bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hydrocephalus in cerebral cysticercosis
Authors: Lobato Ramiro D. , Lamas Eduardo , Portillo Jaime M. , Roger Ricardo , Esparza Javier , Rivas Juan J. , Muñoz Maria J. 
Published: May 2009

✓ The cases of 11 patients with hydrocephalus secondary to cerebral cysticercosis are analyzed. Most of the patients had suffered from epilepsy before they developed hydrocephalic symptoms, and computerized tomography showed that infestation of the parenchyma coexisted with ventricular or cisternal colonization. In four cases, the parasitic vesicles compromised cerebrospinal fluid (CSF) flow in the ventricular system, resulting in internal hydrocephalus. Communicating hydrocephalus, caused by the presence of Cysticercus larvae in the basal cisterns (Cysticercus racemosus), or by the occurrence of a chronic basal meningitis, or both, developed in seven more patients. Changes in CSF pressure were related to the number and location of the cysts and to the leptomeningeal inflammatory reactions evoked by them. The majority of patients presented with a chronic and relatively normotensive hydrocephalus.
All patients except one had identifiable ventricular or cisternal Cysticercus larvae; these patients were treated with open removal of the cysts, and did well. However, most of them had impairment of CSF flow through the basal cisterns and required permanent CSF shunting. Communicating hydrocephalus due to leptomeningeal scarring was also successfully managed with extracranial shunting. Epilepsy was controlled with anticonvulsant therapy. Although good lasting results may be obtained with aggressive treatment of neurocysticercosis, patients are liable to relapse because surgery is only palliative in most instances.
Failure of intravascular volume expansion without hemodilution to elevate cortical blood flow in region of experimental focal ischemia
Authors: Wood James H. , Snyder Lauri L. , Simeone Frederick A. 
Published: May 2009

✓ Cerebrovascular and cardiac alterations evoked by intravascular volume expansion with whole blood, a popular adjunct in the clinical prevention or therapy of the focal ischemic deficits of cerebral vasospasm and acute stroke, were studied in splenectomized dogs. Clipping of the right distal internal carotid and proximal middle cerebral arteries in eight dogs reduced regional cortical blood flow (rCoBF) by 49% to 58% without altering cardiac output (CO), and produced about 10% hemispheric infarction. Eight dogs underwent similar cerebral arterial occlusion and eight dogs underwent arterial manipulation without clipping. Both latter groups received two autologous whole blood infusions within 2 hours, each equal to 20% of the respective dog's total blood volume. Despite significant CO elevations after the infusions, rCoBF in the middle cerebral arterial territory did not rise. These whole-blood infusions did not significantly alter mean arterial blood pressure, hematocrit, intracranial pressure, or, in dogs with clipped cerebral arteries, the relative size of infarction.
These data suggest that nondilutional hypervolemia neither elevates collateral perfusion to ischemic regions of the brain nor reduces infarction. In addition, elevations in CO do not appear to augment blood flow in either ischemic or normal brain.
Effect of intracranial pressure monitoring and aggressive treatment on mortality in severe head injury
Authors: Saul Thomas G. , Ducker Thomas B. 
Published: May 2009

✓ During 1977–1978, 127 patients with severe head injury were admitted and underwent intracranial pressure (ICP) monitoring. All patients had Glasgow Coma Scale (GCS) scores of 7 or less. All received identical initial treatment according to a standardized protocol. The patients' average age was 29 years; 60% had multiple trauma, and 35% needed emergency intracranial operations. Treatment for elevations of ICP was begun when ICP rose to 20 to 25 mm Hg, and included mannitol therapy and drainage of cerebrospinal fluid (CSF) when possible. Forty-three patients (34%) had ICP greater than or equal to 25 mm Hg; of these, 36 (84%) died. The mortality rate of the entire group was 46%.
During 1979–1980, 106 patients with severe head injury were admitted and underwent ICP monitoring. Their average age was 29 years; 51% had multiple trauma, and 31% underwent emergency intracranial surgery. All patients received the same standardized protocol as the previous series, with the exception of the treatment of ICP. In this present series: if ICP was 15 mm Hg or less (normal ICP), patients were continued on hyperventilation, steroids, and intensive care; if ICP was 16 to 24 mm Hg, mannitol was administered and CSF was drained; if ICP was 25 mm Hg or greater, the patients were randomized into a controlled barbiturate therapy study. Twenty-six patients (25%) had ICP's of 25 mm Hg or greater, compared to 34% in the previous series (p < 0.05), and 18 of these 26 patients (69%) died. The overall mortality for this current series was 28% compared to 46% in the previous series (p < 0.0005).
This study reconfirms the high mortality rate if ICP is 25 mm Hg or greater; however, the data also document that early aggressive treatment based on ICP monitoring significantly lessens the incidence of ICP of 25 mm Hg or greater and reduces the overall mortality rate of severe head injury.
Favorable results with syringosubarachnoid shunts for treatment of syringomyelia
Authors: Tator Charles H. , Meguro Kotoo , Rowed David W. 
Published: May 2009

✓ From 1969 to 1979, 20 patients with syringomyelia were treated with a syringosubarachnoid shunt. The principal indications for this procedure were: significant progressive neurological deterioration and absent or minimal tonsillar ectopia. There were 15 patients with idiopathic syringomyelia, four with posttraumatic syringomyelia, and one with syringomyelia secondary to spinal arachnoiditis. The operations were performed with an operating microscope, and attention was directed to preserving the arachnoid membrane to ensure proper placement of the distal end of the shunt in an intact subarachnoid space. In all cases, a silicone rubber ventricular catheter was inserted into the syrinx through a posterior midline myelotomy.
The average follow-up period was 5 years. A favorable result was obtained in 15 of the 20 patients (75%), including an excellent result with improvement of neurological deficit in 11 patients and a good result with cessation of progression in four patients. In the remaining five patients the result was poor with further progression of neurological deficit. A short duration of preoperative symptoms was usually a favorable prognostic feature. Four patients with a history of less than 6 months all had excellent results. Thirteen patients had a syringosubarachnoid shunt only, and all had good or excellent results. Seven patients had other surgical procedures, before, accompanying, or after shunt placement, and two had favorable results. Thus, the syringosubarachnoid shunt is an effective therapeutic modality for many patients with syringomyelia, particularly if there is little or no tonsillar herniation.
Spontaneous carotid-cavernous fistula in osteogenesis imperfecta
Authors: Campos José-Maria de , Ferro Mario O. López , Burzaco Juan A. , Boixadós José R. 
Published: May 2009

✓ A case of spontaneous carotid-cavernous fistula is presented in a patient suffering from osteogenesis imperfecta tarda type I. The patient was operated on under local anesthesia by intraluminal occlusion of the cavernous carotid artery with a Fogarty catheter, in accordance with Prolo's technique, with total remission except for homolateral loss of vision due to postglaucoma atrophy.
The pathogenetic phenomena described in the literature are reviewed, with the suggestion that osteogenesis imperfecta be included with Ehlers-Danlos disease, Marfan's syndrome, and pseudoxanthoma elasticum, as a connective tissue disease with increased weakness of vessel walls that can produce a spontaneous carotid-cavernous fistula. Reports of cases operated on by intraluminal occlusion with various types of balloon-tipped catheters are also reviewed. The good results obtained place this technique among the elective ones for the treatment of carotid-cavernous fistula.
Early decompression and neurological outcome in acute cervical spinal cord injuries
Authors: Wagner Franklin C. , Chehrazi Bahram 
Published: May 2009

✓ To evaluate the effect on neurological outcome of spinal cord compression persisting after a closed injury, the authors reviewed 44 of 62 consecutively managed cases of cervical spinal cord and spine injuries at C3–7, inclusive. Decompression within 48 hours of injury was confirmed by myelography or open reduction. Neurological status, graded numerically on a spinal trauma scale at admission and at follow-up review (an average of 1 year ± 2 months after admission), and percent recovery of neurological deficit were compared to canal narrowing (22 severe, ≥ 30%; versus 22 moderate, 11% to 29%; or mild, ≤ 10%) and to delay before treatment (30 within 8 hours of injury versus 14 treated 9 to 48 hours after injury). Severe narrowing was equated with compression.
Status at admission and at follow-up review was positively correlated. Patients with admission scores of less than 2 recovered a mean of 15% of their deficit, while those with scores more than 2 recovered a mean of 77%. Admission status correlated significantly with spinal canal narrowing but not with vertebral body displacement. Time of treatment had no significant effect upon admission status and percent recovery. No significant difference in the percent of recovery was noted, whether decompression was early (up to 8 hours) or late (9 to 48 hours) after injury. Surgery did not significantly alter the percent of recovery.
The findings indicate that the initial injury to the cervical spinal cord and spine remains the primary determinant of neurological outcome. Severe canal narrowing with cord compression thereafter appears to have comparatively little effect. The conclusion that decompression is without effect is not possible without comparison with a group of patients whose spinal canals remained narrowed at follow-up review.
Effect of sympathectomy on spinal blood flow autoregulation and posttraumatic ischemia
Authors: Young Wise , DeCrescito Vincent , Tomasula John J. 
Published: May 2009

✓ The hypothesis that the paravertebral sympathetic ganglia play a role in spinal blood flow regulation was tested in cats. Five cats were subjected to paravertebral sympathectomy, two to combined sympathectomy-adrenalectomy, three to adrenalectomy alone, and five controls received no treatment. Laminectomy was carried out to expose the T4–10 cord, and autoregulation was tested by measuring blood flow from the lateral columns with the hydrogen clearance technique during manipulation of systemic pressure with intravenous saline infusion and nitroprusside administration. The cord was then contused at T-7 with a 400 gm-cm impact injury. Posttraumatic blood flow was recorded, and neurophysiological function was assessed with somatosensory evoked potential (SEP) monitoring.
Before injury, blood flow in the untreated (control) group had no consistent relationship with mean systemic pressure over the range 80 to 160 mm Hg. In contrast, in all cats with paravertebral sympathectomy, whether accompanied by adrenalectomy or not, blood flows increased with systemic pressure (correlation coefficient 0.86, p < 0.01). After injury, the control and adrenalectomized cats showed blood flow decreases of > 60% to 4 to 6 ml/100 gm/min (p < 0.01) by 2 to 3 hours. However, cats with paravertebral sympathectomy maintained blood flow above 9 ml/100 gm/min for up to 3 hours after injury. All the sympathectomized cats recovered their SEP by the 3rd hour after injury, compared with none of the controls.
Thus, in the absence of the paravertebral sympathetic ganglia, spinal blood flow autoregulation was impaired and the typical posttraumatic loss in blood flow did not occur. The sympathectomy also protected the spinal cords from the neurophysiological loss usually seen in 400 gm-cm injury. The data suggest the need for caution in using acetylcholine blocking agents to paralyze animals in experimental spinal injury, since these agents alter sympathetic activity and may influence the injury process. The spinal cord is an excellent model in which to investigate sympathetic regulation of central nervous system blood flow.
Intradural extramedullary spinal metastasis
Authors: Perrin Richard G. , Livingston Kenneth E. , Aarabi Bizhan 
Published: May 2009

✓ The management of 10 patients with symptomatic localized intradural extramedullary spinal metastasis is reviewed. The single most common primary source was carcinoma of the breast (four cases). The initial symptom in nine patients was pain, with five patients reporting a characteristically severe cramping discomfort with radicular distribution. All patients underwent laminectomy decompression. At the time of surgery, six of the patients were weak but ambulatory and four were bedridden. Following surgery, four patients enjoyed some measure of pain relief, seven patients became ambulatory, and three remained bedridden. Two patients achieved a “satisfactory” result, and were walking and continent 6 months after surgery. Secondary brain tumors were demonstrated or implicated in nine patients, supporting the concept that the spinal metastases represented tertiary deposits following dissemination via the cerebrospinal fluid.
Symptomatic intradural extramedullary spinal metastasis causes a virulent clinical syndrome with poor prognosis and disappointing outcome after treatment. Given the high incidence of associated cerebral metastatic involvement, total neuraxis radiation and/or chemotherapy should be considered when symptomatic spinal metastasis is discovered to be intradural and extramedullary.
Clinical recording of pressure on the spinal cord and cauda equina
Authors: Magnaes Bjørn 
Published: May 2009

✓ When an intraspinal expanding lesion causes a spinal block, a segment of the spinal cord or cauda equina will be subjected to general pressure from the surrounding tissue. This spinal block pressure, the spinal equivalent to intracranial pressure, was measured by lumbar infusion of fluid and simultaneous recording of the volume-pressure curve caudal to the block. The point of deviation from or breakthrough of the exponential volume-pressure curve indicated the spinal block pressure. Spinal block pressure of about 500 mm H2O and more could be determined by this method, and, when it was combined with Queckenstedt's test, lower pressures could be assessed as well. In the static (thoracic) part of the spine, spinal block pressure up to the level of arterial blood pressure was recorded. In the dynamic part of the spine, however, spinal block pressure could exceed arterial blood pressure due to external compressive forces during extension of the spine.
There was a general tendency for more severe neurological deficits in patients with high spinal block pressure; but the duration of the pressure, additional focal pressure, and spinal cord compared with nerve root compression seemed equally important factors.
The recording has implications for diagnosis, positioning of patients for myelography and surgery, selection of high-risk patients for the most appropriate surgical procedure, and detection of postoperative hematoma. There were no complications associated with the recordings.
The activities of noradrenergic and dopaminergic neuron systems in experimental hydrocephalus
Authors: Miwa Soichi , Inagaki Chiyoko , Fujiwara Motokazu , Takaori Shuji 
Published: May 2009

✓ Experimental hydrocephalus was induced in rabbits by intracisternal injection of kaolin suspension, and the concentration of noradrenaline (NA), dopamine (DA), and their metabolites was determined in several brain regions. The NA concentration had decreased in the cerebellum, hypothalamus, and pons plus medulla oblongata, and increased in the caudate nucleus at 2 days after kaolin injection (the stage of early intracranial hypertension). At 1 week (the stage of progressive hydrocephalus), the NA content had returned to control levels in all brain regions studied, and it decreased again at 4 weeks (the stage of chronic hydrocephalus) in the pons plus medulla oblongata. The DA level was unchanged throughout the 4-week period after kaolin injection.
The concentration of 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MOPEG-SO4), the major metabolite of NA, was elevated in all brain regions except the caudate nucleus at all stages after kaolin injection. An increase in MOPEG-SO4 in the caudate nucleus was also observed 1 week after kaolin injection. The content of homovanillic acid (HVA), the major metabolite of DA in the rabbit brain, was decreased in the cerebral cortex at 2 days and at 1 week after kaolin injection, and in the caudate nucleus at 2 days, 1 week, and 4 weeks. The level of HVA was increased in the hypothalamus at 2 days, in the cerebellum at 2 days and at 1 week, in the pons plus medulla oblongata at 2 days, 1 week, and 4 weeks, and in the midbrain at 4 weeks.
These data suggest that, in experimental hydrocephalus in the rabbit, NA release is increased throughout the brain, while DA release is decreased in the cerebral cortex and caudate nucleus, and increased in the cerebellum, hypothalamus, midbrain, and pons plus medulla oblongata.
The effects of gammahydroxybutyric acid on canine cerebral blood flow and metabolism
Authors: Baumann Kent W. , Kassell Neal F. , Olin Julie , Yamada Thoru 
Published: May 2009

✓ Gammahydroxybutyric acid has been proposed as an alternative to high-dose barbiturate therapy for protecting the brain after ischemic or traumatic insult. The cerebral and systemic metabolic and vascular effects of gammahydroxybutyrate and its lactone analogue, gammabutyrolactone, are addressed in this paper. In anesthetized normal dogs, gammahydroxybutyrate or gammabutyrolactone was infused intravenously at a rate of 1 gm/kg/hr. Cerebral blood flow (CBF) decreased progressively with increasing doses of either agent. Cerebral metabolic rate of oxygen (CMRO2) increased initially with gammahydroxybutyrate, but not following gammabutyrolactone. Reduction in CBF exceeded that of CMRO2 at all doses in both series.
The primary systemic effect noted was a severe, lethal metabolic acidosis resulting from infusion of gammabutyrolactone. Gammahydroxybutyrate did not cause a similar acidosis. The imbalance of the CBF-CMRO2 reduction following gammahydroxybutyrate administration suggests that it has no advantage over barbiturates in the management of patients with cerebral vascular insufficiency or intracranial hypertension.
Intravascular aggregation after acute intracranial hypertension by epidural balloon compression in cats
Authors: Fujimoto Shunichiro , Roccaforte Peter , Patel Ashok R. , Moody Robert A. 
Published: May 2009

✓ The authors have studied the effect of acute intracranial hypertension produced by placement of an epidural balloon (control group) in cats, on cerebral perfusion, evoked responses, and hematological parameters. These elements were measured in similarly injured animals which underwent isovolemic hemodilution with dextran 75, after relief of intracranial hypertension. Four hours after balloon deflation, perfusion was markedly impaired in 30% of the control group, and was reduced to 11% in the dextraninfused group. The suppressed N1 amplitude of somatosensory evoked responses on the compression side, the reduced platelet aggregability, and the erythrocyte deformability by intracranial hypertension were all significantly more restored in the dextran-infused group after decompression. The percentage of platelets with volumes between 21.75 and 48.75 cu µ (normal 9.75 to 12.75 cu µ) significantly increased after decompression. Activation of platelets during intracranial hypertension leads to an increase in platelet volume from platelet aggregation, and correlates with a decrease in platelet aggregability. It was also suggested that reduction of erythrocyte deformability was not caused by erythrocyte aggregation.
The authors emphasize the role of intravascular factors such as vascular obstruction by platelet aggregates, and difficulty in passage of erythrocytes through capillaries due to reduced deformability, in the disturbance of the microcirculation following acute intracranial hypertension. The protective effect of dextran 75 by inhibition of platelets as well as hemodilution is stressed.
Spinal cord pathways mediating somatosensory evoked potentials
Authors: Powers Stephen K. , Bolger Catherine A. , Edwards Michael S. B. 
Published: May 2009

✓ Using a CO2 laser, discrete thoracic spinal cord lesions were made in cats anesthetized with ketamine and xylazine (Rompun). Differences in cortical somatosensory evoked potentials (SEP's) produced with high-intensity stimulation (20 times the motor threshold) of each posterior tibial nerve were determined for nine different combinations of unilateral spinal cord lesions.
The results of these studies show that nerve fibers in the ipsilateral dorsal column, the ipsilateral dorsal spinocerebellar tract, and the contralateral ventrolateral tracts with respect to the side of leg stimulation, contribute to cortical SEP's. A lesion of the dorsal spinocerebellar tract affected only the early waves (< 30 msec) of the SEP from leg stimulation ipsilateral to the side of the lesion, whereas a solitary lesion of the ventrolateral tract caused changes primarily in the amplitude of later waves (> 30 msec) of the SEP produced by contralateral leg stimulation. Lesions involving one-half of the dorsal column caused changes in the amplitude of both the early and late waves produced by stimulation ipsilateral to the side of the lesion. The effects of various combinations of lesions on the cortical SEP's were not additive, which indicates significant interaction between afferent pathways.
These findings suggest that high-intensity peripheral nerve stimulation, which activates both C and A fibers, could be used intraoperatively to assess spinal cord function with more accuracy than the current practice of using a stimulus strength of twice the motor threshold. The importance of using anesthetic agents that do not depress cortical activity (which may affect the later components of the SEP) is also emphasized.
Implanted pulsatile balloon device for simulation of neurovascular compression syndromes in animals
Authors: Segal Ricardo , Jannetta Peter J. , Wolfson Sidney K. , Dujovny Manuel , Cook Eugene E. 
Published: May 2009

✓ A self-contained neurovascular compression simulator (NCS) has been designed to function as an artificial artery that pulsates with the heart. When implanted in animals, this device simulates those naturally occurring situations in which there is compression of nervous elements in the region of the brain stem or other areas by aberrant, or ectatic branches of normal arteries. The NCS consists of an intra-aortic balloon, a smaller (cephalic) balloon, a connecting tube, and an injection port, all fabricated of polyurethane-silicone compounds. With each heart systole, the rise in intra-aortic pressure is transmitted to the smaller cephalic balloon in the form of a pulsation. Thus, part of the cardiac ejection energy is transferred to the desired nervous structures. The performance of each NCS is tested in vitro in a pulse duplicator system.
The NCS was chronically implanted for up to 2 years in four dogs and 10 baboons. The cephalic balloon was placed intracranially in the subarachnoid space on the ventrolateral medulla adjacent to the entry zone of the ninth and 10th cranial nerves on the left side of baboons and on the right side of dogs. The position of the balloons was checked by fluoroscopy. Following implantation, the NCS could be inflated or deflated at will using the injection port which served to restart or discontinue the pulsations. No occlusion of the aorta or reduction of blood flow to the lower limbs or trunk was detected. By means of the NCS, an experimental model of neurogenic hypertension was produced in baboons.