12, and an extraspinal thecal sac in the T11—L1 region. Neural tissue was focally absent from T9–12, but neural structures above and below were preserved. Narrowing of the thecal sac on myelograms and sagittal magnetic resonance images signifies in utero focal infarction of the spinal cord after neurulation but before formation of the posterior half of the spinal canal. The infarction resulted in severe focal narrowing of the thecal sac from T10—L1, resembling a premature and duplicated filum terminale; to denote the radiographic appearance of these anomalies, the authors have coined the term “filum intermedium” sign. The extremely unusual radiographic findings in this child illustrate the important interactions between neural tube, neural crest, and somite in the development of the spinal cord and spinal column. Correlation of the radiographic findings with the embryological differentiation and migration of these structures suggests that the spinal anomalies were caused by a focal insult, probably vascular in origin, occurring between the sixth and eighth weeks of gestation. The identification of a focally narrowed thecal sac and spinal cord (the “filum intermedium” sign) localizes the time of the insult to between the first and third month of gestation, and therefore is a useful marker in understanding developmental malformation of the spinal cord.

Spinal Cord Blood Flow in Experimental Transient Traumatic Paraplegia

1980 ◽  
Vol 52 (3) ◽  
pp. 335-345 ◽  
Author(s):  
Dean C. Lohse ◽  
Howard J. Senter ◽  
John S. Kauer ◽  
Richard Wohns
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
White Matter ◽  
Cord Blood ◽  
Spinal Cord Blood Flow ◽  
Flow Measurements ◽  
Content Type ◽  
The Mean ◽  
Blood Flow Measurements ◽  
Fine Print

✓ Blood flow in the lateral funiculus of the thoracic spinal cord was measured in 24 anesthetized cats using the hydrogen clearance method. In a control series of eight nontraumatized animals, blood flow measurements were taken from the T-5 and T-6 segments for 6 consecutive hours. The mean spinal cord blood flow (SCBF) in the control group was 12.8 ± 3.51 (SD) ml/min/100 gm on the basis of 107 measurements over 6 hours. In the experimental groups, 16 animals were similarly prepared. The spinal cords of these animals were then traumatized by dropping a 20-gm weight 5 cm (100 gm-cm trauma) or 13 cm (260 gm-cm trauma) onto the T-5 segment. Previous experiments have shown that these trauma levels lead to a transient paraplegia of less than 10 and 30 days' duration, respectively. Two hundred blood flow measurements from T-5 and T-6 were taken over the 6 hours following trauma. In the seven animals of the 100 gm-cm group, mean SCBF after trauma from the T-5 segment was 12.6 ± 3.45 (SD) ml/min/100 gm on the basis of 50 measurements taken over 6 hours; not significantly different from the controls (p > 0.70). In the 260 gm-cm group, mean SCBF from T-5 for 6 hours after trauma was 17.3 ± 6.60 (SD) ml/min/100 gm; significantly higher than controls (p < 0.001). Mean SCBF 3 to 6 hours after trauma was significantly elevated over controls (p < 0.05). The mean hyperemia in the 260 gm-cm group was found to be due to marked hyperemia in only four animals of the series, while five animals maintained blood flows in the normal range. This experiment provides quantitative evidence that white matter ischemia does not occur in spinal cord injuries that can be expected to produce only transient paraplegia. The data support the concept that white matter ischemia in the acute phase of severe spinal cord trauma may be related to secondary injury and subsequent permanent paraplegia.

Resection of dominant opercular gliosis in refractory partial epilepsy

1992 ◽  
Vol 77 (4) ◽  
pp. 632-639 ◽  
Author(s):  
William G. Obana ◽  
Kenneth D. Laxer ◽  
Philip H. Cogen ◽  
John A. Walker ◽  
Richard L. Davis ◽  
...  
Keyword(s):  
Magnetic Resonance Images ◽  
Partial Epilepsy ◽  
Neurological Deficits ◽  
Cortical Mapping ◽  
Normal Brain ◽  
Dominant Hemisphere ◽  
Content Type ◽  
Refractory Partial Epilepsy ◽  
Normal Speech ◽  
Fine Print

✓ Frontal opercular gliosis in the dominant hemisphere caused medically refractory partial epilepsy in two patients. Both patients were aphasic during their seizures, but otherwise had normal speech. Magnetic resonance images showed well-demarcated lesions resembling tumors in each patient; on heavily T2-weighted images, the lesions were hyperintense compared with normal brain. Cortical mapping with subdural grids localized speech to the area of the lesions; therefore, the resections were performed under local anesthesia and speech was tested throughout the procedure. Postoperatively, both patients were seizure-free and had no new neurological deficits. Well-demarcated lesions, even in the dominant operculum, can be safely removed in patients with medically refractory partial epilepsy.

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