BACKGROUND

Thirteen-and-a-half syndrome consists of a one-and-a half syndrome with an ipsilateral facial and trigeminal nerve palsy. This is due to lesions that affects the ipsilateral paramedian pontine reticular formation (PPRF) or the ipsilateral abducens nerve nucleus (VI), the contralateral medial longitudinal fasciculus (MLF), the facial nerve (VII), and the trigeminal nerve (V) .

This is a case of Thirteen-and-a-half syndrome and stress the importance of a proper neurologic exam to aid in the localization of lesions in the brain.

This patient was monitored during her admission. She underwent a plain cranial CT scan to confirm the suspected hemorrhage and supportive management was done to relieve her symptoms.

A 14-year-old female patient presented with a one day history of right-sided hemiparesis. There was associated binocular diplopia, dizziness, slurring of speech, dropping of the left lip, and three episodes of spontaneous projectile vomiting. Plain cranial CT scan showed a left-sided pontine hemorrhage, and she was then advised admission. There was exotropia of the right eye on primary gaze with -4 on adduction, abducting nystagmus on the right eye, horizontal gaze palsy on the left eye, no convergence, left facial weakness, and decreased left facial sensation with minimal improvement during her admission. On the 1-year follow up, there was significant improvement with full motility on the right eye and a -1 on abduction on the left eye.

This is a case of a Thirteen-and-a-half syndrome in a young female patient. A complete neuro-ophthalmological exam is paramount as it is both sight-saving and life saving.

OBJECTIVES: Clinically, it has been found that some patients with epilepsy are accompanied by cerebellar atrophy that is inconsistent with symptoms, but the pattern of cerebellar atrophy after epilepsy and the role of cerebellar atrophy in the mechanism of epilepsy have not been elucidated. This study aims to explore the specific pattern of cerebellar atrophy after epilepsy via analyzing magnetic resonance images in patients with postepileptic cerebellar atrophy. METHODS: A total of 41 patients with epilepsy, who received the treatment in Xiangya Hospital of Central South University from January 2017 to January 2022 and underwent cranial MRI examination, were selected as the case group. The results of cranial MRI examination of all patients showed cerebellar atrophy. In the same period, 41 cases of physical examination were selected as the control group. General clinical data and cranial MRI results of the 2 groups were collected. The maximum area and signal of dentate nucleus, the maximum width of the brachium pontis, the maximum anterior-posterior diameter of the pontine, and the maximum transverse area of the fourth ventricle were compared between the 2 groups. The indexes with difference were further subjected to logistic regression analysis to clarify the characteristic imaging changes in patients with cerebellar atrophy after epilepsy. RESULTS: Compared with the control group, the maximum width of the brachium pontis and the maximum anterior-posterior diameter of the pontine were decreased significantly, the maximum transverse area of the fourth ventricle was increased significantly in the case group (all P<0.05). The difference in distribution of the low, equal, and high signal in dentate nucleus between the 2 groups was statistically significant (χ²=43.114, P<0.001), and the difference in the maximum area of dentate nucleus between the 2 groups was not significant (P>0.05). The maximum width of the brachium pontis [odds ratio (OR)=3.327, 95% CI 1.454 to 7.615, P=0.004] and the maximum transverse area of the fourth ventricle (OR=0.987, 95% CI 0.979 to 0.995, P=0.002) were independent factors that distinguished cerebellar atrophy after epilepsy from the normal control, while the anterior-posterior diameter of pontine (OR=1.456, 95% CI 0.906 to 2.339, P>0.05) was not an independent factor that distinguished them. CONCLUSIONS In MRI imaging, cerebellar atrophy after epilepsy is manifested as significant atrophy of the brachium pontis, significant enlargement of the fourth ventricle, and increased dentate nucleus signaling while insignificant dentate nucleus atrophy. This particular pattern may be associated with seizures and exacerbated pathological processes.
Humans ; Magnetic Resonance Imaging ; Pons ; Epilepsy/diagnostic imaging* ; Atrophy/pathology* ; Cerebellum/pathology*

The parabrachial nucleus (PBN) integrates interoceptive and exteroceptive information to control various behavioral and physiological processes including breathing, emotion, and sleep/wake regulation through the neural circuits that connect to the forebrain and the brainstem. However, the precise identity and function of distinct PBN subpopulations are still largely unknown. Here, we leveraged molecular characterization, retrograde tracing, optogenetics, chemogenetics, and electrocortical recording approaches to identify a small subpopulation of neurotensin-expressing neurons in the PBN that largely project to the emotional control regions in the forebrain, rather than the medulla. Their activation induces freezing and anxiety-like behaviors, which in turn result in tachypnea. In addition, optogenetic and chemogenetic manipulations of these neurons revealed their function in promoting wakefulness and maintaining sleep architecture. We propose that these neurons comprise a PBN subpopulation with specific gene expression, connectivity, and function, which play essential roles in behavioral and physiological regulation.
Parabrachial Nucleus/physiology* ; Wakefulness/physiology* ; Neurons/physiology* ; Emotions ; Sleep

To explore the changes of cold sensitivity after exposure to acute hypoxia and its mechanisms, Sprague-Dawley rats were divided into normoxia control group (21% O₂, 25 °C), 10% O₂ hypoxia group (10% O₂, 25 °C), 7% O₂ hypoxia group (7% O₂, 25 °C), normoxia cold group (21% O₂, 10 °C) and hypoxia cold group (7% O₂, 10 °C). Cold foot withdrawal latency and preference temperature of each group were measured, skin temperatures were estimated using an infrared thermographic imaging camera, body core temperature was recorded by wireless telemetry system, immunohistochemical staining was used to detect the expression of c-Fos in the lateral parabrachial nucleus (LPB). The results showed that acute hypoxia significantly prolonged the latency of cold foot withdrawal and significantly enhanced the intensity of cold stimulation for foot withdrawal, and the rats under hypoxia preferred cold temperature. Cold exposure (10 °C) for 1 h significantly enhanced the expression of c-Fos in LPB of rats in normoxia, while hypoxia inhibited cold-induced c-Fos expression. Acute hypoxia significantly increased the skin temperature of feet and tails, decreased the skin temperature of interscapular region, and decreased the body core temperature of rats. These results indicate that acute hypoxia can significantly blunt cold sensitivity through the inhibition of LPB, suggesting actively keeping warm measures should be taken at the early stage after ascent to high altitude to prevent the upper respiratory infection and acute mountain sickness.
Rats ; Animals ; Rats, Sprague-Dawley ; Parabrachial Nucleus/physiology* ; Temperature ; Cold Temperature ; Hypoxia ; Proto-Oncogene Proteins c-fos

Objective: To observe the dynamic changes of brainstem locus coeruleus (LC) damage in Parkinson' s disease (PD) -like mice by paraquat (PQ) . Methods: In October 2019, 36 male C57BL/6 mice were randomly divided into the exposure group and the control group, with 18 mice in each group. The mice in the exposure group were given intraperitoneal injection of 15 mg/kg PQ, and the mice in the control group were given intraperitoneal injection of 0.9% saline, twice a week for 8 weeks. Neurobehavioral changes (pole climbing test, swimming test, open field test, tail hanging test, high plus maze test and water maze test) were observed at 4 weeks, 6 weeks and 8 weeks, respectively, and the changes of motor ability, emotion and cognitive function were evaluated. The brain tissue of mice were taken and stained with Hematoxylin-Eosin (HE) to observe the pathological changes of LC. Nissl staining was used to detect the changes of neuronal Nissl bodies in LC. Immunohistochemistry (IHC) staining was used to detect the expression of neuron nuclear antigen (NeuN) , dopamine (DA) neurons and norepinephrine (NE) neuron markers tyrosine hydroxylase (TH) , α-synuclein (α-syn) in substantia nigra (SN) and LC. The expression levels of NeuN, TH and α-syn in the midbrain and brainstem were detected by Western blotting. TUNEL staining was used to detect neuronal apoptosis in LC. Results: Compared with the 4th week of PQ exposure group, the time of pole climbing and swimming immobility were gradually increased, the ratio of open arm residence time of high plus maze test and the number of times of the platform and the residence time of platform quadrant in water maze test were gradually decreased (P<0.05) in the exposure group with the progress of exposure time. The results of HE and Nissl staining showed that the neurons in LC gradually arranged loosely, the nucleus were deeply stained, the cytoplasm was pyknosis, and the number of Nissl bodies gradually decreased (P<0.05) in the exposure group with the progress of exposure time. IHC results showed that the number of NeuN and TH positive cells in SN and LC of mice were gradually decreased, and the positive expression of α-syn was gradually increased (P<0.05) in the exposure group with the progress of exposure time. Western blotting results showed that the expression levels of NeuN and TH in the midbrain and brainstem were gradually decreased, and the expression level of α-syn was gradually increased (P<0.05) in the exposure group with the progress of exposure time. TUNEL staining showed that the apoptosis rates of neurons in LC were gradually increased (P<0.05) in the exposure group with the progress of exposure time. Conclusion: PQ induces progressive damage in the LC area of PD-like mice, which may be caused by the abnormal accumulation of pathological α-syn in the LC area.
Animals ; Dopaminergic Neurons ; Locus Coeruleus/pathology* ; Male ; Mice ; Mice, Inbred C57BL ; Paraquat/toxicity* ; Parkinson Disease/metabolism* ; Substantia Nigra ; Tyrosine 3-Monooxygenase/metabolism*

Humans ; Neurons ; Olivary Nucleus ; Superior Olivary Complex

Acupuncture has remarkable effects on treating functional gastrointestinal diseases, but its central mechanism is not clear. At present, the research has mainly focused on several central nuclei, such as the dorsal vagus complex (DVC), nucleus raphe magnus (NRM), locus coeruleus (LC), subnucleus reticularis dorsalis (SRD), hypothalamic paraventricular nucleus (PVN), cerebellar fastigial nucleus (FN), central amygdala (CeA), etc. It is not clear whether the nuclei are involved in acupuncture regulation of gastric function through certain interrelation. A further summary of related literature indicates that many brain regions or nuclei in the central nervous system are closely related to gastric function, such as DVC, NRM, parabrachial nuclei (PBN), LC, periaqueductal gray (PAG), cerebellum, PVN, arcuate nucleus (Arc), hippocampus, CeA, etc. Most of these nuclei have certain fiber connections with each other, in which DVC is the basic center, and other nuclei are directly or indirectly involved in the regulation of gastric function through DVC. Is DVC the key target in acupuncture regulation of gastric function? Does other nuclei have direct or indirect neural circuit with DVC to participate in the regulation of gastric function by acupuncture, such as the possibility of CeA-DVC neural loop in acupuncture regulating gastric function. Therefore, more advanced techniques such as photogenetics, chemical genetics should be introduced and the central mechanism of acupuncture on regulating gastric function with DVC as center, from the view of nerve loop, will become the focus of further research, which could explain the central integration mechanism of acupoint compatibility by modern neuroscience technology.
Acupuncture Therapy ; Locus Coeruleus ; Paraventricular Hypothalamic Nucleus ; Vagus Nerve

OBJECTIVES: Hearing loss disrupts the balance of auditory-somatosensory inputs in the cochlear nucleus (CN) of the brainstem, which has been suggested to be a mechanism of tinnitus. This disruption results from maladaptive auditory-somatosensory plasticity, which is a form of axonal sprouting. Axonal sprouting is promoted by transforming growth factor (TGF)-β signaling, which can be inhibited by losartan. We investigated whether losartan prevents maladaptive auditory-somatosensory plasticity after hearing loss. METHODS: The study consisted of two stages: determining the time course of auditory-somatosensory plasticity following hearing loss and preventing auditory-somatosensory plasticity using losartan. In the first stage, rats were randomly divided into two groups: a control group that underwent a sham operation and a deaf group that underwent cochlea ablation on the left side. CNs were harvested 1 and 2 weeks after surgery. In the second stage, rats were randomly divided into either a saline group that underwent cochlear ablation on the left side and received normal saline or a losartan group that underwent cochlear ablation on the left side and received losartan. CNs were harvested 2 weeks after surgery. Hearing was estimated with auditory brainstem responses (ABRs). Western blotting was performed for vesicular glutamate transporter 1 (VGLUT1), reflecting auditory input; vesicular glutamate transporter 2 (VGLUT2), reflecting somatosensory input; growth-associated protein 43 (GAP-43), reflecting axonal sprouting; and p-Smad2/3. RESULTS: Baseline ABR thresholds before surgery ranged from 20 to 35 dB sound pressure level. After cochlear ablation, ABR thresholds were higher than 80 dB. In the first experiment, VGLUT2/VGLUT1 ratios did not differ significantly between the control and deaf groups 1 week after surgery. At 2 weeks after surgery, the deaf group had a significantly higher VGLUT2/VGLUT1 ratio compared to the control group. In the second experiment, the losartan group had a significantly lower VGLUT2/VGLUT1 ratio along with significantly lower p-Smad3 and GAP-43 levels compared to the saline group. CONCLUSION: Losartan might prevent axonal sprouting after hearing loss by blocking TGF-β signaling thereby preventing maladaptive auditory-somatosensory plasticity.
Animals ; Axons ; Blotting, Western ; Brain Stem ; Cochlea ; Cochlear Nucleus ; Evoked Potentials, Auditory, Brain Stem ; GAP-43 Protein ; Hearing Loss ; Hearing ; Losartan ; Plastics ; Rats ; Tinnitus ; Transforming Growth Factors ; Vesicular Glutamate Transport Protein 1 ; Vesicular Glutamate Transport Protein 2

It is well known that trigeminal nerve injury causes hyperexcitability in trigeminal ganglion neurons, which become sensitized. Long after trigeminal nerve damage, trigeminal spinal subnucleus caudalis and upper cervical spinal cord (C1/C2) nociceptive neurons become hyperactive and are sensitized, resulting in persistent orofacial pain. Communication between neurons and non-neuronal cells is believed to be involved in these mechanisms. In this article, the authors highlight several lines of evidence that neuron-glial cell and neuron macrophage communication have essential roles in persistent orofacial pain mechanisms associated with trigeminal nerve injury and/or orofacial inflammation.
Cell Communication ; Cervical Cord ; Facial Pain ; Inflammation ; Macrophages ; Neurons ; Nociceptors ; Trigeminal Ganglion ; Trigeminal Nerve ; Trigeminal Nerve Injuries ; Trigeminal Nucleus, Spinal

Ramsay Hunt syndrome with the complication of encephalitis or meningoencephalitis is rarely reported and uncommon in immunocompetent patients. The radiological manifestations of such cases usually involve the cerebellum and brainstem or exhibit the absence of any abnormality. We report a case of a 78-year-old immunocompetent man hospitalized with Ramsay Hunt syndrome, who later developed meningoencephalitis. The cerebrospinal fluid-study excluded other causes of meningoencephalitis, and the clinical diagnosis indicated varicella zoster virus meningoencephalitis. Magnetic resonance imaging revealed increased signal intensities in the bilateral temporal lobe, midbrain, and pons on T2-weighted imaging, and T2 fluid attenuated inversion recovery and contralateral asymmetric pachymeningeal enhancement. Contrast-enhanced T1-weighted imaging revealed ipsilateral facial nerve enhancement.
Aged ; Brain Stem ; Cerebellum ; Diagnosis ; Encephalitis ; Facial Nerve ; Herpes Zoster Oticus ; Herpesvirus 3, Human ; Humans ; Magnetic Resonance Imaging ; Meningoencephalitis ; Mesencephalon ; Pons ; Temporal Lobe