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Biomedical subjects

F F Marciano

Publications and source records attributed to F F Marciano.

At least 19 recordsLinked to original sources
PubMed1998

Long-term graft patency rates and clinical outcomes after revascularization for symptomatic traumatic internal carotid artery dissection.

INTRODUCTION: Surgical management of traumatic internal carotid artery (ICA) dissection remains controversial. Therefore, the delayed outcomes and graft patency rates of patients who underwent bypass procedures for symptomatic traumatic ICA dissection were studied. METHODS: Between September 1989 and August 1996, 13 patients (9 male and 4 female patients; mean age, 30.6 yr) underwent 16 revascularization procedures for symptomatic traumatic ICA dissection. The duration of clinical follow-up averaged 47.3 months (range, 12-94 mo) from the date of diagnosis. The duration of radiographic follow-up (catheter or magnetic resonance angiography, duplex Doppler ultrasonography) averaged 24 months (range, 12-60 mo). RESULTS: ICA dissection was caused by blunt (n = 11) or penetrating trauma (n = 2). Associated angiographic abnormalities included seven ipsilateral ICA occlusions, six dissecting aneurysms, two carotid-cavernous fistulae, and six contralateral traumatic ICA dissections. Patients requiring early revascularization (n = 6) underwent bypass procedures an average of 19.2 days after their injuries. Medically managed patients who developed ischemia later were revascularized a mean of 7.8 months after injury. The mean Glasgow Coma Scale score at the time of presentation was 10 (range, scores of 6-15), and the mean Glasgow Coma Scale score before revascularization was 14 (range, scores of 9-15). There were 14 saphenous vein ICA bypasses (8 cervical-to-petrous, 3 cervical-to-middle cerebral artery, 3 petrous-to-supraclinoid) and 2 superficial temporal artery-to-middle cerebral artery bypasses. There was one early postoperative graft occlusion, which responded to surgical thrombectomy. One patient with multiple other traumatic injuries died as a result of a pulmonary embolus 12 months after revascularization. All remaining patients had Glasgow Outcome Scale scores of 5, with patent bypass grafts confirmed during follow-up. CONCLUSION: Revascularization for persistently symptomatic traumatic ICA dissection eliminated ischemia and was associated with excellent long-term outcomes and graft patency rates.

Adolescent↗
PubMed1997

Acute axis fractures. Analysis of management and outcome in 340 consecutive cases.

STUDY DESIGN: Retrospective review of acute axis fractures treated at a tertiary referral center. OBJECTIVE: To determine the optimal treatment of axis fractures based on 340 cases from a single institution. SUMMARY OF BACKGROUND DATA: Axis fractures account for almost 20% of acute cervical spine fractures. However, their management and the clinical criteria predictive of nonoperative failure remain unclear. METHODS: Admission imaging studies and clinical variables were obtained for 340 consecutive axis fracture patients. Fractures were classified as as odontoid Type I, II, or III with dena displacement on admission roentgenograms; hangman's fractures of Francis grade and Effendi type; and miscellaneous fractures. Treatment methods were documented, and outcomes were based on dynamic lateral roentgenograms, clinical examination, or telephone interviews at last follow-up. RESULTS: Follow-up data were available in 92% of cases. Type II odontoid fractures comprised 35% of all axis fractures, were the most difficult to treat, and had the highest nonunion rate (28.4%). Odontoid displacement of 6 mm or more was associated with Type II nonunion (chi-square = 33.74, P < 0.0001). Patients underwent surgical fusion if fracture alignment could not be maintained by an external orthosis, or if they had odontoid fractures with transverse ligament disruption, Type II odontoid fractures with dens displacement of at least 6 mm, or hangman's fractures of severe Francis grade or Effendi type. CONCLUSIONS: Type II odontoid fractures have the highest nonunion rate and were associated with dens displacement of 6 mm or greater. Early surgical fusion is recommended for acute fracture instability despite external immobilization, transverse ligament disruption, Type II odontoid fractures with dens displacement of at least 6 mm on admission, or severe Francis grade or Effendi-type hangman's fractures. Otherwise, nonoperative management is sufficient.

Adolescent↗
PubMed1997

Completely dislocated hangman's fracture with a locked C2-3 facet. Case report.

The authors report a rare case of a hangman's fracture involving complete dislocation of C-2 onto C-3, accompanied by a C2-3 locked facet and asymptomatic bilateral vertebral artery injuries. The patient, a 25-year-old man who sustained a neck injury in an industrial accident, presented with a mild central spinal cord syndrome. His initial lateral cervical radiograph showed complete anterior dislocation of the C-2 body onto C-3, bilateral neural arch fractures, and a unilateral locked facet. The mechanism was likely flexion and compression. The grossly unstable spine and the locked facet were treated by posterior decompression, reduction, and C1-3 fixation. The patient recovered in several days and is without neurological deficit.

Adult↗
PubMed1996

Impact of traumatic subarachnoid hemorrhage on outcome in nonpenetrating head injury. Part II: Relationship to clinical course and outcome variables during acute hospitalization.

Patients with a nonpenetrating head injury and traumatic subarachnoid hemorrhage (tSAH) on admission head computed tomography scan (n = 240) were compared with patients without tSAH matched in terms of admission postresuscitation Glasgow Coma Scale (GCS) values, age, sex, and the presence of one or more types of intracranial mass lesions. Admission Injury Severity Score was higher only in tSAH patients with admission GCS scores between 13 and 15; GCS values at 6, 24, and 48 hours were lower for tSAH patients. Patients with tSAH underwent fewer craniotomies, but more than twice as many tSAH patients had high intracranial pressure at the time of ventriculostomy placement and 6 hours after admission. tSAH patients underwent more chest procedures and their incidence of hypoxia and hypotension was greater. tSAH patients spent more days in intensive care unit, more total days hospitalized, and had worse Glasgow Outcome Scale scores at acute hospital discharge. Fewer tSAH patients were discharged home, and almost 1.5 times as many tSAH patients died during hospitalization. Given a similar overall degree of injury at admission, patients with tSAH associated with a nonpenetrating head injury had a worse outcome than similar patients without tSAH.

Accidents, Traffic↗
PubMed1996

Pharmacological management of spinal cord injury: current status of drugs designed to augment functional recovery of the injured human spinal cord.

Spinal cord injury often results in devastating physical, psychological, and economic disabilities. Research efforts are directed toward providing prognostic outcome data and animal models that parallel the human disorder, thereby elucidating the mechanisms responsible for its dismal clinical prognosis. Investigators continue to search for pharmacological agents that halt the cascade of events that lead to loss of function after cord injury. The scientific and federal regulatory processes by which new drugs are discovered and implemented clinically permit clinicians to evaluate the potential benefits of any new agent, and provide an estimate of the duration required for promising new agents to be made clinically available. Understanding these processes makes the task of classifying the availability status of new drugs much simpler, allowing rational dissemination of realistic information to patients and their families frequently made desperate for viable alternatives to the prospect of permanent paralysis. In this review, we describe the scientific and regulatory processes necessary for the clinical introduction of new drugs using spinal cord injury as an example. A classification scheme based on current Food and Drug Administration regulations is presented that provides drug availability status at a glance. It is hoped that such an organizational scheme will be of practical benefit to clinicians involved in the management of spinal cord-injured patients.

Animals↗
PubMed1995

Is fusion indicated for lumbar spinal disorders?

STUDY DESIGN: A review of relevant literature and clinical experience with lumbar spinal disorder. OBJECTIVES: To discuss the indications for fusions and lumbar spinal disorders. SUMMARY OF BACKGROUND DATA: Fusion of the lumbar spine is performed frequently, but indications have not been defined clearly. The literature and the authors' experience with these indications are reviewed. METHODS: A comprehensive review of the literature and the authors' clinical experience with lumbar spinal instability was critically examined. Specifically, the role of fusion, with or without instrumentation, versus decompression alone was assessed. From this, a set of definitive and relative indications for spinal arthrodesis in a variety of disorders of the lumbar spine could be established. RESULTS: Once the diagnosis of lumbar spinal instability is established, fusion is indicated. However, fusion without spinal instrumentation has a high pseudarthrosis rate and poorer patient outcome. This spinal instrumentation should be used as an adjunct when considering spinal arthrodesis. CONCLUSIONS: Definitive indications for spinal fusions are trauma, tumor and infection, iatrogenic instability, or ischemic spondylolisthesis. Relative indications for fusions are degenerative spondylolisthesis, abnormal movement visualized on dynamic films with appropriate pain or neurologic deficit, and mechanical pain. Lumbar fusion is rarely indicated for routine discectomy, abnormal results of radiography without appropriate clinical findings, or stable spinal stenosis.

Humans↗
PubMed1995

Novel heuristics of functional neural networks: implications for future strategies in functional neurosurgery.

A hypothesis is proposed that (a) the skeletomotor basal ganglia-thalamocortical loop functions as a model of the behavior of the body and the environment, and that (b) dopaminergic neurons of the substantia nigra pars compacta comprise the substrates of an error distribution system projecting to the striatum. This error signal initiates the learning process in the basal ganglia - learning starts with increasing intensity of the error signal and is complete when the signal is minimized. Parkinson's disease (PD) may be considered as a disruption of learning processes in the basal ganglia that results from progressive degeneration of the substrate that is the error distribution system for this functional motor loop. Numerous clinical and experimental observations obtained from functional procedures for PD that show identical clinical effects in alleviating parkinsonian symptoms, e.g. thermocoagulative lesions and chronic stimulation, can be explained through the use of this conceptual theory of basal ganglia function. Because any controlling neural network must possess a model of the behavior of its controlled object, the heuristics outlined in this theory are broadly applicable for explaining the function of the nervous system, as well as being useful for planning surgical procedures and future strategies in functional neurosurgery.

Basal Ganglia↗
PubMed1995

Anterior communicating artery aneurysm paraparesis syndrome: clinical manifestations and pathologic correlates.

OBJECTIVE: Clinicopathologic evaluation of patients with lower extremity paraparesis/-plegia following rupture and repair of anterior communicating artery (ACoA) aneurysms. DESIGN: Institution-based retrospective review. SETTING: A tertiary neurologic referral center. PATIENTS, PARTICIPANTS: Seven of 101 patients with subarachnoid hemorrhage from ruptured ACoA aneurysms treated between January 1987 and December 1992. MAIN OUTCOME MEASURES: Neurologic status at latest follow-up examination. RESULTS: All patients presented with severe hemorrhage, poor clinical grade, and intracranial hypertension. Motor deficits developed within 7 days of aneurysm rupture and persisted for a mean duration of 39 days. Angiographic evidence of vasospasm in the anterior cerebral artery (ACA) distribution was documented in all cases, and paraparesis persisted beyond the angiographic resolution of vasospasm. All patients had evidence of frontal lobe dysfunction throughout their postoperative courses, and deep venous thrombosis and pulmonary emboli were common causes of morbidity and mortality. Autopsy data supported regional microvascular ischemia within the ACA distribution as the etiology of these motor deficits. CONCLUSIONS: The combination of vasospasm in the ACA distribution and lower extremity weakness associated with cognitive and affective impairment that resolves with time is common in patients with ACoA aneurysms. We propose that this constellation of clinical, radiographic, and pathologic findings be referred to as the "ACoA aneurysm paraparesis syndrome."

Aged↗
PubMed1995

Impact of traumatic subarachnoid hemorrhage on outcome in nonpenetrating head injury. Part I: A proposed computerized tomography grading scale.

The presence of traumatic subarachnoid hemorrhage (tSAH) on admission computerized tomography (CT) scans obtained from patients suffering from severe, nonpenetrating head injury has been shown to be associated with a worse outcome than the injury alone would warrant. However, no previous study has provided a simple means of relating the amount of tSAH, its location, or other abnormal findings on initial head CT scans to outcome in patients with non-penetrating head injury. In this study, admission head CT scans from 252 patients with tSAH, treated at a single institution, were reviewed to ascertain thickness of the tSAH; its location; evidence of mass lesion(s); shift of midline structures (< or = 5 mm vs. > 5 mm); basal cistern effacement; and cortical sulcal effacement. The CT scans were then organized into Grades 1 to 4 with 1 indicating thin tSAH (< or = 5 mm); 2, thick tSAH (> 5 mm); 3, thin tSAH with mass lesion(s); and 4, thick tSAH with mass lesion(s). A stepwise regression analysis of CT features ranked them in descending order of contribution to Glasgow Outcome Scale (GOS) scores at the time of discharge from acute hospitalization as follows: basal cistern effacement, thickness of tSAH, cortical sulcal effacement, presence of mass lesion(s), and location of tSAH. A shift of midline structures was not found to be a significant variable. Further analysis comparing CT grades and admission postresuscitation Glasgow Coma Scale (GCS) scores was highly significant. Patients with lower CT grades had better admission GCS values and discharge GOS scores than those with higher CT grades. From their experience, the authors conclude that their CT grading scale is simple and reliable and relates significantly to outcome at the time of discharge from acute hospitalization.

Adolescent↗
PubMed1994

Transverse atlantal ligament disruption associated with odontoid fractures.

OBJECTIVES: The authors evaluated transverse atlantal ligament integrity in patients with fractures of the odontoid process of the axis. SUMMARY OF BACKGROUND DATA: Injuries of the transverse atlantal ligament can result in atlantoaxial instability after fractures of the atlas or axis, even if osseous healing occurs. METHODS: The clinical histories and follow-up examinations and radiographic data of 30 patients with odontoid fractures were reviewed, using a combination of magnetic resonance (MR) imaging, thin-cut computed tomography (CT), and plain radiographs to evaluate osseous and ligamentous injuries. RESULTS AND CONCLUSIONS: Osteoperiosteal ligamentous avulsion injuries were identified on MR imaging in three patients and were associated with acute and delayed instability and nonunion. The combination of MR imaging, CT, and plain radiographs is useful in evaluating unstable odontoid fractures to facilitate rational treatment planning. Odontoid fractures with transverse ligament injuries should be considered for early surgical stabilization because this combination of injuries is unlikely to heal nonoperatively. Anterior odontoid screw fixation should be avoided when the ligament is injured.

Adolescent↗
PubMed1994

Cardiopulmonary bypass, hypothermic circulatory arrest and barbiturate cerebral protection for the treatment of giant vertebrobasilar aneurysms in children.

Intracranial aneurysms in the pediatric population are rare lesions with a significant proportion occurring as giant aneurysms involving the vertebrobasilar system. The complex anatomy of these lesions frequently creates an extremely difficult management dilemma. We present two patients, a 9-year-old and a 13-year-old, with giant fusiform vertebrobasilar aneurysms, to illustrate the utility of cardiopulmonary bypass, hypothermic circulatory arrest and barbiturate cerebral protection for successful surgical treatment of these complex intracranial vascular lesions in children.

Adolescent↗
PubMed1990

Perineuronal glial responses after axotomy of central and peripheral axons. A comparison.

In each of 6 mature rats, unilateral rubrospinal tractotomy and hypoglossal neurectomy were done at one operative sitting. Paired operated animals were killed by formaldehyde and ethanol-acetic acid perfusion 3, 14 and 28 days later. One pair of unoperated control rats was perfused also. All rats were injected i.p. with [3H]thymidine 24 h before death. Immunohistochemical methods were applied to paraffin sections to visualize glial fibrillary acidic protein (GFAP) and transferrin in astrocytes and oligodendroglia, respectively. Microglia were demonstrated by both lectin-binding and histoautoradiographic methods. Neuroglia and nerve cells were counted in hematoxylin-eosin and azure B stains. Cell areas and the RNA concentration of hypoglossal neurons were determined by the Zeiss Image Scan System. Three days after hypoglossal neurectomy, increased astroglial staining (GFAP) and microglial hyperplasia (radiolabeled nuclei) were evident in the ipsilateral hypoglossal nucleus (HN). Microglial hyperplasia waned rapidly after 3 days and microglial numbers decreased. However, astroglial hypertrophy, demonstrable by GFAP staining, persisted 4 weeks postoperatively when astroglial processes were concentrated in a perineuronal position. Oligodendroglia were unaltered. In contrast to the HN, the axotomized red nucleus (RN) contained few radiolabeled microglia while a slight increase in GFAP-positive astroglial processes was seen only in animals killed 28 days postoperatively. Again, oligodendroglia were unchanged. In neither HN nor RN did axotomy cause nerve cell death. Although axotomized rubral neurons atrophy and become depleted of RNA, no statistically significant changes in somal size and RNA content of axotomized hypoglossal neurons occurred. The apparent absence of a neuroglial response of putatively supportive nature in the environs of axotomized rubral neurons may relate to their failure to regenerate. The neuroglial response likely is originated by the axotomized neuron and its absence may be an innate defect in the reaction of intrinsic neurons to axonic severance. Somas of axotomized peripherally projecting nerve cells appear to have the capacity to summon a neuroglial response.

Animals↗
PubMed1990

Axonal regrowth in the amyelinated optic nerve of the myelin-deficient rat: ultrastructural observations and effects of ganglioside administration.

It has been postulated that myelin degradation products may inhibit regrowth of mammalian central axons and that central nervous system (CNS) myelin and oligodendrocytes may constitute a "nonpermissive substrate" for axonal growth. To address these issues, we utilized an X-linked rat mutant, myelin-deficient or md. In the optic nerve of this mutant, 40 days and more postnatally, normal myelin is absent and oligodendrocytes are few (Dentinger et al. Brain Res. 344:255-266, 1985). Twenty-eight days before sacrifice, we operated on four groups of 50-day-old md rats and age-matched normal littermates according to the following protocols: 1) unilateral intraorbital optic nerve crush; 2) beginning within 1 hour of nerve crush, daily intraperitoneal injection of GM1 ganglioside (20 mg/kg) dissolved in phosphate-buffered saline (PBS); 3) daily intraperitoneal injection of PBS alone, also begun within 1 hour of nerve crush; 4) severance of the optic nerve immediately behind the papilla 16 or 21 days after the primary crush lesions. Additionally, normal and md rats were killed 4 and 14 days after unilateral optic nerve injury. Nerves of unoperated md rats and their normal littermates were also processed. In the operated animals that did not receive GM1, ultrastructural analysis 4, 14, and 28 days after lesioning revealed that md optic nerves contained significantly greater numbers of regenerating axons, including growth cones and varicosities, than nerves of normal rats. Notably, 28 days postoperatively, (group 1), regenerating axons were still abundant in md nerve, whereas, in nerves of normally myelinated littermates, axonal numbers were diminished markedly. Regenerating optic axons of both md and normally myelinated rats were oriented by linear astrocytic arrays and often were enclosed by astrocytic cytoplasm. In normal littermates, GM1 administration (group 2) induced a significant increase in the number of axons within the operative lesion. Paradoxically, GM1 inhibited the ordinarily robust regeneration of md axons. PBS-injected md and normal rats (group 3) showed no significant differences from noninjected, operated animals. Severance of the nerve at the papilla (group 4) 7-12 days before sacrifice confirmed the origination of axonal regrowth by retinal ganglion cells. The data provide in vivo support for a role of myelin breakdown products or the secretory products of oligodendroglia in the inhibition of regenerative axonal sprouting within mammalian CNS.

Animals↗
PubMed1989

Fetal hypothalamic transplants promote survival and functional regeneration of axotomized adult supraoptic magnocellular neurons.

This study investigated the mechanisms by which fetal hypothalamic transplants promote functional recovery in neurohypophysectomized rats. Seven days after neurohypophysectomy (resulting in urine osmolalities of about 800 mOsm), young adult male Long-Evans rats received either fetal hypothalamic grafts (n = 10) or sham transplants (n = 7). Recovery from the lesioned-induced diabetes insipidus was monitored for 6 months and then the transplant sites were evaluated by immunocytochemistry. Surviving host supraoptic magnocellular neurons and neurophysin-positive grafted neurons were counted and their formation of neurohemal contacts evaluated by retrograde transport of systemically injected horseradish peroxidase (HRP). There were significantly more surviving supraoptic magnocellular neurons in neurohypophysectomized animals with median eminence-placed grafts (2236 +/- 261 neurons/animal) than in animals with ectopic tissue grafts (895 +/- 142 neurons/animal) or sham implants (1052 +/- 92 neurons/animal). Almost all surviving host magnocellular neurons were labeled with retrogradely transported HRP while virtually none of the grafted neurophysin positive cells showed evidence of HRP uptake. The degree of functional recovery was directly correlated with the increased survival of host neurons. By 8 weeks post-transplantation, animals with median eminence-placed grafts had recovered from their diabetes insipidus and could concentrate their urine to within normal limits (2,120 +/- 110 mOsm). This recovery was stable for the remainder of the 6 month test period. In contrast, animals with ectopic grafts and sham transplants had permanent deficits in fluid regulation. Our results provide evidence for the long-term capacity of fetal neural tissue implants to rescue host neurons from the cell death that typically occurs in the mature central nervous system after axotomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Telencephalic cholinergic system of the New World monkey (Cebus apella): morphological and cytoarchitectonic assessment and analysis of the projection to the amygdala.

While the cholinergic projection from the nucleus basalis to the cortical mantle has received considerable attention, a similar projection to the magnocellular basal nucleus of the amygdala has not been studied in such detail. The present study analyzed the cholinergic basal forebrain projection to the amygdala in the Cebus apella monkey by using combined tract-tracing and immunocytochemical techniques. As a foundation for this assessment, the morphological and cytoarchitectonic organization of the cholinergic telencephalic system of the New World C. apella monkey was examined by using choline acetyltransferase (ChAT) immunocytochemistry. Although there were minor differences, the telencephalic cholinergic system of Cebus monkeys is similar to that seen in Old World nonhuman primates. ChAT-immunoreactive neurons were observed throughout the Ch1-4 regions of the basal forebrain, with subdivisions of the Ch4 region similar to those previously described (Mesulam et al., '83a). Most cholinergic neurons were hyperchromic and magnocellular; however, some neurons were parvicellular. Like most species, cholinergic neurons were also observed throughout the striatum. However, unlike in rodents, cholinergic perikarya were not observed within the cortex or hippocampus. To analyze the cholinergic fiber projections from the basal forebrain to the amygdala, monkeys received an intraamygdaloid injection of the retrograde tracer horseradish peroxidase conjugated to wheat germ agglutinin. Retrogradely labeled neurons that colocalized ChAT or acetylcholinesterase (AChE) were found predominantly in the anterolateral portion of the CH4 region. Fewer double-labeled neurons were found in the anteromedial and intermediate portion of CH4 and in the CH3 region. Neurons that exhibited retrograde labeling were only occasionally discerned in the posterior portions of the CH4 region, in the medullary laminae of the globus pallidus, or lodged within the internal capsule. These data are discussed in terms of the putative role this cholinergic input might play in cognitive processing in primates.

Acetylcholinesterase↗