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A transient loss of consciousness (TLOC) may have different causes. The term syncope is restricted to an underlying sudden decrease in cerebral perfusion. In most cases, syncopes or other causes of TLOC are recognizable by a basic diagnostic evaluation (history taking, physical examination, ECG, and supine and upright blood pressure measurements). Cues for epileptic seizures, e.g., delayed recovery, should prompt an extended search for an epileptic focus. Unusual features of the attacks without any hint for a syncopal or an epileptic origin require the psychiatric inspection of suspected dissociative (psychogenic) seizures. Neurogenic orthostatic hypotension results from sympathetic failure. The underlying disease (Parkinson's disease, pure autonomic failure, autonomic neuropathy, etc.) has to be identified by neurological examinations.

Background: Standard therapy for acute ischaemic stroke is the intravenous thrombolysis with rtPA. A combined therapy with intravenous bridging and consecutive intraarterial thrombolysis and mechanical thrombectomy is a relatively new option in patients with proximal vessel occlusion., Patients and Methods: 10 Patients with a CTA proven proximal vessel occlusion in the anterior circulation (ACI, carotis bifurcation, MCA) in CTA were treated with a combined therapy with i. v. and i. a. thrombolysis and thrombectomy with a Solitaire FR stent device., Results: All Patients were recanalized, the NIHSS changed from 15.6 to 3.3. 8 out of 10 patients had nearly no symptoms when dismissed. There were no direct therapeutic complications., Conclusion: Combined therapy with i. v. and i. a. thrombolysis and thombectomy with the Solitaire FR stent device is a promising option in patients with acute proximal vessel occlusion in the anterior circulation., (© Georg Thieme Verlag KG Stuttgart · New York.)

Orthostatic circulatory disorders are frequently the cause of orthostatic intolerance, syncope or dangerous falls. A sufficient therapy should be based on a differential diagnosis by means of an active standing test or a tilt-table test. Three typical pathological reactions of blood pressure and heart rate can be differentiated. The hypoadrenergic orthostatic hypotension is characterised by an immediate drop in blood pressure (systolic drop > 20 mmHg below base line within 3 min) with or without compensatory tachycardia. It is caused by peripheral or central sympathetic dysfunction. Tachycardia (> 30 beats per minute above base line within 10 min) without significant blood pressure drop but with a fall of cerebral blood flow indicates a postural tachycardia syndrome. In general, there is no further somatic dysfunction. Increased venous pooling is thought to be the assumed pathomechanism. A reflex mechanism evokes the neurocardiogenic syncope after a certain time of standing: sympathetic inhibition yields a strong blood pressure drop and vagal activation bradycardia. Proved therapies include use of the mineralocorticoide fludrocortison (hypoadrenergic orthostatic hypotension), of the alpha-agonist midodrin (postural tachycardia syndrome) and of beta-blockers (neurocardiogenic syncope).

The clinical significance of quantitative tilt-table examination with TCD monitoring in the diagnosis of neurocardiogenic syncope is evaluated. A 50-year-old male suffered a neurocardiogenic syncope during tilt-table examination with a strong drop in blood pressure, an increase in cerebrovascular resistance as evidenced by transcranial Doppler monitoring, and a 30-s cardiac asystole, followed by a generalized seizure. No further syncope could be elicited during tilt-table examination after beta-blocker treatment. It was hypothesized that hyperactivity of the left ventricular mechanoreceptors due to increased force of ventricular contraction during a state of reduced venous backstream to the heart was responsible for eliciting the neurocardiogenic syncope. Tilt-table examination with an upright position for at least 45 min enables the diagnosis of a neurocardiogenic syncope to be made with sufficient sensitivity and specificity. Several studies have shown that medication with beta-blockers is successful in the treatment of neurocardiogenic syncope. The implantation of cardiac pacemakers should only be considered if medication is not successful.

2D-phase-contrast mapping is a MR method that allows for quantitative measurements of blood flow velocity in intracranial vessels. Using a modified FISP-Sequence with a 1.5 T MR scanner, flow studies were carried out on a phantom. Two matrix sizes (256 x 256 vs. 256 x 512) were compared. In 20 healthy volunteers blood flow velocity and profile of the basal (BA), middle cerebral (MCA), and anterior cerebral artery (ACA) were compared with the corresponding findings of transcranial Doppler (TCD) sonography. 2DPK and TCD yielded equivalent velocity data and profiles of the BA. The blood flow velocity in the MCA determined by 2DPK was lower than the TCD values. Using a 256 x 512 matrix, the acquired data were in better accordance with the TCD findings. Due to significant noise measurements of the ACA and PCA were frequently degraded.

The influence of transcranially applied magnetic stimuli on the function of the afferent (sensory) and efferent (motor) parts of the visual system have been discussed. Excitatory (positive) phenomena are subjective photic sensations (phosphenes) which can be elicited by transcranial magnetic stimulation over occipital parts of the skull. The phosphenes appear on the left or right side of the visual field depending upon the direction of the coil currents, which determines whether the visual cortex of the right or the left hemisphere is activated. The configuration of the phosphene fields hints at an excitation of the primary visual cortex (Brodmann's area 17). However, magnetic brain stimulation also produces inhibitory (negative) phenomena. When strong magnetic field pulses are applied over the primary visual cortex, foveally presented visual stimuli cannot be identified even when no phosphenes are perceived at the same time. Depending on the position of the stimulation coil, this suppression of perception can be restricted to visual stimuli presented on the right, or left of, above or below the fixation point. No generation or disturbance of eye movements by transcranial magnetic stimulation has been reported before, except for a delay of saccades within a reaction time paradigm.