Intracranial aneurysms: is there still a place for neurosurgery?
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Age Factors↗
Biomedical subjects
P Bijlenga
Publications and source records attributed to P Bijlenga.
Early surgery for brainstem cavernomas.
BACKGROUND: The purpose was to review our experience with the surgical management of brainstem cavernomas (BSCs) and especially the impact of the surgical timing on the clinical outcome. METHOD: We retrospectively reviewed 22 patients harboring a BSC, who underwent 23 procedures. FINDINGS: Surgery was carried out during the early stage after the last haemorrhage, with a mean delay of 21.6 days (range 4-90 days). Sixteen procedures were performed after a first bleeding event while seven after multiple bleedings. Complete resection was achieved in 19 patients (86.4%). Early after surgery, 12 patients (52.2%) improved neurologically, 5 (21.7%) were stable and 6 (26.1%) worsened. New postoperative deficits were noted after 9 procedures (39.1%). Statistically significant factors for postoperative aggravation were: late surgery (P = 0.046) and multiple bleedings (P = 0.043). No patient operated on within the first 19 days after bleeding did worsen (n = 11), as opposed to 6 out of 12 who did when operated on later. After a mean follow-up of 44.9 months, 20 patients (90.9%) were improved, 1 patient (4.6%) was worse and 1 patient was lost to follow-up (4.6%), after reoperation for rebleeding of a previously completely resected cavernoma. Late morbidity was reduced to 8.6%. The mean Glasgow Outcome Scale (GOS) at the end of the follow-up period was 4.24, compared to a mean preoperative GOS of 3.22 (P<0.001). Complete neurological recovery of motor deficits, sensory disturbances, cranial nerves (CNs), internuclear ophtalmoplegia and cerebellar dysfunction were respectively 41.7%, 38.5%, 52.6%, 60.0% and 58.3%. Among the most affected CNs: CN 3, CN 5 and CN 7 were more prone to completely recover, respectively in 60.0%, 70.0% and 69.2%. CONCLUSIONS: Surgical removal of BSCs is feasible in experienced hands with acceptable morbidity and good outcome. Early surgery and single bleeding were associated with better surgical results.
Adolescent↗
Inhibition of T-type calcium channels protects neurons from delayed ischemia-induced damage.
Intracellular calcium increase is an early key event triggering ischemic neuronal cell damage. The role of T-type voltage-gated calcium channels in the neuronal response to ischemia, however, has never been studied. Using an in vitro model of ischemia-induced delayed cell death in rat organotypic hippocampal slice cultures, we show that T-type calcium channels inhibitors drastically reduce ischemic cell damage. Immunostaining studies reveal the existence of Ca(V)3.1 and Ca(V)3.2 types of low-voltage-activated calcium channels in rat organotypic hippocampal cultures. Low extracellular calcium (100 nM) or increase of intracellular calcium buffering ability by BAPTA-acetoxymethyl ester significantly reduced ischemia-induced neuronal damage. Pharmacological inhibition of the T-type calcium current by mibefradil, kurtoxin, nickel, zinc, and pimozide during the oxygen-glucose deprivation episode provided a significant protection against delayed neuronal death. Mibefradil and nickel exerted neuroprotective effects, not only if administrated during the oxygen-glucose deprivation episode but also in conditions of postischemic treatment. These data point to a role of T-type calcium currents in ischemia-induced, calcium-mediated neuronal cell damage and suggest a possible new pharmacological approach to stroke treatment.
Animals↗
Nasopharynx paraganglioma with extension in the clivus.
Paraganglioma is a rare benign tumor arising from the sympathetic nervous system. Here we describe an exceptional case of a paraganglioma located in the nasopharynx with an extension through the clivus up to the dura. Atypically, no contact with any major vessels was found. A radical resection of the mass was performed by an anterior transmaxillary approach through a Le Fort I osteotomy. One year follow up reveals no signs of local or distant recurrence. No cosmetic changes can be observed after the surgery and nasal and masticatory functions are unmodified. We review the clinical presentation, workup of paraganglioma, as well as the surgical approaches to the clivus.
Adult↗
Double-lumen balloon microcatheter-assisted occlusion of cerebral vessels with coils: a technical note.
The purpose of this study was to describe a balloon-assisted double-lumen microcatheter technique to perform a controlled and tight coil packing of a vascular segment for vessel occlusion. This technique can be performed immediately after a test occlusion with the balloon kept in place and was, as illustrated in six cases, in our experience safe, straight forward to use and fast.
Adult↗
Dysplastic dens of the axis: case report.
In a patient injured in a bicycle accident, radiological evaluation of the cervical spine revealed an oblique orientation of a dysplastic dens of the axis, which, to our knowledge, has not been reported in the literature. There were no other bony or soft tissue anomalies and no associated instability. This case should draw attention to congenital anomalies of the cranio-cervical junction in trauma patients.
Accidents, Traffic↗
T-type alpha 1H Ca2+ channels are involved in Ca2+ signaling during terminal differentiation (fusion) of human myoblasts.
Mechanisms underlying Ca(2+) signaling during human myoblast terminal differentiation were studied using cell cultures. We found that T-type Ca(2+) channels (T-channels) are expressed in myoblasts just before fusion. Their inhibition by amiloride or Ni(2+) suppresses fusion and prevents an intracellular Ca(2+) concentration increase normally observed at the onset of fusion. The use of antisense oligonucleotides indicates that the functional T-channels are formed by alpha1H subunits. At hyperpolarized potentials, these channels allow a window current sufficient to increase [Ca(2+)](i). As hyperpolarization is a prerequisite to myoblast fusion, we conclude that the Ca(2+) signal required for fusion is produced when the resting potential enters the T-channel window. A similar mechanism could operate in other cell types of which differentiation implicates membrane hyperpolarization.
Calcium↗
Mibefradil (Ro 40-5967) inhibits several Ca2+ and K+ currents in human fusion-competent myoblasts.
1. The effect of mibefradil (Ro 40-5967), an inhibitor of T-type Ca2+ current (I(Ca)(T)), on myoblast fusion and on several voltage-gated currents expressed by fusion-competent myoblasts was examined. 2. At a concentration of 5 microM, mibefradil decreases myoblast fusion by 57%. At this concentration, the peak amplitudes of I(Ca)(T) and L-type Ca2+ current (I(Ca)(L)) measured in fusion-competent myoblasts are reduced by 95 and 80%, respectively. The IC50 of mibefradil for I(Ca)(T) and I(Ca)(L) are 0.7 and 2 microM, respectively. 3. At low concentrations, mibefradil increased the amplitude of I(Ca)(L) with respect to control. 4. Mibefradil blocked three voltage-gated K+ currents expressed by human fusion-competent myoblasts: a delayed rectifier K+ current, an ether-à-go-go K+ current, and an inward rectifier K+ current, with a respective IC50 of 0.3, 0.7 and 5.6 microM. 5. It is concluded that mibefradil can interfere with myoblast fusion, a mechanism fundamental to muscle growth and repair, and that the interpretation of the effect of mibefradil in a given system should take into account the action of this drug on ionic currents other than Ca2+ currents.
Adolescent↗
An ether -à-go-go K+ current, Ih-eag, contributes to the hyperpolarization of human fusion-competent myoblasts.
1. Two early signs of human myoblast commitment to fusion are membrane potential hyperpolarization and concomitant expression of a non-inactivating delayed rectifier K+ current, IK(NI). This current closely resembles the outward K+ current elicited by rat ether-à-go-go (r-eag) channels in its range of potential for activation and unitary conductance. 2. It is shown that activation kinetics of IK(NI), like those of r-eag, depend on holding potential and on [Mg2+]o, and that IK(NI), like r-eag, is reversibly inhibited by a rise in [Ca2+]i. 3. Forced expression of an isolated human ether-à-go-go K+ channel (h-eag) cDNA in undifferentiated myoblasts generates single-channel and whole-cell currents with remarkable similarity to IK(NI). 4. h-eag current (Ih-eag) is reversibly inhibited by a rise in [Ca2+]i, and the activation kinetics depend on holding potential and [Mg2+]o. 5. Forced expression of h-eag hyperpolarizes undifferentiated myoblasts from -9 to -50 mV, the threshold for the activation of both Ih-eag and IK(NI). Similarly, the higher the density of IK(NI), the more hyperpolarized the resting potential of fusion-competent myoblasts. 6. It is concluded that h-eag constitutes the channel underlying IK(NI) and that it contributes to the hyperpolarization of fusion-competent myoblasts. To our knowledge, this is the first demonstration of a physiological role for a mammalian eag K+ channel.
Adolescent↗
Cloning of a human ether-a-go-go potassium channel expressed in myoblasts at the onset of fusion.
An early sign of human myoblast commitment to fusion is the expression of a non-inactivating delayed rectifier K+ current, I(K(NI)), and an associated membrane potential hyperpolarization. We have isolated the full-length coding region of a human ether-a-go-go K+ channel (h-eag) from myoblasts undergoing differentiation. The h-eag gene was localized to chromosome 1q32-41, and is expressed as a approximately 9 kb transcript in myogenic cells and in adult brain tissue. Forced expression of h-eag in undifferentiated myoblasts generates a current with remarkable similarity to I(K(NI)) indicating that h-eag constitutes the channel responsible for this current in vivo.
Adolescent↗
Role of an inward rectifier K+ current and of hyperpolarization in human myoblast fusion.
1. The role of K+ channels and membrane potential in myoblast fusion was evaluated by examining resting membrane potential and timing of expression of K+ currents at three stages of differentiation of human myogenic cells: undifferentiated myoblasts, fusion-competent myoblasts (FCMBs), and freshly formed myotubes. 2. Two K+ currents contribute to a hyperpolarization of myoblasts prior to fusion: IK(NI), a non-inactivating delayed rectifier, and IK(IR), an inward rectifier. 3. IK(NI) density is low in undifferentiated myoblasts, increases in FCMBs and declines in myotubes. On the other hand, IK(IR) is expressed in 28% of the FCMBs and in all myotubes. 4. IK(IR) is reversibly blocked by Ba2+ or Cs+. 5. Cells expressing IK(IR) have resting membrane potentials of -65 mV. A block by Ba2+ or Cs+ induces a depolarization to a voltage determined by IK(NI) (-32 mV). 6. Cs+ and Ba2+ ions reduce myoblast fusion. 7. It is hypothesized that the IK(IR)-mediated hyperpolarization allows FCMBs to recruit Na+, K+ and T-type Ca2+ channels which are present in these cells and would otherwise be inactivated. FCMBs, rendered thereby capable of firing action potentials, could amplify depolarizing signals and may accelerate fusion.
Action Potentials↗
Uncoupling protein-3 expression in rodent skeletal muscle is modulated by food intake but not by changes in environmental temperature.
A new member of the uncoupling protein (UCP) family called UCP3 has recently been cloned and shown to be highly expressed in skeletal muscle of rodents and humans. In the present study, UCP3 was overexpressed in C2C12 myoblasts where it acts as an uncoupling protein. Changes in UCP3 mRNA expression were examined in rodent muscles under conditions known to modulate thermogenesis in brown adipose tissue. In skeletal muscle, UCP3 expression did not change in response to 48 h of cold exposure (6 degrees C), whereas it was decreased by 81% or increased 5.6-fold by 1 week of 50% food restriction or fasting, respectively. It was also decreased by 36% in soleus muscle of obese (fa/fa) as compared with lean Zucker rats. The unexpected rise of UCP3 mRNA level induced by fasting did not change in vitro muscle basal heat production rate but decreased by 31% the capacity to produce heat in response to the uncoupler carbonylcyanide p-trifluoromethoxyphenylhydrazone. This decrease may reflect underlying uncoupling by UCP3. Up-regulation of UCP3 mRNA after a 24-h fast was still observed in mice exposed at thermoneutrality. These results show that the increase in UCP3 expression induced by fasting is associated with the maintenance of thermogenesis measured in muscle in vitro and is not modulated by environmental temperature. The notion that UCP3 expression is modulated by food intake is of importance to better understand the pathophysiology of obesity in humans.
Animals↗
Expression of a voltage-dependent potassium current precedes fusion of human muscle satellite cells (myoblasts).
Using the whole-cell recording patch clamp technique in clonal cultures of human muscle satellite cells (SC), we studied a voltage-gated potassium current analogous to the delayed rectifier current (IKdr) described in adult human skeletal muscle. This current was absent in proliferating SC cultured in a growth medium containing 15% serum, except when the SC approached the end of their replicative life (between 77 and 124 days in culture); at that time, approximately 50% of the SC possessed IKdr. In contrast, IKdr was expressed within less than 4 days in approximately 70% of the SC cultured in a serum-free medium (SFM) and within 24 h in differentiating medium. We believe that IKdr may be a characteristic feature of fusion-component SC and that it may be involved in the fusion process for the following reasons: 1) after the transfer in differentiating medium, cultures of SC in which the expression of IKdr was previously promoted by exposure to SFM were found to fuse immediately, without the initial 24 h lag time observed in control sister cultures; 2) in the latter "naive" SC, IKdr was expressed during the first day in differentiating medium, before SC began to fuse; 3) most of the SC that did not fuse even after weeks of exposure to differentiating medium did not express IKdr; 4) TEA, at a concentration of 3 mM, reduces the amplitude of IKdr by 55% and the fusion index by 55-67%.
Adolescent↗