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L H Sekhon

Publications and source records attributed to L H Sekhon.

15 recordsLinked to original sources
PubMed2001

Epidemiology, demographics, and pathophysiology of acute spinal cord injury.

Spinal cord injury occurs through various countries throughout the world with an annual incidence of 15 to 40 cases per million, with the causes of these injuries ranging from motor vehicle accidents and community violence to recreational activities and workplace-related injuries. Survival has improved along with a greater appreciation of patterns of presentation, survival, and complications. Despite much work having been done, the only treatment to date known to ameliorate neurologic dysfunction that occurs at or below the level of neurologic injury has been intravenous methylprednisolone therapy. Much research over the past 30 to 40 years has focused on elucidating the mechanisms of spinal cord injury, with the complex pathophysiologic processes slowly being unraveled. With a greater understanding of both primary and secondary mechanisms of injury, the roles of calcium, free radicals, sodium, excitatory amino acids, vascular mediators, and apoptosis have been elucidated. This review examines the epidemiology, demographics, and pathophysiology of acute spinal cord injury.

Age Factors↗
PubMed2001

The role and timing of decompression in acute spinal cord injury: what do we know? What should we do?

The management of acute spinal cord injury has traditionally concentrated on preventative measures as well as, for the better part of the previous century, conservative care. Pharmacologic interventions, in particular intravenous methylprednisolone therapy, have shown modest improvements in clinical trials and are still undergoing evaluation. More recent interest has focused on the role of surgical reduction and decompression, particularly "early" surgery. A review of the current evidence available in the literature suggests that there is no standard of care regarding the role and timing of surgical decompression. There are insufficient data to support overall treatment standards or guidelines for this topic. There are, however, Class II data indicating that early surgery (<24 hours) may be done safely after acute SCI. Furthermore, there are Class III data to suggest a role for urgent decompression in the setting of 1) bilateral facet dislocation and 2) incomplete spinal cord injury with a neurologically deteriorating patient. Whereas there is biologic evidence from experimental studies in animals that early decompression may improve neurologic recovery after SCI, the relevant time frame in humans remains unclear. To date, the role of decompression in patients with SCI is only supported by Class III and limited Class II evidence and accordingly can be considered only a practice option. Accordingly, there is a strong rationale to undertake prospective, controlled trials to evaluate the role and timing of decompression in acute SCI.

Acute Disease↗
PubMed1999

Delayed neurological deterioration following resection of arteriovenous malformations of the brain.

OBJECT: The aim of this study was to analyze delayed neurological deficits following surgical resection of arteriovenous malformations (AVMs). METHODS: The authors report on a consecutive series of 200 patients with angiographically proven AVMs of the brain that were surgically resected between January 1989 and June 1998. The 30-day mortality rate for patients in this series was 1%, with one death caused by AVM resection and one death attributed to basilar artery aneurysm repair following successful AVM resection. The Spetzler-Martin grading system correlated well with the difficulty of surgery. No permanent incidence of morbidity resulted from resection of Grade I or II AVMs; the percentage of patients with a significant neurological deficit due to resection was 7.8% for those with Grade III lesions and 33.3% for those with Grade IV or V AVMs. However, this grading system did not accurately predict the development of delayed neurological deficits. Ten patients (5%) developed delayed neurological deficits after recovering from anesthesia and surgery. The delayed deficit was due to hemorrhage in four of the 10 patients and all four had undergone resection of AVMs measuring at least 4 cm in diameter. An increase in blood pressure during the first 8 postoperative days precipitated hemorrhage in these patients. Edema arising as a consequence of propagated venous thrombosis (two patients) was associated with extensive venous drainage networks rather than large AVM niduses. Both hemorrhagic and edematous complications can be included under the umbrella term of "arterial-capillary-venous hypertensive syndrome" to describe the common underlying pathogenesis accurately. An additional four patients developed a delayed deficit as a result of vasospasm. Vasospasm occurred when resection had involved extensive dissection of proximal anterior and middle cerebral arteries; in such cases the incidence of vasospasm was 27%. CONCLUSIONS: On the basis of their analysis of these complications, the authors recommend strict blood pressure control for patients with lesions measuring 4 cm or more in diameter (particularly those with a deep arterial supply). Thromboprophylaxis with aspirin and heparin is prescribed for patients with extensive venous drainage networks, and prophylactic nimodipine therapy and angiographic surveillance for vasospasm are suggested for patients in whom extensive dissection of proximal anterior or middle cerebral arteries has been necessary.

Adolescent↗
PubMed1998

Combined endovascular stent implantation and endosaccular coil placement for the treatment of a wide-necked vertebral artery aneurysm: technical case report.

OBJECTIVE AND IMPORTANCE: We describe a case in humans of the combined application of endovascular stent placement and Guglielmi detachable coil packing in the management of a wide-necked intracranial aneurysm. CLINICAL PRESENTATION: A 56-year-old woman suffered a subarachnoid hemorrhage secondary to a large wide-necked left vertebral artery aneurysm. Because of the size of the neck of the aneurysm and the extent of its calcification evident on computed tomographic scans, it was deemed unsuitable for surgical intervention or for conventional endovascular coiling. Instead, a combined surgical and endovascular therapy was instituted. INTERVENTION: The left vertebral artery was surgically exposed and cannulated to allow for the placement of an endovascular stent across the neck of the aneurysm to act as a buttress against which Guglielmi detachable coils could be packed. The patient suffered no ill effects as a result of this procedure and made a slow but steady recovery. CONCLUSION: This report describes a case of a wide-necked intracranial artery aneurysm treated using a combination of endovascular stent implantation across an aneurysm neck and endosaccular coil placement to obliterate the aneurysm. The technique described provides another treatment to better manage the difficult entity of wide-necked intracranial aneurysms that may be unsuitable for clipping.

Angioplasty, Balloon↗
PubMed1997

Chronic cerebral hypoperfusion: pathological and behavioral consequences.

OBJECTIVE: Although the effects of acute ischemic insults to the brain are well known, the effects related to chronic ischemia are poorly delineated. The pathological and behavioral changes induced by a chronic noninfarctional reduction in cerebral blood flow of 25 to 50% maintained for 6 months were assessed. METHODS: In each of 18 male Sprague-Dawley rats, an arteriovenous fistula was created in the neck via an anastomosis between the right external jugular vein and the right common carotid artery to induce cerebral hypoperfusion. Nineteen age-matched animals comprised a control group. Six months after surgery, the animals were examined using light and electron microscopic techniques, as well as via a battery of behavioral tests (motor, open field, and T-maze). RESULTS: Examination of the hippocampus by using light microscopy revealed disorganization of the CA1 sector with an increased number of astrocytes. Transmission electron microscopy of the CA1 region demonstrated neurons with increased lipofuscin pigment and central nucleoli and astrocytes with more numerous cytosolic mitochondria. Motor performance testing revealed no gross motor deficits, although open-field assessment demonstrated increased exploratory behavior in rats with fistulas. Finally, T-maze testing results suggested that errors in working memory were more common in rats undergoing chronic cerebral hypoperfusion (P < 0.05). CONCLUSIONS: These findings suggest that chronic reductions in cerebral blood flow of a magnitude previously thought to be harmless to neurons (i.e., reduced by 25-50%) do alter neuronal structure and affect whole animal behavior. Such a scenario may be responsible for a symptomatology secondary to arteriovenous steal and severe carotid stenoses. The mechanisms are still unknown.

Animals↗
PubMed1997

Chronic cerebral hypoperfusion inhibits calcium-induced long-term potentiation in rats.

BACKGROUND AND PURPOSE: Long-term potentiation (LTP) in the rat hippocampus induced by tetanic stimulation is impaired by chronic cerebral hypoperfusion. The effects of chronic cerebral hypoperfusion on other forms of LTP are unknown. Such data could help delineate the pathways of cellular alteration caused by chronic cerebral hypoperfusion. The in vitro phenomenon of calcium-induced LTP was thus examined in rat hippocampal CA1 cells that had undergone chronic hypoperfusion with a reduction in cerebral blood flow of between 25% and 50% maintained for 26 weeks. METHODS: Ten Sprague-Dawley rats had a cervical arteriovenous fistula surgically constructed, and an additional 10 animals were used as age-matched controls. Hippocampal slices were prepared after 26 weeks of hypoperfusion, and in vitro extracellular field potential recordings were taken from the Schäffer collateral CA1 region. Properties of LTP induced through transient exposure to a hypercalcemic solution were analyzed. RESULTS: LTP was impaired in animals with an arteriovenous fistula (P < .05). Control animals demonstrated potentiation lasting for the entire 2 hours of recording, whereas fistula animals showed only transient potentiation (< 60 minutes) before returning to baseline values. CONCLUSIONS: Calcium-induced LTP is impaired by chronic cerebral hypoperfusion. This form of LTP is different from that induced by tetanic stimulation. It is the most sensitive test available for in vitro detection of the changes induced in neuronal function by chronic noninfarctional reductions in cerebral blood flow of 25% to 50% and may indicate that the most basic cellular parameters involving calcium homeostasis and metabolism are being altered. The precise mechanisms remain to be elucidated, and several postulates are discussed.

Action Potentials↗
PubMed1997

Normal perfusion pressure breakthrough: the role of capillaries.

Excision of human cerebral arteriovenous malformations (AVMs) can be complicated by postoperative edema and hemorrhage in adjacent brain tissue, despite the complete excision of the malformation. Various theories have purported to explain the hemodynamic basis for this predisposition, including disordered autoregulation causing "normal perfusion pressure breakthrough" and obstruction of venous drainage leading to "occlusive hyperemia." This study did not evaluate the arterial or venous circulations in this scenario, but rather examined the capillaries in adjacent brain parenchyma for any structural deficiencies that would predispose the brain to the postoperative formation of edema and hemorrhage. Arteriovenous fistulas (AVFs) were created surgically in the necks of 10 male Sprague-Dawley rats, which caused chronic cerebral hypoperfusion with a reduction in cerebral blood flow of between 25% and 50%. Ten age-matched animals were used as controls. Twenty-six weeks after AVF formation the animals were killed and perfusion fixed. Their brain tissue was prepared for light microscopic studies by staining for glial fibrillary acidic protein or for transmission electron microscopy. In the CA1 pyramidal cell region of the hippocampus, it was found that in the animals with AVFs there was increased capillary density and absent astrocytic foot processes in some of these vessels. It was concluded that these vessels had developed as a result of neovascularization in response to chronic cerebral ischemia and that their anatomical configuration made them prone to mechanical weakness and instability following the increase in perfusion pressure that occurs in adjacent brain parenchyma after AVM excision. The authors believe that this study pinpoints a structural accompaniment to the hemodynamic changes that occur in brain tissue in the vicinity of cerebral AVMs that predispose these areas to the formation of edema and hemorrhage after AVM excision.

Animals↗
PubMed1995

Chronic cerebral hypoperfusion in the rat: temporal delineation of effects and the in vitro ischemic threshold.

Acute reductions in cerebral blood flow of up to 50% do not affect neuronal function although it has been shown that reductions of a similar magnitude maintained for 26 weeks do induce neuronal changes. In vitro rat hippocampal LTP was evaluated after 10 weeks of cerebral hypoperfusion. An assessment was also made of the possible 'robustness' of hippocampal CA1 pyramidal neurons to combined in vitro hypoxic/ischemic insults because of previously shown differences in hemodynamic autoregulatory curves. No differences were found between controlled and chronically hypoperfused animals in either study. It is concluded that the changes in neuronal function induced by reductions in cerebral blood flow of less than 50% take time to develop and do not induce adaptive changes in affected neurons. The mechanism for these changes remains to be elucidated.

Animals↗
PubMed1994

Chronic cerebral hypoperfusion and impaired neuronal function in rats.

BACKGROUND AND PURPOSE: Studies in acute cerebral ischemia have shown that reductions in cerebral blood flow of up to 50% do not lead to infarction or alterations in neuronal electric activity. Little is known about the effects of chronic reductions in cerebral blood flow. The purpose of this study was to evaluate neuronal electrophysiological function in brain that had been subjected to a chronic reduction of cerebral blood flow of less than 50%. Based on existing knowledge of thresholds of cerebral ischemia, neuronal electrophysiological function should be unaffected by hypoperfusion of this magnitude. METHODS: An arteriovenous fistula model in the rat was used to induce chronic cerebral hypoperfusion with reductions of cerebral blood flow of 25% to 50% as measured previously by 14C-labeled autoradiography. Using in vitro electrophysiological brain slice techniques, long-term potentiation in hippocampal CA1 neurons was examined extracellularly after 6 months of chronic noninfarctional cerebral hypoperfusion. Brains were also examined histologically at this time for evidence of cerebral infarction. RESULTS: There was no evidence of cerebral infarction. Long-term potentiation was produced in 9 of 12 control animals and only 2 of 8 hypoperfused animals. This difference was significant (P < .05) and demonstrated that long-term potentiation was impaired in animals with chronic hypoperfusion. CONCLUSIONS: Noninfarctional reductions in cerebral blood flow of up to 50% do impair neuronal function in chronic cerebral ischemia, a result quite distinct from that seen in acute ischemia. The threshold for neuronal dysfunction in chronic cerebral hypoperfusion is lower than that found in acute cerebral ischemia, suggesting that duration as well as severity of ischemic insult determines cellular viability. Chronic hypoperfusion may lead to a noninfarctional state with impaired neuronal function, a category of chronic cerebral ischemia not previously identified.

Action Potentials↗
PubMed1994

Syndactyly and intracranial arteriovenous malformation: case report.

A case of a 14-year-old boy with syndactyly of all limbs and intracranial dural arteriovenous malformation (AVM) is presented. A failure of differentiation of cerebral vessels, possibly at 3 weeks gestational age, is discussed along with several alternative theories relating to the pathogenesis of dural AVMs. The embryogenesis of syndactyly, occurring as an arrest of normal interdigital tissue regression at 5-7 weeks gestational age, is also reviewed. It is postulated that a single common intrauterine environmental insult of vascular origin occurring during the second month of gestation, is the reason for their simultaneous manifestation.

Adolescent↗
PubMed1994

Extracranial-intracranial saphenous vein bypass for carotid or vertebral artery dissections: a report of six cases.

The management of carotid or vertebral artery dissections has generally been either conservative (with anticoagulation) or surgical (by proximal ligation or trapping procedures). However, identification and management of those patients with a high risk of stroke recurrence have been difficult. Six patients with carotid or vertebral artery dissections underwent a total of seven surgical procedures involving intracranial interpositional saphenous vein bypass grafts anastomosed distally beyond the point of dissection with trapping of the intermediate diseased section of the artery. It is suggested that this procedure be used in patients who have bilateral carotid or vertebral artery disease, persistent angiographic abnormalities (particularly aneurysms), or recurring ischemic events while undergoing anticoagulation therapy, or in whom anticoagulation is undesirable. This procedure has benefits over current surgical options because of the maintenance of high flow, the avoidance of abnormal watershed areas of flow, and the elimination of the risk of emboli. The procedure is compared to previous techniques of extracranial-intracranial bypass.

Adult↗
PubMed1992

Controversies in the management of brainstem cavernous angioma: report of two cases.

Two cases of cavernous angioma involving the medulla oblongata are presented. Both cases underwent surgical excision with excellent outcome. The use of surgery via craniectomy is contrasted with stereotactic radiosurgery in light of the known natural history of the lesions. As a result, it is suggested that surgical excision provides immediate protection from the risks of recurrent haemorrhage, establishes a tissue diagnosis, allows complete removal at the primary intervention, avoids complications of radiation-induced damage and is performed more easily in these vascular anomalies due to the presence of a capsule with surrounding gliotic tissue. Additionally, it is implied that the natural history of lesions in this region is still unclear. For these reasons, it is suggested that surgical excision should be the primary therapeutic intervention for cavernous angiomata that involve the brainstem.

Adult↗
PubMed1991

Pineal teratoma and its relationship to intracerebral development: case report.

A teratoma of the pineal region in a 20-year-old Australian Aborigine is presented in which an unusual location of the straight sinus and tentorium cerebelli suggests that the tumor arose before 4 months of gestation. In addition, this case provides some insight into the development of the falx cerebri, which might arise from the midline fusion of the left and right tentoria cerebelli caused by the dorsal development of the telencephalon.

Adult↗