Wilhelm Nacimiento

Contralateral early blink reflex in patients with facial nerve palsy: indication for synaptic reorganization in the facial nucleus during regeneration

Fifty patients with Bells palsy and 30 patients with etiologically different symptomatic peripheral facial nerve palsy were studied by means of electrically evoked blink reflexes 1-23 days after onset of paresis. Their results were compared with a normal control group of 30 healthy subjects. In a significant number of patients (64% in Bells palsy and 53% in symptomatic facial nerve palsy) a contralateral early blink reflex response (R1) could be elicited upon stimulation of the normal side as compared to 13% in the control group. It is suggested that this result may be explained by synaptic reorganization of the facial nucleus leading to functional unmasking of pre-existing crossed trigemino-facial reflex pathways during regeneration. This view is in line with previous experimental data in animals on the time course of structural changes in the facial nucleus after lesioning of the ipsilateral facial nerve.

Astrocytes re-express nestin in deafferented target territories of the adult rat hippocampus

Up-regulation of the intermediate filament protein, nestin, is a sensitive indicator for the extent of astrocytic activation in regions of CNS close to the point of injury. However, it remains unclear whether activated astrocytes in distant, deafferented CNS territories are also capable of nestin re-expression. Here, we demonstrate that traumatic injury to the dentate gyrus is followed by the rapid but transient expression of nestin in astrocytes located in the stratum lucidum of field CA3. Up-regulation of nestin was first detected at 1 day, was still visible at 14 days, and returned to close to control levels by 28 days post-injury. The present investigation clearly demonstrates the sensitivity of nestin expression as a indicator of astroglial activation in hippocampal target territories undergoing deafferentation-related changes.

Spontaneous orientation of transplanted olfactory glia influences axonal regeneration.

TRANSPLANTED olfactory ensheathing cells (OECs) have previously been demonstrated to support axonal growth and myelination in the adult rat CNS. Here, the capacity of donor OECs to control the direction of axonal regeneration has been investigated following transplantation, as elongated columns, into the thalamus of adult rats. The OECs formed a ‘glial bridge’ which extended from the thalamus to the hippocampus. Transplanted OECs rapidly adopted a spindle-shaped morphology which was orientated along the vertical axis of the transplant. Numerous host axons grew into the transplants and followed the highly orientated OEC cell matrix across the choroid fissure. Thus, the spontaneous elongation and orientation of donor OECs may support highly directional host axonal growth across natural barriers within the CNS.

MRI follow-up of herpes simplex virus (type 1) radiculomyelitis

Most genital infections by herpes simplex virus (HSV) are associated with HSV-2, whereas HSV-1 has rarely been implicated in these conditions.1 Following primary genital infection, the virus persists in a latent stage within neurons of dorsal root ganglia (DRG). Occasionally, HSV reactivation may be followed by radiculomyelitis, which variably affects the cauda equina, conus, and thoracic spinal cord.1 We report a 48-year-old immunocompetent man with acute HSV-1 radiculomyelitis that occurred in the absence of any preceding or concomitant herpetic skin lesions. The patient was admitted to the hospital owing to progressive numbness, which started in both feet the day before and ascended proximally to the legs. He also complained of gait disturbance and urinary incontinence. On neurologic examination, signs of meningeal irritation were absent and cranial nerves were normal. Deep-tendon reflexes were ++ in both arms and absent in the legs; plantar responses were flexor. Muscle strength was normal in the arms and slightly reduced in the legs (4/5). There was a severe sensory loss for all modalities in both legs and in the perianal region, as well as marked sensory ataxia of the lower limbs with corresponding gait disturbance. Anal sphincter muscle tone was reduced, resulting in stool incontinence; there was also overflow urinary incontinence. Motor nerve …

Intermittent hypoglossal nerve palsy caused by a calcified persistent hypoglossal artery: an uncommon neurovascular compression syndrome.

Neurovascular compression is assumed to cause symptoms like trigeminal neuralgia, hemifacial spasm and vestibular paroxysmia. We present a patient with recurrent episodes of transient dysarthria due to isolated right hypoglossal nerve (HN) palsy. We describe the first case of a calcified persistent hypoglossal artery (PHA) as the putative cause of a hypoglossal neurovascular compression syndrome. Our patient received a daily low-dose medication of carbamazepine resulting in complete relief of symptoms. In conclusion, PHA is not only an anatomic variation but also a possible cause of a neurovascular compression syndrome leading to intermittent HN palsy.

Aktuelle Aspekte der Neuroregeneration nach Rückenmarktrauma

ZusammenfassungAusgeprägte Rückenmarktraumen führen regelmäßig zu einem persistierenden Querschnittsyndrom mit entsprechender lebenslanger Behinderung. Ursache ist eine funktionell unzureichende Regeneration durchtrennter Nervenfasern im zentralen Nervensystem. In den vergangenen 20 Jahren konnten eine Reihe zellulärer und molekularer Mechanismen der abortiven Nervenregeneration und der komplexen Reorganisation nach Rückenmarktrauma tierexperimentell identifiziert werden. Auf der Grundlage dieser Erkenntnisse konnten im Rahmen zahlreicher experimenteller Therapiestrategien partielle funktionelle Restitutionen erzielt werden. Eine klinische Anwendung dieser Behandlungskonzepte bei querschnittgelähmten Patienten ist jedoch noch nicht absehbar. Die folgende Übersicht fasst die wichtigsten neurobiologischen Aspekte der Regeneration nach Rückenmarktrauma zusammen und skizziert die Prinzipien der experimentellen Behandlungsstrategien.AbstractIn recent years, our neurobiological knowledge of the various cellular mechanisms that mediate successful peripheral nerve regeneration, and also of those that prevent repair of damaged nerve fibre pathways following traumatic injury to the central nervous system (CNS), has become more precise. On the basis of this knowledge, a range of experimental therapies for promoting axonal regeneration and functional recovery after spinal cord injury have been developed in animal models. Such intervention strategies focus on the molecular inactivation of glial-associated growth-inhibitory factors and on the application of trophic molecules and cellular substrates that enhance the postlesional regenerative capacity of intrinsic CNS neurons. At present, these experimental therapies cannot be applied in the clinical situation for the treatment of spinal cord-injured patients. This overview briefly summarizes current progress in the neurobiology of spinal cord trauma.

Gefäßveränderungen des Hirnstamms

ZusammenfassungDie klinische Relevanz von vaskulären Fehlbildungen des Hirnstamms soll mit den Befunden der bildgebenden Diagnostik verglichen werden.Acht Patienten mit vaskulären Fehlbildungen des Hirnstamms wurden magnetresonanztomographisch und teilweise angiographisch untersucht. Zusätzlich wurden klinischneurologische und elektrophysiologische Untersuchungen durchgeführt.In jeweils der Hälfte der Fälle wurden die vaskulären Veränderungen des Hirnstamms nach der MRT als venöse Dysplasie (DVA) und kapilläre Teleangiektasie eingestuft. Begleitende Kavernome wurden bei zwei Patienten gefunden, Übergangsformen einmal. Als Ursache klinischer Symptome wurden zweimal die Kavernome identifiziert, in einem Fall mit Trigeminusneuralgie die Drainagevene der DVA. Einmal bestand ein möglicher Zusammenhang zwischen einer kapillären Teleangiektasie und einer latenten Hemiparese. In den anderen Fällen bestand kein Zusammenhang.Die erste Methode zur Diagnostik der Gefäßveränderungen des Hirnstamms ist die MRT. Die differentialdiagnostische Abgrenzung zu pathologischen Hirnstammprozessen ist mittels Dünnschichtuntersuchung bei Kenntnis der Malformation fast immer möglich. Die klinische Relevanz von Kavernomen ist gesichert, von DVA und kapillärer Teleangiektasie nur in Ausnahmefällen. Es gibt Übergangsformen zwischen den venösen Veränderungen des Hirnstamms.AbstractTo compare the clinical findings in patients with venous anomalies of the brainstem with imaging findings.Eight patients with venous anomalies of the brainstem were examined with magnetic resonance imaging. In addition, intraarterial angiographies were obtained in 4 patients with developmental venous anomalies. All patients were evaluated clinically and electrophysiologically.The lesions were classified as developmental venous anomalies (DVA) in 4 cases and as capillary telangiectasia in the other 4. Concomitant cavernomas were discovered in 2 patients, borderline lesions in 1. The clinical symptoms were attributable to the cavernomas in 2 cases, to the draining vein of the DVA in 1 patient. A slight subclinical hemiparesis may have been caused by a capillary telangiectasia in 1 patient. A causative link between the unspecific complains of the other patients and a brainstem vascular dysplasia could not be established.MRI is the imaging method of choice for the imaging of vascular brainstem anomalies. Safe diagnosis is nearly always possible if the typical imaging appearance of vascular malformations is appreciated. The clinical relevance of cavernomas has long been established. The clinical significance of DVA and capillary telangiectasia seems to be exceptional.