[Facial nerve neurography involving magnetic stimulation techniques can be used to assess the intracranial segment of the facial nerve and the entire facial motor pathway, as opposed to the traditional neurography, involving only extracranial electric stimulation of the nerve. Both our own experience and data published in the literature underline the value of the method in localising facial nerve dysfunction and its role in clinical diagnosis. It is non-invasive and easy to perform. Canalicular hypoexcitability has proved to be the most useful and sensitive parameter, which indicates the dysfunction of the nerve between the brain stem and the facial canal. This is an electrophysiological finding which offers for the first time positive criteria for the diagnosis of Bell’s palsy. The absence of canalicular hypoexcitability practically excludes the possibility of Bell’s palsy. The technique is also able to demonstrate subclinical dysfunction of the nerve, which can be of considerable help in the etiological diagnosis of facial palsies. For example, in a situation where clinically unilateral facial weakness is observed, but facial nerve neurography demonstrates bilateral involvement, etiologies other than Bell’s palsy are more likely, such as Lyme’s disease, Guillain-Barré syndrome, meningeal affections etc. Furthermore, the technique differentiates reliably between peripheral facial nerve lesion involving the segment in the brain stem or the segment after leaving the brainstem.]

[symptoms. In two thirds of the cases the cause is unknown, this is called “idiopathic peripheral facial palsy or Bell’s palsy”, but several different diseases have to be considered in the differential diagnosis. In this paper we reviewed the case histories of 110 patients treated for “peripheral facial palsy” in the Department of Neurology, Semmelweis University, Budapest in a five year period, 2000-2004. We studied the age, gender distribution, seasonal occurance, comorbidities, sidedness, symptoms, circumstances of referral to the hospital, the initial diagnoses and therapeutic options. We also discuss the probable causes and consequences of diagnostic failures. Results: the proportion of males and females was equal. There was no considerable difference between sexes regarding agedistribution. Of the 110 patients 106 was diagnosed with idiopathic Bell’s palsy, three cases with otic herpes zoster and one patient with Lyme disease. In our material, peripheral facial palsy was significantly more frequent in the cold period of late autumn, winter, and early spring. Diabetes mellitus and hypertension were more frequent than in the general population. 74% of the patients were admitted within two days from the onset of the symptoms. In 37% preliminary diagnosis was unavailable. In 15% cerebrovascular insult was the first, incorrect diagnosis, the correct diagnosis of “Bell’s palsy” was provided only in 16%. The probable causes of diagnostic failures may be the misleading symptoms and accompanying conditions. We examined the different therapies applied and reviewed the literature in this topic. We conclude that intravenous corticosteroid treatment in the early stage of the disease is the therapy of choice.]

[Motor neuron diseases. Analysis of our cases of amyotrophic lateral sclerosis. Experimental immune-mediated substantia nigra damage. Role of ansa galeni in the laryngeal protective reflex - intraoperative neuromyographic studies in dogs. Prognostic role of conduction velocity measurements in Bell's palsy. Nervous system inflammation. A subtype case of meningoencephalitis. Ophthalmoplegia in herpes zooster (two cases presented). Differential diagnostic problems in cases of Guillain-Barré syndrome. A case of central nervous system complication associated with SLE (clinicopathological presentation). Ventriculo-peritoneal (vp) shunt in basal arachnitis with severe cerebrospinal fluid (CSF) circulatory disturbance. Pain syndrome. Spect and TCD studies in cluster headache. Incidence of migraine in our department. Treatment of trigeminal neuralgia with glycerol infiltration of the Meckel's pouch. Pain syndromes caused by osteoporosis. Other neurological problems. Neuropsychiatric aspects of hypoparathyroidism. Practice in the preoperative evaluation of patients with therapy-resistant bitemporal epilepsy (case presentation). A case report of a tumor of the corpus callosum. Co-occurrence of meningioma and basilar giant aneurysm (case report). The value of cervical duplex ultrasound in the care of cerebrovascular patients (experience of 700 studies). Experience in ultrasound examination of the carotid artery in patients with lower extremity vascular stenosis. Laser Doppler circulatory testing for monitoring cochlear autoregulation. New possibilities in ABR studies using the dantec counterpoint MK-2 EMG/EP. Use of HBS-Madopar in Parkinson's syndrome with special reference to nocturnal dystonia. Role of HBS-Madopar in different types of on-off.]

Background and purpose – There is growing evidence for the viral origin of the Bell’s facial palsy, vestibular neuritis and sudden sensorineural hearing loss, however their exact pathophysiology is still unknown. We investigated the possibility of brainstem infections following peripheral viral inoculations in rats. Methods – Pseudorabies virus, a commonly used neurotropic viral retrograde tracer was injected into the nasolabial region of rats. Five and 6 days after injections, infected brainstem nuclei were demonstrated by immunohistochemical techniques. Results – Infected neurons were found in the motor facial, the medial vestibular, and the sensory trigeminal nuclei, as well as in the medial nucleus of the trapezoid body. Conclusion – Pseudorabies virus infects auditory and vestibular sensory neurons in the brainstem through facial inoculation. The possible routes of infections: 1. trans-synaptic spread constituted by facio-vestibular anastomoses: primarily infected motor facial neuron infects neurons in the medial vestibular nucleus, 2. via trigeminal sensory nerves: the sensory trigeminal complex innervated by GABAergic medial vestibular neurons, and 3. one bisynaptical route: infected facial motoneurons may receive indirect input from the medial vestibular nucleus and the trapezoid body via connecting neurons in the sensory trigeminal complex. We may assume that latent infections of these areas may precede the infections of the peripheral organs and the reactivation of the virus exerts the symptoms.