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Biomedical subjects

W H Pilcher

Publications and source records attributed to W H Pilcher.

At least 19 recordsLinked to original sources
PubMed2004

AMPA receptor alterations precede mossy fiber sprouting in young children with temporal lobe epilepsy.

Following neurological injury early in life numerous events, including excitotoxicity, neural degeneration, gliosis, neosynaptogenesis, and circuitry reorganization, may alone or in concert contribute to hyperexcitability and recurrent seizures in temporal lobe epilepsy. Our studies provide new evidence regarding the temporal sequence of key elements of hippocampal reorganization, mossy fiber sprouting and glutamate receptor subunit up-regulation, in a subset of young temporal lobe epileptic patients. Without evidence of mossy fiber sprouting, the youngest age group (3-10 years old) of mesial temporal lobe epileptic patients demonstrated enhanced glutamate receptor subunit profiles, suggesting that the dendritic change precedes axonal sprouting. However, sclerotic hippocampal specimens from epileptic patients ages 12-15 years old had the characteristic features of glutamate receptor up-regulation and mossy fiber sprouting first identified in the adult, indicating that reconstructed circuits appear early in the course of the disease. Non-sclerotic hippocampal specimens from lesion associated temporal lobe epileptic patients of all age groups showed minimal cell loss, sparse staining of glutamate receptor subunits in the dentate gyrus, and little or no mossy fiber sprouting. These compelling findings suggest a progressive sequence of events in the reorganization of the dentate gyrus of sclerotic hippocampal specimens. We suggest that cell loss and up-regulation of glutamate receptor subunits appear early in temporal lobe epilepsy and contribute to the synaptic plasticity that may facilitate the subsequent sprouting of mossy fiber collaterals which compound an already precipitous state of decline. The combination of pre-synaptic and post-synaptic changes serves as a potential substrate for hyperexcitability.

Adolescent↗
PubMed1999

Fibro-osseous lesions of the central nervous system: report of four cases and literature review.

Fibro-osseous lesions, also reported as calcifying pseudoneoplasms of the neural axis, are uncommon lesions of the CNS. We report four additional cases: two extraaxial and two intraaxial, in patients ages 33, 47, 49, and 59 years at presentation. Fibro-osseous lesions involving the CNS demonstrate variable proportions of fibrous stroma, bone, palisading spindle to epithelioid to multinucleated cells in association with a highly distinctive, perhaps pathognomonic, chondromyxoid-like matrix often distributed in a nodular pattern. This histopathologically distinctive lesion can be seen in many regions of the neuraxis, often with a dural association, and most commonly along the vertebral column. It appears to be a slow-growing lesion and, with wide excision, the prognosis is excellent. The etiology remains unclear, but the preponderance of data favors a reactive rather than neoplastic process. If this putative pseudotumor is not recognized histopathologically, a neoplastic or infectious differential might result in inappropriate investigations and potentially harmful therapies.

Adult↗
PubMed1998

Malignant ependymomas in a patient with Turcot's syndrome: case report and management guidelines.

BACKGROUND: Turcot's Syndrome is the association of multiple adenomatous polyps of the colon with a primary tumor of the central nervous system. We present the first reported case of Turcot's Syndrome in a patient with malignant ependymomas. Recent advances in the elucidation of the genetic basis for the hereditary forms of colon cancer have provided a clearer understanding of the etiology of Turcot's Syndrome. This new information is relevant to the neurosurgical community and provides updated guidelines in the diagnosis and management of patients with this complex disease process. RESULTS: Turcot's Syndrome is related to two distinct genetic errors. The first involves a germ-line mutation in the adenomatous polyposis coli (APC) gene, which is postulated to act as a tumor suppressor gene. The second is a germ-line defect in one of a group of genes responsible for DNA nucleotide mismatch repair. CONCLUSION: The elucidation of the gene defects responsible for the hereditary forms of colon cancer has provided a clearer understanding of the molecular basis of Turcot's Syndrome. Patients with hereditary forms of colon cancer and neurologic symptoms require immediate and thorough investigation because of their significantly increased risk of developing CNS tumors. Previously healthy patients diagnosed with a CNS tumor with a family history of adenomatous polyposis coli should undergo screening and surveillance colonoscopy as the CNS lesion may precede colonic symptoms. CNS screening guidelines for asymptomatic patients with adenomatous polyposis coli requires further risk analysis studies. All patients diagnosed with Turcot's Syndrome should be tested for the gene defect, including the CNS tumor tissue to provide further data on the genetic relationship between Turcot's Syndrome and the hereditary forms of colon cancer.

Adenomatous Polyposis Coli↗
PubMed1996

Distribution of AMPA receptor subunits in the hippocampal formation of temporal lobe epilepsy patients.

The immunocytochemical distribution of the AMPA-selective receptor subunits GluR1 and GluR2/3 were mapped in the human hippocampal formation obtained from surgery for medically intractable temporal lobe epilepsy. GluR2/3 immunoreactivity was detected in all principal cell types of the hippocampal formation, including hilar neurons, granule cells of the dentate gyrus, and pyramidal cells of the cornu ammonis fields and subiculum. GluR2/3 immunostaining typically filled the cell bodies and processes of neurons. A comparison of GluR2/3 immunoreactivity in a sclerotic specimen versus a non-sclerotic specimen demonstrated a profound loss of staining, specifically in the areas where neuronal dropout was occurring, including CA1, CA3 and the hilus. An analysis of GluR1 immunoreactivity in non-sclerotic specimens revealed that it was predominantly localized to cellular processes throughout the cornu ammonis fields, with a sparse staining of the dentate gyrus outer molecular layer and little to no staining of the dentate gyrus inner molecular layer. Similar to the GluR2/3-immunostained patterns, GluR1 immunoreactivity was lost in the cornu ammonis fields of sclerotic hippocampal specimens, corresponding to patterns of neuronal dropout. Our most compelling finding was a unique extensive pattern of GluR1 and Glu2/3 immunoreactivity throughout the molecular layers of the dentate gyrus of severely compromised hippocampi. The altered staining of GluR1 and GluR2/3 complements some of the patterns of axonal sprouting already described for the dentate gyrus, with a conjecture that their anatomy and distribution pattern underlies to some degree the reorganization of the sclerotic hippocampus. A combination of enhanced glutamatergic transmission and changes in neuropeptides that modulate hippocampal circuitry could greatly affect the degree of excitability in the hippocampal formation. The alterations of GluR1 and GluR2/3 immunoreactivity in the dentate gyrus add another component to the concept of reorganization in the epileptic sclerotic hippocampus.

Adolescent↗
PubMed1996

Adrenocorticotropic hormone immunoreactivity in the hippocampal formation of temporal lobe epilepsy patients.

PURPOSE: We wished to identify immunocytochemically the distribution of proopiomelanocortin-related peptides in the hippocampal formation of patients with epilepsy. METHODS: Surgical hippocampal specimens from temporal lobe epilepsy (TLE) patients and autopsy control tissue were examined immunocytochemically for ACTH, alpha-melanocyte-stimulating hormone (alpha-MSH) and beta-endorphin. RESULTS: There was a dense distribution of ACTH-immunoreactive neurons in the hippocampal formation of patients with mesial TLE syndrome (MTLE). These hippocampal specimens showed significant cell loss. ACTH-positive neurons were most prominent in the subiculum, with scattered ACTH-immunoreactive neuronal elements distributed in the cornu ammonis fields and hilus. Light ACTH immunoreactivity was detected in the tumor-related epileptic hippocampal specimens, which showed minimal cell loss. Although autopsy control tissue from the hypothalamus showed intense ACTH staining patterns in cells and fibers, there was little or no ACTH immunoreactivity in the autopsy hippocampal tissue. The expression of ACTH immunoreactive elements was correlated with patterns of cell loss. No alpha-MSH- or beta-endorphin-immunoreactive neurons were detected in any of the hippocampal specimens. CONCLUSIONS: ACTH has anticonvulsant properties, and its novel expression in the glutamatergic subicular neurons, which provide the main outflow of the hippocampal formation, may represent an attempt by the damaged hippocampal circuit to restore the balance of excitatory/inhibitory neurotransmission in TLE.

Adrenocorticotropic Hormone↗
PubMed1994

Nuclear factor-kappa B in rat brain: enhanced DNA-binding activity following convulsant-induced seizures.

The DNA-binding protein nuclear factor-kappa B (NF-kappa B) is a pleiotropic transcription factor which regulates the transcription of specific target genes such as cytokines. The existence of NF-kappa B has not been reported in brain tissue. This is the first report demonstrating the expression of NF-kappa B in the rat brain. After pentylene tetrazole (s.c.)-induced clonic-tonic seizures at an LD50 dose of 85 mg/kg, we have shown a gradual increase in NF-kappa B expression reaching a maximum at 24 h, a decrease at 48 h and again increased at 96 and 120 h. A similar time-dependent pattern was observed for the NF-kappa B subunit p50 expression. The NF-kappa B subunit p65 was not expressed at all. These data suggest a possible underlying mechanism of signal transduction and transcriptional regulation of late-response genes after perturbations in the CNS milieu.

Animals↗
PubMed1993

Late solitary cerebral metastases from renal cell carcinoma: report of two cases.

We report two cases of solitary cerebral metastases from renal cell carcinoma 15 and 18 years after nephrectomy. In a review of the literature, only two cases of solitary brain metastasis from renal cell carcinoma with latency periods greater than 10 years have been documented. Our two cases represent the longest latency periods reported between nephrectomy and detection of a solitary cerebral metastasis. Histologic examination and immunohistochemical profile of the primary renal tumors and metastatic cranial tumors showed identical morphology and immunophenotype.

Aged↗
PubMed1993

Intraoperative electrocorticography during tumor resection: impact on seizure outcome in patients with gangliogliomas.

Gangliogliomas are indolent neoplasms that are often associated with long-standing intractable seizures. The seizure-free outcome following ganglioglioma resection alone (or "lesionectomy") has been generally favorable, ranging in most series from 50% to 65%. Thus, the value of resection of epileptogenic cortex in addition to tumor with regard to seizure outcome has been the subject of controversy. The authors describe a series of 12 patients with frontal or temporal lobe gangliogliomas associated with long-standing intractable seizures. In these patients, intraoperative electrocorticography was used to guide the resection of epileptogenic cortex along with tumor. Functional brain mapping, interictal and ictal monitoring of seizures, as well as thorough neuropsychological assessments were performed prior to resection in all cases. Outcome with regard to seizures, tumor recurrence, and neurological deficits was assessed with a mean follow-up period of 3.1 years. There was universal freedom from seizures postoperatively in 11 patients in whom complete or near-complete resection of epileptogenic cortex was achieved. In one patient in whom complete tumor resection and subtotal removal of epileptogenic cortex was achieved, a 95% reduction in seizure frequency was identified. No tumor recurrence or neurological deficits were observed. In a subset of four patients, neuropsychological and cognitive function were evaluated pre- and postoperatively. In these four, a clear trend toward improvement was noted in most functions. Thus, resection of epileptogenic cortex along with tumor may improve seizure outcome in selected patients with tumor-associated epilepsy without engendering identifiable neurological or cognitive deficits attributable to the incremental resection.

Adolescent↗
PubMed1993

Complications of epilepsy surgery.

In the treatment of patients with medically intractable epilepsy, neurosurgeons are involved in the application of invasive monitoring procedures and definitive surgical therapies, including resective and disconnection surgery. Each alternative intervention carries with it a unique set of potential adverse outcomes or complications, which provides the principal focus of this article.

Brain↗
PubMed1992

Acute subdural hematoma after aneurysmal rupture; evacuation with aneurysmal clipping after emergent infusion computed tomography: case report.

A 74-year-old woman sought treatment after an initial subarachnoid hemorrhage verified on computed tomographic scan with no focal neurological deficit. Shortly after admission, she sustained a second subarachnoid hemorrhage with acute neurological decompensation. A repeat computed tomographic scan revealed increased blood along the right medial temporal region, as well as in the interhemispheric fissure and bilateral sylvian cisterns. Also evident was a right hemispheric acute subdural hematoma. The patient's rapidly deteriorating neurological status precluded a cerebral angiogram; therefore, a double-dose infusion computed tomographic scan was performed. This revealed a cerebral artery aneurysm adjacent to the right medial temporal hematoma. She was taken to the operating room on the basis of this study. After evacuation of the right hemispheric subdural hematoma and clipping of the right posterior communicating artery aneurysm, the patient made a rapid, full neurological recovery.

Aged↗
PubMed1992

Ultrasonographic and electrophysiological adjuncts to surgery within the brain stem: technical note.

The surgical approach to intrinsic lesions within the brain stem is undertaken by the surgeon knowing the potential for significant operative morbidity. We report the use of real-time intraoperative ultrasound and electrophysiological mapping techniques to aid in the localization and resection of an intrinsic brain-stem tumor in a child. These techniques permitted an aggressive surgical approach without encountering adverse postoperative neurological sequelae.

Brain Mapping↗
PubMed1991

Resection of intrinsic tumors from nondominant face motor cortex using stimulation mapping: report of two cases.

We report two right-handed patients who underwent resection of intrinsic glial tumors from the nondominant hemisphere, face motor cortex. Both patients underwent preoperative assessment with computed tomography and magnetic resonance imaging localizing the tumor in the inferior region of the Rolandic cortex. With the patients under general anesthesia and without muscular paralysis, the tumor volume was determined by intraoperative ultrasound and resective surgery accomplished with the aid of cortical and subcortical stimulation mapping techniques. Radical resection of the tumor from the face motor cortex was achieved in both patients. A transient contralateral facial weakness and apraxia were noted in each patient, and this resolved within 6 to 8 weeks following surgery. Removal of intrinsic tumors involving the nondominant face motor cortex may be safely achieved using brain mapping techniques to localize inferior Rolandic cortex and avoid resection of the hand motor cortex and descending subcortical motor pathways. Permanent disability will be prevented due to the bilateral representation of face motor function at the neocortical level. However, due to language localization in cortical zones contiguous with the dominant hemisphere, face motor cortex, we do not recommend resection of this region.

Adolescent↗