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Biomedical subjects

Devin K Binder

Publications and source records attributed to Devin K Binder.

At least 19 recordsLinked to original sources
PubMed2006

Transsylvian functional hemispherectomy.

OBJECTIVE: To describe the technique of transsylvian-transventricular functional hemispherectomy developed at our institution. METHODS: We review appropriate patient selection and evaluation, timing of surgery, selection of surgical approach, preoperative preparation, details of operative procedure, and postoperative management. CONCLUSIONS: The transsylvian "keyhole" functional hemispherectomy technique involves a smaller craniotomy than other functional hemispherectomy techniques and consists of transsylvian exposure, resection of mesial temporal structures, transventricular frontobasal disconnection, callosotomy, and occipitoparietal disconnection. The key advantages of this approach compared to the Rasmussen's "classic" functional hemispherectomy are smaller exposure, shorter operative time, and lower blood loss. The efficacy of functional hemispherectomy procedures in achieving seizure freedom appears to be at least as good compared to resective procedures. The long-term complication rate will require longer follow-up times.

Cerebral Cortex↗
PubMed2006

Increased seizure duration and slowed potassium kinetics in mice lacking aquaporin-4 water channels.

The glial water channel aquaporin-4 (AQP4) has been hypothesized to modulate water and potassium fluxes associated with neuronal activity. In this study, we examined the seizure phenotype of AQP4 -/- mice using in vivo electrical stimulation and electroencephalographic (EEG) recording. AQP4 -/- mice were found to have dramatically prolonged stimulation-evoked seizures after hippocampal stimulation compared to wild-type controls (33 +/- 2 s vs. 13 +/- 2 s). In addition, AQP4 -/- mice were found to have a higher seizure threshold (167 +/- 17 microA vs. 114 +/- 10 microA). To assess a potential effect of AQP4 on potassium kinetics, we used in vivo recording with potassium-sensitive microelectrodes after direct cortical stimulation. Although there was no significant difference in baseline or peak [K(+)](o), the rise time to peak [K(+)](o) (t(1/2), 2.3 +/- 0.5 s) as well as the recovery to baseline [K(+)](o) (t(1/2), 15.6 +/- 1.5 s) were slowed in AQP4 -/- mice compared to WT mice (t(1/2), 0.5 +/- 0.1 and 6.6 +/- 0.7 s, respectively). These results implicate AQP4 in the expression and termination of seizure activity and support the hypothesis that AQP4 is coupled to potassium homeostasis in vivo.

Action Potentials↗
PubMed2006

Three distinct roles of aquaporin-4 in brain function revealed by knockout mice.

Aquaporin-4 (AQP4) is expressed in astrocytes throughout the central nervous system, particularly at the blood-brain and brain-cerebrospinal fluid barriers. Phenotype analysis of transgenic mice lacking AQP4 has provided compelling evidence for involvement of AQP4 in cerebral water balance, astrocyte migration, and neural signal transduction. AQP4-null mice have reduced brain swelling and improved neurological outcome in models of (cellular) cytotoxic cerebral edema including water intoxication, focal cerebral ischemia, and bacterial meningitis. However, brain swelling and clinical outcome are worse in AQP4-null mice in models of vasogenic (fluid leak) edema including cortical freeze-injury, brain tumor, brain abscess and hydrocephalus, probably due to impaired AQP4-dependent brain water clearance. AQP4 deficiency or knock-down slows astrocyte migration in response to a chemotactic stimulus in vitro, and AQP4 deletion impairs glial scar progression following injury in vivo. AQP4-null mice also manifest reduced sound- and light-evoked potentials, and increased threshold and prolonged duration of induced seizures. Impaired K+ reuptake by astrocytes in AQP4 deficiency may account for the neural signal transduction phenotype. Based on these findings, we propose modulation of AQP4 expression or function as a novel therapeutic strategy for a variety of cerebral disorders including stroke, tumor, infection, hydrocephalus, epilepsy, and traumatic brain injury.

Action Potentials↗
PubMed2006

Functional changes in astroglial cells in epilepsy.

Epilepsy comprises a group of disorders characterized by the periodic occurrence of seizures, and pathologic specimens from patients with temporal lobe epilepsy demonstrate marked reactive gliosis. Since recent studies have implicated glial cells in novel physiological roles in the CNS, such as modulation of synaptic transmission, it is plausible that glial cells may have a functional role in the hyperexcitability characteristic of epilepsy. Indeed, alterations in distinct astrocyte membrane channels, receptors and transporters have all been associated with the epileptic state. This review integrates the current evidence regarding astroglial dysfunction in epilepsy and the potential underlying mechanisms of hyperexcitability. Functional understanding of the cellular and molecular alterations of astroglia-dependent hyperexcitability will help to clarify the physiological role of astrocytes in neural function as well as lead to the identification of novel therapeutic targets.

Animals↗
PubMed2005

Transcortical cooling inhibits hippocampal-kindled seizures in the rat.

PURPOSE: When epileptogenic regions encroach on eloquent brain, surgery may incur unacceptable deficits. Reversible cooling may control seizures while preserving function. We describe the effects of cooling kindled seizures in awake, freely moving rats. METHODS: We kindled rats after placement of a bipolar electrode and a copper cooling coil in dorsal hippocampus. Fully kindled animals (three consecutive grade 5 seizures) were cooled to one of two target temperatures (24 degrees or 27 degrees C) for 3 min preceding a kindling stimulation and 2 minutes after. We compared seizure score (0-5) and afterdischarge duration (ADD) with and without cooling. Target temperatures were confirmed in identical animals by using a needle thermocouple advanced to the kindling target while circulating coolant. RESULTS: Circulation of 16 degrees C and 8 degrees C coolant reliably achieved transcortical cooling of the hippocampal target to 27.0 +/- 1.2 degrees C and 23.8 +/- 2.0 degrees C, respectively, by 180 s. Cooling with 16 degrees C coolant (n = 5) significantly reduced seizure scores from 5 to 2.57 +/- 1.56, and ADD from 142 +/- 94.5 s to 45.7 +/- 20.5 s. Cooling with 8 degrees C coolant (n = 5) reduced seizure scores from 5 to 2.0 +/- 0.42, and ADD from 132.3 +/- 29.6 s to 55.5 +/- 25.9 s. In 33.3% of all cooled stimulations, grade 0 seizures resulted; grade 5 seizures recurred during subsequent stimulations when cooling was withheld. CONCLUSIONS: Fully kindled, tonic-clonic seizures can be suppressed or aborted with periictal cooling of the kindling target. Anticonvulsant activity occurred at temperatures well above those known to result in tissue injury or inhibition of normal neurologic function. These findings have important implications for the potential use of implantable cooling devices in humans with refractory epilepsies in or near eloquent cortex or dominant hippocampal formations.

Animals↗
PubMed2005

Expression of the aquaporin-1 water channel in human glial tumors.

OBJECTIVE: Malignant glial tumors are associated with cerebral edema. The aquaporins (AQPs) are a family of membrane proteins that provide a major pathway for water transport in mammals. In the central nervous system, AQP1 is selectively expressed in the choroid plexus and thought to participate in cerebrospinal fluid production. Prior studies have suggested that AQP1 may be up-regulated in glial tumors, potentially contributing to tumor-associated edema. The objective of this study was to investigate the expression of AQP1 in a large series of human glial tumors. METHODS: Thirty-six human glial tumors were obtained from the University of California, San Francisco Neurosurgery Tissue Bank. AQP1 expression was evaluated by reverse transcriptase polymerase chain reaction, complementary deoxyribonucleic acid gene array, Western blot analysis, and immunohistochemical analyses. RESULTS: AQP1, normally restricted to choroid epithelia, was highly expressed in glioblastomas. Complementary deoxyribonucleic acid array, Western blot analysis, and immunohistochemical analysis revealed intense up-regulation of AQP1 expression in all glioblastomas studied. CONCLUSION: The abnormal up-regulation of AQP1 in glial tumors suggests a potential pathological role for this membrane water channel and raises the possibility that selective AQP1 inhibition might offer a new therapeutic target for treatment of tumor-associated edema.

Adult↗
PubMed2005

Risk factors for hemorrhage during microelectrode-guided deep brain stimulator implantation for movement disorders.

OBJECTIVE: Although hemorrhage is a well-known complication of microelectrode-guided deep brain stimulation (DBS) surgery, risk factors for the development of hemorrhage have not been well defined. We analyzed the risk factors for symptomatic and asymptomatic hemorrhage in a large series of DBS implantations into the subthalamic nucleus, ventrolateral thalamus, and internal globus pallidus. METHODS: All DBS procedures performed by a single surgeon at our institution between June 1998 and May 2004 were included in this study. All patients had postoperative imaging (magnetic resonance imaging or computed tomography) 4 to 24 hours after surgery. Hematomas were noted and scored as symptomatic or asymptomatic. Statistical correlation of factors affecting risk of hematoma formation was performed by use of logistic regression analysis. RESULTS: The total number of lead implantations was 481. There were 6 symptomatic hematomas and 10 asymptomatic hematomas. Three of the symptomatic hematomas resulted in permanent new neurological deficit. The risk of hematoma (of any type) per lead implantation was 3.3%, whereas the risk of permanent deficit from hematoma was 0.6%. Patients who developed hematomas had a slightly greater number of microelectrode recording penetrations than patients who did not have hematomas, but this difference did not reach statistical significance. There was not a statistically significant relationship between risk of hematoma and patient age or diagnosis. There was a significant effect of brain target (P = 0.001), with only 1 hemorrhage detected after thalamic DBS. CONCLUSION: DBS is generally safe, with only 0.6% of implantations associated with permanent neurological deficit. The incremental risk of successive serial microelectrode penetrations is small.

Aged↗
PubMed2005

Neurocutaneous melanosis presenting with hydrocephalus. Case report and review of the literature.

Neurocutaneous melanosis (NCM) is a rare congenital neurocutaneous syndrome characterized by large or multiple congenital melanocytic nevi and benign or malignant melanocytic tumors of the leptomeninges. The authors report the case of a 5-month-old girl with congenital giant melanocytic nevi who presented with symptomatic hydrocephalus. A right frontal ventriculostomy was performed in the patient. Magnetic resonance imaging demonstrated melanocyte accumulation within the hippocampi, medulla, and cerebellum. Cerebrospinal fluid cytology revealed no presence of melanocytes. A ventriculoperitoneal shunt was placed; the patient's neurological condition improved and she was discharged home in good condition. The diagnosis of neurocutaneous melanosis should be considered in a case in which an infant or child presents with hydrocephalus and either large or multiple (> or = 3) congenital melanocytic nevi. Although our patient's neurological status improved following treatment for hydrocephalus, there is no definitive therapy for NCM and symptomatic patients have a poor prognosis. Our case illustrates to the neurosurgeon the importance of recognizing the likelihood of underlying pathological conditions of the central nervous system in a child with cutaneous melanocytic nevi.

Female↗
PubMed2005

Spontaneous intracranial hypotension associated with transdural thoracic osteophyte reversed by primary. dural repair. Case report.

Spontaneous intracranial hypotension (SIH) is an increasingly recognized syndrome associated with a specific set of clinical and imaging findings; however, determining the site of spinal cerebrospinal fluid (CSF) leakage in these patients is often difficult, and indications for surgical intervention need to be better defined. The authors report on a 55-year-old woman who presented with posture-related headache, disorientation, and memory impairment. Imaging features were consistent with SIH. Computerized tomography myelography demonstrated a large T2-3 anterior transdural osteophyte associated with a CSF fistula. After an unsuccessful trial of conservative therapy, the patient underwent median sternotomy, T2-3 discectomy and removal of osteophyte, which allowed adequate exposure for primary dural repair. Postoperatively, there was immediate and prolonged resolution of all of her symptoms. This case of SIH was caused by transdural penetration by an anterior osteophyte and CSF leakage in the upper thoracic spine, which was treated effectively by anterior exposure and primary dural repair. Aggressive surgical intervention may be required to treat upper thoracic CSF leaks refractory to other measures.

Diskectomy↗
PubMed2004

Enhanced macromolecular diffusion in brain extracellular space in mouse models of vasogenic edema measured by cortical surface photobleaching.

Diffusion of solutes and macromolecules in brain extracellular space (ECS) is important for normal brain function and efficient drug delivery, and is thought to be impaired in edematous brain. Here we measured the diffusion of an inert macromolecular fluorescent marker (FITC-dextran, 70 kDa) in the ECS by fluorescence recovery after photobleaching after staining the exposed cerebral cortex in vivo. In a brain tumor model of vasogenic (leaky capillary) edema, FITC-dextran diffusion was reduced more than fourfold in hypercellular tumor and surrounding astrogliotic tissue; however, diffusion in brain away from the tumor was approximately 30% faster than in normal contralateral brain. The increased diffusion was abolished by dexamethasone pretreatment. Enhanced ECS diffusion was also found in uninjured brain near a region of leaky brain vessels produced by focal cortical freeze injury. In contrast, ECS diffusion was slowed more than sixfold in cytotoxic brain edema caused by anoxia. Diffusion results were related semiquantitatively to ECS volume fraction and matrix viscosity from in vitro photobleaching studies in a model system consisting of silica particles in a fluorescent water/glycerol matrix. Our data provide in vivo evidence for enhanced ECS diffusion in vasogenic brain edema, yet greatly slowed diffusion in cytotoxic edema and in and around tumors.

Animals↗
PubMed2004

In vivo measurement of brain extracellular space diffusion by cortical surface photobleaching.

Molecular diffusion in the brain extracellular space (ECS) is an important determinant of neural function. We developed a brain surface photobleaching method to measure the diffusion of fluorescently labeled macromolecules in the ECS of the cerebral cortex. The ECS in mouse brain was labeled by exposure of the intact dura to fluorescein-dextrans (M(r) 4, 70, and 500 kDa). Fluorescein-dextran diffusion, detected by fluorescence recovery after laser-induced cortical photobleaching using confocal optics, was slowed approximately threefold in the brain ECS relative to solution. Cytotoxic brain edema (produced by water intoxication) or seizure activity (produced by convulsants) slowed diffusion by >10-fold and created dead-space microdomains in which free diffusion was prevented. The hindrance to diffusion was greater for the larger fluorescein-dextrans. Interestingly, slowed ECS diffusion preceded electroencephalographic seizure activity. In contrast to the slowed diffusion produced by brain edema and seizure activity, diffusion in the ECS was faster in mice lacking aquaporin-4 (AQP4), an astroglial water channel that facilitates fluid movement between cells and the ECS. Our results establish a minimally invasive method to quantify diffusion in the brain ECS in vivo, revealing stimulus-induced changes in molecular diffusion in the ECS with unprecedented spatial and temporal resolution. The in vivo mouse data provide evidence for: (1) dead-space ECS microdomains after brain swelling; (2) slowed molecular diffusion in the ECS as an early predictor of impending seizure activity; and (3) a novel role for AQP4 as a regulator of brain ECS.

Animals↗
PubMed2004

Primary brachial plexus tumors: imaging, surgical, and pathological findings in 25 patients.

OBJECT: The authors report on the treatment of primary brachial plexus tumors in 25 patients at the University of California, San Francisco. They compare their findings with those obtained in similar series. METHODS: The authors reviewed the electronic and medical records, radiological images, operative reports, and pathological findings in 25 consecutive cases of primary brachial plexus tumors. Cases of metastatic lesions or adjacent neoplasms extending into and involving the brachial plexus were excluded. At presentation patients ranged in age from 19 to 71 years (mean 47-15 years), and neurofibromatosis was present in eight patients (32%). Presenting signs and symptoms included palpable mass (60%), numbness/paresthesias (44%), radiating pain (44%), local pain (16%), and weakness (12%). Duration of symptoms ranged from 2 months to 10 years. Neuroimaging revealed lesions ranging widely in size (volume approximately 1 to 100 ml). Pathological diagnoses included schwannoma (15 [60%]), neurofibroma (five [20%]), malignant peripheral nerve sheath tumor (four [16%]), and desmoid tumor (one [4%]). CONCLUSIONS: Primary tumors arising in the brachial plexus are rare. Careful workup, surgical technique, and attention to pathological diagnosis optimize management.

Adult↗
PubMed2004

Increased seizure threshold in mice lacking aquaporin-4 water channels.

Mice deficient in the glial water channel aquaporin-4 (AQP4) show decreased cerebral edema and improved neurological outcome following water intoxication or ischemic challenge. In this report, we tested seizure susceptibility in AQP4 mice. AQP4 mice and wild-type controls were given the chemoconvulsant pentylenetetrazol (PTZ) and monitored for seizure activity. At 40 mg/kg PTZ, all wild-type mice exhibited seizure activity, whereas six of seven AQP4 mice did not exhibit seizure activity. At 50 mg/kg PTZ, both groups exhibited seizure activity; however, the latency to generalized (tonic-clonic) seizures was significantly lower in wild-type than AQP4 mice. These results suggest that glial water channels may modulate brain excitability and the initiation and generalization of seizure activity.

Action Potentials↗
PubMed2004

The role of BDNF in epilepsy and other diseases of the mature nervous system.

The neurotrophin brain-derived neurotrophic factor (BDNF) is ubiquitous in the central nervous system (CNS) throughout life. In addition to trophic effects on target neurons, BDNF appears to be part of a general mechanism for activity-dependent modification of synapses in the developing and adult nervous system. Thus, diseases of abnormal trophic support (such as neurodegenerative diseases) and diseases of abnormal excitability (such as epilepsy and central pain sensitization) can be related in some cases to abnormal BDNF signaling. For example, various studies have shown that BDNF is upregulated in areas implicated in epileptogenesis, and interference with BDNF signal transduction inhibits the development of the epileptic state. Further study of the cellular and molecular mechanisms by which BDNF influences cell survival and excitability will likely provide novel concepts and targets for the treatment of diverse CNS diseases.

Age Factors↗
PubMed2004

Brain-derived neurotrophic factor.

Since the purification of BDNF in 1982, a great deal of evidence has mounted for its central roles in brain development, physiology, and pathology. Aside from its importance in neural development and cell survival, BDNF appears essential to molecular mechanisms of synaptic plasticity. Basic activity-related changes in the central nervous system are thought to depend on BDNF modification of synaptic transmission, especially in the hippocampus and neocortex. Pathologic levels of BDNF-dependent synaptic plasticity may contribute to conditions such as epilepsy and chronic pain sensitization, whereas application of the trophic properties of BDNF may lead to novel therapeutic options in neurodegenerative diseases and perhaps even in neuropsychiatric disorders.

Animals↗
PubMed2004

A history of Todd and his paralysis.

OBJECTIVE: To describe the history of Robert Bentley Todd (1809-1860) and certain of his contributions to medicine, including his original and subsequent descriptions of "epileptic hemiplegia," which came to be called "Todd's paralysis." METHODS: The author conducted a comprehensive review of English-language literature, modern and historical, related to "Todd's paralysis" and examined Todd's original case histories and commentary by Todd, his contemporaries, and his successors. RESULTS: Todd held that some patients "who recover from a severe fit, or from frequently repeated fits of epilepsy, are often found to labor under hemiplegia, or other modifications of palsy." He believed that this resulted from "undue exaltation. [resulting in] a state of depression or exhaustion." Interestingly, Todd was the first to present an electrical theory of epilepsy, supported by his own animal experimentation, well before his better-known successor John Hughlings Jackson (1835-1911) (famous for his investigations of partial epilepsies and the eponymous "Jacksonian march"). CONCLUSION: Many neurologists and investigators followed Todd in acknowledging transient postictal paralysis as a distinct clinical entity. Yet whether the pathophysiology of "Todd's paralysis" is related to "neuronal exhaustion" or excessive inhibition is still controversial.

History, 19th Century↗