By L. R. Caplan (auth.), Prof. Dr. Louis R. Caplan, Prof. Dr. Hanns Christian Hopf (eds.)
The localization of small vascular lesions in the brain-stem is the focus of this quantity which correlates scientific exam, evoked potentials, brain-stem reflexes and imaging ideas in a single evaluation. For the 1st time, a bunch of specialists has been introduced jointly to summarize a number of the tools for detecting practical disturbances of specialised buildings, to correlate those findings with morphologic standards (MRI) and, eventually, to intricate styles of irregular findings that are attribute of small brain-stem lesions. you're therefore expert approximately neuro-physiological recommendations that are better to imaging innovations in neighborhood brain-stem pathology.
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Extra resources for Brain-Stem Localization and Function
Electronystagmography (ENG) is used for monitoring eye movements. The potential between the cornea (the positive pole) and the retina (the negative pole) is measured (corneoretinal potential). Gaze is investigated for the presence of spontaneous, gaze-provoked, or positional nystagmus. Tests for vestibular ocular reflex function using caloric testing and visual ocular control regarding saccades and pursuit eye movements are performed. Different structures in the brain-stem and cerebellum are part of the oculomotor system [2, 10, 31].
Electrical stimulation of the supraorbital nerve elicits two separate responses of the orbicularis oculi muscle: the early ipsilateral R1 component via a pontine pathway and the late ipsi- and contralateral R2 and R2c components relayed through a more complex route involving the pons and lateral medulla. These anatomic correlations originate from studies in Multifocal Ischemic Brain-Stem Lesions 25 patients with localized brain-stem lesions and from animal experiments [8, 17, 27]. Blink reflex latencies reflect conduction along the entire length of the supraorbital and facial nerves: therefore, pathological alterations of latencies do not necessarily indicate a pathological process within the brainstem.
The finding of an isolated wave I usually is rather stable, but wave I can also finally disappear, presumably due to decreased perfusion by the internal auditory artery (Fig. 3). An interesting phenomenon is the increase in amplitude of wave I that occasionally occurs before it disappears [5, 17,32]. This may be explained by the loss of an inhibitory centrifugal tract to the cochlea. Alternatively, it could reflect the increased excitability that some neurons show under hypoxic conditions .