Cerebral hyperperfusion, a state in which blood flow exceeds the metabolic needs of brain, may complicate a number of neurological and neurosurgical conditions. It may account for the propensity with which hemorrhage, cerebral edema, or seizures follow embolic stroke, carotid endarterectomy, or the excision of large arteriovenous malformations, and for some of the morbidity that accompanies acute severe head injury, prolonged seizures, and acute severe hypertension. Hyperperfusion syndromes have in common acute increases in blood pressure, vasodilatation, breakdown of the blood-brain barrier, and the development of cerebral edema. These common features suggest the possibility that they share the same pathogenic mechanisms. It was believed until recently that reactive hyperemia was caused primarily by the generation of vasoactive metabolites, which induced vasodilatation through relaxation of vascular smooth muscle. However, the authors have recently established that the release of vasoactive neuropeptides from perivascular sensory nerves via axon reflex-like mechanisms has a significant bearing upon a number of hyperperfusion syndromes. In this article, the authors summarize their data and discuss possible therapeutic implications for blockade of these nerves or their constituent neuropeptides.

Background and Purpose: Hemodynamic changes associated with acute ischemia cannot be measured with conventional nuclear magnetic resonance imaging. In this study, we used dynamic susceptibilitycontrast magnetic resonance imaging to measure the changes in vascular transit time and relative cerebral blood volume in a feline occlusion-reperfusion model.Methods: Dynamic susceptibility-contrast measurements were obtained before and during 10 minutes of global cerebral ischemia and for up to 3 hours after the onset of reperfusion. A cerebral blood flow index was calculated from the vascular transit time and relative cerebral blood volume measurements. Functional maps were constructed to demonstrate the regional hemodynamic differences resulting from the induced ischemia.Results: During the early phase after reperfusion, both the relative cerebral blood volume and blood flow index rose sharply, followed by a fall to near-basal levels at 45 minutes (lxcontrol and 1.3xcontrol, respectively). Thereafter, the volume rose slowly, whereas the flow index continued to drop. At 3 hours, cerebral blood volume had reached 1.6 times its control value, whereas the flow index had returned to its base value.Conclusions: The hemodynamic behavior we observed in our model reflects the independent responses of the cerebral blood volume and flow index to ischemic insult. Measurements acquired by our method were consistent with the temporal behavior reported in previous radionuclide studies. Susceptibilitycontrast nuclear magnetic resonance tomographic imaging proved to be valuable in detecting and quantifying both immediate and subsequent changes in the hemodynamic state of the ischemic and

Object Posterior epidural migration of a free disc fragment in the lumbar region is a very rare condition that has only been reported in isolated cases to date. Patients with this condition present with radiculopathy or major neurological deficits. Difficulties in diagnosis and the choice and timing of surgical treatment are important in these cases. In this clinical case series, features of cases with posterior epidural migration of free lumbar disc fragments accompanied by cauda equina syndrome are discussed. Methods Eight cases (0.27%) of posterior epidural migration of disc fragments were detected among 2880 patients surgically treated for lumbar disc herniation between 1995 and 2008. Seven of these patients had cauda equina syndrome. The mean duration of symptoms in the 8 cases was 4.2 days (range 1–10 days). The group included 6 men and 2 women, with a mean age of 48 years (range 34–72 years). The sequestered disc fragments were at the L3–4 level in 6 patients (75%) and the L4–5 level in 2 (25%). Magnetic resonance imaging showed tumor-like ring contrast enhancement around sequestered fragments in 5 patients. The patients' motor, sensory, sexual, and urological functions were evaluated postoperatively, and modified Odom criteria and a visual analog scale were used in the assessment of postoperative outcomes. Results A microsurgical approach was used in all cases. Sequestrectomy with minimal hemilaminotomy and removal of the free segments were performed. The patients were followed up for a mean period of 28.5 months. Three patients (37.5%) had excellent results, 3 (37.5%) had good results, 1 patient (12.5%) had fair results, and only 1 patient had poor results according to the Odom criteria. The main factors affecting the long-term outcomes were the presence of cauda equina syndrome and the time period between onset of symptoms and surgery. Conclusions Patients with posterior migration of a disc fragment present with severe neurological deficits such as cauda equina syndrome. Because the radiological images of disc fragments may mimic those of other more common posterior epidural space–occupying lesions, definite diagnosis of posteriorly located disc fragments is difficult. All of these lesions can be completely removed with hemilaminotomy and sequestrectomy, and early surgical treatment is important as a first choice to prevent severe neurological deficits.

Five cases of primary spinal column sarcomas are presented. Sarcomas primarily originating from paravertebral soft tissues were excluded. Patients' age ranged from 1 to 14 years (mean 8.4 years). The male:female ration was 2:3. Two patients had Ewing's sarcoma (ES) originating from L5-S1 and L4-5 pedicles, respectively; two patients had mesenchymal chondrosarcoma (MCS) originating from L1-2 pedicles and L5 body, respectively; and one patient had osteogenic sarcoma (OS) of C4 body. All patients clinically presented with pain and progressive weakness of the extremities. The time that elapsed between the onset of symptoms and diagnoses ranged from one to five months. All cases were treated with chemotherapy, radiotherapy and subtotal tumour resection with spinal canal decompression. Two cases received posterior spinal fusion operations. Three patients were alive 10 to 98 months following diagnosis. Only the case with ES of L5-S1 pedicles was in complete remission and off therapy at the 98th postoperative month. The two MCS cases were in partial remission, and were receiving chemotherapy at the time of analysis. These tumours caused similar clinical findings and prognoses, and required combined treatment, which consisted of surgery, radiotherapy and chemotherapy; histologically three different types of malignant tumours are presented in the same category. We preferred surgical decompression and stabilization procedures especially for neurologically symptomatic patients, even if they had extensive tumours with high grades. By spinal canal decompression and stabilisation, we did not intend to cure the disease; however, we intended to provide neurological improvement, spinal stabilisation, improved quality of life, early mobilisation of the patient, and cytoreduction by means of surgical tumour ablation, which could render the chemotherapy more effective.

Tumor-to-tumor metastasis is a well recognized phenomenon. Although any tumor may be potential recipient of metastasis, renal cell carcinoma and meningioma are the most common malignant and benign recipients, respectively, whereas the lung and breast are the most common metastatic donors respectively, in both settings. Patients with hereditary cancer syndromes may be at higher risk for the development of tumor-to-tumor metastases. The most common pattern of tumor-to-tumor metastasis for intracranial neoplasms is the type in which an aggressive high-grade malignancy serves as the source of tumor and a more indolent neoplasm serves as the recipient tumor. The development of tumor metastasis from a second primary malignancy is uncommon and remains biologically puzzling. Its low incidence has made its full biological characterization evasive. Although rare, neurosurgeons should be aware of the entity of tumor-to-tumor metastasis. KeywoRds: Tumor, Metastasis, Central nervous system ÖZTümörden tümöre metastaz, iyi bilinen bir fenomendir. Herhangi bir tümör, metastazlar için potansiyel hedef olsa da en sık yayıldıkları malign ve benign tümörler sırasıyla renal hücreli karsinom ve menenjiyomlardır, en sık kaynaklandıkları bölgeler ise akciğer ve memedir. Herediter kanser sendromlarına sahip olan hastalar tümörden tümöre metastaz gelişimi açısından daha fazla risk taşıyabilirler. İntrakranial neoplazilerde tümörden tümöre metastazların en sık görülen şekli, saldırgan ve yüksek evreli bir tümörün daha iyi huylu bir tümöre metastazı ile olandır. Tümör metastazının ikinci bir primer malign tümörden gelişmesi az görülür ve biyolojik olarak halen şaşırtıcıdır. Bu durumun insidansının düşük olması biyolojik tanımlamanın tam olarak yapılmasını da zorlaştırmaktadır. Nadir olsa bile nöroşirürjiyenler, bir antite olarak tümörden tümöre metastaz hakkında bilgi sahibi olmalıdırlar.

Sympathetic pathways mediating chronotropic, dromotropic, and inotropic responses during ansae subclavia stimulation were determined by sequential dissection around major cardiac vessels. Right sympathetic (RS) projections influencing ventricular contractile force converge at the common pulmonary artery and within the pulmonary artery nerves (PAN). RS projections influencing left atrial contractile force course within the PANs. RS pathways to pacemaker and right atrial contractile tissue were localized between the superior vena cava and ascending aorta. RS projections influencing conductile tissue converge between the common pulmonary artery and proximal right pulmonary artery. Left sympathetic (LS) projections to ventricular contractile tissue were localized at the common pulmonary artery, within the PANs, and in the ventral lateral cardiac nerve (VLCN). LS pathways influencing heart rate and conductile tissue were localized at the left pulmonary artery and coursing between the right pulmonary artery and left superior pulmonary vein. LS projections to atrial contractile tissue were localized within the PANs and coursing between the right pulmonary artery and left superior pulmonary vein. We conclude that there are parallel, yet distinct, projections of sympathetic efferents to automatic, conductile, and contractile tissue of the canine heart.

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Summary: Marked hyperemia accompanies reperfusion after ischemia in the brain, and may account for the pro pensity of cerebral hemorrhage to follow embolic stroke or carotid endarterectomy, and for the morbidity that fol lows head injury or the ligation of large arteriovenous malformations. To evaluate the contribution of trigeminal sensory fibers to the hyperemic response, CBF was de termined in 12 symmetrical brain regions, using micro spheres with up to five different isotopic labels, in four groups of cats. Measurements were made at 15-min inter vals for up to 2 h of reperfusion after global cerebral ischemia induced by four-vessel occlusion combined with systemic hypotension of either 10-or 20-min duration. In normal animals, hyperemia in cortical gray matter 30 min after reperfusion was significantly greater after 20 min (n = 10) than after 10 min (n = 7) of ischemia (312 milIOO g/min versus 245 ml/100 g/min; p < 0.01). CBF returned to preischemic levels �45 min after reperfusion and was reduced to �65% of basal CBF for the remaining 75 min. In cats subjected to chronic trigeminal ganglionectomy (n 261tery (MCA) territory, and was confined to regions known to receive a trigeminal innervation. In these animals, sub stance P (SP) levels in the MCA were reduced by 64% (p < 0.01), and the density of nerve fibers containing calci tonin gene-related peptide (but not vasoactive intestinal polypeptide or neuropeptide Y) was decreased markedly on the lesioned side. Topical application of capsaicin (100 nM; 50 f.LI) to the middle or posterior temporal branch of the MCA 10-14 days before ischemia decreased SP levels by 36%. Postocclusive hyperemia in cortical gray matter was attenuated throughout the ipsilateral hemisphere by up to 58%, but the cerebral vascular response to hyper capnia (PaC02 = 60 mm Hg) was unimpaired. The dura tion of hyperemia and the severity of the delayed hypo perfusion were not influenced by trigeminalectomy, cap saicin application, or the intravenous administration of ATP. These data demonstrate the importance of neuro genic mechanisms in the development of postischemic hyperperfusion, and suggest the potential utility of strat egies aimed at blocking axon reflex-like mechanisms to reduce severe cortical hyperemia.