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Evaluation of Balance
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
There are three important reticular saccadic areas. A small central region in the pontomedullary junction (nucleus raphe interpositus (RIP)) which is the gateway for all saccadic movements; small lesions in this area can produce absence or slowness of saccades and quick phases of nystagmus in all directions.The paramedian pontine reticular formation (PPRF) which generates the high frequency neuronal burst required to accelerate the eyes; this area is responsible for ipsilateral horizontal saccadic velocity so that a right side pontine lesion produces absence or slowness of saccades towards the right.The midbrain reticular formation, in particular the rostral interstitial nucleus of the medial longitudinal fasciculus (RIMLF) responsible for the generation of vertical saccades. Lesions in this area can cause selective up, down or complete vertical saccadic gaze palsy or slowing, according to location and extension.
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
At the opposite extreme are Noback and Demarest (1981), who give a very extensive list of limbic structures (p. 466, 473). They include the limbic lobe (i.e., septal area, cingulate gyrus and its isthmus, and parahippocampal gyrus with its uncus—p.465 [Fig. 15–21], the hippocampal formation, the amygdala, the olfactory system and its pathways (i.e., olfactory nerve, bulb, tract, and striae, and primary olfactory cortex, [including the anterior perforated substance], in addition to areas in the limbic lobe and amygdala already mentioned—p. 454), the fornix, the stria terminalis. the ventral amygdalofugal fibers, the preoptic area, “many nuclei of the hypothalamus,” the stria medullaris thalami, the habenula, the dorsomedial and “anterior ventral” nuclei of the thalamus, the prefrontal cortex (including the orbitofrontal cortex), neocortex of the medial temporal lobe and of the insula, the median midbrain reticular formation, the interpeduncular nucleus, the dorsal and ventral tegmental nuclei of Gudden, the periaqueductal gray matter, and the paramedian tegmentum of the upper pons, including the superior central nucleus. If Noback and Demarest also intend to include additional “connections of the limbic system” (p. .474 [Fig. 15–6], 475 [Fig. 15–7], 476 [Fig. 15–8]) as components of the system, a point which is not clear to me, then their list would also include the mamillothalamic tract, the cingulum, the medial forebrain bundle, the fasciculus retroflexus, the dorsal longitudinal fasciculus, and the central tegmental tract!
The Internal Milieu Brain and Body
Published in Rolland S. Parker, Concussive Brain Trauma, 2016
SCN output: There are descending nerve impulses, via the superior cervical ganglia, to sympathetic postganglionic fibers (noradrenergic), which innervate the pineal gland. This completes the circuit by which light and dark affects levels of endocrine secretion (Reichlin, 1998, p. 216). Thus, pineal function could be vulnerable to neck trauma. The SCN projects to the medial preoptic hypothalamic region (MePO/AH), lateral hypothalamus, retrochiasmic region, and a region immediately ventral to the PVN. MePO neurons are involved in sleep induction through connections with the adjacent basal forebrain. Projections from the SCN to the PVN appear to be important for circadian regulation of pineal and autonomic function. The PVN in turn projects to the preganglionic sympathetic neurons innervating the superior cervical ganglion. Noradrenergic neurons of the superior cervical ganglion project to the pineal gland. Sympathetic inputs stimulate synthesis of melatonin by the pineal gland. This pathway may be responsible for the light suppression of melatonin. Both warm-sensitive neurons of the MePO/AH and “sleep active” neurons in the basal forebrain inhibit activity of neurons of the midbrain reticular formation and posterior hypothalamus that are part of the reticular arousal system.
Eight-and-a-half syndrome caused by a pontine haemorrhage: a case report and review of the literature
Published in International Journal of Neuroscience, 2018
Nian-ge Xia, Yan-yan Chen, Jia Li, Xi Chen, Zu-sen Ye, Si-yan Chen, Zhen-guo Zhu
Eight-and-a-half syndrome variants include eight-and-a-half syndrome with vertical gaze palsy and bilateral gaze palsy with unilateral peripheral facial palsy. Marquart et al. [17] reported a case of eight-and-a-half syndrome combined with ipsilateral vertical gaze palsy, which was caused by the blood of the dorsal pons. The ipsilateral vertical gaze palsy may be the result of the impairment of midbrain reticular formation (MRF) incoming to the left-third (subnucleus rectus superi or inferior) in the dorsal tegmentum of midbrain. In 2009, Felicio et al. documented a case of a patient with bilateral horizontal gaze palsy and unilateral peripheral facial paralysis caused by pontine tegmentum infarction. This variant was similar to the classic type of eight-and-a-half syndrome but developed bilateral horizontal gaze palsy [18].
Evaluating Auditory Pathway by Electrical Auditory Middle Latency Response and Postoperative Hearing Rehabilitation
Published in Journal of Investigative Surgery, 2019
Bin Wang, Keli Cao, Chaogang Wei, Zhiqiang Gao, Huan Li
Since the waveform of auditory brainstem response is identified, the response recorded in the far-field of auditory cortex at 10–100 ms after stimulus onset are called AMLR.2 The neural sources of AMLR are different from those of auditory brainstem response, and the waveform usually has 5 peaks, which are labeled as Po, Na, Pa, Nb and Pb. Current evidence suggests the putative generator sites of AMLR include the primary auditory cortex, midbrain reticular formation, nonspecific nuclei in the hypothalamus and the medial geniculate nucleus.3 Pa wave is believed to be generated from the primary auditory cortex and Na wave is from the subcortical structures.3 The average threshold value of AMLR we recorded using Bio-logic brand auditory evoked potential measurement system in normal hearing subjects was 12.5 ± 8.6 dB nHL, comparable with the value (10.5 ± 7.7 dB nHL) reported from the literature.4 The activity from thalamus to cortex in adults by artificial cochlear device was recorded by Firszt et al.5 Similar EMLR waveforms was reported in an 8.5 years old child with cochlear implant.6 A systematical study evoked potentials, and described the waveforms and thresholds of EMLR in detail, including stimulating between electrodes 4 and 10 of a 24 Nucleus implant with a pulse width of 50 µsec at 7 pulses per second.7 The actual behavioral threshold of this patient under the same condition was 190 Nucleus clinical units, and as depicted the threshold of EMLR was also 190 clinical units, which is more comparable than that of EABR or nerve response telemetry (NRT).